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Traumatic brain injury general surgery. Traumatic brain injury. Osteoplastic trepanation in the occipital region

Traumatic brain injury (TBI)

Among people under 50 years of age, head injuries are more likely to cause death and disability than any other neurological disease, despite the fact that the brain is protected by the thick bones of the skull.

The brain can be damaged even if the integrity of the skull bones is preserved. Many of its injuries are associated with the sudden acceleration that the skull acquires following a shock caused by a strong blow to the head or a sudden stop when colliding with a stationary object, and brain damage can occur both at the point of impact and on the opposite side.

TBI includes all types of injuries that are accompanied by general cerebral and focal symptoms, which are signs of damage to the brain, meninges and cranial nerves, regardless of the violation of the integrity of the skull bones.

General cerebral symptoms include:

loss of consciousness;
headache;
dizziness;
amnesia;
nausea and vomiting;
noise in ears;
tachycardia, bradycardia;
meningeal symptoms (stiff neck - the patient cannot reach the chest with his chin; Kernig - a leg bent at the hip and knee joint does not straighten at the knee; Brudinsky - when the head is tilted, the legs involuntarily bend);
convulsive syndrome.

Focal symptoms:

asymmetry of the face (the corner of the mouth is drooping, the cheek is “swallowing”);
anisocoria;
paresis and paralysis;
disorders of speech, vision, hearing, swallowing, etc.

Types of traumatic brain injury:

closed and open (penetrating and non-penetrating);
with and without damage to the skull bones:
- - fractures of the cranial vault: depressed, perforated, comminuted, complete and incomplete;
- - fracture of the base of the skull;
- - damage to the facial skull;
with and without damage to brain structures:
- concussion;
- brain contusion (of varying severity);
- compression of the brain.

All types of TBI are divided according to severity:

for the lungs - concussion, mild brain contusion;
moderate severity - moderate brain contusion, subarachnoid hemorrhage, skull fractures;
severe - fracture of the base of the skull, destruction of brain matter, compression of the brain.

However, at the prehospital stage, there are no special examination methods and a mild TBI can suddenly develop into a severe one, so the ambulance paramedic needs to treat any head injury as severe.

An open injury is considered to be one that is accompanied by damage to the aponeurosis and penetrating damage to the integrity of the dura mater.

Examination methods:

Consultations with a neurologist and an ophthalmologist are required.

A blow to the head with a blunt hard object or a blow to the head against a hard object can be accompanied by crushing of the skin, subcutaneous tissue, damage to the aponeurosis, and fracture of the skull bones. The angle of injury matters. Direct mild bruises of the soft tissues of the head result in the formation of a “bump” - a subcutaneous hematoma. With tangential blows, a forcible displacement of the aponeurosis occurs with damage to the loose subaponeurotic tissue and the formation of an extensive and flat hematoma in it. Bone fractures with closed trauma without skull deformation are detected only by x-ray.

First aid for damage to the soft tissues of the head, superficial wounds: the hair around is cut off widely, the wound is washed with hydrogen peroxide, furatsilin, its edges are treated with an antiseptic and a dry sterile (“cap”) or pressure (“bridle”) bandage is applied. You cannot check the depth of damage with your finger or probe.

Victims with extensive injuries, suspected fractures of the skull bones, damage to the aponeurosis, or damage to brain structures are transported to the hospital in a lateral decubitus position.

Facial wounds heal primarily. Wounds of the scalp are prone to suppuration.

Brain concussion. Trauma causes functional disorders of the brain without morphological damage. As a rule, it manifests itself only as general cerebral symptoms, the duration and severity of which depends on the severity of the injury. A short-term spasm of blood vessels is replaced by their dilation, which leads to cerebral edema and an increase in intracranial pressure.

The victim briefly loses consciousness and may vomit. After the return of consciousness, memory loss occurs (retrograde amnesia), headache, nausea, tinnitus, dizziness, asymmetry of blood pressure when measured in both arms, low-grade fever, sleep disturbance, etc. persist for a long time.

Brain contusion. This type of injury is classified as severe and is always accompanied by anatomical (morphological) damage to the brain substance. Bruises can be mild (petechial hemorrhages), moderate (soaked in blood) and severe (destruction of brain matter). In this regard, in addition to general cerebral symptoms, there are focal symptoms, and focal symptoms appear from the moment of injury. The number and brightness of the manifestation of focal symptoms depend not so much on the degree of destruction of brain tissue, but on the localization of the affected area (for example, destruction of the optic nuclei causes loss of vision, damage to the nuclei of the facial nerve causes facial asymmetry, etc.). Contusions of the “silent” parts of the brain (frontal lobes) do not produce focal symptoms, but subsequently manifest as a decrease in intelligence. The bruise is often combined with hemorrhages of various locations, hematomas and is accompanied by focal or general traumatic cerebral edema. Bruised areas liquefy and dissolve, forming cysts or scars.

Compression of the brain. Traumatic compression of the brain occurs with depressed fractures, damage to cerebral vessels and vessels of the meninges, even without bone damage. More often, the middle cerebral artery or venous sinuses formed by the dura mater in places where it is incompletely adjacent to the bones of the skull are damaged. In this regard, a distinction is made between epidural and subdural hematomas. Damage to the meninges may be accompanied by damage to adjacent areas of the brain. Intracerebral hematomas occur.

The classic picture of compression of the brain by a hematoma at the first moment resembles the clinic of a concussion, but after some time after the improvement of the condition, called the light interval, the victim’s condition begins to quickly deteriorate. General cerebral and focal symptoms appear and increase (anisokaria, mydriasis on the side of compression, facial asymstria, grinning, deviation of the tongue, paresis, paralysis, etc.), and the patient falls into a coma. The severity and duration of improvement, the so-called light interval, depend on the location and rate of growth of the hematoma. With depressed fractures, there is no light gap. Focal symptoms are more pronounced with epidural localization of the hematoma. Blood during lumbar puncture is detected in subdural localization and intracerebral hematomas communicating with the ventricles of the brain.

Without timely assistance, death occurs from herniation of the brain into the foramen magnum.

Fracture of the base of the skull. A fracture of the base of the skull occurs as a result of indirect trauma. The fracture line may begin at the cranial vault and extend to the base.

The victim is usually unconscious with impaired breathing and hemodynamics, the severity of which depends on the severity of the injury. There are symptoms of contusion or compression of the brain. The injury is often accompanied by bleeding from the nose (damage to the ethmoid bone), ears, and leakage of cerebrospinal fluid (damage to the dura mater). In the first hours, the cerebrospinal fluid mixes with the blood. To determine the presence of cerebrospinal fluid in the blood, it is necessary to moisten gauze with bloody liquid. If there is cerebrospinal fluid on the gauze, a light ring (rim) forms around the bloody spot. Leakage of brain matter is extremely rare. There are signs of paresis and paralysis of the cranial nerves exiting the base of the skull. Usually, the next day, bruises appear around the eyes - a “symptom of glasses”, in the area of the mastoid processes (injury of the posterior cranial fossa), under the mucous membrane of the pharynx.

The prognosis is poor, especially for fractures of the middle cranial fossa, since here surgical intervention is almost impossible, and the chances of infection entering the cranial cavity are very high.

In its pure form, bruise and compression of the brain, damage to the meninges are rare.

In differential diagnosis, it is important to consider the following:

a concussion is manifested only by general cerebral symptoms;
with brain contusion (destruction of brain matter), focal symptoms appear immediately after the injury;
intracranial hematoma is characterized by the presence of a light gap - the period between the restoration of consciousness immediately after the injury and its repeated loss;
with an epidural hematoma, the light gap is short and there will be no blood in the cerebrospinal fluid. There will be no blood even with a hematoma inside the brain tissue if it does not communicate with the ventricles of the brain;
a subdural hematoma has a longer clear gap and there will be blood in the cerebrospinal fluid, since the subdural space communicates with the intrathecal space of the spinal cord.

It must also be remembered that brain damage and hematoma can be localized on the opposite side of the injury.

Urgent Care for various types of TBI. At concussion:

treat and bandage the wound;
for excessive arousal: intravenously 2-L ml of 0.5% diazepam solution per 20 ml of 0.9% sodium chloride solution or 20 ml of 40% glucose;
mandatory hospitalization in a hospital (surgical or neurological department).

At bruises and compression of the brain:

stabilization of the cervical spine - Shants collar until the nature of the injury is clarified;
restoration of patency of the upper respiratory tract (triple dose of Safar, removal of mucus, sputum, foreign objects from the oral cavity, installation of an air duct);
oxygen inhalation - start with 100%, then gradually reduce the concentration to 40%;
in the presence of apnea, hypopnea, or increasing cyanosis, transfer the patient to mechanical ventilation in the mode of moderate hyperventilation (RR - 16-20 per minute, tidal volume - 600-800 ml);
hospitalization in a hospital with a neurosurgical service; in case of respiratory and cardiac dysfunction - hospitalization in the intensive care unit;
During transportation, take all measures to prevent tongue retraction and blood leakage into the respiratory tract. It should be remembered that loss of consciousness, cardiac and respiratory arrest can occur at any time during transportation.

Bruises and compression of the brain can be accompanied by convulsions, hypertension and pain syndromes.

At excitement and convulsions:

Intravenous administration of 2-4 ml of 0.5% diazepam solution (10-20 mg - 0.2 mg/kg) at a rate of 2-5 mg/min per 10 ml of 0.9% sodium chloride solution or 20 ml 5% glucose (if the seizures do not stop, intravenous administration of diazepam in the same dose is repeated after 15 minutes).

At presence of signs of hypertension syndrome:

intravenous administration 2-A ml of 1% solution of furosemide (in case of decompensated blood loss or associated trauma, do not administer furosemide);
intravenous administration of 30-90 mg of prednisolone or 4-12 mg of dexamethasone;
Ventilation in hyperventilation mode (RR 16-20 per minute, tidal volume - 600-800 ml).

At pain syndrome:

Intravenous administration of 2 ml of a 50% solution of metamizole or 50-100 mg of tramadol (1-2 ml of a 5% solution), or jet or intramuscular administration of 10-30 mg of ketorolac per 10 ml of 0.9% sodium chloride solution .

Principles of treatment of victims with TBI. In the hospital, victims with severe TBI are hospitalized in intensive care if they require mechanical ventilation, or in the neurosurgical department. The necessary diagnostic procedures are performed, patients are examined by a neurologist, neuro-oculist. In the absence of indications for surgery (hematomas, depressed fractures), drug therapy is prescribed aimed at decompressing the brain (diuretics, magnesium sulfate, 40% glucose), improving its blood supply and protecting against hypoxia; when excited - sedatives.

Complications of open TBI: encephalitis, meningitis, brain abscesses, traumatic hydrocephalus (impaired outflow of cerebrospinal fluid), traumatic epilepsy.

The problem of treating severe traumatic brain injury (TBI) is relevant in modern medicine and is of great socio-economic importance. In Moscow, from 1997 to 2012, the number of victims with TBI increased from 10,000 to 15,000; more than 2,000 patients a year require surgical treatment. The main contingent of victims are people of working age (from 20 to 50 years). In the structure of mortality from all types of injuries, 30-50% are due to TBI. The overall mortality rate for TBI, including mild and moderate TBI, is 5-10%. In severe forms of TBI with the presence of intracranial hematomas and foci of brain contusion, mortality increases to 41-85%.

In 20-25% of cases, TBI is combined with damage to other organs and systems: the musculoskeletal system, organs of the thoracic and abdominal cavities, the spine and spinal cord. Mortality among victims with combined trauma with extremely severe multiple injuries and massive blood loss can reach 90-100%.

TBI remains one of the main causes of disability in the population. The number of people with permanent disability as a result of a TBI reaches 25-30%. In this regard, TBI ranks first in terms of the total medical, social and economic damage caused among all types of injuries.

Surgical treatment of TBI is one of the main areas of scientific activity of the Department of Neurosurgery of the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky. Over the years, monographs and a large number of articles in scientific journals have been devoted to the problems of studying the pathogenesis of TBI, the development of new methods of diagnosis and surgical treatment, prevention and treatment of complications.

Reducing mortality and improving the functional outcomes of treatment cannot be achieved without constant improvement and introduction into practice of the department of modern standards of treatment and rehabilitation of victims with TBI, new methods of diagnosis and neuromonitoring, and surgical technologies. The Department of Emergency Neurosurgery of the Institute is one of the leading methodological centers in Russia for organizing the treatment of patients with TBI and training specialists in this field. Employees of the department participate in Russian and foreign congresses and conferences, exchange experiences with colleagues, and regularly conduct seminars, educational cycles and master classes on the problems of treating TBI.

The main scientific directions of studying TBI in the emergency neurosurgery clinic of the NIISP named after. N.V. Sklifosovsky include a study of epidemiology, determination of the characteristics of the clinical course of traumatic brain injury and combined injuries, study of the pathophysiology of brain injury based on data from modern neuroimaging tools (computer and magnetic resonance imaging, ultrasound methods), biochemical studies including specific markers of brain damage, analysis of the mechanisms of evolution of lesions brain contusion, improvement of methods of surgical treatment of dislocation syndrome, post-traumatic epilepsy, complications and consequences of TBI, prognosis of functional treatment outcomes.

Patient about traumatic brain injury

In Russia, the main causes of injury in TBI are a fall from a height (in 70% of cases during alcohol intoxication) and criminal trauma - about 65%. Road traffic accidents (RTAs) (drivers, passengers and pedestrians), falls from heights and other causes account for another 20%.

The mechanisms of injury vary greatly between young and elderly victims and also depend on the time of year. In summer, “criminal” trauma predominates in young victims; in winter, trauma to the skull and brain is more often recorded in patients of older age groups, and the leading cause is falls from height. Road traffic casualties peak in January and September, with a significant decline observed in the summer months.

Brain injury most often occurs at the site of injury, but a significant number of injuries occur on the opposite side of the skull in the impact zone.

Depending on the severity, the following types of traumatic brain injury are distinguished:

mild: concussion, mild brain contusion;
moderate severity: moderate brain contusion;
severe: severe brain contusion, acute compression of the brain.

They also distinguish between isolated (when there are no extracranial injuries), combined (the simultaneous presence of TBI and damage to other organs and systems) and combined traumatic brain injury (if several types of energy are simultaneously exposed - mechanical, radiation, chemical, etc.).

Closed TBI includes injuries in which there are no violations of the integrity of the scalp, while open TBI includes injuries in which there are wounds to the soft tissues of the head. Penetrating is a traumatic brain injury accompanied by damage to the dura mater, which may be accompanied by the leakage of cerebrospinal fluid (CSF) or the penetration of air into the cranial cavity. With open and especially penetrating traumatic brain injury, purulent-infectious complications can develop much more often.

By type of brain damage there are:

Brain concussion
Brain contusion:

mild brain injury
moderate brain contusion
severe brain injury

Brain compression:

intracranial hematoma
depressed fracture

Diffuse axonal brain injury (DABI)

Compression of the head.

Concussion is a condition that occurs more often as a result of exposure to a small traumatic force and is characterized by a predominance of reversible functional changes in the brain. Occurs in almost 70% of victims with TBI. When a concussion occurs, victims usually lose consciousness for a short time - from 1-2 to 10-15 minutes or a decrease in the degree of wakefulness. Patients are worried about headache, nausea, less often vomiting, dizziness, weakness, pain when moving the eyeballs. Victims often do not remember the circumstances of the incident. Symptoms of a concussion disappear after 5-8 days. It should be remembered that more severe forms of traumatic brain injury - brain contusions and intracranial hematomas - can have a similar clinical picture. Despite the fact that a concussion is a mild TBI, up to 50% of victims have various residual effects that reduce their ability to work. Patients with a concussion must be examined by a neurosurgeon or neurologist, who will determine the need for additional studies - CT or MRI of the brain, electroencephalography. Concussion is a single form and is not divided into degrees of severity. Most patients with a concussion do not require admission to a neurosurgery unit. The patient should undergo outpatient treatment under the supervision of a neurologist.

Brain contusion– with this type of traumatic brain injury, damage to the brain substance occurs, often with hemorrhage. Based on the clinical course and severity of damage to brain tissue, brain contusions are divided into mild, moderate and severe bruises.

Mild brain contusion. Damage to the brain substance in this type of pathology is minimal. Skull fractures are detected in 25% of patients. Vital functions (breathing, cardiac activity) are not impaired. CT scans of the brain often do not reveal pathological changes, but foci of post-traumatic ischemia may be observed. Neurological symptoms are moderate and regress within 2 to 3 weeks.

Moderate brain contusion– a much more severe type of injury. Possible disturbances in mental activity and transient disorders of vital functions (brady or tachycardia, increased blood pressure). Meningeal and focal symptoms are determined (impaired pupillary reactions, paresis of the limbs, pathological foot reflexes). With a bruise of moderate severity, CT scans often reveal fractures of the vault and base of the skull, signs of subarachnoid hemorrhage and small focal changes in the brain substance corresponding to the focus of the bruise (Fig. 1). During treatment, these changes undergo reverse development on repeat CT.

Rice. 1. CT scan of the brain. Axial slice. Hemorrhagic contusion of the left temporal lobe of the brain.

Severe brain contusion. The brain matter is damaged to a significant extent. Foci of hemorrhage can involve several lobes of the brain. Victims lose consciousness for a period of several hours to several weeks. Severe disturbances in vital functions are observed, as a result of which patients are hospitalized in intensive care units. CT scans often reveal fractures of the vault and base of the skull, massive subarachnoid and intraventricular hemorrhage, large areas of brain contusion, and intracranial hematomas (Fig. 2).

Rice. 2. CT scan of the brain, axial section. Severe brain contusion. Foci of contusion and traumatic intracerebral hematomas in both frontal and left temporal lobes.

Diffuse axonal brain damage. A special form of brain contusion is diffuse axonal brain injury (DAI). DAP most often develops in car accidents. With diffuse axonal damage to the brain, long processes of nerve cells - axons - are damaged or ruptured, and the conduction of nerve impulses is disrupted. In victims with diffuse axonal damage, there is primary damage to the brain stem in which vital functions are disrupted - breathing, blood circulation and the patient requires mandatory drug and hardware correction. A decrease in the degree of wakefulness is a characteristic clinical sign of DAP, and in 25% of victims the duration of loss of consciousness exceeds 2 weeks. Mortality in diffuse axonal brain damage is very high and reaches 80-90%, and survivors develop apallic syndrome, i.e. functional separation of the brain stem and cerebral hemispheres. Patients can remain in this state for a long time.

CT and MRI with diffuse axonal damage reveal cerebral edema, against which small hemorrhagic foci are found in the white matter of the cerebral hemispheres, the corpus callosum, subcortical and brainstem structures (Fig. 3).

Rice. 3. MRI of the brain, coronal section. Diffuse axonal brain damage. Against the background of cerebral edema, small foci of increased MR signal (hemorrhage) are visualized in the corpus callosum.

Brain compression occurs due to the accumulation of blood - the formation of hematomas in the cranial cavity and a decrease in the intracranial space. A feature of the clinical course of brain compression is the manifestation of clinical symptoms not immediately after the injury, but after a certain period of time (the so-called “bright period”, which is characterized by a period of relatively normal well-being).

Depending on the anatomical relationship of the skull bones and the dura mater, the following types of traumatic intracranial hematomas are distinguished:

epidural hematomas that are localized above the dura mater (Fig. 4a);
subdural hematomas
intracerebral hematomas

A) b) V)

Rice. 4. CT scan of the brain, axial sections: a) epidural hematoma; b) subdural hematoma; c) intracerebral hematoma.

Fig.5. Intraoperative photography. Acute subdural hematoma.

When the brain is compressed, the brain stem is pinched in the naturally rigid structures of the skull and dura mater, resulting in a disruption of the vital functions of breathing and circulation. Therefore, compression of the brain is an indication for emergency surgery to eliminate the hematoma causing compression and prevent further herniation of the brain stem.

Diagnosis of TBI

Establishing an accurate diagnosis of the nature of damage to the brain and bones of the vault and base of the skull during TBI is of paramount importance - this determines the outcome of the injury and the likelihood of various complications (cerebrospinal fluid leakage, meningitis, convulsive syndrome, etc.).

In the first hours of injury, it can be very difficult to establish an accurate diagnosis, which is due to the severity of the condition of the victims, associated trauma, and often the alcohol intoxication of the patients.

The most common signs found in patients with traumatic brain injury are:

loss of consciousness
headache
damage (abrasions, wounds, bruises) to the soft tissues of the head
discharge of fluid from the nose or ears
bruises in the area behind the ear or around the eyes (Fig. 6).

A) b) V)

Rice. 6. Signs of a fracture of the base of the skull: a) curvature of the face (paresis of the right facial nerve), lagophthalmos; b) paraorbital hematomas; c) retroauricular hematoma.

CT and MRI of the brain are currently the main instrumental methods of examination for TBI. The method of choice in emergency neurotraumatology is CT, which allows you to quickly diagnose the type, number, location and volume of intracranial foci of brain damage, determine the presence of edema and the degree of brain dislocation, and assess the condition of the ventricular system. Following what was developed at the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky emergency examination protocol, all patients with a history of high-intensity trauma (fall from a height, road traffic accidents) along with a CT scan of the brain, patients simultaneously undergo a CT scan of the spine.

In case of trauma to the facial skeleton, in addition to routine CT of the skull and brain, the Research Institute for Emergency Medicine urgently performs a spiral CT of the facial skull according to a special protocol developed in the department of emergency neurosurgery.

In the diagnosis of traumatic brain injury, the MRI method is widely used, which has greater sensitivity than the CT method in diagnosing foci of contusions and brain ischemia, including in the brain stem, periventricular zone, and in the region of the posterior cranial fossa. MRI allows you to visualize the capsule in chronic hematomas, the direction of displacements and deformations of the brain in dislocation syndrome. MRI is used as the method of choice in patients with diffuse axonal damage, trauma to the posterior cranial fossa, subacute and chronic intracranial hematomas (Fig. 7).

Fig.7. MRI in a patient with bilateral chronic subdural hematomas.

Diffusion-weighted MRI allows for differential diagnosis of vasogenic and cytotoxic cerebral edema, as well as diagnosis of ischemic changes in the first hours of their development, which is especially important in the diagnosis of secondary post-traumatic ischemic brain damage. Important is the ability of MR diffusion to evaluate not only the zone of deep necrosis, but the penumbra zone along the periphery of the lesion, where hypoxia is still reversible. Diffusion tensor MRI is used to determine the state of the brain pathways, which makes it possible to assess the degree of compression and damage to nerve fibers in patients who have suffered acute dislocation syndrome and DAP. Proton MR spectroscopy demonstrates the extent of brain damage by assessing metabolic processes in different areas of the brain, although the technique is still less popular due to its time-consuming and high cost.

Proton MR spectroscopy provides insight into the metabolism of individual brain regions, which is necessary in the treatment of victims with DAP, brain contusions and the risk of their evolution, as well as for assessing the severity of secondary ischemic changes.

The use of perfusion CT in patients with severe TBI makes it possible to visually and quantitatively assess cerebral blood flow and tissue perfusion in different parts of the brain, diagnose disorders of regional blood flow in the brain already in the first minutes after the development of ischemia, monitor the dynamics of its recovery and assess the development of collateral circulation. Currently, the department is conducting a study to study the state of cerebral blood flow and diagnose secondary cerebral ischemia in victims with bruises and acute dislocation syndrome (Fig. 8).

Rice. 8. CT perfusion in a patient with secondary ischemic changes due to brain contusion: a) color CBF perfusion map, there is a local decrease in the volumetric velocity of cerebral blood flow (CBF) in the right temporal and occipital lobes of the brain (indicated by an arrow); b) color CBV perfusion map, there is a twofold decrease in cerebral blood volume (CBV) in the right temporal and occipital lobes compared to the opposite side (indicated by an arrow); c) color MTT perfusion map, in the right temporal and occipital lobes due to vasospasm there is an increase in the average blood transit time (MTT) (indicated by the arrow).

TBI surgery

Based on the clinical picture and CT and MRI data, not only the indications for surgery or conservative treatment are determined, but also the prognosis for TBI.

Acute supratentorial meningeal (epidural, subdural) and intracerebral hematomas must be completely removed. Indications for surgical treatment are determined depending on the volume and location of such hematomas, as well as the severity of perifocal edema and the degree of brain dislocation.

Indications for surgical treatment of acute epidural hematomas are:

Epidural hematomas with a volume of more than 40 ml, regardless of the degree of wakefulness of the victim. For epidural hematomas located at the base of the middle cranial fossa, surgical treatment may be indicated when the hematoma volume is 20 ml.
Epidural hematomas of any volume, causing displacement of the midline structures of the brain by 5 mm or more or compression of the surrounding cistern.
Epidural hematomas of any volume, accompanied by a clinical picture of dislocation syndrome.

Indications for surgical treatment of acute subdural hematomas are:

Subdural hematomas of any volume with a thickness of more than 10 mm or causing a displacement of the midline structures by more than 5 mm, regardless of the degree of depression of the victim’s wakefulness.
Subdural hematomas of any volume with a thickness of less than 10 mm and displacement of the midline structures of less than 5 mm in the presence of depression of wakefulness to the point of stupor or coma, or with a decrease in the level of wakefulness noted since the moment of injury by 2 points or more on the Glasgow Coma Scale (GCS).

Indications for surgical treatment of traumatic acute intracerebral hematomas are:

Intracerebral hematomas with a volume of more than 30 ml or if the diameter of the hematoma is more than 4 cm, when the hematoma is localized in the parietal and temporal lobes.
When an intracerebral hematoma is localized in the basal parts of the temporal lobe, surgical intervention may be required for a hematoma of a smaller volume (15-20 ml).
Intracerebral hematomas of any volume in the presence of suppression of the level of wakefulness to the point of stupor or coma or displacement of the midline structures by more than 5 mm and/or deformation of the surrounding cistern.

When treating patients with severe brain contusion, accompanied by depression of the level of wakefulness to coma, it is necessary to monitor intracranial pressure (ICP). Indications for surgical treatment are a persistent increase in ICP above 20 mmHg. Art., refractory to conservative therapy methods.

When removing foci of contusion and crush injury to the brain during surgery, an operating microscope and microsurgical instruments should be used to inspect the contusion cavity and carry out high-quality hemostasis in order to prevent recurrent bleeding.

Conducted at the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky's study made it possible to clarify the clinical picture and determine the tactics of surgical treatment of traumatic hematomas of the posterior cranial fossa. The absolute indications for removal of intracranial foci of brain damage in the posterior cranial fossa (PCF) are the simultaneous presence of: 1) a lesion localized in the PCF and causing compression and dislocation of the IV ventricle and/or occlusive hydrocephalus and 2) a decrease in the level of wakefulness of the victim 14 or less GCS scores and/or the presence of a neurological deficit.

One of the stages of emergency surgical intervention for severe TBI accompanied by compression of the brain is craniotomy. The method of craniotomy (osteoplastic - KPTCH or decompressive - DTC) is a significant factor in the outcome of surgical treatment.

In order to determine the optimal method of craniotomy for severe TBI at the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky conducted two independent studies:

assessment of ICP dynamics during surgery and in the postoperative period with different methods of craniotomy (KPTCH and DTC),
A prospective randomized study examining the choice of craniotomy method (CPT or DTC) in patients with severe TBI.

In terms of its design, the study is the first randomized trial in the Russian Federation and has no analogues to date. Both studies included victims with severe TBI and depression of the level of wakefulness from 4 to 9 points on the GCS.

In the course of a randomized study, it was revealed that when planning a method of craniotomy in patients with severe TBI, it is necessary to take into account the dynamics of ICP during surgery and the postoperative period, the clinical picture and CT data of the brain. KPTCH is indicated in the absence of signs of edema and swelling of the brain during surgery, depression of the level of consciousness no deeper than moderate coma, type 1 dynamics of ICP (with a normotensive course), in the absence of episodes of hypotension, the value of ICP-2 is more than 9%. DTC is indicated in the presence of types 2 and 3 of ICP dynamics (with gradual or acute development of intracranial hypertension and cerebral edema), as well as in cases of persistent increase in ICP above a critical level, refractory to conservative treatment.

Increased ICP is one of the pathogenetic mechanisms that determine the course and outcome of TBI. ICP monitoring, as a component of multimodal neuromonitoring, allows you to continuously monitor ICP fluctuations and promptly apply different intensive care methods. The indication for monitoring ICP in patients with TBI is a decrease in the degree of wakefulness of less than 9 points on the GCS.

The main causes of unfavorable outcomes in victims with severe TBI are progressive intracranial hypertension and acute dislocation syndrome, leading to displacement and compression of the brain stem with subsequent disruption of the vital functions of breathing and circulation. The problem of treating dislocation syndrome is key in the surgery of severe TBI. With the improvement of neuroimaging tools and the improvement of surgical techniques, surgery for dislocation syndrome is developing.

In the neurosurgical department of the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky developed a technique for performing DP in combination with resection of the inferomedial parts of the temporal lobe and open tentoriotomy for the surgical treatment of temporotentorial herniation in patients with severe TBI. The technique consists of performing a unilateral wide infratemporal DST, radical removal of foci of brain damage, followed by selective microsurgical resection of the anterior sections of the middle and inferior temporal gyri, the uncus of the hippocampus and the parahippocampal gyrus (Fig. 9).

A) b) V) G)

Rice. 9. a, b) CT scan of the brain upon admission. Axial projection. Depressed fracture of the right temporal and parietal bones. Traumatic intracerebral hematoma in the right temporal and parietal lobes with a volume of 40 cm3. Displacement of the midline structures to the left by 12 mm. Lack of visualization of the parasellar, covering and quadrigeminal cisterns. Dislocation of the brain stem to the left. c, d) CT scan of the brain 1 day after DST in the right fronto-parietal-temporal region in combination with resection of the lower parts of the temporal lobe. In the area of resection of the inferomedial parts of the temporal lobe, an area of pneumocephalus and hemorrhagic impregnation is determined. There is no displacement of the median structures. The parasellar, circumflex and quadrigeminal cisterns can be traced and are not deformed.

The obtained data from clinical and instrumental examination of patients in the postoperative period confirm the effectiveness of this method of internal brain decompression. In patients who underwent DST in combination with resection of the lower parts of the temporal lobe, there was a more rapid recovery of the level of wakefulness after surgery than in patients with conventional DST, a lower level of ICP in the postoperative period and a halving of the number of lethal outcomes of treatment (in the group In patients with temporal resection, the mortality rate was 40%, in patients with conventional DST – 80%). Data from a brain CT scan performed in the postoperative period in patients with resection of the lower parts of the temporal lobe confirm the elimination of temporotentorial herniation, which is expressed in the absence of signs of compression of the basal cisterns and dislocation of the brain stem.

At the Research Institute of Emergency Medicine named after. N.V. Sklifosovsky developed and implemented a fundamentally new original method of minimally invasive surgery for TBI - puncture aspiration and local fibrinolysis of traumatic intracranial hematomas using frameless neuronavigation. Accurate construction of the shape, calculation of the volume and coordinates of the intracerebral hematoma makes it possible to intraoperatively place a catheter for the introduction of fibrinolytics according to the maximum diagonal of the hemorrhage, and select the trajectory of the drainage immersion along a functionally insignificant area of the brain, for example, through the pole of the frontal lobe.

Indications for the use of the method of puncture aspiration and local fibrinolysis in the surgery of traumatic intracranial hemorrhages are: hematomas of intracerebral localization, subdural hematomas located above 1-2 lobes of the brain, residual traumatic hemorrhages, traumatic intracranial hematomas in victims with combined trauma, elderly patients and persons with severe concomitant pathology.

In patients with traumatic intracranial hematomas, the technique is used in the absence or beginning signs of progression of dislocation syndrome (depression of consciousness, anisokaria, bradycardia) in cases where the total volume of the pathological focus (hematoma, focus of contusion and area of perifocal edema) does not exceed 40 cm3 (Fig. 10 ).

A) b) V) G)

Rice. 10. Computer tomograms of patient O., 68 years old: a) before surgery: a traumatic intracerebral hematoma of the right temporal lobe is determined 30 cm3, transverse dislocation of the brain to the left by 5 mm; b) determining the trajectory of catheter insertion for fibrinolysis using a frameless neuronavigation system; c) after 24 hours of local fibrinolysis with recombinant prourokinase: the volume of the residual intracerebral hematoma of the right temporal lobe is 3 cm3, there is no transverse dislocation, a catheter for fibrinolysis is visualized in the hematoma cavity; d) catheter for fibrinolysis.

A contraindication to local fibrinolysis of epidural hematomas is the localization of the hematoma in projection a. meningea media. The use of the local fibrinolysis method allows for a good outcome with complete removal of the hematoma and clinical regression of symptoms in 82% of patients and a mortality rate of 8%.

The use of the videoendoscopic method for some types of TBI ensures a reduction in the volume and trauma of surgical access while maintaining its radicality. Modern rigid and flexible neuroendoscopes, with a movable distal segment with a diameter of 0.5 - 6 mm, high illumination and a wide field of view, have significantly increased the efficiency of endoscopic operations. The neuroendoscopic technique can be used in the treatment of patients with subacute and chronic intracranial hematomas, as well as in the treatment of traumatic intracerebral hematomas located in functionally significant areas of the brain (Fig. 11, 12).

The main contraindications for neuroendoscopy when removing chronic subdural hematomas are the multi-chamber structure of the hematoma, the presence of hyperdense areas according to CT and MRI, excessively trabecular and recurrent hematomas.

Modern principles of diagnosis and intensive care of victims with severe TBI are based on multimodal neuromonitoring, which includes a wide range of methods that allow dynamic monitoring of the state of the cerebral system and conduct targeted therapy aimed at preventing secondary ischemic brain damage.

ICP control is one of the most important components of neuromonitoring; it allows not only to assess the degree of intracranial hypertension, but also to calculate cerebral perfusion pressure (CPP). In the department, monitoring of intraventricular and intraparenchymal pressure is used in patients with severe symptoms. Also, during multimodal monitoring, patients with TBI are implanted with sensors for measuring oxygen tension in the brain (PbrO2) and sensors for tissue microdialysis.

Fig. 13. Multimodal neuromonitoring in a patient with TBI.

The use of new technologies in the diagnosis and treatment of patients with TBI in the Department of Neurosurgery of the NIISP named after. N.V. Sklifosovsky allowed to significantly reduce postoperative mortality in patients operated on for severe TBI, which in 2002 was 41% and by 2010 decreased to 30%.

According to the mechanism of action on the skull and brain, impact trauma is distinguished, in which mechanical damage localized at the site of application of traumatic force, anti-shock, when brain damage is localized at a distance from the force applied to the skull, and their combination.

By type of injury TBI divided into closed and open, the latter in turn divided into those that do not penetrate the cranial cavity and those that penetrate. Closed TBI includes injuries to the skull and brain that are not accompanied by soft tissue wounds and damage to the dura mater. Such lesions are most resistant to the occurrence of purulent infection. Open TBI includes injuries to the skull and brain, in which there are wounds to the soft tissues of the head. With such injuries, due to the presence of anastomoses between the venous and arterial systems, a purulent infection may develop

To penetrating TBI include injuries to the skull and brain, accompanied by damage to the dura mater. In 40.3% of patients, fractures of the base of the skull are accompanied by micro- or macrocerebrospinal fluid leakage from the nose (in case of damage to the anterior cranial fossa) or ear (in case of a fracture of the temporal bone). The fistulas that arise in this case are the entrance gates and can cause the development of intracranial purulent infection.

Skull fractures. There are fractures of the vault and fractures of the base of the skull. Fractures of the base of the skull are most often presented in the form of cracks in the bottom of the anterior (frontal, ethmoid, sphenoid bone), middle (temporal bone, its squama and pyramid, sphenoid bone) or posterior (occipital bone) cranial fossa.

Cranial vault fractures can be in the form of single or multiple cracks, comminuted (depressed or non-depressed) fractures - isolated or multiple. It should be noted that the severity of the victim’s condition is determined not so much by the nature of the skull fractures as by the severity of the brain damage.

The following are distinguished: types of brain damage.

Brain concussion. In quantitative terms, this is the main type of TBI (up to 70-75%). A concussion occurs when there is a relatively minor mechanical injury to the head due to the acceleration imparted to the brain at the time of injury. There are many ambiguities and controversial positions in the pathogenesis of concussion. The opinion of S. Scheidegger (1948) remains relevant: “It is easier to say what is not a concussion than to define this concept.”

For fresh concussions There are no traumatic macrostructural changes in the brain substance

Brain contusion. This term currently refers to the focus of macroscopic damage to the brain substance that occurs at the time of injury. Brain contusions are clinically divided into mild, moderate and severe bruises.

Diffuse axonal brain injury is a special type of TBI. Most often, such injuries are formed as a result of rotational movements of the brain, which can occur both with rotational trauma (trauma with rotational acceleration) and with local exposure to trauma (blows to the head, a fall from a height, a kick to the chin). In this case, rotation of the more mobile hemispheres of the brain occurs while its trunk is fixed. With local trauma, such as a kick to the chin, individual layers of the brain can become displaced in relation to each other. Even a slight displacement of individual layers of the brain can lead to rupture of nerve fibers and blood vessels, to asynapsia (impaired conduction of nerve impulses at the synapse level).

Brain compression. There are increasing and non-increasing compression. Increasing compression of the brain occurs with intracranial hematomas, non-increasing compression is observed with pressure on the brain from bone fragments during depressed skull fractures. This division, however, is very arbitrary, since under the influence of secondary factors, when bone fragments put pressure on the brain, local and then widespread cerebral edema occurs, which leads to increasing pressure on the brain, an increase in both intracranial and intracerebral pressure.
Most dangerous to the patient's life intracranial hematomas.

Intracranial traumatic hematomas according to the course they are divided into acute, subacute and chronic. Chronic hematomas include hematomas with a formed capsule, which usually occurs in the middle to the end of the 3rd week after injury. Before capsule formation, hematomas are considered acute. Subacute hematomas include those in which the capsule has not completely formed, and its clinical manifestations are characterized by blurred symptoms.

By location, intracranial hematomas are divided into epidural (blood accumulates between the bones of the skull and the dura mater), subdural (blood accumulates between the brain and the dura mater) and intracerebral (blood accumulates in the brain parenchyma).

There are also multiple intracranial hematomas, which are particularly difficult.

Features of shock in combined TBI. As a rule, shock during TBI develops against the background of massive bleeding. Decrease in blood pressure below 70 mm Hg. leads to cerebral ischemia, which complicates the process of restoring its functions. Violations of central and peripheral hemodynamics lead to an increase in cerebral edema and dislocation

With combined TBI, shock may develop against the background of the victim’s unconscious state (coma) and be accompanied by bradycardia. The erectile shock phase in such patients is usually longer. Blood pressure, despite massive blood loss, may be normal or even slightly elevated. Pulse pressure decreases or (much less frequently) increases slightly. With normal systolic pressure, a pulse of weak filling is detected.

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Traumatic brain injury (TBI) is one of the most common types of injuries and accounts for up to 50 % of all types of injuries, and in recent decades is characterized by both an increasing trend in the proportion of brain injuries and their severity.

Traumatic brain injury(TBI) is one of the most common types of injuries and accounts for up to 50 % of all types of injuries, and in recent decades is characterized by both an increasing trend in the proportion of brain injuries and their severity. Thus, TBI is increasingly becoming a multidisciplinary problem, the relevance of which is increasing for neurosurgeons, neurologists, psychiatrists, traumatologists, radiologists, etc. At the same time, recent observations show insufficient quality and non-compliance with the continuity of conservative therapy.

There are several main types of interrelated pathological processes:

1) direct damage to the brain substance at the time of injury;

2) cerebrovascular accident;

3) violation of liquor dynamics;

4) disturbances of neurodynamic processes;

5) formation of scar-adhesive processes;

6) processes of autoneurosensitization.

The basis of the pathological picture of isolated brain injuries is primary traumatic dystrophies and necrosis; circulatory disorders and organization of tissue defect. Concussions are characterized by a complex of interconnected destructive, reactive and compensatory-adaptive processes occurring at the ultrastructural level in the synaptic apparatus, neurons, and cells.

Brain contusion is an injury characterized by the presence in the substance of the brain and in its membranes of macroscopically visible foci of destruction and hemorrhage, in some cases accompanied by damage to the bones of the vault and base of the skull. Direct damage to the hypothalamic-pituitary, brainstem structures and their neurotransmitter systems during TBI determines the uniqueness of the stress response. Impaired metabolism of neurotransmitters is the most important feature of the pathogenesis of TBI. Cerebral circulation is highly sensitive to mechanical influences.

The main changes that develop in the vascular system are expressed by spasm or dilation of blood vessels, as well as increased permeability of the vascular wall. Directly related to the vascular factor is another pathogenetic mechanism for the formation of the consequences of TBI—a violation of liquor dynamics. Changes in the production of cerebrospinal fluid and its resorption as a result of TBI are associated with damage to the endothelium of the choroid plexuses of the ventricles, secondary disorders of the microvasculature of the brain, fibrosis of the meninges, and in some cases, liquorrhea. These disorders lead to the development of liquor hypertension, and less commonly, hypotension.

In TBI, hypoxic and dysmetabolic disorders play a significant role in the pathogenesis of morphological disorders, along with direct damage to nerve elements. TBI, especially severe, causes respiratory and circulatory disorders, which aggravates existing cerebral dyscirculatory disorders and collectively leads to more pronounced brain hypoxia.

Currently (L. B. Likhterman, 1990) there are three basic periods during traumatic brain disease: acute, intermediate, and remote.

The acute period is determined by the interaction of the traumatic substrate, damage reactions and defense reactions, and is the period of time from the moment of the damaging effects of mechanical energy until the stabilization at one or another level of impaired cerebral and general body functions or the death of the victim. Its duration ranges from 2 to 10 weeks, depending on the clinical form of TBI.

The intermediate period is characterized by the resorption and organization of areas of damage, and the development of compensatory and adaptive processes until complete or partial restoration or stable compensation of impaired functions. The length of the intermediate period for non-severe TBI is up to 6 months, for severe TBI – up to a year.

The long-term period is the completion or coexistence of degenerative and reparative processes. The length of the period for clinical recovery is up to 2-3 years, for a progressive course it is not limited.

All types of TBI are usually divided into closed brain injuries (CBI), open and penetrating. Closed TBI is a mechanical injury to the skull and brain, resulting in a number of pathological processes that determine the severity of the clinical manifestations of the injury. TO open TBI should include injuries to the skull and brain in which there are wounds to the integument of the skull (damage to all layers of the skin); penetrating damage involves a violation of the integrity of the dura mater.

Classification of traumatic brain injury(Gaydar B.V. et al., 1996):

brain concussion;
brain contusion: mild, moderate, severe;
compression of the brain against the background of a bruise and without a bruise: hematoma - acute, subacute, chronic (epidural, subdural, intracerebral, intraventricular); hydro wash; bone fragments; edema-swelling; pneumocephalus.

It is very important to determine:

condition of the intrathecal spaces: subarachnoid hemorrhage; CSF pressure - normotension, hypotension, hypertension; inflammatory changes;
condition of the skull: no bone damage; type and location of the fracture;
condition of the skull: abrasions; bruises;
associated injuries and diseases: intoxication (alcohol, drugs, etc., degree).

It is also necessary to classify TBI according to the severity of the victim’s condition, the assessment of which includes the study of at least three components:

1) state of consciousness;

2) the state of vital functions;

3) the state of focal neurological functions.

There are five gradations of the condition of patients with TBI

Satisfactory condition. Criteria:

1) clear consciousness;

2) absence of violations of vital functions;

3) absence of secondary (dislocation) neurological symptoms; absence or mild severity of primary focal symptoms.

There is no threat to life (with adequate treatment); the prognosis for recovery is usually good.

Moderate condition. Criteria:

1) state of consciousness - clear or moderate stun;

2) vital functions are not impaired (only bradycardia is possible);

3) focal symptoms - certain hemispheric and craniobasal symptoms may be expressed, often appearing selectively.

The threat to life (with adequate treatment) is insignificant. The prognosis for restoration of working capacity is often favorable.

Serious condition. Criteria:

1) state of consciousness - deep stupor or stupor;

2) vital functions are impaired, mostly moderately according to 1-2 indicators;

3) focal symptoms:

a) brainstem - moderately expressed (anisocoria, decreased pupillary reactions, limited upward gaze, homolateral pyramidal insufficiency, dissociation of meningeal symptoms along the body axis, etc.);

b) hemispheric and craniobasal - clearly expressed both in the form of symptoms of irritation (epileptic seizures) and loss (motor disorders can reach the degree of plegia).

The threat to life is significant and largely depends on the duration of the serious condition. The prognosis for restoration of working capacity is sometimes unfavorable.

Extremely serious condition. Criteria:

1) state of consciousness - coma;

2) vital functions - gross violations in several parameters;

3) focal symptoms:

a) stem - expressed roughly (plegia of upward gaze, gross anisocoria, divergence of the eyes along the vertical or horizontal axis, a sharp weakening of the pupils’ reactions to light, bilateral pathological signs, hormetonia, etc.);

b) hemispheric and craniobasal - pronounced.

The threat to life is maximum and largely depends on the duration of the extremely serious condition. The prognosis for restoration of working capacity is often unfavorable.

Terminal state. Criteria:

1) state of consciousness - terminal coma;

2) vital functions - critical impairment;

3) focal symptoms:

a) stem - bilateral fixed mydriasis, absence of pupillary and corneal reflexes;

b) hemispheric and craniobasal - blocked by general cerebral and brainstem disorders.

Survival is usually impossible.

Clinical picture of acute traumatic brain injury

Brain concussion. Clinically, it is a single functionally reversible form (without division into degrees). With a concussion, a number of general cerebral disorders occur: loss of consciousness or, in mild cases, short-term blackout from several seconds to several minutes. Subsequently, a stunned state persists with insufficient orientation in time, place and circumstances, an unclear perception of the environment and a narrowed consciousness. Retrograde amnesia is often detected - loss of memory for events preceding the injury, less often anterograde amnesia - loss of memory for events subsequent to the injury. Speech and motor agitation are less common.

Brain contusion severe severity is clinically characterized by loss of consciousness after injury lasting from several hours to several weeks. Motor agitation is often pronounced, and severe, threatening disturbances in vital functions are observed. The clinical picture of severe UHM is dominated by brainstem neurological symptoms, which overlap focal hemispheric symptoms in the first hours or days after TBI. Paresis of the limbs (up to paralysis), subcortical disturbances of muscle tone, reflexes of oral automatism, etc. may be detected. Generalized or focal epileptic seizures are noted. Focal symptoms regress slowly; gross residual effects are frequent, primarily in the motor and mental spheres. Severe UHM is often accompanied by fractures of the vault and base of the skull, as well as massive subarachnoid hemorrhage.

An undoubted sign of fractures of the base of the skull is nasal or auricular liquorrhea. In this case, the symptom of a spot on a gauze napkin is positive: a drop of bloody cerebrospinal fluid forms a red spot in the center with a yellowish halo along the periphery.

Suspicion of a fracture of the anterior cranial fossa arises with the delayed appearance of periorbital hematomas (a symptom of glasses). With a fracture of the temporal bone pyramid, Battle's symptom (hematoma in the mastoid region) is often observed.

Brain compression- a progressive pathological process in the cranial cavity that occurs as a result of trauma and causes dislocation and infringement of the trunk with the development of a life-threatening condition. In TBI, cerebral compression occurs in 3-5 % of cases, both with and without UGM. Among the causes of compression, the first place is occupied by intracranial hematomas - epidural, subdural, intracerebral and intraventricular; This is followed by depressed fractures of the skull bones, areas of crushing of the brain, subdural hygromas, and pneumocephalus.

The clinical picture of compression of the brain is expressed by a life-threatening increase in a certain period of time (the so-called light interval) after the injury or immediately after it of cerebral symptoms, the progression of impaired consciousness; focal manifestations, stem symptoms.

Complications of traumatic brain injury

Violations of vital functions - a disorder of the basic life support functions (external respiration and gas exchange, systemic and regional circulation). In the acute period of TBI, the causes of acute respiratory failure (ARF) are dominated by pulmonary ventilation disorders associated with impaired airway patency caused by the accumulation of secretions and vomit in the nasopharynx with their subsequent aspiration into the trachea and bronchi, and retraction of the tongue in comatose patients.

Dislocation process: temporotentorial inclusion, representing a displacement of the mediobasal sections of the temporal lobe (hippocampus) into the fissure of the tentorium of the cerebellum and herniation of the cerebellar tonsils into the foramen magnum, characterized by compression of the bulbar sections of the trunk.

Purulent-inflammatory complications are divided into intracranial (meningitis, encephalitis and brain abscess) and extracranial (pneumonia). Hemorrhagic - intracranial hematomas, cerebral infarctions.

Scheme of examination of victims with traumatic brain injury

Organization and tactics of conservative treatment of victims with acute TBI

In general, victims with acute TBI should go to the nearest trauma center or medical facility where initial medical examination and emergency medical care are provided. The fact of injury, its severity and the condition of the victim must be confirmed by appropriate medical documentation.

Treatment of patients, regardless of the severity of TBI, should be carried out in an inpatient setting in a neurosurgical, neurological or trauma department.

Primary medical care is provided for urgent reasons. Their volume and intensity are determined by the severity and type of TBI, the severity of the cerebral syndrome and the possibility of providing qualified and specialized care. First of all, measures are taken to eliminate airway and cardiac problems. For convulsive seizures and psychomotor agitation, 2-4 ml of diazepam solution is administered intramuscularly or intravenously. If there are signs of compression of the brain, diuretics are used; if there is a threat of cerebral edema, a combination of loop and osmodiuretics is used; emergency evacuation to the nearest neurosurgical department.

To normalize cerebral and systemic circulation during all periods of traumatic illness, vasoactive drugs are used; in the presence of subarachnoid hemorrhage, hemostatic and antienzyme agents are used. The leading role in the treatment of patients with TBI is given to neurometabolic stimulants: piracetam, which stimulates the metabolism of nerve cells, improves cortico-subcortical connections and has a direct activating effect on the integrative functions of the brain. In addition, neuroprotective drugs are widely used.

To increase the energy potential of the brain, the use of glutamic acid, ethylmethylhydroxypyridine succinate, and vitamins B and C is indicated. Dehydration agents are widely used to correct liquorodynamic disorders in patients with TBI. To prevent and inhibit the development of adhesive processes in the membranes of the brain and to treat post-traumatic leptomeningitis and choreoependymatitis, so-called “absorbable” agents are used.

The duration of treatment is determined by the dynamics of regression of pathological symptoms, but requires strict bed rest in the first 7-10 days from the moment of injury. The duration of hospital stay for concussions should be at least 10-14 days, for mild bruises - 2-4 weeks.

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Closed traumatic brain injury includes concussion, brain contusion and brain compression. This division is conditional; their combination is often observed - traumatic brain disease.
The cause of a closed craniocerebral injury is often direct trauma (a blow to the head with a heavy object, a fall on the head).

Brain concussion. The most common pathology of all skull injuries. As a rule, no damage to the skull bones is observed with a concussion. The impact of a short and strong blow sets the brain and the liquid component (cerebrospinal fluid, blood) in motion. Morphologically, very minor changes are observed: short-term spasm of blood vessels followed by their dilation, venous stagnation, swelling of the brain and membranes, pinpoint hemorrhages. The duration of these changes is 1-2 weeks.
Clinical picture. The leading symptoms of a concussion are loss of consciousness from several minutes to several hours and retrograde amnesia (the patient does not remember what happened to him). Vomiting may occur. There is pallor of the skin of the face and, less commonly, hyperemia. Breathing is shallow. With a mild concussion, the pulse quickens (tachycardia); with a severe concussion, on the contrary, it slows down (bradycardia). A uniform narrowing or dilation of the pupils and a slight smoothing of the nasolabial fold may be observed. Subsequently, headache, dizziness, tinnitus, heaviness in the head, aching in the eyes appear, aggravated by their movement and bright lighting (Mann-Gurevich symptom). During spinal puncture, there is usually no pathological changes in the cerebrospinal fluid, but its pressure may be increased. A few days after the injury, insomnia, irritability, sweating, general weakness, and divergent strabismus when reading (Sedona symptom) develop.
Depending on the severity of the injury, according to the Petit classification, three degrees of concussion are distinguished: mild (short-term loss of consciousness without retrograde amnesia), moderate (with retrograde amnesia, but without general or focal craniocerebral disorders) and severe (with significant brain disorders).
Treatment. The basis of treatment is strict bed rest. For a mild concussion it is prescribed for 1-2 weeks, for a moderate concussion - for 2-3 weeks, for a severe one - for 3-4 weeks. Neuroplegic, antihistamine and vitamin preparations are widely used. When cranial pressure increases, 40-60 ml of a 40% glucose solution, 10-20 ml of a 10% sodium chloride solution, 5-10 ml of a 40% solution of hexamine are administered intravenously, 10 ml of a 20% solution of magnesium sulfate is administered intramuscularly, and diuretics are prescribed. A salt-free diet with fluid restriction is indicated.
In cases of cerebral edema, an additional 5-10 ml of 2% is administered intravenously. hexonium solution, 1-2 ml of 2% diphenhydramine solution, 50-100 mg of cortisone or hydrocortisone. When intracranial pressure decreases, saline or distilled water is injected subcutaneously or intravenously.
Brain contusion. A bruise has a more severe clinical picture compared to a concussion. Morphologically, foci of destruction of the medulla (rupture, softening, crushing, hemorrhage, etc.) are noted in the brain tissue. The affected area is most often located in the cortex, subcortical layer and meninges. Bruises and hemorrhages in the brain stem, cerebellum, and cerebral ventricles are especially dangerous.
The clinical picture resembles a severe concussion: loss of consciousness occurs for a longer period of time, followed by lethargy for several days or even weeks. Retrograde amnesia is more pronounced. The temperature rises, neutrophilic leukocytosis, and a constant admixture of blood in the cerebrospinal fluid are noted.
In case of brain contusion, local central symptoms predominate: paralysis and paresis of cranial nerves and limbs, hemiplegia, pathological reflexes.
Treatment is carried out according to the same scheme as for a concussion, but the condition of the internal organs, depending on brain stem disorders, is taken into account. In case of breathing problems, mucus is sucked out from the trachea and bronchi through the intubated larynx and oxygen is given at the same time. The patient is administered lobeline and cititon. When these phenomena increase, a tracheostomy is applied and controlled breathing is established. To normalize blood circulation, cardiovascular drugs (caffeine, cordiamine, etc.) are used.
Compression of the brain. A more severe course is noted. Pathoanatomical changes boil down to a gradual increase in compression of the brain due to its edema and growing hematoma (vascular rupture). Based on their location, hematomas are divided into: subdural (under the dura mater), epidural (above the dura mater), subarachnoid (under the pia mater) and intracerebral (into the substance of the brain).
Clinical picture. When the brain is compressed, especially due to a hematoma, there is a so-called light interval from several minutes to several hours, followed by loss of consciousness. Bradycardia appears up to 40-50 beats per minute. The pupils are initially constricted, then dilate. Vomiting occurs and the act of swallowing is disrupted. During the daytime, severe headache and dizziness are observed.
In differential diagnosis between different types. For hematomas, clinical presentation and spinal puncture indicators are of great importance. With an epidural hematoma, loss of consciousness occurs quite quickly, and cerebrospinal fluid pressure is increased. With a subdural hematoma, the light gap is longer and there is blood in the cerebrospinal fluid. With a subarachnoid hematoma, the lucid interval can last up to several days, and loss of consciousness may not occur at all. There is a large admixture of blood in the cerebrospinal fluid.
As general cerebral symptoms increase, the focal symptomatology of compression and dislocation of the brain becomes more pronounced: paresis and paralysis of the cranial nerves on the side of the hemorrhage (anisocoria, ptosis of the upper eyelid, constriction followed by dilation of the pupil, strabismus), paresis and paralysis of the muscles of the limbs (monoplegia with pathological reflexes, epileptiform convulsions) - on the opposite side.
Treatment is mainly surgical. The essence of the operation is craniotomy, emptying the hematoma and stopping bleeding (decompressive craniotomy). If there is no significant damage to the brain matter and the bleeding has been reliably stopped, the defect in the skull bones is closed using the preserved bone flap. If it is impossible to perform primary plastic surgery of the bone defect, it is carried out after several months.
Fractures of the cranial vault. The mechanism is direct trauma. By nature, a fracture of the skull vault can be in the form of a crack, a splintered fracture and bone tissue defects. The latter type of fractures is observed mainly in gunshot wounds.
Fractures can be complete, that is, spread over the entire thickness of the bone, and incomplete, when only the outer or inner plates of the cranial vault are broken. With comminuted fractures, as well as a fracture of the internal plate, the meninges and medulla are damaged. The same picture can occur with open fractures.
Clinical picture. There are general cerebral symptoms associated with concussion and cerebral edema, and focal symptoms caused by damage to certain parts of the brain, which can increase.
Treatment. In case of closed skull fractures and the absence of intracranial bleeding, treatment is carried out according to the same scheme as for closed craniocerebral injury. For intracranial bleeding, fragmentation and open fractures, surgical intervention is indicated. The operation is based on the principle of removing depressed bone fragments and stopping bleeding.
Fractures of the base of the skull. The mechanism of injury is a fall from a height onto the head or legs. In this case, damage occurs to the bones of the base of the skull (basal and temporal bones).
Clinical picture. In diagnosis, the main role is played by anamnestic data, localization of bruises and bleeding. If the anterior cranial fossa is damaged, bruises appear in the eyelid area and around the eyes - a “symptom of glasses” (Fig. 124), as well as nosebleeds; if the middle and posterior cranial fossae are damaged, bruises in the throat area and bleeding from the ears appear. If the posterior cranial fossa is damaged, there will be bruising in the area of the mastoid processes. Sometimes there is a leakage of cerebrospinal fluid from the nose and ears. When the base of the skull is fractured, the cranial nerves are often damaged: the facial, abducens and oculomotor. Due to irritation of the meninges, the phenomena of meningism (stiff neck muscles) occur.
Treatment is carried out according to the same principle as the treatment of a concussion. A spinal tap that releases cerebrospinal fluid reduces intracranial pressure, which leads to a reduction in headaches and dizziness. To prevent infection, antibiotics are prescribed. If there is bleeding, it is not recommended to rinse the ear canal and nose due to the possibility of infection. Nasal tamponade is performed only if there is severe bleeding.