Traumatic brain injury: classification, symptoms and treatment. Closed craniocerebral injury

Traumatic brain injury - mechanical damage to the skull and (or) intracranial formations (brain, meninges, blood vessels, cranial nerves). It accounts for 25-30% of all injuries, and among deaths due to injuries, its share reaches 50-60%. As the cause of death of persons of young and middle age Ch. t. ahead of cardiovascular and oncological diseases.

Traumatic brain injury is divided into 3 stages according to severity: mild, moderate and severe. To easy Ch. t. include concussion and mild brain contusions; to moderate severity - bruises of the brain of an average degree; to severe - severe brain contusions, diffuse axonal damage and compression of the brain.

The main clinical forms of traumatic brain injury are concussion, brain contusion (mild, moderate and severe), diffuse axonal brain injury and brain compression.

Brain concussion observed in 60-70% of the victims. Light diffuse craniocerebral injury, characterized by impaired consciousness. Although the short-term nature of this disruption is often pointed out, there is no clear agreement on its duration. Usually there is no macro- and microscopic damage to the medulla. There are no changes on CT and MRI. It is also believed that loss of consciousness is not mandatory. Possible changes in consciousness: confusion, amnesia (the main symptom of CGM) or complete loss of consciousness. After the restoration of consciousness, complaints of headache, dizziness, nausea, weakness, tinnitus, flushing of the face, sweating are possible. Other autonomic symptoms and sleep disturbance. The general condition of patients improves rapidly during the 1st, less often the 2nd week. after injury.

Contusion (contusion) of the brain. Distinguish brain bruises mild, moderate and severe.

Mild brain injury it is noted at 10 — 15% of patients with H. - m. m. It is characterized by impaired consciousness after injury, the duration is possible up to several minutes. After recovery of consciousness, complaints of headache, dizziness, nausea, etc. are typical. Neurological symptoms are usually mild (nystagmus, signs of mild pyramidal insufficiency in the form of reflex paresis in the extremities, meningeal symptoms), often regressing for 2-3 weeks. after injury. The treatment is conservative, it is initially mandatory in the stationary conditions of the neurosurgical department.

Moderate brain injury observed in 8-10% of victims. It is characterized by loss of consciousness after an injury lasting from several tens of minutes to several hours. Amnesia is expressed (retro-, con-, anterograde). The headache is often severe. There may be repeated vomiting. Sometimes there are mental disorders. Focal symptoms are clearly manifested, the nature of which is due to the localization of the brain contusion; pupillary and oculomotor disorders, paresis of the extremities, disorders of sensitivity, speech, etc. These symptoms gradually (within 3-5 weeks) smooth out, but can also last for a long time. Treatment, in most cases, is conservative in the neurosurgical department. In some cases, the course of this type of injury is complicated by the appearance of secondary hemorrhages and even the formation of an intracerebral hematoma, when surgical assistance may be required.

Severe brain injury observed in 5-7% of victims. It is characterized by a loss of consciousness after an injury lasting from a day to several weeks. This type of injury is especially dangerous because it is manifested by a violation of the brain stem functions, there are severe violations of vital functions - respiration and systemic hemodynamics. The patient is admitted to the intensive care unit. Treatment is collegially handled by a neuroresuscitator and a neurosurgeon. Cerebral and focal symptoms regress slowly. Racks of residual phenomena in the form of mental disorders, motor deficits are characteristic.

In the case of the formation of an intracerebral hematoma, which is the cause of compression of the brain, surgical treatment is indicated - craniotomy, removal of the hematoma.

Intracerebral hematoma of the right temporal lobe.

Diffuse axonal brain injury characterized by a prolonged (up to 2-3 weeks) coma, pronounced stem symptoms (paresis of upward gaze, eye separation along the vertical axis, bilateral inhibition or loss of pupillary light reaction, impaired or absent oculocephalic reflex, etc.). Often there are violations of the frequency and rhythm of breathing, hemodynamic instability. A characteristic feature of the clinical course of diffuse axonal damage is the transition from a prolonged coma to a persistent or transient vegetative state, the onset of which is evidenced by the appearance of a previously absent opening of the eyes spontaneously or in response to various stimuli. At the same time, there are no signs of tracking, fixing the gaze, or following at least elementary instructions (this condition is called apallic syndrome). The vegetative state in such patients lasts from several days to several months and is characterized by functional and/or anatomical dissociation of the cerebral hemispheres and the brain stem. As the vegetative state emerges, the neurological symptoms of dissociation are replaced predominantly by symptoms of prolapse. Among them, the extrapyramidal syndrome dominates with severe muscle stiffness, discoordination, bradykinesia, oligophasia, hypomimia, minor hyperkinesis, and ataxia. At the same time, mental disorders are clearly manifested: pronounced aspontaneity (indifference to the environment, untidiness in bed, lack of any urge to any activity), amnestic confusion, dementia, etc. At the same time, gross affective disorders are observed in the form of anger, aggressiveness.

CT scan with diffuse-axonal brain damage (diffuse edema, many small hemorrhages).

The treatment of this type of injury is carried out conservatively with the participation of a neuroresuscitator, a neurosurgeon, a doctor and an exercise therapy instructor (early motor rehabilitation is carried out in order to prevent the formation of contractures in the joints).

Compression (compression) of the brain observed in 3-5% of victims. It is characterized by an increase in a certain period of time after an injury or immediately after it of cerebral symptoms (appearance or deepening of impaired consciousness, increased headache, repeated vomiting, psychomotor agitation, etc.), focal (appearance or deepening of hemiparesis, focal epileptic seizures, and etc.) and stem symptoms (the appearance or deepening of bradycardia, increased blood pressure, upward gaze restriction, tonic spontaneous nystagmus, bilateral pathological signs, etc.).

Among the causes of compression in the first place are intracranial hematomas (epidural, subdural, intracerebral, intraventricular). The cause of compression of the brain can also be depressed fractures of the bones of the skull, foci of crushing of the brain, subdural hygromas, pneumocephalus.

epidural hematoma on a computed tomogram, it looks like a biconvex, less often plano-convex zone of increased density adjacent to the cranial vault. The hematoma is limited and, as a rule, is localized within one or two lobes.

Epidural hematoma of the posterior cranial fossa.

Treatment of acute epidural hematomas.

Conservative treatment:

Epidural hematoma with a volume of less than 30 cm3, a thickness of less than 15 mm, with a displacement of the median structures of less than 5 mm in patients with a GCS level of consciousness of more than 8 points and the absence of focal neurological symptoms. Clinical control is carried out within 72 hours with a frequency of every 3 hours.

Surgical treatment

1. Emergency surgery

acute epidural hematoma in a patient in a coma (less than 9 GCS points) in the presence of anisocoria.

2. Urgent surgery

epidural hematoma more than 30 cm3, regardless of the degree of depression of consciousness according to the GCS. In some cases, with a slight excess of the specified volume of epidural hematoma and a completely compensated state of the victim with no symptoms, conservative tactics with dynamic CT control of the situation are acceptable.

Absolute indications for surgical treatment for injuries of the posterior cranial fossa are epidural hematomas > 25 cm3, cerebellar lesions of lateral localization > 20 cm3, occlusive hydrocephalus, lateral dislocation of the IV ventricle

Operation methods:

2. Osteoplastic trepanation

For subdural hematoma on a computed tomogram, the presence of a crescent-shaped zone of altered density of plano-convex, biconvex, or irregular shape is more often characteristic.

subdural hematoma.

Treatment of acute subdural hematomas.

Surgical treatment

1. In acute subdural hematoma >10 mm thick or displacement of median structures >5 mm, regardless of the patient's neurological status according to the GCS.

2. Injured in a coma with subdural hematoma thick< 10 мм и смещением срединных структур < 5 мм, если наблюдается ухудшение неврологического статуса в динамике - нарастание глубины комы, появление стволовой симптоматики. У пострадавших с острой субдуральной гематомой, при наличии показаний к операции, хирургическое вмешательство должно быть выполнено в экстренном порядке. Удаление острой субдуральной гематомы осуществляется путем краниотомии в большинстве случаев с удалением костного лоскута и пластикой твердой мозговой

Treatment of depressed skull fractures.

Surgical treatment is indicated in the presence of signs of damage to the dura mater (DM), significant intracranial hematoma, depression more than 1 cm, involvement of the airways, cosmetic defect.

Principles of surgical treatment..

early surgical intervention is recommended to reduce the risk of infection; elimination of depression and surgical treatment of the wound are the main elements of the operation. In the absence of wound infection, primary bone grafting is possible.

Comminuted fracture of the skull bones with depression in the cranial cavity.

Forecast at easy Ch. m. (concussion, mild brain contusion) is usually favorable (subject to the recommended regimen and treatment for the victim).

With a moderate injury (medium-degree brain contusion), it is often possible to achieve a complete restoration of the labor and social activity of the victims. A number of patients develop leptomeningitis and hydrocephalus, which cause asthenia, headaches, vegetovascular dysfunction, disturbances in statics, coordination, and other neurological symptoms.

In severe trauma (severe brain contusion, diffuse axonal damage, brain compression), mortality reaches 30-50%. Among the survivors, disability is significant, the leading causes of which are mental disorders, epileptic seizures, gross motor and speech disorders. At open Ch. t. inflammatory complications (meningitis, encephalitis, ventriculitis, brain abscesses), as well as liquorrhea, may occur.

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

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

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

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

Principles of classification of traumatic brain injury

According to biomechanics, the following types of TBI are distinguished

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

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

By type of damage

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

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

According to the genesis of the injury

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

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

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

By type of TBI

According to the type of traumatic brain injury, they are usually divided into:

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

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

Isolated appearance - the presence of extracranial lesions is not characteristic.
Combined type - characterized by the presence of damage of the extracranial type, as a result of mechanical influence.
Combined view - it is characterized by the combination of various types of damage (mechanical, radiation or chemical, thermal).

The nature

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

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

According to the mechanism of occurrence of TBI

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

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

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

The following clinical forms of TBI are distinguished

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

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

The course of each of the listed forms of TBI has acute, intermediate and remote periods. In time, each of the periods lasts differently, it all depends on the severity and type of injury. For example, the acute period can last from 2 to 10-12 weeks, while the intermediate period can last up to six months, and the remote period can last up to several years.

Brain concussion

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

Diagnosis

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

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

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

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

As you know, a concussion is not inherent in fractures of the bones of the skull. At the same time, the index of craniocerebral pressure, as well as the biochemical composition of the cerebrospinal fluid, remain unchanged. CT or MRI is considered an accurate diagnostic method, but does not reveal intracranial spaces.

Clinical picture

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

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

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

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

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

Treatment

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

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

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

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

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

Forecast

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

Mild brain injury

Diagnostics

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

Clinical picture

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

Loss of consciousness may continue for the next 30 minutes. In some cases, the duration of this state reaches several hours. At the same time, congrade, retrograde or anterograde types of amnesia have a special severity. The patient is not excluded severe vomiting and headache. In some cases, there may be a violation of important vital functions.

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

Other possible symptoms include:

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

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

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

Moderate brain injury

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

Diagnosis

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

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

Clinical picture

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

Vomiting may occur periodically with repetitions. At the same time, all vital functions are preserved. Very often, tachycardia and bradycardia occur in victims, and blood pressure can sometimes be elevated. As for breathing, it remains unchanged, as well as body temperature, which remains normal. Individual symptoms of a neurological nature may regress after 2 weeks.

Severe brain injury

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

In this case, the following disorders of the vital functions of a person can be noted:

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

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

Among other things, symptoms of oral automatism, as well as paresis and focal epileptic seizures, can be expressed. It will be extremely difficult to restore the shaken functions. Very often, after recovery, patients experience residual disorders in the motor apparatus and there may be obvious mental disorders.

With a severe brain injury, the patient's condition is considered critical. For a person, a coma is inherent, lasting from several hours to several days. The patient may be in a state of psychomotor agitation, alternating with a depressed mood.

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

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

Often severe bruises lead to death.

Diagnostics

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

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

Diffuse axonal brain injury

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

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

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

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

Diagnosis

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

Brain compression

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

Diagnosis

With the help of CT, a biconvex or flat-convex limited zone can be detected, which is characterized by increased density, adjacent to the cranial vault or located within the boundaries of one or even two lobes. If several sources of bleeding were identified, then the zone of increased density can become even larger, differing in its crescent shape.

Treatment of traumatic brain injury

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

inspection;
skull x-ray;
Ultrasound of the chest and abdomen;
laboratory research;
urine tests and consultations with various specialists.

Checkup for TBI

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

skull x-ray

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

Laboratory research

Laboratory tests include a complete blood count and urine test, a biochemical blood test, a blood sugar test, and an electrolyte test. In the future, such laboratory studies should be carried out regularly.

Additional diagnostic measures

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

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

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

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

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

Post-treatment therapy

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

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

Speaking about the methods of nutrition, two of the most common should be distinguished: enteral and parenteral. In order to stop epileptic seizures, anticonvulsants are prescribed with a minimum dosage. These drugs include, for example, levetiracetam and valproate.

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

Prognosis for traumatic brain injury

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

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

The content of the article

Closed injuries of the skull and brain

In all developed countries of the world over the past decades, both in peacetime and in wartime, injuries have been steadily increasing and, accordingly, the number of traumatic brain injury.

Classification of traumatic brain injury

The existing numerous classifications of traumatic brain injury are based mainly on the classification of Petit, who in 1774 identified three main forms of these injuries - commotio (concussion), contusio (bruise) and compressio cerebri (brain compression). All craniocerebral injuries are divided into two main groups.
1. Closed skull injuries and the brain, which include all types of trauma while maintaining the integrity of the skin or injuring the soft tissues of the skull, but without damaging its bones. Under these conditions (if we exclude fractures of the paranasal sinuses and ear), the possibility of infection of the dura mater, cerebrospinal fluid spaces and the brain is small.
2. Open damage, which should be considered as primary bacterially contaminated.
In clinical conditions, with a high degree of conditionality, three main types of closed craniocerebral injury can be distinguished:
1) concussion as the mildest brain injury;
2) brain contusion of moderate severity with the presence of cerebral and focal hemispheric symptoms, often with stem disorders of a non-vital degree;
3) severe craniocerebral injury, in which a prolonged loss of consciousness comes to the fore, with life-threatening symptoms of damage to the trunk and subcortical formations; at the same time, in approximately 60% of the damaged brain contusion is combined with its “pressure, primarily due to intracranial hematomas. A more detailed classification of a closed craniocerebral injury is presented in Scheme No. 1.

Concussion and brain injury

Pathogenesis.
The starting point of all pathophysiological processes in traumatic brain injury is, of course, the action of a mechanical factor. Features of damage to the intracranial contents are determined by two main conditions: the nature of the impact of the traumatic agent and the complexity of the intracranial topography. In this case, first of all, the magnitude, direction and area of application of the mechanical factor are taken into account.

Concussion (commotio cerebri)

This is a traumatic injury, characterized by symptoms of diffuse brain damage with a predominance of stem disorders in the acute period. A concussion is observed in almost all cases of a closed craniocerebral injury, and against its background, symptoms of contusion and compression of the brain may appear. Widespread dystrophic changes in nerve cells (in the form of central chromatolysis) and nerve fibers are considered as primary damage to brain tissue during concussion. Dyscirculatory disorders can exacerbate the primary damage to neurons.
Intracranial hemorrhages occur, apparently, in all or in most cases in which the symptoms of a closed craniocerebral injury are clinically clearly manifested.
Typical localization of paraventricular petechial hemorrhages is at the border of the transition of the wide part of the ventricles to the narrow one - and vice versa, namely, at the level of Monro's holes, in the caudal sections of the III ventricle when it passes into the Sylvian aqueduct and in the oral sections of the IV ventricle at the border of the midbrain and the brain bridge . These hemorrhages occur regardless of the point of application of the blow to the skull and are called Dure hemorrhages.
Recent observations indicate the importance of neurohumoral changes in the pathogenesis of vasomotor disorders resulting from the direct impact of trauma or cerebrospinal fluid shock on the central humoral mechanisms of mediator metabolism disorders with the release of free acetylcholine into the cerebrospinal fluid. Traumatic brain injury causes a complex set of morphological and functional disorders that affect each other, which is especially pronounced in severe cases.

Clinic of concussions and bruises of the brain

A mild degree of concussion, observed in most cases, is characterized by a short-term loss of consciousness for several seconds or minutes, nausea, vomiting, headache, followed by a satisfactory condition of the patient, the disappearance of complaints during the first week, the absence or slight severity of objective symptoms, the absence of residual phenomena. With an average degree of concussion, after a short or longer loss of consciousness, neurogenic and psychogenic symptoms appear; it is possible that in this case there is a combination of concussion with a bruise of those parts of it, damage to which in the acute stage of the disease can manifest itself only with the symptoms observed during concussion.
In severe forms of craniocerebral injury, when reversible or irreversible damage to vital functions is observed, along with concussion, bruises are detected (in particular, the basal parts of the hypothalamic-pituitary and stem regions), therefore, in such cases, the term "severe craniocerebral injury" is used. trauma”, and not “severe concussion”, thus emphasizing that in these cases concussion and brain contusion are combined. The group "severe craniocerebral injury" also includes cases of a combination of concussion and brain contusion with massive intracranial hematomas.
With a mild degree of concussion against the background of a relatively short-term loss of consciousness, pallor of the skin, hypotension or atony of the muscles of the extremities, a decrease in the reaction of the pupils to light, a slowdown or increase in the pulse with insufficient tension are noted. There is often vomiting. With an average degree of concussion after the stage of turning off consciousness, various forms of its disintegration, retrograde amnesia, adynamia, asthenia, headache, dizziness, nausea, vomiting, spontaneous nystagmus, autonomic disorders, cardiovascular disorders, etc. are observed. brain injury is covered below in the Treatment of Concussion and Brain Contusion section.
The main symptom of a concussion is loss of consciousness. With a combination of concussion and brain contusion, all intermediate phases can be observed between short-term, complete or partial switching off of consciousness to a coma. The duration and severity of unconsciousness are the most important prognostic signs. If it is reliably known that the duration of the unconscious state exceeded 4-5 minutes, then such an injury cannot be regarded as light. An important test that helps to assess the depth of impaired consciousness is the study of the pharyngeal reflex. Violation of the act of swallowing with the ingress of liquid into the respiratory tract against the background of other stem symptoms is extremely unfavorable for the prognosis.
A bad prognostic sign is an increase in breathing up to 35-40 per minute, especially if the correct rhythm of breathing is disturbed and it becomes wheezing. Cheyne-Stokes respiration indicates a severe lesion of the brain stem.

Subarachnodial hemorrhages

Subarachnodial hemorrhages are often observed with a closed craniocerebral injury. Even when the clinical process proceeds as a mild degree of concussion, it is often possible to detect a small admixture of fresh blood in the cerebrospinal fluid. With subarachnoid hemorrhage in cases of moderate craniocerebral injury, the phenomena of psychomotor arousal of varying intensity come to the fore. Patients complain of intense pain, which sometimes has basal-shell features with localization in the supraorbital and occipital regions, photophobia, difficulty in moving the eyeballs, pain and discomfort in them. Vasomotor lability and other autonomic disorders are sufficiently pronounced.
If the amount of blood in the cerebrospinal fluid is significant, then it tends to gradually descend into the lower sections of the spinal canal, which leads to the occurrence of lumbosacral radicular pain syndrome. Meningeal symptoms are pronounced and usually increase during the first days after the injury.
With subarachnoid hemorrhages, either subfebrile temperature is observed, or its increase to 38-39 ° C during the first week after injury, followed by gradual normalization. The blood shows leukocytosis with a slight shift to the left. Critical to the diagnosis of subarachnoid hemorrhage is the presence of blood in the cerebrospinal fluid. With an increase in the severity of the injury, the frequency of detection of subarachnoid hemorrhage and, to some extent, the quantitative admixture of blood to the fluid, usually increase. It should be noted that if subarachnoid hemorrhage is suspected, spinal puncture is indicated. In cases where the clinic gives indications of the possibility of brain dislocation, puncture is contraindicated due to the possibility of increasing this dislocation.

Brain contusion (contusio cerebri)

Brain contusion (contusio cerebri) is a traumatic injury to the brain tissue. Crushing of the brain tissue is the most severe degree of its damage and is characterized by gross destruction of the tissue with rupture of the meninges, the release of brain detritus to the surface, rupture of blood vessels and outpouring of blood into the subarachnoid space. In this case, hematomas of various sizes are formed, which in turn entails further destruction of the brain tissue, its deformation, expansion and displacement. Usually, the brain crush is localized in the area of head contusion, especially often in the presence of depressed fractures and tearing of the dura mater. Characterized by localization of crushing by the type of counterblow (contre coup) in the basal regions of the frontal lobes, pole and basal regions of the temporal lobes.
Brain injuries of the type of counterblow can be the result of a bruise on the bony irregularities of the skull located far from the place of direct application of force, skull deformity, bruising on the processes of the dura mater, the formation of a vacuum, complex rotational movements of the brain.
Of particular importance are contusion foci in the brain stem, located both on its outer surface and paraventricularly. Contusion foci on the outer surface of the brain stem are found in more than 1/3 of cases of traumatic brain injury ending in death. They are observed when a traumatic force is applied to different parts of the cranial vault. In relation to the point of application of this force, contusion foci in the trunk are shockproof and arise as a result of the impact of the trunk on the Blumenbach slope, the bone edge of the foramen magnum and the sharp edge of the cerebellar tenon at the time of displacement and deformation of the brain.

Brain Injury Clinic

Symptoms of contusion of the cerebral hemispheres with a closed craniocerebral injury are much less pronounced and more reversible than with penetrating injuries. In a complex clinical picture, when symptoms and syndromes of concussion, bruise and compression of the brain are closely intertwined, it is necessary to single out local signs of bruising or compression, which is of great practical importance. Symptoms that depend on concussion tend to disappear quickly over the next few days after the injury, while symptoms of brain contusion remain constant or progress from the 2-3rd day after the injury, and their regression begins no earlier than from the 2nd week after injury. The symptomatology of a brain contusion and its dynamics are determined by the nature of the main lesion and perifocal phenomena, depending on the violation of blood and blood circulation. When the contusion focus is located in the functionally significant parts of the brain, persistent phenomena of prolapse usually remain. Perifocal phenomena are characterized by a later development and increase in symptoms, as well as their early and complete regression in the recovery stage. Focal epileptic seizures, especially of the Jacksonian type, in the acute period of brain contusion with a closed injury are relatively rare and almost always indicate the presence of a local hematoma to be removed. In the late period after injury, these seizures are common.
Contusion of the basal parts of the brain (hypothalamic-pituitary region and trunk) is clinically manifested by prolonged loss of consciousness and severe neurovegetative syndrome, the main components of which are respiratory, cardiovascular and thermoregulation disorders, metabolic, humoral and endocrine disorders.

Treatment for concussion and brain injury

With mild and moderate degrees of closed craniocerebral injury in the acute period, the following therapeutic measures are appropriate. 1. Bed rest for 10-20 days, depending on the course of the disease.
2. Symptomatic treatment of headache (analgesics orally or intramuscularly), dizziness, nausea (platifillin, bellaspon), repeated vomiting (chlorpromazine, diprazine - pipolfen, atropine) and insomnia (hypnotics).
3. Appointment for motor or psychomotor agitation of hypnotics, tranquilizers, neuroleptics (phenobarbital, eunoctin, seduxen, elenium, levomepromazine, chlorpromazine). In case of pronounced arousal, short-acting barbituric acid preparations (hexenal, petotal) are indicated; at the same time, a short narcotic sleep can be extended by 6-12 hours with hypnotics (barbamil, phenobarbital). Sedative, narcotic and neuroleptic drugs are contraindicated in cases of suspected intracranial hematoma.
4. Dehydration therapy - glucocorticoids (prednisolone, etc.), glycerol, diuretics - lasix, uregit, mannitol (to reduce intracranial and intracerebral pressure). In this case, it is necessary to take into account the relative short duration of the positive effect of most hypertonic solutions and the phenomenon of the subsequent rise in intracranial pressure above the initial one.
Therefore, drugs such as hypertonic solutions of glucose, sodium chloride, magnesium sulfate should not be used.
Dehydration therapy is not indicated for a decrease in intracranial pressure (hypotension), which is clinically detected by measuring the pressure of the cerebrospinal fluid and occurs in approximately 8-10% of cases of closed head injury.
5. Diagnostic lumbar puncture is contraindicated in the syndrome of a pronounced increase in intracranial pressure, especially if there is a suspicion of the possibility of brain dislocation.
Treatment with "unloading" spinal punctures is indicated for subarachnoid hemorrhages, when blood and its decay products accumulate in the lower parts of the spinal canal. After a 2-3-fold unloading puncture (remove 10-20 ml of liquid), the normalization of the composition of the cerebrospinal fluid is accelerated by increasing its production and resorption, which reduces the effects of acute aseptic meningitis and the risk of developing adhesive1 membrane process in the future.
6. Cervical vagosympathetic and lumbar novocaine blockades, less commonly used in the treatment of concussion.
7. Surgical intervention with the removal of bone fragments, indicated for depressed skull fractures. Sometimes there are indications for the early removal of foci of bruising or crushing of the brain, which contribute to increased cerebral edema and the development of its dislocation, in order to prevent these terrible complications.
In the later stages of the disease, with paresis or paralysis of the extremities as a result of a brain injury, physiotherapy and therapeutic exercises are indicated, and with aphasia, rehabilitation treatment under the supervision of a speech therapist. With the development of late traumatic epilepsy (Conservative treatment consists of anticonvulsant therapy, the appointment of dehydrating agents to reduce swelling and swelling of the brain, as well as general strengthening treatment. Sometimes pneumoencephalography is effective, which is performed to separate loose meningeal adhesions. In the absence of effect (conservative methods of treatment and the severity of symptomatic epilepsy, there may be indications for surgical intervention.With significantly pronounced residual effects of brain injury, the patient must be taught new professions, taking into account the remaining ability to work.
It is necessary to dwell in more detail on the treatment of severe forms of traumatic brain injury.
The most characteristic signs of an extremely severe traumatic brain injury are pronounced and prolonged disturbances of consciousness from soporous to transcendental coma in combination with progressive disorders of the so-called vital functions of the body, which are combined by the term "neurovegetative syndrome". The importance of pathological changes in the brain stem in extremely severe traumatic brain injury should be emphasized. There are two main causes of violation of vital functions in extremely severe traumatic brain injury associated with brain damage.
1. Primary and early damage to the trunk, diencephalic region and subcortical formations intimately associated with them, the morphological manifestation of which is vasodilation, perivascular hemorrhages, edema, chromatolysis and other changes in the cell nuclei and areas of softening.
2. Secondary damage to the trunk during the progression of intracranial hypertension, dislocation, cerebral edema and cerebrovascular disorders, which most often occurs with an increase in intracranial hematomas and contusion foci in the brain.
The main components of neurovegetative syndrome in severe traumatic brain injury are:
a) respiratory failure of the central and peripheral (tracheobronchial obstruction) types, with the development of general hypoxia and local hypoxia of the brain;
b) cardiovascular disorders (hemodynamic disorders);
c) violations of thermoregulation;
d) metabolic, humoral and endocrine disorders (metabolic disorders).
Resuscitation measures for severe traumatic brain injury should begin in the ambulance, continue during transportation and in the hospital. The treatment complex is a consistent application of measures aimed at normalizing numerous disorders in the whole organism, on the one hand, and the impact on the processes unfolding in the cranial cavity, on the other, and primarily includes the following activities:
1) ensuring free airway patency using, if necessary, intubation and tracheostomy;
2) combating hypoxia and hypercapnia (or hypocapnia), ensuring adequate breathing, if necessary, a complete replacement of the respiratory function - artificial respiration;
3) the fight against concomitant shock and blood loss, with the obligatory replenishment of the volume of circulating blood to the proper degree to create conditions for normal hemodynamics.
It should be noted that among those who died from traumatic brain injury in 14% of cases, the direct cause of death is the aspiration of blood and vomit, and in another 26% these factors additionally play an important role in the outcome of the disease) . All this emphasizes the importance of the time factor in providing proper care for traumatic brain injury.
Hemodynamic disorders are manifested in a variety of deviations from the norm of frequency and rhythm, as well as heart contractions, as well as blood pressure and peripheral blood flow. In addition to damage to the brain centers, concomitant traumatic shock and blood loss can be the causes of hemodynamic disturbances.
If a patient who is taken to a hospital, 20-30 minutes after a craniocerebral injury, shows a clinical picture of shock with a sharp decrease in blood pressure, then this usually indicates a combination of trauma to the brain and its membranes with one of the following damage:
1) extensive fracture of the bones of the vault or base of the skull;
2) severe bruises of the body;
3) compression of the chest with rib fractures (sometimes lung rupture and hematsiracooma);
4) fracture of the bones of the limbs or pelvis, in rare cases - the spine;
5) damage to internal organs with bleeding into the abdominal cavity.
In children, shock sometimes develops with an isolated craniocerebral injury with extensive subaponeurotic or epidural hematoma.
These additional injuries require urgent measures in the form of novocaine blockade and immobilization of limb fractures, or surgery in the abdominal or thoracic cavity. In other cases, treatment of traumatic brain injury and shock should be limited. If the cause of the state of shock lasting for hours is not clear, then especially careful observation of the surgeon is required in order to timely detect damage to internal organs. Regardless of their cause, shock and collapse sharply worsen the course of severe traumatic brain injury, are closely intertwined with the symptoms of stem lesions and require urgent therapeutic measures.
The elimination of acute circulatory disorders and shock symptoms is achieved by normalizing the volume of circulating blood by intravenous administration of a sufficient amount of blood, plasma, high-molecular solutions (polyglucin, syncole) and other blood-substituting fluids. Sometimes there are indications for intra-arterial blood transfusion.
Along with the introduction of fluid into the body during shock and collapse, analeptic drugs (cordiamin, etc.) should also be used that stimulate the central nervous system and can bring it out of a state of oppression, as well as adrenomimetic drugs (adrenaline, mezaton, ephedrine), which excite active adrenore systems and can quickly raise blood pressure. It should, however, be cautioned against the use of these drugs without the introduction of fluid into the body, because in this case, after a rapid increase in blood pressure, a catastrophic fall, often irreversible, usually develops.
Violations of thermoregulation in the form of central hyperthermia are observed in severe traumatic brain injury quite often. Often the cause of hyperthermia are inflammatory complications (pneumonia, meningitis), as well as metabolic disorders. Severe metabolic disorders are observed in all patients with a prolonged coma. They are manifested by disorders of water, electrolyte, protein, fat and carbohydrate metabolism and are the result of traumatic damage to higher autonomic centers located in the hypothalamic and stem parts of the brain, shock, impairment of the filtering ability of the kidneys as a result of circulatory failure or very low blood pressure, hypoxia, etc. .
Correction of metabolic disorders and energy balance is achieved:
1) correction of violations of acid-base balance (with respiratory forms of this disorder - the regulation of external respiration with the provision of normal ventilation of the lungs, with acidosis - the introduction of sodium bicarbonate, with alkalosis - the introduction of chlorine compounds "not containing sodium);
2) regulation of violations of ion: and protein balance (introduction of dry and native plasma, solutions of potassium chloride, calcium chloride, etc.);
3) hormonal therapy (administration of glucocorticoids in case of insufficiency of the adrenal cortex, confirmed by laboratory data, or in case of acute insufficiency of the hypothalamic-pituitary-adrenal system);
4) regulation of energy balance (parenteral and tube nutrition);
5) the introduction into the body of 2-3 liters of fluid per day, because the lack of fluid exacerbates metabolic disorders, and leads to even greater fluid retention in the tissues of the body;
6) the fight against cerebral edema and intracranial hypertension (moderate hardware hyperventilation, the introduction of hypertonic solutions, but strict indications of mannitol or urea);
7) measures aimed at increasing the resistance of the brain to hypoxia (long-term general moderate hypothermia (craniocerebral hypothermia, hyperbaric oxygenation).
Attention should be paid to the fight against infectious and trophic complications (pneumonia, bedsores, thrombophlebitis, etc.).
In a number of cases, it is possible to isolate the predominant lesion of certain parts of the diencephalic-thiophyseal and stem regions of the brain and, depending on this, develop a differentiated treatment strategy.
With the most severe bruises of the brain, the following forms are distinguished:
1) diencephalic-estrapyramidal, which develops in the case of primary and secondary lesions of the diencephalic parts of the brain with relative preservation of the function of the trunk. Clinically, this form is manifested by loss of consciousness, a change in breathing according to the diencephalic type with its increase to 40-60 per minute (often with the presence of slow periodic changes in the amplitude of breathing), a persistent increase in vascular tone and blood pressure, a rise in temperature (often to hyperthermia); often this is accompanied by an extrapyramidal aindrome with an increase in muscle tone according to the plastic type, sometimes with the appearance of hyperkinesis;
2) mesencephalic-bulbar, which occurs with primary damage to the midbrain, pons and medulla oblongata (or in the case of a secondary lesion of these formations) and is clinically manifested by neurological signs of damage to the trunk, as well as respiratory and circulatory disorders of the mesencephalic-bulbar nature;
3) cerebrospinal, in which combined symptoms of damage to the trunk and adjacent parts of the spinal cord appear.
Depending on the clinical form of brain contusion, appropriate targeted therapy is prescribed. So, for example, diencephalic syndrome, especially (With the presence of hyperthermia, it is advisable to stop it in a timely manner, at the very first signs of its development, with the help of hibernation and physical cooling, which reduce the intensity of pathologically increased and perverted metabolism in the body and reduce elevated body temperature to 35-36 ° C. In the mesencephalic-bulbar form, the task of compensating for breathing with the help of mechanical ventilation, maintaining vascular tone, pharmacological stimulation of breathing and cardiac activity comes to the fore.
Brain compression. The most common causes of brain compression in blunt traumatic brain injury are intracranial hematomas, less often subdural hygromas; a smaller role is played by depressed skull fractures and edema - swelling of the brain.
Acute intracranial hematomas occur in approximately 2-4% of all cases of traumatic brain injury. The importance of timely diagnosis of intracranial hematomas should be emphasized, because all non-operated patients with intracranial hematomas of a significant volume die, while after removal of the hematoma, many recover. Lethal postoperative outcomes depend primarily on delayed diagnosis and surgery, as well as concomitant severe traumatic brain injury. Despite the use of modern methods of diagnosis and treatment, cases of delayed or erroneous diagnosis of acute intracranial hematomas of traumatic etiology are not uncommon (according to some authors, life-time diagnosis occurs in about 60% of victims, and in the rest, hematomas are detected at autopsy), and postoperative mortality among in patients operated on at a late stage of the disease or with a combination of hematoma with brain contusion in a deep coma, approaches 70-80% of cases. The progression of symptoms in patients with traumatic brain injury gives grounds to suspect, first of all, the formation of an intracranial hematoma.
Epidural hematomas account for about 20% of the total number of patients with intracranial hematomas. These hematomas are located between the dura mater and the bone, and upon reaching a significant volume, they cause a clinic of brain compression.

Epidural hematomas

Epidural hematomas in closed injuries are usually localized in the region of a skull fracture, most often its vault. Difficulties in diagnosing this complication are sometimes exacerbated by the fact that epidural hematomas are often observed in the absence of bone fractures or on the side opposite to the fracture.
There are three types of epidural hemorrhages:
1) from the branches of the meningeal arteries, most often from the middle artery;
2) from the veins of the outer surface of the dura mater and the veins of the diploe;
3) from the sinuses and veins going to the sinuses.
Damage to the middle meningeal artery usually occurs in the area of application of the injury and much less often in the area of the counterblow. Bleeding from the branches of this artery usually increases during the first day. Due to the high pressure in the arterial system, the hematoma reaches a significant volume and, peeling the dura mater from the bone, breaks off the veins of the epidural space. Symptoms of brain compression usually appear 12-36 hours after the rupture of the meningeal artery, when the hematoma reaches 4-5 cm in diameter and 2-4 cm thick, forming a saucer-shaped depression on the surface of the brain. With extensive cracks or fractures of the bones, several branches of the artery may be injured. Relatively rare are epidural hemorrhages from the anterior and posterior meningeal arteries.
Local symptoms depend on the location of the most massive parts of the hematoma.
The following localization of epidural hematomas is distinguished:
1) anterior (frontotemporal);
2) the most frequently observed middle (temporal-parietal);
3) back (parietal-temporal-occipital);
4) basal-temporal.
The most typical for an epidural hematoma that has developed as a result of a rupture of the middle meningeal artery against the background of concussion and mild or moderate brain contusion is the following clinical picture:
1) a light interval lasting usually 3-12 hours, after which, as the volume of the hematoma increases and reactive changes in the brain tissue increase, general signs of brain compression gradually increase (lethargy, soporous and, finally, coma);
2) focal symptoms in the form of pupil dilation on the side of the hematoma and pyramidal symptoms on the opposite side.
The symptomatology of an epidural hematoma depends on the concomitant concussion and brain contusion. In some cases, with very severe concussions and bruises of the brain with an initial coma, the symptoms of epidural hematoma recede into the background, in others, with concussions and bruises of mild to moderate degree, they come to the fore (epidural hematoma clinic).
Usually, with epidural hematomas, which form a deep dent in the brain tissue and cause compression of the brain, 70-100 ml of liquid blood and clots are found, and the amount of 150 ml is usually incompatible with life. Clinical observations clearly indicate that, along with the amount of blood poured into the cranial cavity, the time factor is of primary importance - the speed of development of acute cerebrovascular accidents and cerebral edema, as well as the features of dislocation syndromes, the severity of concussion and brain injury and the age of the patient.
The most important symptom of a hematoma is the expansion of the pupil on the side of the lesion. However, slight and fluctuating aiaisoxria has no significant diagnostic value.
Diagnostic value has a progressive and relatively stable expansion of the pupil to a size 3-4 times larger than the size of the pupil on the opposite side. Typically for a growing epidural hematoma, at first, the absence of anieocoria, then a relatively short period of slight pupillary constriction on the side of the lesion, a. in subsequent stages - a characteristic increasing expansion of the pupil on the side of the lesion almost until the disappearance of the iris. At first, the pupil responds satisfactorily to the light, and then becomes immobile, not narrowing with light stimulation. In the next stage of compression, the maximum expansion of both pupils occurs; this stage is already considered irreversible.
Most authors believe that the expansion of the pupil on the side of the lesion is associated with a herniated tentorial herniation of the medial parts of the temporal lobe, which exerts direct pressure on the oculomotor nerve. Often, anisocoria is observed with moderate and severe forms of closed brain injury and in the absence of a massive intracranial hematoma, however, a pronounced and persistent mydriasis always indicates the possibility of a massive hematoma on the side of the focus. At the same time, this most important symptom with epidural hematoma appears in approximately half of the cases. It should be noted that sometimes the expansion of the pupil is observed on the opposite side of the hematoma.
Pyramidal symptoms in epidural hematomas are often detected and, as a rule, on the opposite side, manifesting themselves either as signs of irritation in the form of Jacksonian epileptic seizures, or as symptoms of prolapse in the form of progressive paresis and paralysis. Identification of the side of paresis or paralysis of the limbs is possible in almost all patients, regardless of the degree of loss of consciousness. Movement of the limb in response to a shout, pricks, irritation of the cornea of the eye, nasal mucosa, external auditory canal, position of the paralyzed lower limb with normal outward rotation and sagging of the foot, faster fall and extension of the raised paralyzed limb compared to the limb on the opposite side, along with other pyramidal signs allow you to set the side of the lesion.
The following course of the disease is most characteristic. After the disappearance of acute concussion phenomena with the restoration of consciousness, the condition of the patients becomes relatively satisfactory, but after a few hours or 1-1/2 days, progressing cerebral and local symptoms are noted in the form of hamolateral pupillary dilation and contralateral gamiparesis. Sometimes there are concomitant convulsions in the affected limbs, hemitype sensory disturbances and pyramidal signs. The so-called light interval with epidural hematomas usually lasts from 3 to 12 hours, but sometimes reaches l.5 days. One of the most important symptoms of increasing brain compression is a gradual increase in workload, the development of a soporous and, finally, a coma, which indicates a delay in the correct diagnosis. It is very important to monitor the degree of impairment of consciousness and determine the indications for surgery even before complete loss of consciousness develops. In some cases
it is possible to clearly identify the clinic of a growing epidural hematoma without previous symptoms of a concussion, and then the recognition of a hematoma does not present any particular difficulties. In many cases, a light gap cannot be caught. The reason that makes it difficult to identify the open period can be very severe concussions and contusions of the brain, against the background of which the progression of symptoms of compression cannot be detected, or a rapid increase in compression with a very short light interval. However, with careful neurological monitoring of the dynamics of the disease, even against the background of an unconscious state, it is possible to identify symptoms of an increase in brain compression.
Usually, with an epidural hematoma in the avetous gap, the following dynamics of the disease is observed. In good condition and full consciousness of the patient, the pulse rate and blood pressure are usually within normal limits. When intracranial hypertension disappears, drowsiness and congestion increase, the pulse first slows down, and sometimes an increase in blood pressure is detected. In an unconscious state, bradacardia is observed, sometimes reaching up to 40 beats per minute with sufficient filling of the pulse! In some cases, the stage of bradycardia cannot be identified. Finally, circulatory decompensation occurs, the pulse becomes rapid, arrhythmic and thready, blood pressure falls. During this period, breathing disorders appear first in the form of increased frequency, then difficulty in breathing, irregular rhythm, wheezing and, finally, shallow breathing. Cheyne-Stoke respiration a is a poor prognostic sign. The rise in temperature to 39 ° C and above in the absence of infectious complications is a symptom of decompensation. Vomiting is a common symptom of mild compression of the brain, but it is absent in the stage of decompensation. According to the increase in brain compression, bilateral pathological reflexes appear, then areflexia, atony, and lack of control over natural functions. Often in the stage of decompensation, decerebranion rigidity occurs, but with the timely and successful removal of the hematoma, patients recover even after terrible phenomena of decerebrate rigidity.
Only in 18-20% of cases, slow development of epidural hematoma is observed, and at the same time, symptoms of brain compression appear 5-6 days or more after the injury. With a distinct clinic of growths of intracranial hematoma, spinal puncture is contraindicated due to the danger of strengthening the dislocation of the brain.
Significant assistance in the diagnosis of hematoma is provided by echoancephalography, which reveals a pronounced displacement of the median structures of the brain in hematoma.
There are indications in the literature that epidural hematomas in children occur much less frequently than in adults, which is associated with the elasticity of the children's skull and intimate fusion of the dura mater and a. meningea media with the inner surface of the bone and the transfer of diffuse mechanical effects on the area of especially elastic connective tissue fontanelles. In children, especially at an early age, it is often very difficult to establish the duration and loss of consciousness, but lethargy, drowsiness, and then motor restlessness developing after an injury, followed by increased drowsiness and lethargy, indicate the possibility of intracranial hemorrhage.
In difficult-to-diagnose cases, angiography of the brain should be performed or a burr hole should be applied to examine the dura mater. With large epidural hematomas, arteriograms reveal a shift in the vascular system of the brain. A particularly informative method for detecting intracranial hematomas is computed tomography.

Treatment of epidural hematomas

At the slightest suspicion of a massive epidural hematoma, one should not hesitate and wait, as this can lead to an irreversible stage of the disease. An urgent consultation with a neurosurgeon is necessary, and if an intracranial hematoma is established, an urgent surgical intervention is necessary.
In any, even the most difficult condition of the patient, the operation to remove an epidural hematoma is absolutely indicated and often leads to recovery, despite the supposedly irreversible condition in the preoperative period.
Postoperative mortality after removal of epidural hematomas, according to different authors, ranges from 15-40%.
In rare cases, usually in the presence of a crack in the scales of the occipital bone, epidural hematomas form in the region of the cerebellar hemispheres. This reveals a clinical picture of compression of the cerebellum and trunk at the level of the posterior cranial fossa and infringement of the tonsils in the foramen magnum. In these cases, an arch operation is indicated for applying a diagnostic burr hole above the cerebellar hemisphere, and if a hematoma is detected, this hole is expanded and the hematoma is removed.

Subdural hematomas

Acute subdural hematomas account for about 40% of the total number of acute intracranial hematomas. This name refers to a massive accumulation of blood or bloody fluid in the subdural space. Most subdural hematomas are of traumatic etiology, less often they are the result of an inflammatory lesion of the meninges in the elderly and in patients with alcoholism.
The source of obdural hematomas in a closed craniocerebral injury is usually stray veins that run along the convexital surface of the brain to the sagittal sinus and tear at the time of injury due to oscillatory displacements of the brain. When a vein is torn off at the site of its confluence with the sagittal sinus, the hole in it may remain gaping and blood flows into the subdural space. Much less often, the source of bleeding is ruptured occipital veins flowing into the transverse sinus. In newborns, a massive subdural hematoma compressing the brain is usually the result of birth trauma, and primarily the application of forceps, but is also observed in cases where this intervention was not used.
From a clinical point of view, the following division of subdural hematomas is advisable:
1) acute hematoma in combination with a severe degree of concussion and brain contusion, the end of the hematoma symptoms appear during the first 3 days after the injury;
2) acute hematoma with concussion and contusion of the brain of moderate and mild degree;
3) subacute hematoma, when symptoms appear 4-14 days after injury;
4) chronic hematoma, when the symptoms of a hematoma begin to appear from the 3rd week after the injury and can be especially clearly revealed several months after the injury.
Subdural hematomas are usually located on the convexital surface of the cerebral hemisphere over a fairly extensive extent. Most often they are unilateral, sometimes bilateral. Severe clinical symptoms are usually observed with the development of a hematoma of a large volume.
In acute subdural hematomas, to an even greater extent than in epidural, against the background of a very serious condition of the patient and brain contusion, the symptoms of hematoma recede into the background.
In pathoanatomical examination, in 80% of patients with subdural hematomas, massive contusion foci of the brain are also detected. The clinic of acute and subacute subdural hematoma appears more clearly against the background of concussion and brain contusion of mild and moderate severity.

Clinic of acute and subacute subdural hematomas

The clinic of acute and subacute subdural hematomas is somewhat similar to the clinic of epidural hematomas. Differences are revealed due to the presence of two points:
1) with epidural hematomas, bleeding is arterial, and therefore the clinical picture of brain compression manifests itself quickly - over 0.5-1.5 days, with subdural hematoma, bleeding is venous, which leads to a slow increase in symptoms of brain compression for several days and even weeks, although in in some cases, pronounced compression can occur on the first day after the injury;
2) subdural hematomas usually spread over a wide area, while epidural hematomas form a more limited deep dent in the brain. The so-called light gap with subdural hematomas is less pronounced than with epidural, although it is often observed.
Along with general epochal phenomena, the clinical picture of acute subdural hematomas reveals local symptoms, usually corresponding to the areas of the greatest accumulation of blood. When compared with epidural hematomas in rubdural hematomas, less clarity of local symptoms and progressive brain compression syndrome attracts attention. The picture of a severe concussion and bruise of the brain comes to the fore. Pupil dilation on the side of a subdural hematoma is less common than with an epidural hematoma.
In the acute period of severe traumatic brain injury, even pronounced pyramidal symptoms do not always help to correctly recognize the side of the location of the subdural hematoma. Paresis of the limbs on the opposite side are detected in approximately 60%, and on the side of the hematoma - in 30% of cases. The presence of pyramidal symptoms on the homolateral side, apparently, is a consequence of the fact that with pronounced lateral displacements of the brain, a displacement of the contralateral brain stem is also observed, which is pressed against the sharp edge of the tentorial notch and damaged in this area. On the contrary, with the development of chronic subdural hematoma, pyramidal symptoms almost always correctly indicate the direction of the hematoma. It should be emphasized that in most cases, a neurological examination can correctly assess the relationship of manifesting pyramidal symptoms with either a brain contusion or a progressive subdural hematoma. While the pyramidal symptoms, depending on the brain contusion, are relatively constant, with a hematoma, this symptomatology increases.
The symptoms of chronic subdural hematomas resemble those of a benign brain tumor and are manifested by an increasing increase in intracranial pressure and local symptoms. Significant assistance in the diagnosis is provided by echoencephalography, which reveals a pronounced displacement of the median structures of the brain with a hematoma.
In unclear cases, angiography is indicated, which reveals a picture that is extremely typical for subdural hematomas or the imposition of one or more diagnostic burr holes.

Treatment of acute and subacute subdural hematomas

In acute and subacute subdural hematomas, urgent surgical intervention is indicated, in chronic cases, the timing of surgical intervention varies depending on the patient's condition. In some cases, spontaneous resorption of subdural hematomas is observed and at the same time, expectant management is acceptable, but such patients must be in a neurosurgical hospital under constant monitoring of their condition, the dynamics of echoencephalographic and angiographic data so that, if indicated, it is possible to perform an urgent or accelerated operation. hematoma emptying. High postoperative mortality in acute and subacute subdural hematomas is mainly due to their frequent combination with brain contusion and intracerebral hemorrhage.
In newborns, in whom machine subdural hematomas are usually the result of birth trauma or forceps, the hematoma is emptied by puncturing the subdural space through the lateral part of the large fontanelle with blood aspiration.
Subdural hygromas occur in about 5% of cases to the total number of patients with intracranial hematomas. They represent a limited subdural accumulation of a clear or hemorrhagically colored fluid, which, increasing in volume up to 100-150 ml during the first days, and more often months or years after the injury, causes compression of the brain. According to most authors, at the time of injury, a small tear of the arachnoid membrane occurs and fluid pours into the subdural space, while this tear functions as a valve valve, preventing the fluid from returning to the subarachnoid space.
It is almost never possible to distinguish a subdural ligroma from a hematoma in the preoperative period. Treatment - operational.
Intracerebral hematomas account for approximately 9% of cases in the total number of patients with intracranial hematomas. It should be clearly distinguished intracerebral hemorrhage and intracerebral hematoma; the latter is understood as a massive accumulation (from 30 to 150 ml) of liquid blood or clots in the brain tissue. The allocation of large focal hematomas to a special group is dictated by practical problems, since when these hematomas are localized in the cerebral hemispheres and cerebellum, surgical intervention is indicated to empty the hematoma.
Symptoms of intracerebral hematoma develop in parallel with the increase in its volume and concomitant edema - swelling of the brain. At the same time, the phenomena of increasing compression of the brain with clear local signs are revealed. Often it is not possible to differentiate with certainty epidural or subdural hematoma from intracerebral. Almost all the signs of increasing compression of the brain, which were discussed when describing the clinic of epidural hematomas, can be observed with massive intracerebral hematomas of the cerebral hemispheres. And therefore, often on the basis of neurological symptoms, it is possible to establish the diagnosis of intracranial hematoma without specifying whether there is an epidural, subdural or intracerebral hematoma of the cerebral hemispheres, and only during the operation a more accurate localization of the hematoma is revealed.
The increase in clinical phenomena in intracerebral hematomas during the first days after injury may be associated not so much with an increase in the amount of blood in the hematoma cavity, but with progressive perifocal or general cerebral edema, as well as with diapedesis into the hematoma cavity and into the perifocal brain tissue as a result of local disorders permeability vascular loom. If with epidural and subdural massive hematomas, angiography can reliably establish the diagnosis, then three intracerebral hematomas this method sometimes gives fuzzy or questionable data.
It should be emphasized that, in most cases, the clinic of severe brain compression manifests itself during the first 7-IV2 out after the injury. However, there are often cases of a more protracted course, when in the first weeks after the injury, the signs of hematoma are relatively often expressed, the condition of patients is moderate, and 2-4 weeks after the injury, a pronounced clinical picture of intracerebral hematoma appears. Timely surgical intervention with emptying of the hematoma and in these cases often ends in recovery.
Cerebellar hematomas. In the presence of a large hematoma in the cerebellum, symptoms of acute compression of the formations of the posterior cranial fossa appear, sometimes with a clear symptom complex of infringement of the tonsils in the foramen magnum and compression of the lower sections of the medulla oblongata. Most often, there is a crack in the lower parts of the cup of the occipital bone, which facilitates local diagnosis. In these cases, urgent surgical intervention is indicated.
It should be noted that often: (in about 20% of cases of the total number of patients with hematomas) there are multiple hematomas, unilateral and bilateral.

skull fractures

The skull has a certain elasticity and can withstand significant trauma without breaking the integrity of its bones. However, severe damage to the brain itself can be observed. If the impact of the mechanical factor on the skull exceeds its elasticity, then a fracture occurs. It is advisable to subdivide skull fractures into fractures of the vault, and fractures of the base of the skull.
Fractures of the base of the skull, in turn, can be divided into two groups:
1) combined damage to the vault and base of the skull, when the line of fracture of the frontal, temporal and occipital bones passes to the base of the skull;
2) fractures of the base of the skull. Most skull base fractures are located in the anterior cranial fossa; in second place are fractures of the anterior cranial fossa and in third place are fractures of the posterior cranial fossa.
The clinic of fractures of the base of the skull depends on the severity of the traumatic brain injury and the localization of the fracture and consists of symptoms of concussion and moderate or severe brain contusion, pronounced stem disorders, damage to the nerves of the base of the brain, meningeal symptoms, liquorrhea, and bleeding from the ears and nose.
The nature of the impact of the traumatic factor makes it natural to involve the basal parts of the brain, including its stem parts, in the process. With severe tinnitus of the basal-diencephalic parts of the brain or the posterior cranial fossa, patients usually die within the next day after the injury. In other cases of a fracture of the base of the skull, the condition of the patients may be of moderate severity or even satisfactory. Bleeding from the external auditory canal is observed with a fracture of the pyramid in combination with a rupture of the tympanic membrane.
In case of fractures of the base of the skull, bleeding from the ear acquires diagnostic significance only when combined with the corresponding neurological symptoms, if its occurrence is excluded as a result of direct damage to the auricle, external auditory canal, middle ear with a rupture of the tympanic membrane, but without a fracture of the base of the skull and pyramid. To an even greater extent, this applies to bleeding from the nose, which is often the result of damage to the soft tissues and bones of the facial skeleton, but may also be the result of a fracture of the base of the skull in the paranasal sinuses. The same applies to diffuse hemorrhages in the conjunctiva and hemorrhages in the periorbital tissue (the so-called glasses), which can be the result of both a bruise of the face and a fracture of the anterior cranial fossa.
Liquorrhea from the ears and nose is an unconditional sign of a fracture of the base of the skull with a rupture of the dura mater. The outflow of cerebrospinal fluid from the ears, as a rule, stops in the acute period of the disease and usually lasts one or several days, less often weeks. Persistent leakage of cerebrospinal fluid from the ears in the chronic stage of the disease is rare and requires surgical intervention, as it often leads to outbreaks of recurrent infectious meningitis.
Fissures of the base of the skull can be the cause of reversible and irreversible dysfunctions of the cranial nerves, “especially the facial and auditory, which in frequency occupy the first place among the lesions of the cranial nerves in fractures of the base of the skull (pyramid). However, not in all cases, when damage to the facial nerve of the peripheral type or the auditory nerve (hearing loss up to unilateral deafness) is detected after an injury, a fracture of the base of the skull necessarily occurs. Hearing loss may be the result of a hemorrhage in the tympanic cavity, rupture of the tympanic membrane, a violation of the auditory ossicles, and paralysis of the facial nerve - the result of bruising or compression in the canal of the facial nerve.
Treatment for skull base fractures is basically the same as for moderate to severe concussion and brain contusion. Indications for surgery occur with comminuted and depressed fractures of the parabasal parts of the skull, accompanied by damage to the air cavities (primarily the frontal sinus).

Open injuries of the skull and brain in peacetime

In peacetime there are:
a) open non-gunshot injuries;
b) gunshot wounds of the skull and brain.
Open non-gunshot injuries are 2-3 times less common than closed ones - with bruised, chopped, cut and stab wounds of the head.
Open injuries should be classified into:
a) non-penetrating, in which there is no defect in the dura mater; this minimizes the possibility of wound infection spreading to CSF spaces and brain tissue;
b) penetrating, in which the presence of a defect in the dura mater contributes to the infection of the brain and cerebrospinal fluid.
In peacetime, penetrating and non-penetrating gunshot wounds to the skull and brain can be inflicted both by firearms used in a combat situation (for example, during explosions of anti-tank and anti-personnel mines, grenade fuses, rupture of rifle cartridges, etc.), and when using hunting rifles (rupture of the breech of a gun or a shot in the head) or artisanal revolvers (“self-propelled guns”). Peacetime gunshot wounds most often occur in children with careless handling of explosive projectiles. At the same time, due to the close distance from the explosion site, multiple severe penetrating craniocerebral injuries are often observed with simultaneous damage to the face and eyes.
With open craniocerebral injuries in peacetime, the following therapeutic measures are indicated.
1. In case of circulatory and respiratory disorders - their normalization.
2. Early floor-by-floor primary surgical debridement, the radical nature of this debridement and the simultaneous nature of all surgical manipulations on the skull and brain. The most favorable terms for the primary surgical treatment of wounds are the first 3 days from the moment of injury, but if for some reason these periods are missed, then a trimmed primary treatment performed 4qpe3 3-6 days after the injury is quite acceptable and appropriate.
3. Completion of the primary surgical treatment of the wound (in the absence of contraindications):
a) sealing of the subarachnoid space by plastic closure of defects in the dura mater;
b) plastic closure of a skull defect (cranioplasty);
c) a deaf suture of the integument of the skull.
4. Fight against cerebral edema and purulent complications (encephalitis, brain abscesses, etc.).

Penza State University

medical institute

department of TO and VEM

course "Extreme and military medicine"

Traumatic brain injury

Penza 2003

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

Traumatic brain injury belongs to the category of the most common injuries and accounts for > 40% of their total number, mortality in severe injuries of the skull and brain reaches 70-80%. The mechanism of traumatic brain injury can be direct and indirect. An example of an indirect mechanism is a traumatic brain injury as a result of a fall from a height onto the legs or pelvis. When landing and stopping the movement of the skeleton, the skull, due to inertia, is, as it were, placed on the spine and a fracture of the base of the skull may occur. If this does not happen, the skull stops, and the brain, continuing to move, hits its base and standing bones.

Classification of traumatic brain injuryTable 1.

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

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

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

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

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

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

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

Dizziness. Instability in the Romberg position.

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

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

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

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

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

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

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

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

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

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

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

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

Lower stem(bulbar) syndrome is characterized by a more severe condition. Consciousness is absent - coma. Respiratory distress reaches an extreme degree, pathological forms of respiration occur. The pulse is weak and frequent. Blood pressure drops to 70/40 mm Hg. and below. The pupils are wide, the reaction to light is barely perceptible. Swallowing is severely impaired. Thermoregulation is reduced.

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

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

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

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

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

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

Additional research methods

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

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

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

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

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

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

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

Rice.2

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

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

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

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

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

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

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

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

CLINIC AND DIAGNOSIS OF INDIVIDUAL

NOSOLOGICAL FORMS OF CRANIO-BRAININJURIES

Brain concussion

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

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

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

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

brain contusion

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

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

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

There are three degrees of brain injury.

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

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

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

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

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

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

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

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

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

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

COMPRESSION OF THE BRAIN

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

Compression of the brain by bone fragments and foreign bodies

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

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

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

Preliminary data make it possible to diagnose brain contusion (of varying severity), which actually accompanies depressed fractures and foreign bodies of the skull with brain compression. The final diagnosis is made after craniography, computed tomography, echoencephalography, which reveal depressed skull fractures or foreign bodies in it, and the clinical data and the results of additional research methods on the topography of the location of the ingredient that causes pressure on the brain tissue must match.

Compression of the brain by intracranial hematomas

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

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

The clinical manifestations of various hematomas are not the same, but a number of patterns can be traced in their course, which allow us to consider intracranial hematomas in one group. Schematically, it looks like this: a history of head trauma with loss of consciousness (often for a short period). Upon the return of consciousness, cerebral symptoms are revealed, on the basis of which a diagnosis of "Concussion of the brain" can be made. In the best case, the patient is hospitalized and appropriate treatment is prescribed: rest, sedatives, etc. In some cases, victims may not seek help, since a short bed rest, as a rule, relieves cerebral symptoms. Moderate headaches and amnesia persist. The patient's condition improves significantly. Thus, the rupture of an intracranial vessel at the time of injury due to the absence of a clinical picture of brain compression remains unnoticed. As compression increases, meningeal and then local symptoms appear (anisocaria, mono- or hemiparesis, etc.). There comes a disorder of consciousness according to the cortical type. There is psychomotor and speech excitement, which later turns into depressed consciousness (stupor), often with convulsive seizures and subsequent cerebral coma. The outcome of compression of the brain in the absence of treatment, as a rule, is death. Thus, an intracranial hematoma is characterized by a three-phase course: trauma with loss of consciousness - improvement of the condition ("light gap") - deterioration of the condition with a tragic outcome.

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

What determines the duration of the light 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 gap. The reason is that the brain is not "squeezed" into the skull, but has certain spaces between it and the membranes with a certain intracranial pressure. A hematoma that has formed at an early stage does not cause pronounced compression of the brain, since, like any living organ, it loses its volume to a certain limit, while compensating for the functional state. Gradual vascular disorders, hypoxia, increasing edema, and then swelling of the brain lead to an increase in its volume and a sharp increase in pressure over the area of contact between the hematoma and the brain. There comes a breakdown of the compensatory capabilities of the central nervous system, which is expressed in the end of the light interval. A further increase in the volume of the brain leads to a shift in the median structures, and then the dislocation of the brain stem into the opening of the cerebellar tenon and the occipitocervical dural funnel.

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

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

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

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

Epidural hematomas

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

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

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

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

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

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

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

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

There is persistent nausea, repeated vomiting, frightening dizziness - everything floats before my eyes. The pulse rate slows down, moderate bradycardia sets in (51-59 bpm), blood pressure increases (from 140/80 to 180/100 mm Hg). Breathing moderately quickens (21-30 breaths per minute). At this stage, focal microsymptoms may appear: mild anisocaria - a slight dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, moderate deviation of the tongue. With percussion of the skull, it is possible to identify areas of increased pain (usually above the hematoma), to which the patient reacts with a suffering grimace of the face.

In the stage of inhibition, the behavior of the patient changes radically. He no longer rages and asks for nothing. There comes a secondary disorder of consciousness, starting with stunning and turning into a stupor. The victim is indifferent to the environment, his gaze is pointlessly directed into the distance. There is an increase in bradycardia (41-50 bpm) and tachypnea (31-40 breaths per minute). There is an asymmetry in blood pressure. On the opposite hand from the lesion, the blood pressure will be 15-20 mm Hg. higher than on the arm from the side of the hematoma. Increasing focal symptoms. Among them, the main diagnostic role is played by: pupil dilation on the side of the hematoma, smoothness of the nasolabial fold, grin disturbances, tongue deviation, spastic hemiparesis with a predominant lesion of the arm on the opposite half of the body. Reveal meningeal signs in the form of stiff neck and positive symptoms of Kernig and Brudzinski.

The final stage of untreated epidural hematoma is the stage of cerebral coma. It is caused by displacement and infringement of the brain. It is characterized by dislocation signs: the transition of bradycardia into tachycardia (120 bpm and above), tachypnea into pathological types of breathing, blood pressure begins to steadily decrease, reaching critical numbers (below 60 mm Hg), swallowing disorder, a symptom of floating gaze, gross anisocaria and dissociation of meningeal symptoms, muscle tone and reflexes along the axis of the body. In the final phase, bilateral mydriasis with no pupillary response to light, areflexia, muscle atony, and death occur.

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

An ophthalmological examination reveals congestion in the fundus.

Subdural hematomas

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

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

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

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

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

subdural hygroma

Subdural hygroma - this is a limited accumulation of cerebrospinal fluid in the space under the dura mater resulting from trauma.

Subdural hygromas are much less common than hematomas of a similar situation. The question of the pathogenesis of hygromas has not been finally resolved. The reasons for the limited accumulation of cerebrospinal fluid under the dura mater are considered damage to the arachnoid by the type of valve that allows the cerebrospinal fluid to move in only one direction - from the subarachnoid to the subdural space. Hygromas can also occur due to changes in the vessels of the dura mater, which create conditions for blood plasma to leak into the subdural space, or as a result of severe brain damage, when there are messages between the intrathecal spaces, the lateral ventricles.

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

If the hygroma arose in isolation, then its clinic is very similar to that of a subdural hematoma, especially the three-phase flow. As a rule, after an injury with a short-term loss of consciousness, a lucid interval occurs, more often lasting 1-3 days and with typical cerebral symptoms. Then the headache intensifies, stupor appears and grows, meningeal and local symptoms appear in the form of paresis of the facial nerve, mono- or hemiparesis, and sensitivity disorders.

However, in the classical clinic of intracranial hematoma, one can notice some features typical of subdural hygroma, or signs that are most common with it. This is a large light interval (1-10 days) - hygromas often have a subacute course. Headaches are paroxysmal, radiating to the eyeballs, the cervical-occipital region. Characterized by photophobia and local pain on percussion of the skull. The general condition of patients worsens slowly, as do the signs of brain compression, which grow relatively softer and gradually. Often there are mental disorders according to the type of frontal syndrome (decrease in criticism of one's condition, euphoria, disorientation, apathetic-abulic symptoms), proboscis and grasping reflexes appear. Psychomotor agitation often develops.

Paresis of spastic limbs with hypertonicity and revitalizationreflexes. Quite often, patients with hygromas have convulsive seizures that begin with the muscles of the face or on the contralateral side. Subdural hygromas are characterized by a gradual, undulating deepening of secondary disturbances of consciousness. So, in the early stages, after a convulsive seizure, consciousness is restored and you can make contact with the patient.

For acute hygromas, the absence of anisocaria is characteristic, and if it is, then, unlike hematomas, the reaction of the pupil to light is preserved.

Intracerebral hematomas

Intracerebral hematoma - This is a post-traumatic hemorrhage in the substance of the brain with the formation of a cavity filled with blood in it. The frequency of formation of intracerebral hemorrhages is approximately 5-7% of all intracranial hematomas. The favorite localization is the frontotemporal lobe. The size of intracerebral hematomas is relatively small and is 1–3 cm in diameter, but can reach 7–8 cm.

The source of cerebral hemorrhages are damaged vessels of the substance of the brain when it is bruised or other types of craniocerebral injury.

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

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

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

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

Intraventricular hematomas

Intraventricular hematomas - These are post-traumatic hemorrhages in the cavity of the lateral, III and IV ventricles of the brain. This type of hemorrhage occurs only against the background of a severe brain contusion and practically does not happen in isolation.

Intraventricular hematomas account for 1.5 to 4% of all intracerebral hemorrhages. The cause of their occurrence is the rupture of the choroid plexuses of the ventricles as a result of hydrodynamic impact at the time of injury. More often one of the lateral ventricles suffers. 40-60 and even 100 ml of blood can pour into it.

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

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

Neurological symptoms in intraventricular hematomas are usually bilateral.

Quite early, violations of the regulation of breathing appear in the form of tachypnea (30-70 breaths per minute), which stubbornly progress, reaching pathological forms (Cheyne-Stokes, Biota). Subsequently, there are signs of brain dislocation (transition of bradycardia into tachycardia, reaching up to 160 or more beats per minute with bilateral mydriasis, the occurrence of pathological reflexes from the feet.

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

Lumbar puncture reveals an abundant admixture of blood in the cerebrospinal fluid.

Subarachnoid hemorrhage.

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

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

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

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

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

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

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

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

FRACTURES OF THE SKULL BONES

Skull fractures make up to 10% of fractures of all bones of the skeleton and belong to the category of severe injuries, because they are unthinkable without damage to the underlying structures - the membranes and substance of the brain. 18-20% of all severe traumatic brain injuries are accompanied by skull fractures. Distinguish between fractures of the facial and cerebral skull, and in the damage to the brain skull, fractures of the arch and base are distinguished.

Fractures of the base of the skull

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

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

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

In direct trauma, bruising occurs immediately after the impact. They are not symmetrical and often go beyond the orbit, painful on palpation. There are signs of direct mechanical impact: skin abrasions, wounds, hemorrhages in the sclera, bruises of inhomogeneous color, etc.

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

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

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

Fractures of the calvaria

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

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

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

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

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

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

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

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

Linear fractures have a number of distinguishing features:

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

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

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

Sometimes along with cracks there is a divergence of seams.

Treatment of patients with traumatic brain injury

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

Assistance to victims with traumatic brain injury can be divided into three periods: assistance at the prehospital stage, treatment in a hospital (hospital stage) and aftercare in outpatient conditions (outpatient stage) or under the supervision of a family doctor.

Assistance at the prehospital stage is as follows:

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

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

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

Cold to the head.

Give oxygen inhalation.

According to indications, they are used: analeptics (cordiamin, cytiton, lobelin), cardiac glycosides (strophanthin K, corglicon).

In an emergency, transport the patient (necessarily in a supine position) to a medical facility.

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

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

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

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

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

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

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

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

5. Antihistamines(diphenhydramine, fenkarol, diazolin).

As a result of vascular disorders and hypoxia of the brain, destruction and resorption of intracranial hemorrhages, decay of the destroyed brain substance, a mass of histamine-like substances (serotonin, etc.) is formed, so the appointment of antihistamines is mandatory.

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

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

Unloading lumbar punctures directly reduce cerebrospinal fluid pressure, when 8-12 ml of cerebrospinal fluid is slowly released after the lumbar puncture.

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

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

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

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

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

If a fracture is detected during the revision of the wound, then it is necessary to carefully remove all small free-lying fragments with tweezers and examine the dura mater. In the absence of its damage, normal color, preserved ripple, the shell is not opened. The edges of the bone wound are cut with wire cutters to a width of 0.5 cm. Hemostasis is performed and the wound is sutured.

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

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

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

When the brain is compressed by hematomas or hygroma, resection or osteoplastic surgery can be performed. The first version of the operation is that in the projection of the alleged hematoma, a search burr hole is applied. If a hematoma is detected, the hole is expanded by gradual resection of the bone to the desired size (6x6, 7x7 cm). Through the created window, an intervention is performed on the brain and membranes. The operation is completed by suturing the soft tissue, leaving a large defect in the bones of the skull. Such an operation creates a good decompression of the brain, especially when the compression of the brain is combined with severe contusion. But resection trepanation also has negative sides. After it, one more intervention is necessary to close the skull defect with a synthetic material (steractyl) or an autobone taken from the rib. If this is not done, posttrepanation syndrome will develop. Changes in intracranial pressure caused by physical stress (straining, coughing, sneezing, etc.) lead to frequent displacements of the medulla into the "window" of the skull defect. Traumatization of the brain on the edge of the burr hole causes the development of a fibrous process in this area. Adhesions are formed between the brain and the membranes, bones and integuments of the skull, which cause local and headaches, and later epileptic seizures. Osteoplastic trepanation does not leave skull defects requiring subsequent plasty. Produce a semi-oval base downward incision of the soft tissue to the bone. Five burr holes are drilled along the incision line, without separating the soft tissue flap - two at the base of the flap and three along the arc. the flap on the pedicle is turned down.The further course of the operation depends on the type of injury.After the intervention in the cranial cavity is completed, the bone flap is placed in place and the soft tissues are sutured in layers.

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

Mechanisms of traumatic brain injury.

Classification of traumatic brain injury.

List the general symptoms.

Name the local symptoms.

List the meningeal symptoms.

Name the stem symptoms.

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

How is a concussion diagnosed?

What is the diagnosis of brain injury based on?

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

Causes of brain compression.

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

Clinic of cerebral compression by intracerebral and intraventricular hematomas.

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

What is a subdural hygroma?

The difference between the clinic of concussion, contusion and compression by epi- and subdural hematomas.

Clinic of subarachnoid hemorrhage.

Fracture of the base of the skull, diagnosis.

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

Fractures of the cranial vault, diagnosis, tactics.

First aid for traumatic brain injury.

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

Conservative treatment of brain damage in the recovery period.

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

Technique of various types of trepanation, the necessary tools.

What is posttrepanation syndrome, its treatment.

Outcomes and long-term consequences of TBI.

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 single), headache, dizziness, weakness, painful eye movements, etc. There are no focal symptoms in the neurological status. Macrostructural changes in the substance of the brain during concussion are not detected.

Clinically, it is a single functionally reversible form (without division into degrees). With a concussion, a number of cerebral disorders occur: loss of consciousness or, in mild cases, its short-term darkening from several seconds to several minutes. Subsequently, a stunned state persists with insufficient orientation in time, place and circumstances, an unclear perception of the environment and a narrowed consciousness. Retrograde amnesia is often found - loss of memory for events preceding the trauma, less often anterograde amnesia - loss of memory for events following the trauma. Speech and motor excitation is less common. Patients complain of headache, dizziness, nausea. Vomiting is an objective symptom.

Neurological examination usually reveals minor diffuse symptoms:

symptoms of oral automatism (proboscis, nasolabial, palmar-chin);

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

moderately pronounced or non-permanent pyramidal pathological signs (symptoms of Rossolimo, Zhukovsky, less often Babinsky).

Cerebellar symptoms are often clearly manifested: nystagmus, muscle hypotension, intentional 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.

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

Brain contusion (UGM)

Brain contusion is characterized by focal macrostructural lesions of the medulla 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 is characterized by loss of consciousness up to 1 hour after injury, complaints of headache, nausea, and vomiting. In the neurological status, rhythmic twitching of the eyes when looking to the sides (nystagmus), meningeal signs, asymmetry of reflexes are noted. Roentgenograms may show skull fractures. In the cerebrospinal fluid - an admixture of blood (subarachnoid hemorrhage). A brain contusion of mild severity is clinically characterized by a short-term loss of consciousness after an injury up to several tens of minutes. Upon its recovery, complaints of headache, dizziness, nausea, etc. are typical. As a rule, retro-, con-, anterograde amnesia, vomiting, sometimes repeated, are noted. Vital functions are usually without pronounced disturbances. 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 on the 2-3rd week after TBI. With mild UGM, unlike concussion, fractures of the bones of the cranial vault and subarachnoid hemorrhage are possible.

Moderate brain contusion is clinically characterized by loss of consciousness after an injury lasting up to several tens of minutes or even hours. Moderate brain injury. Consciousness is switched off for several hours. Loss of memory (amnesia) for the events preceding the trauma, the trauma itself and the events after it is expressed. Complaints of headache, repeated vomiting. Short-term respiratory disorders, heart rate, 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 disorders, weakness in the limbs, etc. Craniography often reveals fractures of the vault and base of the skull. Lumbar puncture showed significant subarachnoid hemorrhage. .Con-, retro-, anterograde amnesia is expressed. Headache, often severe. There may be repeated vomiting. There are mental disorders. 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; subfebrile condition. Meningeal symptoms are often expressed. Stem symptoms are also detected: nystagmus, dissociation of meningeal symptoms, muscle tone and tendon reflexes along the axis of the body, bilateral pathological signs, etc. Focal symptoms are clearly manifested, determined by the localization of the brain contusion: pupillary and oculomotor disorders, paresis of the extremities, sensitivity disorders, etc. . Organic symptoms are gradually smoothed out over 2-5 weeks, but individual symptoms can be observed for a long time. Often there are fractures of the bones of the vault and base of the skull, as well as significant subarachnoid hemorrhage.

Severe brain injury. A severe brain contusion is clinically characterized by loss of consciousness after an injury lasting from several hours to several weeks. It is characterized by a prolonged shutdown of consciousness (lasting up to 1-2 weeks). Gross violations of vital functions are revealed (changes in pulse rate, pressure level, frequency and rhythm of breathing, temperature). In the neurological status, there are signs of damage to the brain stem - floating movements of the eyeballs, swallowing disorders, changes in muscle tone, etc. There may be weakness in the arms and legs up to paralysis, as well as convulsive seizures. A severe contusion is usually accompanied by fractures of the vault and base of the skull and intracranial hemorrhages. .Motor excitation is often expressed, severe threatening violations of vital functions are observed. The clinical picture of severe UGM is dominated by stem neurological symptoms, which in the first hours or days after TBI overlap focal hemispheric symptoms. Paresis of the extremities (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 phenomena are frequent, primarily from the motor and mental spheres. Severe UGM 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 ear liquorrhea. In this case, the “spot symptom” on the gauze is positive: a drop of bloody cerebrospinal fluid forms a red spot in the center with a yellowish halo around the periphery.

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

Brain compression

Brain compression is a progressive pathological process in the cranial cavity that occurs as a result of trauma and causes dislocation and infringement of the trunk with the development of a life-threatening condition. With TBI, brain compression occurs in 3-5% of cases, both against the background of UGM and without them. Among the causes of compression in the first place are intracranial hematomas - epidural, subdural, intracerebral and intraventricular; this is followed by depressed skull fractures, brain crush foci, subdural hygromas, pneumocephalus. Brain compression. The main cause of brain compression in 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), intracerebral (in the white matter of the brain and intraventricular (in the cavity of the ventricles of the brain)) hematomas are isolated. there may also be depressed fractures of the bones of the cranial vault, especially the penetration of bone fragments to a depth of more than 1 cm.

The clinical picture of cerebral compression is expressed by a life-threatening increase in a certain period of time (the so-called light period) after an injury or immediately after it of cerebral symptoms, 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 light 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, pupil dilation on one side, a slowing of the pulse (frequency 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.