What does a traumatic brain injury entail? Traumatic brain injury Closed injuries to the skull and brain

Basic principles of classification: severity (mild traumatic brain injury, moderate traumatic brain injury, severe traumatic brain injury), combination (isolated, combined, combined), type of damage (focal, diffuse), nature (closed, open non-penetrating, open penetrating), genesis of damage (primary, secondary).

The following clinical forms of traumatic brain injury are distinguished:
Brain concussion
Mild brain contusion
Moderate brain contusion
Severe brain contusion
Diffuse axonal injury
Brain compression

To understand how dangerous head injuries are, it is enough to know that every hundredth death occurs as a result of a traumatic brain injury. This is one of the most common types of injuries, accounting for approximately half of injuries. Most often, such injuries, which are often incompatible with life, are suffered by people leading an active lifestyle, and you can protect yourself by observing basic safety measures. Today we have learned to treat traumatic brain injury of the head and do it successfully in many institutions, and a positive prognosis depends on the correct diagnosis and choice of medical institution.

Types and main symptoms of TBI

Many uninitiated people are interested in what types of traumatic brain injuries are, to which the answer can be that there are two main types of head injuries: open and closed. In the first case, damage occurs to the surface of the scalp, skull bone and dura mater, which often leads to irreversible consequences. Fortunately, less dangerous types of traumatic brain injuries most often occur, such as concussions of varying degrees, compression of the brain under the influence of external factors, head contusions, subarachnoid hemorrhages and others.

The symptoms of most traumatic brain injuries are similar, and as a rule, severe headaches and nausea can be a reason to sound the alarm. It should be borne in mind that there are three degrees of severity of TBI, so the symptoms can differ significantly. As a rule, with a concussion, in addition to nausea and vomiting, a short-term loss of consciousness occurs; with a mild brain contusion, a person may regain consciousness only after an hour. A moderate bruise precedes the onset of amnesia, while the respiratory rate increases, heart function is disrupted, and blood pressure increases. The cause of severe contusion is a fracture of the base of the skull and intracranial hemorrhage, as a rule. When the brain is compressed, loss of consciousness can recur, and it is especially difficult to diagnose the disease in a person in a coma.

Diagnosis and treatment of TBI

High-quality treatment for traumatic brain injury in Moscow is offered, among other institutions, by specialists from the Burdenko Research Institute, where, based on preliminary research data, a correct diagnosis will be made and an effective treatment regimen will be prescribed. Diagnosis of traumatic brain injury is carried out using MRI and computed tomography devices, but it is also important that the patient is closely monitored by specialists who must monitor breathing, measure pulse and blood pressure.

The most effective treatment for TBI is in the acute period, because in this case the main thing is to prevent secondary brain damage, which is much more difficult to treat. Treatment of TBI in a hospital is considered the most effective, where medical workers will take, if necessary, all measures to support the patient’s breathing and prevent the consequences of circulatory disorders. Treatment is often carried out using conservative methods, but surgical intervention is often necessary. At the same time, the cost of TBI surgery depends on the severity of the disease and the timeliness of contacting a medical institution, therefore, if you discover unwanted syndromes, you should immediately contact the nearest medical institution.

Among the causes of death in young and middle age, trauma ranks first. Traumatic brain injury (TBI) is one of the most common types of injuries and accounts for up to 50% of all types of injuries. In injury statistics, brain injuries account for 25-30% of all injuries, accounting for more than half of deaths. Mortality from traumatic brain injury accounts for 1% of total mortality.

Traumatic brain injury is damage to the bones of the skull or soft tissues, such as brain tissue, blood vessels, nerves, and meninges. There are two groups of traumatic brain injuries - open and closed.

Classification of TBI

Open damage

With an open craniocerebral injury, the skin and aponeurosis are damaged and the bottom of the wound is bone or deeper tissue. A penetrating injury is one in which the dura mater is damaged. A special case of penetrating trauma is otoliquorrhea resulting from a fracture of the bones of the base of the skull.

Closed damage

In a closed head injury, the aponeurosis is not damaged, although the skin may be damaged.

All traumatic brain injuries are divided into:

• A concussion is an injury in which there are no permanent disturbances in the functioning of the brain. All symptoms that occur after a concussion usually disappear over time (within a few days). Persistent symptoms are a sign of more serious brain damage. The main criteria for the severity of a concussion are the duration (from several seconds to hours) and the subsequent depth of loss of consciousness and the state of amnesia. Non-specific symptoms - nausea, vomiting, pale skin, cardiac dysfunction.
• Compression of the brain (hematoma, foreign body, air, contusion).
• Brain contusion: mild, moderate and severe.
• Diffuse axonal damage.
• Subarachnoid hemorrhage.

At the same time, various combinations of types of traumatic brain injury can be observed: bruise and compression by a hematoma, bruise and subarachnoid hemorrhage, diffuse axonal damage and bruise, brain contusion with compression by a hematoma and subarachnoid hemorrhage.

Symptoms of TBI

symptoms of impaired consciousness - stupor, stupor, coma. Indicate the presence of a traumatic brain injury and its severity.
symptoms of damage to the cranial nerves indicate compression and contusion of the brain.
symptoms of focal brain lesions indicate damage to a certain area of ​​the brain; they occur with a bruise or compression of the brain.
stem symptoms are a sign of compression and contusion of the brain.
meningeal symptoms - their presence indicates the presence of a brain contusion or subarachnoid hemorrhage, and a few days after the injury it can be a symptom of meningitis.

Treatment for concussion

All victims with a concussion, even if the injury seems mild from the very beginning, must be transported to an emergency hospital, where, to clarify the diagnosis, radiography of the skull bones is indicated; for a more accurate diagnosis, if equipment is available, a CT scan of the brain can be performed.

Victims in the acute period of injury should be treated in the neurosurgical department. Patients with a concussion are prescribed bed rest for 5 days, which is then gradually expanded, taking into account the characteristics of the clinical course. In the absence of complications, discharge from the hospital on the 7-10th day for outpatient treatment lasting up to 2 weeks is possible.

Drug treatment for concussion is aimed at normalizing the functional state of the brain, relieving headaches, dizziness, anxiety, and insomnia.

Typically, the range of drugs prescribed upon admission includes analgesics, sedatives and hypnotics:

Painkillers (analgin, pentalgin, baralgin, sedalgin, maxigan, etc.) select the most effective drug for a given patient.

For dizziness, choose one of the available medications (cerucal)
Sedatives. They use infusions of herbs (valerian, motherwort), drugs containing phenobarbital (Corvalol, Valocordin), as well as tranquilizers (Elenium, Sibazon, phenazepam, nozepam, rudotel, etc.).

Along with symptomatic treatment for a concussion, it is advisable to conduct a course of vascular and metabolic therapy for a faster and more complete recovery of brain dysfunction and the prevention of various post-concussion symptoms. Prescription of vasotropic and cerebrotropic therapy is possible only 5-7 days after injury. A combination of vasotropic (Cavinton, Stugeron, Teonicol, etc.) and nootropic (nootropil, aminolon, picamilon, etc.) drugs is preferable. Take Cavinton three times a day, 1 tablet. (5 mg) and nootropil 1 cap. (0.4) for 1 month.

To overcome frequent asthenic phenomena after a concussion, multivitamins such as “Complivit”, “Centrum”, “Vitrum”, etc. are prescribed, 1 tablet each. in a day.

Tonic preparations include ginseng root, eleutherococcus extract, and lemongrass fruit.

A concussion is never accompanied by any organic lesions. If any post-traumatic changes are detected on CT or MRI, it is necessary to talk about a more serious injury - brain contusion.

Brain contusion due to TBI

A brain contusion is a violation of the integrity of the brain matter in a limited area. It usually occurs at the point of application of the traumatic force, but can also be observed on the side opposite to the injury (contusion from a counter-impact). In this case, destruction of part of the brain tissue, blood vessels, and histological cell connections occurs, with the subsequent development of traumatic edema. The area of ​​such violations varies and is determined by the severity of the injury.
There are mild, moderate and severe brain contusions.

Mild brain contusion

A mild brain contusion is characterized by loss of consciousness after injury lasting from several to tens of minutes.

• After regaining consciousness, typical complaints are headache, dizziness, nausea, etc.
• As a rule, retro-, con-, and anterograde amnesia is noted. Amnesia (Greek: amnesia forgetfulness, memory loss) is a memory impairment in the form of loss of the ability to retain and reproduce previously acquired knowledge.
• Vomiting, sometimes repeated. Moderate bradycardia may be observed. Bradycardia is a decrease in heart rate to 60 or less per minute in an adult.
• tachycardia - an increase in heart rate over 90 beats per minute for adults.
• sometimes - systemic arterial hypertension; hypertension - increased hydrostatic pressure in blood vessels, hollow organs or body cavities.
• Breathing and body temperature without significant deviations.
• Neurological symptoms are usually mild (clonic nystagmus - involuntary rhythmic biphasic movements of the eyeballs, drowsiness, weakness)
• slight anisocoria, signs of pyramidal insufficiency, meningeal symptoms, etc., often regressing within 2-3 weeks. after injury.

It is almost impossible to differentiate between a concussion and a mild cerebral contusion (concussion) by the duration of coma and post-traumatic amnesia, as well as by clinical manifestation.

The classification adopted in Russia allows for the presence of linear fractures of the cranial vault with mild brain contusion.
An analogue of a mild brain contusion in the domestic classification is a minor head injury by American authors, which implies a condition that meets the following criteria:

1) more than 12 points on the Glasgow Coma Scale (during observation in the clinic);
2) loss of consciousness and/or post-traumatic amnesia not exceeding 20 minutes;
3) hospitalization for less than 48 hours;
4) absence of clinical signs of contusion of the brainstem or cortex.

Unlike a concussion, with a brain contusion, the structure of the brain tissue is disrupted. So, with a mild bruise, a mild damage to the brain substance is microscopically determined in the form of areas of local edema, pinpoint cortical hemorrhages, possibly in combination with limited subarachnoid hemorrhage as a result of rupture of the pial vessels.

With subarachnoid hemorrhage, blood enters under the arachnoid membrane and spreads through the basal cisterns, grooves and fissures of the brain. Hemorrhage can be local or fill the entire subarachnoid space with the formation of clots. It develops acutely: the patient suddenly experiences a “blow to the head”, severe headache, vomiting, and photophobia appear. There may be one-time generalized seizures. Paralysis, as a rule, is not observed, but meningeal symptoms are pronounced - rigidity of the neck muscles (when the head is tilted, the patient’s chin cannot touch the sternum) and Kernig’s sign (the leg bent at the hip and knee joints cannot be straightened at the knee joint). Meningeal symptoms indicate irritation of the membranes of the brain due to bleeding.

Moderate brain contusion

Moderate brain contusion is characterized by loss of consciousness after injury lasting from several tens of minutes to several hours. Amnesia is pronounced (retro-, con-, anterograde). The headache is often severe. Repeated vomiting may occur. Mental disorders are sometimes observed. Transient disorders of vital functions are possible: bradycardia or tachycardia, increased blood pressure, tachypnea - rapid shallow (not deep) breathing without disturbing the rhythm of breathing and airway patency, low-grade fever - increased body temperature within 37-37.9 ° C.

Often, meningeal and brainstem symptoms, dissociation of muscle tone and tendon reflexes along the body axis, bilateral pathological signs, etc. are detected. Focal symptoms are clearly manifested, the nature of which is determined by the localization of the brain contusion; pupillary and oculomotor disorders, paresis of the limbs, disorders of sensitivity, speech, etc. These symptoms gradually (within 3-5 weeks) smooth out, but can persist for a long time. With moderate brain contusion, fractures of the bones of the vault and base of the skull, as well as significant subarachnoid hemorrhage, are often observed.

Computed tomography in most cases reveals focal changes in the form of high-density small inclusions, non-compactly located in a zone of reduced density, or a moderate homogeneous increase in density (which corresponds to small hemorrhages in the bruise area or moderate hemorrhagic impregnation of brain tissue without gross destruction). In some observations, with a clinical picture of a moderate bruise, a computed tomogram reveals only zones of reduced density (local edema) or signs of brain injury are not visualized at all.

Severe brain contusion

Severe brain contusion, intracerebral hematomas (limited accumulation of blood due to closed and open injuries to organs and tissues with rupture (injury) of blood vessels; a cavity is formed containing liquid or coagulated blood) of both frontal lobes.

Severe brain contusion is characterized by loss of consciousness after injury lasting from several hours to several weeks. Motor agitation is often pronounced. Severe disturbances in vital functions are observed: arterial hypertension (sometimes hypotension), bradycardia or tachycardia, disorders of the frequency and rhythm of breathing, which may be accompanied by disturbances in the patency of the upper respiratory tract. Hyperthermia is pronounced. Primary brainstem neurological symptoms often dominate (floating movements of the eyeballs, gaze paresis, tonic nystagmus, swallowing disorders, bilateral mydriasis or ptosis - drooping of the upper eyelid, divergence of the eyes along the vertical or horizontal axis, changing muscle tone, decerebrate rigidity, depression or increased tendon reflexes, reflexes from the mucous membranes and skin, bilateral pathological foot signs, etc.), which in the first hours and days after injury obscures focal hemispheric symptoms. Paresis of the limbs (up to paralysis), subcortical disorders of muscle tone, reflexes of oral automatism, etc. can be detected. Generalized or focal epileptic seizures are sometimes observed. Focal symptoms regress slowly; gross residual effects are frequent, primarily in the motor and mental spheres. Severe brain contusion is often accompanied by fractures of the vault and base of the skull, as well as massive subarachnoid hemorrhage.

Computed tomography reveals focal brain lesions in the form of a heterogeneous increase in density in 1/3 of cases. An alternation of areas with increased (density of fresh blood clots) and decreased density (density of edematous and/or crushed brain tissue) is determined. In the most severe cases, the destruction of the brain substance spreads in depth, reaching the subcortical nuclei and the ventricular system. Observation over time shows a gradual decrease in the volume of compaction areas, their merging and transformation into a more homogeneous mass already in 8-10 days. The volumetric effect of the pathological substrate regresses more slowly, indicating the existence of unresolved crushed tissue and blood clots in the focus of the contusion, which by this time become equally dense in relation to the surrounding edematous substance of the brain. The volume effect disappears by 30-40 days. after injury indicates the resorption of the pathological substrate and the formation in its place of zones of atrophy (a decrease in the mass and volume of an organ or tissue, accompanied by a weakening or cessation of their function) or cystic cavities.

In approximately half of the cases of severe brain contusion, computed tomography reveals significant areas of intense homogeneous increase in density with unclear boundaries, indicating a significant content of liquid blood and its clots in the area of ​​traumatic brain injury. The dynamics show a gradual and simultaneous decrease over 4-5 weeks. the size of the destruction area, its density and the resulting volumetric effect.

Damage to the structures of the posterior cranial fossa (PCF) is one of the severe types of traumatic brain injury (TBI). Their peculiarity lies in their extremely difficult clinical diagnosis and high mortality. Before the advent of computed tomography, the mortality rate for PCF injury was close to 100%.

The clinical picture of damage to the PCF structures is characterized by a severe condition that occurs immediately after the injury: depression of consciousness, a combination of cerebral, meningeal, cerebellar, and brainstem symptoms due to rapid compression of the brainstem and impaired cerebrospinal fluid circulation. If there is significant damage to the substance of the cerebrum, hemispheric symptoms are added.
The proximity of the location of damage to the PCF structures to the liquor-conducting pathways causes their compression and disruption of liquor circulation by a small-volume hematoma. Acute occlusive hydrocephalus - one of the most severe complications of damage to the structures of the posterior follicle - is detected in 40%.

Treatment of brain contusion

Mandatory hospitalization!!! Bed rest.

The duration of bed rest for a mild bruise is 7-10 days, for a moderate bruise up to 2 weeks. depending on the clinical course and results of instrumental studies.
In case of severe traumatic brain injury (foci of crush injury, diffuse axonal damage), resuscitation measures are necessary, which begin at the prehospital stage and continue in a hospital setting. In order to normalize breathing, ensure free patency of the upper respiratory tract (freeing them from blood, mucus, vomit, introducing an air duct, tracheal intubation, tracheostomy tracheostomy (an operation of dissecting the anterior wall of the trachea with subsequent insertion of a cannula into its lumen or the creation of a permanent opening - stoma)) , use inhalation of an oxygen-air mixture, and, if necessary, perform artificial ventilation.

Surgical treatment is indicated for brain contusion with crushing of its tissue (most often occurs in the region of the poles of the frontal and temporal lobes). The essence of the operation: osteoplastic trephination (a surgical operation consisting of creating a hole in the bone in order to penetrate into the underlying cavity) and washing out brain detritus with a stream of 0.9% NaCl solution, stopping bleeding.

The prognosis for mild TBI (concussion, mild brain contusion) is usually favorable (subject to the recommended regimen and treatment for the victim).

In case of moderate injury (moderate brain contusion), it is often possible to achieve complete restoration of work and social activity of the victims. A number of patients develop leptomeningitis and hydrocephalus, causing asthenia, headaches, vegetative-vascular dysfunction, disturbances in statics, coordination and other neurological symptoms.

With severe trauma (severe brain contusion, diffuse axonal damage, brain compression), mortality reaches 30-50%. Among survivors, disability is significant, the leading causes of which are mental disorders, epileptic seizures, gross motor and speech disorders. With an open head injury, inflammatory complications can occur (meningitis, encephalitis, ventriculitis, brain abscesses), as well as liquorrhea - the leakage of cerebrospinal fluid (CSF) from natural holes or holes formed due to various reasons in the bones of the skull or spine, which occurs when integrity is violated.

Half of all deaths from traumatic brain injury are caused by road traffic accidents. Traumatic brain injury is one of the leading causes of disability in the population.

What is traumatic brain injury (TBI)?

Traumatic brain injury includes all types of head injury, including minor bruises and cuts to the skull. More serious injuries from traumatic brain injury include:

skull fracture;

concussion, concussion. A concussion is manifested by a short, reversible loss of consciousness;

accumulation of blood above or below the dural membrane of the brain (the dural membrane is one of the protective films that envelop the brain), respectively, epidural and subdural hematoma;

intracerebral and intraventricular hemorrhage (bleeding into the brain or into the space around the brain).

Almost every person has experienced at least once in their life a minor traumatic brain injury - a bruise or cut to the head that required minimal or no treatment.

What are the causes of traumatic brain injury?

Causes of traumatic brain injury may include:

skull fracture with tissue displacement and rupture of the protective membranes around the spinal cord and brain;

bruises and ruptures of brain tissue due to concussions and blows in a confined space inside the hard skull;

bleeding from damaged vessels into the brain or into the space around it (including bleeding due to a ruptured aneurysm).

Brain damage can also occur due to:

direct injury to the brain by objects penetrating the cranial cavity (for example, bone fragments, bullets);

increased pressure inside the skull as a result of cerebral edema;

a bacterial or viral infection that penetrates the skull in the area of ​​its fractures.

The most common causes of traumatic brain injury are motor vehicle accidents, sports injuries, assaults, and physical abuse.

Traumatic brain injury can develop in anyone at any age because it is the result of trauma. Brain damage can occur during childbirth.

Classification of traumatic brain injuries (TBI).

The following main clinical forms of traumatic brain injury: concussion, mild, moderate and severe brain contusion, compression of the brain.

According to the risk of infection of the brain and its membranes traumatic brain injury is divided into closed and open.

With a closed craniocerebral injury, the integrity of the soft tissues of the head is not violated or there are superficial wounds of the scalp without damage to the aponeurosis.

With an open traumatic brain injury, fractures of the bones of the vault or base of the skull are observed with injury to adjacent tissues, bleeding, leakage of cerebrospinal fluid from the nose or ear, as well as damage to the aponeurosis in wounds of the soft integument of the head.

When the dura mater is intact, open craniocerebral injuries are classified as non-penetrating, and when it is ruptured, they are classified as penetrating. If there are no extracranial injuries, the traumatic brain injury is isolated. When extracranial injuries occur simultaneously (for example, fractures of limbs, ribs, etc.), they speak of a combined traumatic brain injury, and when exposed to different types of energy (mechanical or chemical, radiation or thermal) - a combined one.

Based on severity, traumatic brain injury is divided into mild, moderate and severe. A mild traumatic brain injury includes a mild concussion and contusion, a moderate traumatic brain injury includes a moderate brain contusion, a severe traumatic brain injury includes a severe brain contusion and compression of the brain in the acute period.

There are several main types of interrelated pathological processes that occur at the time of injury and some time after it:

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- damage characterized by the presence in the substance of the brain and in its membranes of macroscopically visible foci of destruction and hemorrhages, 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. Another pathogenetic mechanism for the formation of the consequences of TBI is directly related to the vascular factor - 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, there are three basic periods during traumatic brain disease: acute, intermediate, and long-term.

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 level or another 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 deployment 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 of clinical recovery - up to 2-3 years with a progressive course - is not limited.

All types of TBI are usually divided into closed brain injuries (CBI), open and penetrating. Closed TBI is a mechanical damage to the skull and brain, resulting in a number of pathological processes that determine the severity of the clinical manifestations of the injury. 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 injuries involve disruption of the integrity of the dura mater.

Classification of traumatic brain injury according to Gaidar:

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; cerebrospinal fluid 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:

state of consciousness;

state of vital functions;

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; 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.

Clinic of various forms of traumatic brain injury

Clinical picture (symptoms) of acute traumatic brain injury

Brain concussion.

A concussion is characterized by a short-term loss of consciousness at the time of injury, vomiting (usually one-time), headache, dizziness, weakness, painful eye movements, etc. There are no focal symptoms in the neurological status. Macrostructural changes in the brain substance during a concussion are not detected.

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, a short-term blackout from several seconds to several minutes. Subsequently, a stunned state persists with insufficient orientation in time, place and circumstances, unclear perception of the environment and 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. Patients complain of headache, dizziness, nausea. An objective sign is vomiting.

Neurological examination usually reveals minor, diffuse symptoms:

symptoms of oral automatism (proboscis, nasolabial, palmomental);

unevenness of tendon and skin reflexes (as a rule, there is a decrease in abdominal reflexes and their rapid exhaustion);

moderately expressed or unstable pyramidal pathological signs (Rossolimo, Zhukovsky, less often Babinsky symptoms).

Cerebellar symptoms are often clearly manifested: nystagmus, muscle hypotonia, intention tremor, instability in the Romberg position. A characteristic feature of concussions is the rapid regression of symptoms; in most cases, all organic signs disappear within 3 days.

Various vegetative and, above all, vascular disorders are more persistent in cases of concussions and mild bruises. These include fluctuations in blood pressure, tachycardia, acrocyanosis of the extremities, diffuse persistent dermographism, hyperhidrosis of the hands, feet, and armpits.

Brain contusion (CBM)

Brain contusion is characterized by focal macrostructural damage to the brain matter of varying degrees (hemorrhage, destruction), as well as subarachnoid hemorrhages, fractures of the bones of the vault and base of the skull.

Mild brain contusion characterized by loss of consciousness up to 1 hour after injury, complaints of headache, nausea, vomiting. In the neurological status, rhythmic twitching of the eyes when looking to the sides (nystagmus), meningeal signs, and asymmetry of reflexes are noted. X-rays may reveal fractures of the cranial vault. There is an admixture of blood in the cerebrospinal fluid (subarachnoid hemorrhage). .Mild brain contusion is clinically characterized by a short-term loss of consciousness after the injury, up to several tens of minutes. Upon its recovery, typical complaints are headache, dizziness, nausea, etc. As a rule, retro-, con-, anterograde amnesia, vomiting, and sometimes repeated are noted. Vital functions are usually without significant impairment. Moderate tachycardia and sometimes arterial hypertension may occur. Neurological symptoms are usually mild (nystagmus, mild anisocoria, signs of pyramidal insufficiency, meningeal symptoms, etc.), mostly regressing 2-3 weeks after TBI. With mild UHM, in contrast to concussion, fractures of the calvarial bones and subarachnoid hemorrhage are possible.

Moderate brain contusion clinically characterized by a loss of consciousness after injury lasting up to several tens of minutes or even hours. Moderate brain contusion. Consciousness turns off for several hours. There is a marked loss of memory (amnesia) for the events preceding the injury, the injury itself, and the events after it. Complaints of headache, repeated vomiting. Short-term disorders of breathing, heart rate, and blood pressure are detected. There may be mental disorders. Meningeal signs are noted. Focal symptoms manifest themselves in the form of uneven pupil size, speech impairment, weakness in the limbs, etc. Craniography often reveals fractures of the vault and base of the skull. Lumbar puncture revealed significant subarachnoid hemorrhage. Con-, retro-, anterograde amnesia is expressed. Headache, often severe. Repeated vomiting may occur. Mental disorders occur. Transient disorders of vital functions are possible: bradycardia or tachycardia, increased blood pressure; tachypnea without disturbances in the rhythm of breathing and patency of the tracheobronchial tree; low-grade fever. Meningeal symptoms are often prominent. Brainstem symptoms are also detected: nystagmus, dissociation of meningeal symptoms, muscle tone and tendon reflexes along the body axis, bilateral pathological signs, etc. Focal symptoms are clearly manifested, determined by the localization of the brain contusion: pupillary and oculomotor disorders, paresis of the limbs, sensitivity disorders, etc. . Organic symptoms gradually smooth out over 2-5 weeks, but some symptoms can persist for a long time. Fractures of the bones of the vault and base of the skull, as well as significant subarachnoid hemorrhage, are often observed.

Severe brain contusion. Severe brain contusion is clinically characterized by loss of consciousness after injury lasting from several hours to several weeks. Characterized by prolonged loss of consciousness (lasting up to 1-2 weeks). Gross violations of vital functions are detected (changes in pulse rate, pressure level, frequency and rhythm of breathing, temperature). The neurological status shows signs of damage to the brain stem - floating movements of the eyeballs, swallowing disorders, changes in muscle tone, etc. Weakness in the arms and legs, up to paralysis, as well as convulsive seizures may be detected. A severe bruise is usually accompanied by fractures of the vault and base of the skull and intracranial hemorrhages. .Motor agitation is often expressed, and severe, threatening disturbances in vital functions are observed. The clinical picture of severe UHM is dominated by brainstem neurological symptoms, which in the first hours or days after TBI overlap focal hemispheric symptoms. Paresis of the limbs (up to paralysis), subcortical disorders of muscle tone, reflexes of oral automatism, etc. can 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, a “spot symptom” 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

Compression of the brain is a progressive pathological process in the cranial cavity that occurs as a result of trauma and causes dislocation and infringement of the brainstem with the development of a life-threatening condition. With TBI, compression of the brain occurs in 3-5% of cases, both with and without UGM. Among the causes of compression, intracranial hematomas come first - epidural, subdural, intracerebral and intraventricular; This is followed by depressed fractures of the skull bones, areas of brain crushing, subdural hygromas, and pneumocephalus. .Compression of the brain. The main cause of brain compression during traumatic brain injury is the accumulation of blood in a closed intracranial space. Depending on the relationship to the membranes and the substance of the brain, epidural (located above the dura mater), subdural (between the dura mater and the arachnoid mater), intracerebral (in the white matter of the brain and intraventricular (in the cavity of the ventricles of the brain) hematomas are distinguished. The cause of compression of the brain can be There may also be depressed fractures of the bones of the cranial vault, especially penetration of bone fragments to a depth of more than 1 cm.

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

In most cases, there is loss of consciousness at the time of injury. Subsequently, consciousness can be restored. The period of restoration of consciousness is called the lucid interval. After a few hours or days, the patient may again fall into an unconscious state, which, as a rule, is accompanied by an increase in neurological disorders in the form of the appearance or deepening of paresis of the limbs, epileptic seizures, dilation of the pupil on one side, slowing of the pulse (rate less than 60 per minute), etc. .d. According to the rate of development, acute intracranial hematomas are distinguished, which appear in the first 3 days from the moment of injury, subacute - clinically manifested in the first 2 weeks after injury, and chronic, which are diagnosed after 2 weeks from the moment of injury.

How does traumatic brain injury manifest?
Symptoms of traumatic brain injury:

loss of consciousness;

Strong headache;

increasing drowsiness and lethargy
vomit;

discharge of clear fluid (cerebrospinal fluid or cerebrospinal fluid) from the nose, especially when tilting the head face down.

Call emergency medical services immediately for a person with a traumatic brain injury, no matter how minor the injury.

If you think you have suffered a traumatic brain injury, get medical help or ask someone to help you.

With extensive head wounds penetrating into the cranial cavity, there is a high probability of brain damage. However, in 20% of cases, death after a traumatic brain injury occurs without the presence of skull fractures. Therefore, a person with a traumatic brain injury in the presence of the above symptoms must be hospitalized

Diagnosis of traumatic brain injury.

If the patient is conscious, careful identification of the circumstances and mechanism of injury is necessary, since the cause of a fall and head injury may be a stroke or an epileptic seizure. Often the patient cannot remember the events preceding the injury (retrograde amnesia), those immediately following the injury (anterograde amnesia), as well as the moment of injury itself (cograde amnesia). It is necessary to carefully examine the head to look for signs of injury. Hemorrhages over the mastoid process often indicate a fracture of the temporal bone. Bilateral hemorrhages in the orbital tissue (the so-called “spectacles symptom”) may indicate a fracture of the base of the skull. This is also indicated by bleeding and liquorrhea from the external auditory canal and nose. With fractures of the calvarium, a characteristic rattling sound is heard during percussion - the “symptom of a cracked pot.”

To objectify disturbances of consciousness during traumatic brain injury, a special scale has been developed for nursing staff - the Glasgow Coma Scale. It is based on the total score of 3 indicators: eye opening to sound and pain, verbal and motor responses to external stimuli. The total score ranges from 3 to 15.

Severe traumatic brain injury corresponds to 3-7 traumatic brain injury points, moderate - 8-12 points, mild - 13-15.

Glasgow Coma Scale

A qualitative assessment of consciousness in traumatic brain injury should be performed. Clear consciousness means wakefulness, complete orientation in place, time and environment. Moderate confusion is characterized by drowsiness, mild errors in time orientation, and slow comprehension and execution of instructions. Deep Stun characterized by deep drowsiness, disorientation in place and time, following only basic instructions (raise your hand, open your eyes). Sopor- the patient is motionless, does not follow commands, but opens his eyes, defensive movements are expressed in response to local painful stimuli. At moderate coma it is not possible to wake up the patient, he does not open his eyes in response to pain, defensive reactions without localization of painful stimuli are uncoordinated. Deep coma characterized by a lack of response to pain, pronounced changes in muscle tone, respiratory and cardiovascular disorders. At terminal coma There is bilateral dilation of the pupils, immobility of the eyes, a sharp decrease in muscle tone, absence of reflexes, severe disturbances of vital functions - breathing rhythm, heart rate, drop in blood pressure below 60 mm Hg. Art.

A neurological examination allows you to assess the level of wakefulness, the nature and degree of speech disorders, the size of the pupils and their reaction to light, corneal reflexes (normally, touching the cornea with a cotton swab causes a blinking reaction), strength in the limbs (a decrease in strength in the limbs is called paresis, and a complete absence in their active movements - paralysis), the nature of twitching in the limbs (convulsive seizures).

An important role in the diagnosis of traumatic brain injury is played by instrumental research methods, such as echoencephalography, skull radiography and computed tomography of the head, including computed tomography with contrast (angiography).

What examinations are needed after a traumatic brain injury?

Diagnosis of traumatic brain injury:

assessment of airway patency, respiratory and circulatory function;

assessment of the visible area of ​​skull damage;

if necessary, X-rays of the neck and skull, CT (computed tomography), MRI (magnetic resonance imaging);

monitoring the level of consciousness and vital functions of the body (pulse, breathing, blood pressure).

In cases of severe traumatic brain injury, it may be necessary to:

observation by a neurosurgeon or neurologist;

MRI and CT as necessary;

monitor and treat increased pressure inside the skull due to swelling or bleeding;

surgical intervention for blood accumulation (hematoma);

prevention and treatment of seizures.

Scheme of examination of victims with traumatic brain injury

1. Identifying the history of the injury: time, circumstances, mechanism, clinical manifestations of the injury and the amount of medical care before admission.

2. Clinical assessment of the severity of the victim’s condition, which is of great importance for diagnosis, triage and provision of stage-by-stage assistance to victims. State of consciousness: clear, stunned, stupor, coma; the duration of loss of consciousness and the sequence of exit are noted; memory impairment, antero- and retrograde amnesia.

3. State of vital functions: cardiovascular activity - pulse, blood pressure (a common feature in TBI - the difference in blood pressure on the left and right limbs), breathing - normal, impaired, asphyxia.

4. Condition of the skin - color, moisture, bruises, presence of soft tissue damage: location, type, size, bleeding, liquorrhea, foreign bodies.

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

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

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

8. Echoencephaloscopy.

9. X-ray of the skull in two projections; if damage to the posterior cranial fossa is suspected, a posterior semi-axial image is taken.

10. Computer or magnetic resonance imaging of the skull and brain.

11. Ophthalmological examination of the condition of the fundus of the eye: swelling, congestion of the optic nerve head, hemorrhages, condition of the vessels of the fundus.

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

13. Computed tomography with contrast in the case of hemorrhagic stroke (in the presence of blood in the cerebrospinal fluid of step 12) and suspected aneurysm rupture, or other additional diagnostic methods at the discretion of the doctor.

14. Making a diagnosis. The diagnosis reflects: the nature and type of brain damage, the presence of subarachnoid hemorrhage, compression of the brain (cause), liquor hypo- or hypertension; condition of the soft covers of the skull; fractures of the skull bones; the presence of concomitant injuries, complications, intoxications.

First aid for victims with severe traumatic brain injury

The results of treatment of traumatic brain injury largely depend on the quality of prehospital care and the speed of hospitalization of the victim. It is unlikely to find another type of injury where a delay in transporting the patient to the hospital for an hour or two made a significant difference. Therefore, it is generally accepted that an ambulance service that is unable to transport a victim with a severe traumatic brain injury to a neurosurgical hospital within a few minutes is not doing its job. In many countries, patients with severe traumatic brain injury are transported to hospitals by helicopter.

When providing first aid at the scene of an accident, it is first necessary to restore the airway. Along with oxygen starvation (hypoxia), a frequent complication of traumatic brain injury is increased accumulation of carbon dioxide in the body (hypercapnia). During transport, patients must breathe 100% oxygen. In case of multiple injuries accompanied by shock, intravenous administration of Ringer's solution, rheopolyglucin, etc. is simultaneously started. Ischemia, hypoxia or hypotension for a short period, even with a moderate traumatic brain injury, can lead to irreversible consequences in the future. If a high spinal cord injury is suspected, the cervical spine should be immobilized.

Bleeding must be stopped by applying a tight bandage or quickly suturing the wound. Damage to the scalp, especially in the elderly, can lead to a sharp worsening of the condition.

Indications for hospitalization for TBI

The generally accepted criteria for hospitalization for traumatic brain injury are:

1) a clear decrease in the level of consciousness,

2) focal neurological disorders (paresis of the limbs, uneven pupil width, etc.),

3) open fractures of the skull bones, bleeding or liquorrhea from the nose or ear canal,

4) epileptic seizures,

5) loss of consciousness as a result of injury,

6) significant post-traumatic amnesia.

Patients with severe headaches, restless, and disoriented are hospitalized until these symptoms disappear.

Treatment is carried out in neurosurgical hospitals.

Caring for patients with severe traumatic brain injury involves preventing bedsores and hypostatic pneumonia (turning the patient in bed, massage, skin toilet, cupping, mustard plasters, suction of saliva and mucus from the oral cavity, sanitation of the trachea).

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.

What is the prognosis for traumatic brain injury?
Chances of recovery

The outcome of a traumatic brain injury can vary, just as the response to a traumatic brain injury varies from person to person. Some extensive penetrating wounds of the skull ultimately result in the patient’s complete recovery, while fairly minor wounds can have the most serious consequences. Usually the damage is more severe in cases of severe cerebral edema, increased intracranial pressure and prolonged loss of consciousness.

A fairly small number of people may remain in a permanent vegetative state after a traumatic brain injury. Qualified neurological and neurosurgical treatment in the early stages after traumatic brain injury can significantly improve the prognosis.

Recovery from traumatic brain injury can be very slow in severe cases, although improvement may last up to 5 years.

Consequences of traumatic brain injury.

The outcomes of traumatic brain injury are largely determined by the age of the victim. For example, with severe traumatic brain injury, 25% of patients under 20 years of age and up to 70-80% of victims over the age of 60 die. Even with mild traumatic brain injury and moderate traumatic brain injury, the consequences become apparent over a period of months or years. The so-called “post-traumatic syndrome” is characterized by headache, dizziness, increased fatigue, decreased mood, and memory impairment. These disorders, especially in old age, can lead to disability and family conflicts. To determine the outcomes of traumatic brain injury, the Glasgow Outcome Scale (GOS) has been proposed, which provides five outcome options.

Glasgow Outcome Scale

We can talk about outcomes 1 year after the traumatic brain injury, since in the future there are no significant changes in the patient’s condition. Rehabilitation measures include physical therapy, physiotherapy, taking nootropic, vascular and anticonvulsant drugs, and vitamin therapy. The results of treatment largely depend on the timeliness of assistance at the scene of the incident and upon admission to the hospital.

What are the consequences of traumatic brain injury?

The consequences of traumatic brain injury can be associated with damage to a specific area of ​​the brain or be the result of general brain damage with swelling and high blood pressure.

Possible consequences of traumatic brain injury:

epilepsy,
decrease in a certain degree of mental or physical abilities,
depression,
memory loss,
personal changes,

How is traumatic brain injury treated?

First of all, an accurate diagnosis of the nature of the injury is important; the method of treatment depends on this. A neurological examination is performed to assess the level of damage and the need for further rehabilitation and treatment.

Surgery is necessary to remove the blood clot and reduce intracranial pressure, restore the integrity of the skull and its membranes, and prevent infection.

Medicines are needed to control the degree of increased pressure inside the skull, swelling of the brain, and improve blood flow to the brain.

After discharge from the hospital, it may be necessary to observe various specialists: a neurologist, a therapist, etc.

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 assistance. 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.

The brain is protected from external (mechanical) factors better than any other organ. In addition to the bones of the skull, the meninges protect it from damage. The fluid that bathes the brain also acts as a shock absorber. However, traumatic brain injury (TBI) is one of the most common reasons for seeking help from medical institutions. In the overall structure of injuries, TBI accounts for over 50% of cases, and in recent years there has been a tendency to increase their number, as well as to worsen the injuries themselves. This is not least due to the increase in the pace of life (especially in cities) and the increase in the number of vehicles on the roads. Treatment of traumatic brain injury is the task of traumatologists and neurosurgeons. In some cases, patients require the help of neurologists and even psychiatrists.

Consequences of traumatic brain injury

A victim may experience the following as a result of a head injury:

• mechanical disruption of the integrity of brain tissue;
• disturbance of cerebrospinal fluid dynamics;
• hemodynamic disorders;
• neurodynamic disorders;
• formation of scars and adhesions.

During concussions, reactive and compensatory changes develop at the level of synapses, neurons and cells.

Bruises are characterized by the presence of visible lesions and hematomas.

If during a traumatic brain injury there is damage to the stem structures or the hypothalamic-pituitary system, a specific stress response develops due to a disturbance in the exchange of neurotransmitters.

The cerebral circulatory system is particularly sensitive to traumatic injuries. With TBI, spasm or dilation of regional vessels occurs, and the permeability of their walls increases. A direct consequence of vascular disorders are disorders of liquorodynamics.

Dysmetabolic disorders and hypoxia develop against the background of TBI. Severe injuries can provoke respiratory and hemodynamic disorders.

The so-called “traumatic disease” includes 3 periods:

• spicy;
• intermediate;
• remote.

Depending on the severity and type of TBI, the duration of the first period is from 2 weeks to 2.5 months. Acute phase determined by a combination of damaging factors and defense reactions. This is the time interval from the onset of exposure to a traumatic factor until the restoration of body functions or death.

IN intermediate period the processes of lysis and repair actively occur in damaged areas. At this stage, compensatory and adaptive mechanisms are activated, contributing to the return of impaired functions to normal levels (or stable compensation). The duration of the second period can be from 6 months to 1 year.

Final (remote) period characterized by the completion of degeneration and recovery. In some cases they continue to coexist. The duration of the phase against the background of clinical recovery is 2-3 years, and with further development of the process it is very uncertain.

Classification of traumatic brain injury

Note:injuries in this category are divided into closed, open and penetrating.

Closed TBI– these are head injuries accompanied by the development of clinical symptoms, but without serious damage to the skin.

Open– these are injuries with damage to the layers of skin and aponeurosis of the skull.

Penetrating injuries characterized by a violation of the integrity of the hard shell.

Condition assessment

During the initial examination and examination of the patient in a medical facility, the following factors must be taken into account:

The severity of a traumatic brain injury is assessed by 3 factors:

• state of consciousness;
• vital functions;
• neurological symptoms.

Severity of TBI

1. Satisfactory The patient’s condition is considered if he has clear consciousness, there are no impairments of the most important functions, and there are no primary and secondary neurological clinical signs. With timely and correctly carried out therapeutic measures, nothing threatens life, and working capacity is fully restored.
2. For moderate injuries consciousness is clear or there is some stupor. Vital functions are not affected, but the number of heartbeats may decrease. Individual focal signs can be diagnosed. There is practically no threat to life if qualified assistance is provided in a timely manner. The prognosis for full recovery after such a traumatic brain injury is quite favorable.
3. In severe condition The patient experiences severe stupor or develops stupor - depression of consciousness, in which loss of voluntary activity occurs and reflex activity persists. Impaired respiratory and circulatory functions are recorded, and neurological symptoms are present. Paresis, paralysis, etc. are possible. The threat to life is quite obvious, and the degree of danger is determined by the duration of the acute phase. The prospects for full recovery after severe TBI are rather doubtful.
4. Signs very serious condition are coma, inhibition of a number of important functions and pronounced neurological symptoms (both primary and secondary). The threat to life is very serious, and full recovery from injury usually does not occur.
5. The most dangerous condition is terminal . It is characterized by coma, critical impairment of vital functions, as well as deep stem and cerebral disorders. Unfortunately, it is extremely rare to save the victim in such a situation.

Symptoms of traumatic brain injury

Clinical symptoms allow us to draw preliminary conclusions about the nature of the traumatic brain injury.

Concussion is accompanied by reversible cerebral disorders.

Characteristic symptoms:

• short-term darkening or (up to several minutes);
• slight stupor;
• some difficulties with orientation in space;
• loss of memory of the period of time after the injury;
• motor agitation (rare);
• (cephalgia);
• (not always);
• decreased muscle tone;
• nystagmus (involuntary eye vibrations).

During the neurological examination, instability in the Romberg position may be noted. Symptoms usually regress quickly. Organic signs disappear without a trace in the next 3 days, but vegetative disorders persist much longer. The patient may complain of vascular symptoms - decreased or increased blood pressure, coldness and blue fingers, as well.

Bruises (UGM)

Clinically, there are 3 degrees of UGM – mild, moderate and severe.

Signs of a mild brain injury:

• loss of consciousness (up to 20-40 minutes);
• vomit;
• amnesia;
• cardiopalmus;
• (may be missing).

Moderate neurological symptoms regress within 2-3 weeks after such a traumatic brain injury.

Note:The fundamental difference between a bruise and a concussion is the possibility of fracture of the bones of the vault and the presence of subarachnoid hematomas.

Signs of moderate UGM:

A neurological examination reveals meningeal and brainstem symptoms. The main organic manifestations disappear within 2-5 weeks, but some clinical signs of a traumatic brain injury make themselves felt for a long time.

Signs of severe UGM:

• consciousness is absent for up to several weeks;
• there are life-threatening impairments of essential functions;
• motor agitation;
• paralysis;
• hypo- or hypertonicity of muscles;
• convulsions.

The reverse development of symptoms is slow, and residual disorders often occur, including mental disorders.

Important:a sign that is 100% likely to indicate a fracture of the base of the skull is the release of cerebrospinal fluid from the ear or nose.

The appearance of symmetrical hematomas around the eyes (“glasses”) gives reason to suspect a fracture in the area of ​​the anterior cranial fossa.

Compression

Compression often accompanies bruises. Its most common causes are hematomas of various locations and damage to the bones of the arch with their depression. Less commonly, damage is caused by swelling of the brain tissue and pneumocephalus.

Symptoms of compression can increase sharply immediately after a traumatic brain injury or after a certain (“bright”) time period.

Characteristic signs of compression:

• progressive impairment of consciousness;
• cerebral disorders;
• focal and stem signs.

Possible complications of TBI

The greatest danger in the acute phase is from dysfunctions of the respiratory system (respiratory depression and gas exchange disorders), as well as problems with central and regional (cerebral) circulation.

Hemorrhagic complications are cerebral infarctions and intracranial hemorrhages.

With severe traumatic brain injuries, dislocation (displacement) of parts of the brain is possible.

Against the background of TBI, the likelihood of complications of a purulent-inflammatory nature is quite high. They are divided into intra- and extracranial. The first group includes abscesses, and, and the second, for example,.

Note:Possible complications include post-traumatic and.

First aid for traumatic brain injury

Important:Pre-medical care for a traumatic brain injury consists of providing the victim with complete rest. He needs to be given a horizontal position with his head raised. If the patient is unconscious, he cannot be moved, since the possibility of spinal injury cannot be ruled out. It is advisable to apply a heating pad with cold water or an ice pack to your head. If breathing or cardiac activity stops, before the ambulance arrives, resuscitation measures must be carried out - indirect cardiac massage and artificial respiration.

Primary care for patients is provided at the nearest medical facility. The scope of primary care is determined by the severity of the patient’s condition and the capabilities of physicians. The primary task of doctors is to maintain respiratory and circulatory functions. It is extremely important to restore the patency of the airways (it is often impaired as a result of aspiration of blood, secretions or vomit).

TBI– damage by mechanical energy to the skull and intracranial contents (brain, meninges, vessels and cranial nerves).

TBI is in first place in the structure of neurosurgical pathology, the most common cause of death and disability in the adult population under the age of 45 years.

Highlight open(the cranial cavity communicates with the external environment) and closed(without violating the integrity of the skin of the head; with soft tissue wounds without damage to the aponeurosis; fractures of the bones of the calvarium, which are not accompanied by injury to the adjacent soft tissues and aponeurosis) TBI.

Closed TBI

A. GM concussion

b. GM injury
V. GM compression

Based on severity, closed TBIs are divided into:

a) mild: loss of consciousness (primary coma) 5-10 minutes

b) moderate degree: loss of consciousness 15-25 minutes

c) severe: loss of consciousness for more than 30 minutes

In addition, when determining the degree of severity, the presence of fractures, hemorrhages, focal injuries, and stem symptoms are taken into account.

Conventionally, it is possible to distribute various types of closed TBI according to severity:

1. Mild TBI:

a) concussion;

b) mild brain contusion;

2. Moderate TBI:

a) moderate brain contusion;

b) subacute and chronic compression of the brain;

3. Severe TBI:

a) severe brain contusion;

b) diffuse axonal damage to the brain;

c) acute compression of the brain;

d) compression of the head

Brain contusion.

Brain contusion differs from concussion by macroscopically detectable areas of damage to the brain matter.

Bruises are often accompanied by subarachnoid hemorrhages, fractures of the bones of the vault and base of the skull. Local and generalized cerebral edema is observed. Most often, the convex surface of the brain hemispheres is damaged, thereby compromising the integrity of the brain tissue. The damaged area has a yellowish color, in places there are foci of hemorrhage and softening, covered with intact membranes of the brain.

Mild bruises are characterized by the presence of local edema, moderate bruises are characterized by extensive areas of hemorrhagic impregnation, and severe bruises are characterized by decomposition of areas of the brain and the formation of brain detritus.

GM contusion can be limited or widespread.

Clinic: focal + cerebral symptoms, which depend on the location, size and severity of the injury

a) contusion of the frontal lobe: paresis and paralysis of the limbs (usually mono-); motor aphasia; violation of combined head and eye rotation; frontal psyche; grasp reflexes

b) bruise of the parietal lobe: sensitivity disorders, body diagrams; apraxia; asteroagnosia (loss of the ability to recognize objects by touch)

c) contusion of the temporal lobe: sensory or amnestic aphasia

d) contusion of the occipital lobe: visual disturbances (hemianopsia, visual agnosia)

e) contusion of the base of the brain: disorders of consciousness, breathing, cardiac activity, thermoregulation

f) contusion of the brain stem: respiratory and cardiac disorders

General cerebral symptoms are caused by a concussion (see concussion clinic).

Treatment: see question 110.

Compression of the brain.

Compression of the brain can cause:

ü intracranial hematomas (epidural, subdural, intracerebral, intraventricular, multiple);

ü depressed fractures of the bones of the cranial vault;

ü areas of crush injury with perifocal edema;

ü subdural hygromas;

ü pneumocephalus.

Clinic: compression of the brain, regardless of the cause, is characterized by a steady increase in general cerebral and focal symptoms; a period of imaginary well-being is characteristic (the time between the injury and the first signs of intracranial hypertension), which lasts minutes, the patient’s condition at this time is satisfactory; the light gap may be expanded, erased or absent; after a light interval, the degree of consciousness disorder increases, contralateral hemiparesis, bradycardia and dyspnea, anisocoria with mydriasis on the side of the hematoma, attacks of Jacksonian epilepsy in the opposite limbs, signs of congestion in the fundus.

Suspicion of an intracranial traumatic hematoma is the basis for urgent magnetic resonance imaging or computed tomography, and in their absence, carotid angiography.

Treatment: if an intracranial hematoma is identified as the cause of compression of the brain, emergency surgery (osteoplastic or resection craniotomy) is indicated.

For subdural hematomas In the trepanation window, a bluish, tense, non-pulsating dura mater is visible. It is opened and blood and clots are removed from the subdural space, then hemostasis is performed, the dura mater is sutured and a bone flap is placed, after which the skull is restored. Drainage is left in the wound for a day.

For intracerebral hematomas trephination of the skull with dissection of the brain substance and emptying of the hematoma is indicated.

The rest of the treatment – ​​see question 110.

Brain concussion.

GM Concussion– traumatic injury, characterized by symptoms of diffuse brain damage with a predominance of brainstem syndrome in the acute period.

A concussion is based on a mechanical impact (impact), causing a change in the physicochemical properties of brain tissue, the functional state of membranes and swelling of synapses, which leads to disruption of communication between neurons. Characteristic changes in the tone of the vascular walls contribute to the leakage of plasma into the intercellular space.

Clinic: characterized by the presence of general cerebral symptoms in the absence of focal

a) mild concussion: short-term loss of consciousness (5-10 minutes), after which the patient comes to his senses; general condition quickly normalizes; patients complain of general weakness, dizziness, noise in the head, slight headache, and sometimes vomiting; usually these phenomena disappear within the first week

b) moderate concussion of the brain: loss of consciousness for 15-25 minutes; bradycardia; vomit; retrograde amnesia; decreased periosteal and tendon reflexes; pale skin; superficial tachypnea; dizziness and headache

c) severe concussion: loss of consciousness for more than 30 minutes; coma; brady- or tachycardia; the pharyngeal reflex is absent; all tendon and periosteal reflexes are suppressed; urinary and fecal incontinence; retrograde amnesia; headache; nystagmus; dizziness; sleep disorders; At first the patient is inhibited, stunned, then irritable, hot-tempered, touchy, and tearful.

Providing first aid for TBI:

1. At the scene of the incident: place the patient on his side; eliminate tongue retraction; clear the upper airways

2. First aid: clear the airways of blood, mucus, vomit; stop the bleeding; if blood pressure drops - hydrocortisone; for fractures - splints, analgesics

3. Emergency room: upper airway suction, airway, intubation or tracheostomy

Treatment of TBI:

1. Bed rest

2. Analgesics (citramon, sedalgin, pentalgin, in severe cases - promedol), sedatives and hypnotics (seduxen, elenium).

NB! Sedatives and antipsychotics are contraindicated in cases of suspected intracranial hematoma.

3. Diuretics to combat cerebral edema (furosemide, mannitol)

4. Sodium hydroxybutyrate to increase brain resistance to hypoxia

5. Prevention of bleeding (vicasol, aminocaproic acid)

6. For low cerebrospinal fluid pressure, use endolumbar saline solution.

7. Antibiotic therapy for the prevention of infectious complications

8. In the recovery period – resorption therapy (aloe, FIBS, vitreous)

Penza State University

medical school

department of technical and electrical engineering

course "Extreme and military medicine"

Traumatic brain injury

Penza 2003

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

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

Classification of traumatic brain injuryTable 1.

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

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

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

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

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

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

Dizziness. Instability in the Romberg pose.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Additional research methods

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

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

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

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

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

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

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

Rice.2

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

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

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

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

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

The manipulation is performed with the patient lying on his side, on a hard table with his legs bent towards the stomach. The back is bent as much as possible. The place for puncture is the space between the III and IV lumbar vertebrae. Treat the skin with iodine tincture, then with alcohol until traces of iodine disappear, the entry of which into the lumbar canal is extremely undesirable. The puncture site is anesthetized with a 1% novocaine solution in an amount of 5-10 ml. The puncture is performed with a special needle with a mandrel, directing its course strictly sagittally and at an angle to the frontal plane. The angle corresponds to the inclination of the spinous processes. The sensation of needle failure usually corresponds to the needle being in the subarachnoid space. When removed from the mandrin needle, cerebrospinal fluid begins to flow out. The pressure is measured with a manometer, and then 2 ml of cerebrospinal fluid is taken for examination. In case of high blood pressure, the cerebrospinal fluid should be slowly released by drip 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 in return produced mainly by the choroid plexuses of the ventricles.

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

CLINICAL AND DIAGNOSTICS OF INDIVIDUAL

NOSOLOGICAL FORMS OF CRANIOBRAININJURIES

Brain concussion

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

Nystagmus, slight asymmetry of the face may appear due to the smoothness of the nasolabial fold and drooping of the corner of the mouth, deviation of the tongue. These and other local “microsymptoms” usually occur within 1-2 days. Longer persistence of these signs indicates the presence of a brain contusion.

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

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

Brain contusion

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

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

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

There are three degrees of brain contusions.

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

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

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

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

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

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

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

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

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

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

BRAIN COMPRESSION

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

Compression of the brain by bone fragments and foreign bodies

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

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

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

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

Compression of the brain by intracranial hematomas

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

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

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

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

What determines the duration of the light interval?

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

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

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

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

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

Epidural hematomas

Epidural hematoma - This is a limited accumulation of blood between the bones of the skull and the dura mater of the brain. Suprathecal hemorrhages occur as a result of a 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 epidural hematoma formation most often is 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 and is fused with them along the suture lines, therefore the area of ​​epidural hematomas is limited and most often is 6-8 cm in diameter.

Suprathecal hematomas usually have a hemispherical shape with a height in the central part of up to 4 cm. The amount of blood poured into the epidural space is 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.

The history reveals the presence of a head injury, accompanied by loss of consciousness. Upon return of consciousness, only general cerebral symptoms are found in the patient.

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

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

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

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

During the inhibition stage, the patient's behavior changes radically. He no longer rages or asks for anything. A secondary disorder of consciousness occurs, beginning with stupor and progressing to stupor. The victim is indifferent to his surroundings, his gaze is pointlessly directed into the distance. Bradycardia (41-50 beats/min.) and tachypnea (31-40 breaths per minute) increase. Asymmetry in blood pressure appears. On the arm opposite to the lesion, blood pressure will be 15-20 mmHg. higher than on the arm on the side of the hematoma. Focal symptoms increase. Among them, the main diagnostic role is played by: dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, abnormal grins, deviation of the tongue, spastic hemiparesis with a predominant lesion of the arm on the opposite half of the body. Meningeal signs are identified in the form of stiff neck and positive Kernig and Brudzinski signs.

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

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

An ophthalmological examination reveals congestion in the fundus.

Subdural hematomas

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

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

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

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

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

Subdural hygroma

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

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

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

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

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

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

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

Intracerebral hematomas

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

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

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

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

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

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

Intraventricular hematomas

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

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

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

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

Neurological symptoms with intraventricular hematomas are usually bilateral.

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

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

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

Subarachnoid hemorrhage.

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

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

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

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

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

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

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

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

SKULL FRACTURES

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

Fractures of the base of the skull

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

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

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

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

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

In case of a fracture of the middle cranial fossa, characteristic signs should be considered a bruise in the posterior wall of the pharynx and liquorrhea from the ear canals.

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 region. It should be noted that all bruises from a fracture of the base of the skull appear, as well as the symptom of “glasses”, no earlier than 12-24 hours from the moment of injury. The clinic is the leader in diagnosing fractures of the base of the skull, since primary radiographs in standard settings can detect bone damage in only 8-9% of 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 places of the base of the skull. For reliable diagnosis, special techniques are required, which cannot always be used due to the severity of the patient’s condition.

Cranial vault fractures

Cranial vault fractures result from a direct mechanism of injury, where the point of application of force and the site of injury coincide. An indirect mechanism is also possible when the skull, which has a spherical shape, is compressed; the fracture occurs at the point of intersection of the force lines with an extreme load, and not in the pressure zone.

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

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

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

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

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

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

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

Linear fractures have a number of distinctive features:

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

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

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

Sometimes, along with cracks, seams come apart.

Treatment of patients with traumatic brain injury

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

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

Providing assistance at the prehospital stage is as follows:

Place the patient in a horizontal position. Create peace of mind with the means at hand: pillow, bolsters, clothes.

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

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

Cold to the head.

Give oxygen inhalation.

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

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

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

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

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

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

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

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

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

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

5. Antihistamines(diphenhydramine, fenkarol, diazolin).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Mechanisms of traumatic brain injury.

Classification of traumatic brain injury.

Name the general cerebral symptoms.

Name local symptoms.

Name meningeal symptoms.

Name the stem symptoms.

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

How is a concussion diagnosed?

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

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

Causes of compression of the brain.

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

Clinic of brain compression by intracerebral and intraventricular hematomas.

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

What is a subdural hygroma?

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

Clinic of subarachnoid hemorrhage.

Fracture of the base of the skull, diagnosis.

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

Fractures of the cranial vault, diagnosis, tactics.

First aid for traumatic brain injuries.

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

Conservative treatment of brain damage during the recovery period.

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

Techniques of various types of trepanations, necessary instruments.

What is post-trepanation syndrome, its treatment.

Outcomes and long-term consequences of TBI.