Combined traumatic brain injury statistics. Chapter vi combined injuries of the bones of the facial skeleton

CHAPTER VI COMBINED DAMAGES TO THE BONES OF THE FACIAL SKELETON. TRANO BRAIN INJURY.

CHAPTER VI COMBINED DAMAGES TO THE BONES OF THE FACIAL SKELETON. TRANO BRAIN INJURY.

Combined injury- is simultaneous damage by one traumatic agent to two or more of the seven anatomical areas of the body.

The concept of “polytrauma” involves simultaneous damage to several parts of the body, organs or systems, when there is at least one life-threatening injury.

1. Combined traumatic brain injury.

With combined traumatic brain injury (CTBI), the facial skeleton, cranial bones and brain are simultaneously damaged. A closed traumatic brain injury (TBI) without damage to the skull bones, combined with fractures of the facial skeleton, is possible.

Fractures of the facial bones in combination with TBI are diagnosed in 6.3 - 7.5% of patients. The fairly high frequency of craniofacial injuries is due not only to their anatomical proximity, but also to the fact that some bones of the facial skeleton take part in the formation of the base of the skull.

The characteristics of TBI are based on the relationship between two defining factors:

1. Localization of extracranial damage.

2. The ratio of cranial and extracranial damage according to their severity.

In more than 1/3 of cases, TBI is accompanied by shock.

Erectile its phase is significantly extended in time and can occur against the background of impaired consciousness (as opposed to the classic one), accompanied by bradycardia, severe disturbances in external respiration, hyperthermia, meningeal signs, and focal neurological symptoms. In addition, the peculiarities of the anatomical relationship of the bones of the facial and cerebral skull lead to the fact that fractures of the facial bones, for example the upper jaw, zygomatic bone, as a rule, extend beyond their anatomical boundaries and the broken bone fragment often includes the bones of the base of the skull. In this regard, it is worth recalling the anatomical data relevant to the issue under consideration.

The anterior cranial fossa (fossa cranii anterior) is separated from the middle one by the posterior edge of the small wings of the sphenoid bone. It is formed by the orbital surface of the frontal bone, the ethmoid, sphenoid (lesser wings and part of its body) bones. It is known that they take part in the formation of the upper, inner and outer walls of the orbit, along which the fracture gap of the upper jaw passes in the middle and upper types.

The middle cranial fossa (fossa cranii media) is formed by the anterior surface of the pyramid and the scales of the temporal bone, the body and large wing of the sphenoid bone, which take part in the formation of the inner and outer walls of the orbit.

Between the lesser and greater wings, as well as the body of the sphenoid bone, there is the superior orbital fissure. The orbital surface of the upper jaw, together with the orbital margin of the greater wings of the sphenoid bone, limits the inferior orbital fissure.

Fractures of the upper jaw can be accompanied not only by fractures of the base of the skull, but also by concussion or contusion of the brain, the formation of intracranial

hematomas. To determine the correct tactics for examining and treating such patients, the dental surgeon must remember the main clinical signs of these injuries.

It is known that combined injury from a pathophysiological point of view, it is a pathological process different in content than equivalent damage to any one vital organ (for example, the brain). Her cannot be considered as a simple sum of damage to two or more anatomical areas.

The combined injury is severe in terms of the overall reaction of the body, despite the possible relatively minor damage to each of the organs involved. Possible disturbances in breathing, circulation, and liquor dynamics characteristic of TBI potentially lead to cerebrovascular insufficiency. Brain hypoxia and disturbances in its metabolism cause cerebral edema and central respiratory impairment. All this contributes to even greater brain swelling.

Thus, a vicious circle closes: damage to the brain causes disruption of all types of metabolism, and damage to other areas (maxillofacial, chest, etc.) enhances such changes and creates the preconditions for suppression of brain activity.

The mortality rate of patients with combined trauma ranges from 11.8 to 40% or more.

When systolic blood pressure decreases below 70 - 60 mm Hg. column, self-regulation of blood circulation in the brain is disrupted, which is accompanied first by functional and then morphological changes in the brain.

Respiratory failure is a serious complication that poses a threat to the life of the victim. In case of combined injuries, it can be of three types: respiratory disorder due to:

Central type

Peripheral type

Mixed type.

Breathing disorder central type is caused by brain injury, more precisely, by the respiratory centers located in the brain stem. In this case, the patency of the peripheral airways is not impaired. Clinically, this is manifested by a violation of the rhythm, frequency, amplitude of breathing: bradypnea, tachypnea, periodic rhythms of Cheyne-Stokes and Biot, spontaneous stopping.

Providing assistance for central-type breathing disorder consists of intubating the patient and providing assisted breathing.

Breathing disorders peripheral type can be caused not only by brain injury, but also by damage to the maxillofacial area. They arise due to obstruction of the upper respiratory tract, as well as the trachea and bronchi with vomit, mucus, blood from the mouth, nose and nasopharynx (especially with a jaw fracture), retraction of the tongue or displacement of the soft tissue flap, which acts as a valve that prevents the passage of air into the lungs.

Providing assistance with this type of breathing disorder consists of sanitation of the tracheobronchial tree, removal of a foreign body from the mouth and oropharynx.

Breathing disorders are more common mixed type, due to one and other reasons. It should be remembered that occlusion of the tracheobronchial tree leads to hypercapnia.

Restoring airway patency is accompanied by a decrease in CO2 levels in the blood, which can lead to respiratory arrest. In this clinical situation, artificial respiration is indicated until spontaneous breathing is restored.

2. Fracture of the base of the skull.

The base of the skull is weakened by numerous openings through which blood vessels and nerves pass. In case of a fracture of the base of the skull, the fracture gap is located in the

the path of least resistance, which determines the ambiguity of its location. Therefore, it is advisable to recall which holes are located in the anterior and middle cranial fossae, within which a fracture of the base of the skull can occur in patients with a fracture of the upper jaw. IN front the cranial fossa contains:

1. The cribriform plate of the ethmoid bone (Lamina cribrosa ossis etmoidalis) with numerous holes in it through which the olfactory filaments pass.

2. Blind opening (foramen coecum), which communicates with the nasal cavity.

3. Optic foramen (foramen opticum), through which the optic nerve passes. IN average The cranial fossa has the following openings:

1. Superior orbital fissure (fissura orbitalis superior).

2. Round hole (foramen rotundum).

3. Oval hole (foramen ovale).

4. Spinous foramen (foramen spinosum).

5. Ragged hole (foramen lacerum).

6. Internal carotid foramen (foramen caroticum interna).

7. Opening of the facial canal (hiatus canalis fasialis).

8. Superior opening of the tympanic tubule (apertura superior canalis tympanici). As an example, we can cite the most common location of the fracture gap of the base of the skull:

1) From the round foramen of one side through the sella turcica towards the ragged and spinous foramen of the other side.

2) From the foramen spinosum through the oval and round foramen to the optic foramen, spreading to the orbital surface of the frontal bone. Possible damage to the cavernous sinus.

3) From the canal of the hypoglossal nerve through the jugular foramen and the internal auditory canal (posterior cranial fossa) it goes to the spinous foramen, and then along the scales of the temporal bone. The pyramid of the temporal bone breaks.

If the base of the skull is fractured, the basal parts of the brain, brain stem, and cranial nerves may be damaged. Therefore, it is possible to establish general cerebral symptoms, brainstem disorders, and signs of damage to the cranial nerves. Bleeding from the ear (fracture of the pyramid of the temporal bone with rupture of the mucous membrane of the internal auditory canal and eardrum), from the nose (rupture of the mucous membrane of the upper wall of the nasal cavity, fracture of the ethmoid bone), from the mouth and nasopharynx (fracture of the sphenoid bone and rupture of the mucous membrane) can often be noted. membranes of the pharyngeal vault).

A Le Fort I and Le Fort II type fracture of the upper jaw is accompanied by a fracture of the base of the skull. When a fracture occurs in the anterior cranial fossa, hemorrhage occurs in the area of ​​the periorbital tissue (strictly in the area of ​​the orbicularis oculi muscle), subcutaneous emphysema, and nosebleeds. Nosebleeds occur when there is a fracture of the bottom of the anterior cranial fossa in the area of ​​the roof of the nose, the posterior wall of the frontal sinus or the lateral wall of the ethmoid sinus and a mandatory rupture of the nasal mucosa covering these bones.

When the wall of the frontal or ethmoid sinuses is fractured, emphysema periorbital region, forehead, cheek. One of the clinical signs of a fracture of the base of the skull is the late appearance of "symptom of glasses"(hematoma in the eyelid area) in the absence of local signs of applied force to the soft tissues of this area. This is due to the fact that blood from the base of the skull in the area of ​​the upper wall of the orbit penetrates the retrobulbar fatty tissue and gradually permeates the loose tissue of the eyelids.

May be liquorrhea from the nose (rhinorrhea). It should be recalled that for rhinorrhea to occur, in addition to a fracture of the base of the skull, a rupture of the dura mater and nasal mucosa at the site of the fracture is necessary. Nasal liquorrhea occurs when

fracture of the anterior cranial fossa only: in the area of ​​the perforated plate, frontal, main (sphenoid) sinuses, cells of the ethmoid bone. The leakage of cerebrospinal fluid into the nose is possible through the openings of the ethmoid bone even in the absence of bone damage due to separation of the fibers of the olfactory nerve.

The liquorrhea stops a few days after the injury, when the wound of the dura mater, nasal mucosa and the fracture gap in the bone is sealed with clotted blood (fibrin).

It is known that post-traumatic liquorrhea is the leakage of cerebrospinal fluid from the cranial cavity when the bones of the base or vault of the skull, dura mater and integumentary tissues (skin, mucous membrane) are damaged. It is possible when the tightness of the subarachnoid space is violated (subarchnoid liquorrhea), when the walls of the ventricles are injured (ventricular liquorrhea), basal cisterns (cistern liquorrhea).

In case of fractures of the facial skeleton extending to the base of the skull, liquorrhea is of great clinical importance, since the cranial cavity freely communicates with the microbially contaminated nasal cavity, with the frontal, ethmoid, sphenoid sinuses, and cells of the mastoid process. The cerebrospinal fluid, becoming infected, flows into these sinuses, and there is a real threat of developing meningitis. Ear liquorrhea spontaneously stops in the first 2 to 3 days after injury.

The leakage of cerebrospinal fluid leads to a decrease in cerebrospinal fluid pressure. This is accompanied by headache and vestibular disorders. Patients are adynamic, occupy a forced position - they tend to lower their head down. If cerebrospinal fluid flows into the pharynx, a cough is provoked due to irritation of its mucous membrane. When the patient's position in bed changes (from back to side), the cough may stop.

According to the degree of increase in the risk of initial liquorrhea, fractures of the bones of the face and skull are located in the following sequence: fracture of the bones of the nose, upper jaw, Le Fort type I, Le Fort type II, ethmoid bone fractures. Liquor rhea is observed in more than 30% of patients with a fracture of the base of the skull. In 70% of patients with liquorrhea, hypotensive syndrome develops. Therefore, the observation of cerebrospinal fluid hypotension in patients with a basal skull fracture should make one think about cerebrospinal fluid leakage.

When fragments of a broken upper jaw are displaced, the cranial nerves located in the region of the ethmoid bone (I pair - olfactory), the body and small wings of the sphenoid bone (II pair - optic nerve), passing through the superior orbital fissure, i.e. are often damaged. between the large and small wings of the sphenoid bone (III pair - oculomotor, IV trochlear pair, VI pair - abducens).

A decrease or loss of smell in a patient with a Le Fort type I and II fracture of the upper jaw indicates damage to the olfactory nerve (I pair).

If there is a decrease in visual acuity, loss of parts of the visual fields, i.e. central and paracentral scotomas, this indicates injury to the optic nerve (II pair).

If the patient does not open the eye partially or completely, the oculomotor nerve (II pair) is damaged.

If the fracture occurs in the area of ​​the superior orbital fissure, oculomotor disturbances may occur - signs of damage to the III, IV, VI pairs of cranial nerves. So, if the patient does not open his eyes, there is divergent strabismus, vertical separation of the eyeballs, impaired mobility of the eyeball up, down, inward, ptosis, mydriasis, then there is damage to the oculomotor nerve.

Deviation of the eyeball upward and inward, limitation of movement of the eyeball downward and outward, and diplopia when looking down are characteristic of damage to the trochlear nerve.

Convergent strabismus, impaired outward mobility of the eyeball, double vision in the horizontal plane are signs of damage to the abducens nerve.

Fractures of the anterior cranial fossa lead to its communication with the orbit or paranasal cavities.

Fractures of the middle cranial fossa (transverse, oblique, longitudinal) most often pass through the pyramid of the temporal bone, parasellar structures (tissues located around the sella turcica), and openings of the base of the skull. Damage to the III, IV, VI, VII, VIII pairs of cranial nerves may occur. As a result, the patient either partially or completely does not open his eyes. There may be restrictions on the movement of the eyeball inwards, convergent strabismus, hearing loss, tinnitus, dizziness, nystagmus, loss of coordination of movements, paresis of the facial muscles, taste disturbance on the anterior 2/3 of the tongue on the side of the lesion of the intermediate nerve in the internal auditory canal.

Bruising is localized in the area of ​​the mastoid process and temporal muscle. There may be bleeding from the ear, liquorrhea in the case of a fracture of the temporal bone pyramid, rupture of the dura mater, the mucous membrane of the internal auditory canal and the eardrum. If its integrity is not broken, then blood and cerebrospinal fluid from the middle ear flow through the eustachian tube into the nasopharynx, and then into the nasal cavity and mouth.

It is extremely rare that heavy bleeding from the nose occurs as a result of rupture of the internal carotid artery, as well as damage to the wall of the sphenoid sinus (Blagoveshchenskaya N.S., 1994).

In a patient with liquorrhea from the nose or ear in the early period, strict bed rest is indicated. It is advisable to prevent coughing and sneezing. A protective sterile cotton-gauze bandage should be applied (on the nose or ear). It is better to give the victim’s head an elevated position, turning and tilting it towards the flow of cerebrospinal fluid. Antibiotics are prescribed prophylactically.

With a fracture of the base of the skull, there may be subarachnoid hemorrhages. The location of the fracture is determined by analyzing craniogram data, the presence of auricular or nasal liquorrhea, and signs of damage to certain cranial nerves. Dehydration therapy is indicated, which reduces pressure and production of cerebrospinal fluid, as well as unloading repeated lumbar punctures.

In addition to a fracture of the base of the skull, traumatic brain injury may cause concussions, brain contusion, and intracranial hematomas. The symptoms of their manifestation also need to be known to the dentist in order to determine treatment tactics for patients.

3. Concussion.

In case of a concussion, microstructural changes in the brain substance were not detected. However, there is damage to cell membranes. Clinically, it is characterized by a loss of consciousness - from stunning to a stop of varying duration (from several seconds to 20 minutes). Sometimes there is loss of memory for events during, before and after the injury, congrade, retrograde, anterograde amnesia. The latter is for a narrow period of events after injury. There may be nausea or occasional vomiting. Patients always report headache, dizziness, weakness, tinnitus, sweating, flushing of the face, and sleep disturbances.

Breathing is shallow, pulse is within the physiological norm. Blood pressure - no significant changes. There may be pain when moving the eyes and reading, divergence of the eyeballs, vestibular hyperesthesia.

With a mild concussion, the pupils are constricted; in severe concussions, their pupils dilate. Sometimes - anisocoria, transient oculomotor disturbances.

Neurological examination sometimes reveals asymmetry of facial muscles, labile rough asymmetry of tendon and skin reflexes, unstable small-scale nystagmus, and occasionally minor membrane symptoms that disappear in the first 3 to 7 days.

A concussion should be considered the mildest form of closed craniocerebral injury. However, these patients in the acute period should be in the hospital under the supervision of a specialist. It is known that symptoms of organic brain damage appear after a light interval. In addition, it is necessary to treat the autonomic and vascular disorders that occur with this brain injury. Bed rest for 5-7 days, the use of sedatives and vasodilators, and antihistamines are indicated.

4. Brain contusion.

With a brain contusion (loss of consciousness for more than 20 minutes), focal microstructural damage to the brain substance of varying severity occurs, edema and swelling of the brain, and changes in the cerebrospinal fluid-containing spaces are observed.

For easy The degree of brain contusion is characterized by loss of consciousness from several minutes to one hour, headache, dizziness, nausea, vomiting. Con-, retro- and anterograde amnesia, moderate bradycardia, clonic nystagmus, mild anisocoria, signs of pyramidal insufficiency, and meningeal symptoms are noted.

Brain contusion average degree of severity is characterized by a longer loss of consciousness (up to several hours), more pronounced focal neurological symptoms, mild transient disturbances of vital functions, and a more severe course of the acute period.

At severe The degree of brain contusion is characterized by loss of consciousness for a long period - from several hours to several weeks. Neurological symptoms with disruption of the vital functions of the body increase. Con-, retro- and anterograde amnesia, severe headache, repeated vomiting, bradycardia or tachycardia, increased blood pressure, tachypnea are expressed.

Meningeal symptoms, nystagmus, and bilateral pathological signs are common. Focal symptoms due to the localization of brain contusion are clearly identified: pupillary and oculomotor disorders, paresis of the limbs, sensitivity and speech disorders. Subarachnoid hemorrhages are common.

In 35–45% of cases with TBI, the temporal lobe of the brain is damaged. Sensory aphasia is characteristic, which is referred to as “verbal okroshka”.

Conservative therapy for brain contusion includes, in addition to the drugs used in patients with concussion, antibacterial treatment for the prevention of meningitis and meningoencephalitis, repeated lumbar punctures before sanitizing the cerebrospinal fluid. From 5 to 10 ml of cerebrospinal fluid can be withdrawn at once. Bed rest is required for 2 to 4 weeks, depending on the severity of the brain damage.

5. Intracranial hematomas.

Facial bone fractures combined with TBI may be accompanied by the formation of intracranial hematomas. According to the literature, they occur in 41.4% of patients with this type of TBI (Fraerman A.B., Gelman Yu.E., 1977).

Epidural hematoma- accumulation of spilled blood between the inner surface of the skull bones and the dura mater. The prerequisite for its formation is the rupture of the vessels of the dura mater - most often the middle meningeal artery and its branches, when struck in the inferior parietal or temporal region. They are localized in the temporal, temporo-parietal, temporo-frontal, temporo-basal regions. The diameter of the hematomas is 7 cm, the volume is from 80 to 120 ml.

An epidural hematoma compresses the underlying dura mater and brain matter, forming a dent in its shape and size. General and local compression of the brain occurs. Characterized by a short loss of consciousness with

its complete recovery, moderate headache, dizziness, general weakness, con- and retrograde amnesia. There may be moderate asymmetry of the nasolabial folds, spontaneous nystagmus, anisoreflexia, and moderate meningeal symptoms.

A relatively favorable state can last for several hours. Then the headache intensifies to the point of unbearable, vomiting occurs, which can be repeated. Possible psychomotor agitation. Drowsiness develops and consciousness turns off again. Bradycardia and increased blood pressure are noted.

Initially, a moderate dilation of the pupil on the side of the hematoma is determined, then with extreme mydriasm (dilation of the pupil) and the absence of its reaction to light.

To diagnose an epidural hematoma, a triad of signs is used: a lucid interval, the absence of cerebral, focal neurological symptoms against the background of temporary restoration of consciousness, homolateral mydriasis, contralateral hemiparesis. Important signs are also bradycardia, hypertension, localized headache, including with percussion of the skull.

The side of brain compression can be determined by damage to the oculomotor nerve - dilation of the pupil on the side of compression, drooping eyelids, divergent strabismus, gaze paresis, decreased or loss of pupillary response to light, dilated on the side of the hematoma.

Contralateral monoor hemiparesis and speech disorder are determined. On the side of the compression, swelling of the optic nerve sometimes occurs, on the opposite side - pyramidal insufficiency. Treatment is only surgical.

Subdural hematomas are characterized by the fact that the spilled blood is localized between the dura mater and the arachnoid mater. It causes general or local compression of the brain. Sometimes - both at the same time.

A subdural hematoma can occur both on the side where force is applied and on the opposite side. Place of impact - occipital, frontal, sagittal areas. Subdural hematomas are the most common among intracranial hematomas. Their dimensions are 10 by 12 cm, the volume ranges from 80 to 150 ml.

The classic version of a hematoma of this localization is characterized by a three-phase change in consciousness: primary loss at the time of injury, an expanded lucid interval, and secondary loss of consciousness. The light period can last from 10 minutes to several hours and even up to 1-2 days.

During this period, patients complain of headache, dizziness, and nausea. Retrograde amnesia is determined. Focal symptoms are not clearly expressed. Subsequently, there is a deepening of stunning, the appearance of drowsiness, and psychomotor agitation. The headache increases sharply, and repeated vomiting occurs. Homolateral mydriasis, contralateral pyramidal insufficiency and sensitivity disorder are detected.

Along with the loss of consciousness, a secondary brainstem syndrome develops with bradycardia, increased blood pressure, changes in breathing rhythm, bilateral vestibuloculomotor pyramidal disorders, and tonic convulsions.

Thus, subdural hematomas are characterized by a slower development of cerebral compression, longer light intervals, the presence of meningeal symptoms and the presence of blood in the cerebrospinal fluid. The remaining symptoms resemble those of an epidural hematoma.

At subarachnoid In a hematoma, spilled blood accumulates under the arachnoid membrane of the brain. Hematomas of this location accompany brain contusions. Blood breakdown products, being toxic, have a mainly vasotropic effect. They can cause cerebral vasospasm and cerebrovascular accident.

The clinical picture of subarachnoid hematoma is characterized by a combination of cerebral, meningeal and focal neurological symptoms. The patient's consciousness is disturbed and he experiences intense headache, dizziness, nausea, vomiting, and psychomotor agitation. Meningeal symptoms may be detected: photophobia, painful movement of the eyeballs, stiff neck, Kerning sign, Brudzinski sign. There may be insufficiency of the VII, XII pairs of cranial nerves of the central type, anisoreflexia, mild pyramidal symptoms.

The body temperature is elevated for 7-14 days due to irritation of the hypothalamic thermoregulation center and the meninges by the spilled blood.

Lumbar puncture is important in diagnosis: the presence of blood indicates subarachnoid hemorrhage.

Intracerebral a hematoma is a hemorrhage located in the substance of the brain. In this case, a cavity is formed filled with blood or blood mixed with brain detritus. In patients with intracerebral hematoma, focal symptoms predominate compared to cerebral symptoms. Of the focal symptoms, pyramidal insufficiency is most often noted, which is always contralateral to the side of the hematoma. Hemiparesis is pronounced. They are accompanied by central paresis of the facial (VII pair) and hypoglossal (XII pair) nerves. More often than with meningeal hematomas, there is a combination of pyramidal and sensory disorders on the same limbs, which can be supplemented by the same hemianopsia. This is explained by the proximity of the intracerebral hematoma to the internal capsule. When these hematomas are localized in the frontal lobe and other “silent” areas, the focal pathology is not clearly expressed. Treatment is surgical.

Very often the brain stem is involved in the pathological process. Stem phenomena significantly complicate the diagnosis of hematomas, distorting their manifestation.

Trunk lesions may be primary(at the time of injury) and secondary when compression is possible by displaced areas of the brain. In addition, dislocation of the trunk itself due to swelling of brain tissue cannot be ruled out.

When the trunk is damaged, a deep coma, severe respiratory distress and abnormalities in cardiac activity, tonic disorders with bilateral pathological signs, and dysfunction of the oculomotor nerves are noted.

To diagnose intracranial hematomas, lumbar puncture cannot be performed due to the risk of developing midbrain compression syndrome (compression of the mesencephalic trunk), or compression of the medulla oblongata, or secondary bulbar syndrome (herniation of the bulbar trunk in the area of ​​the foramen magnum).

6. Treatment of patients with combined traumatic brain injury consists of solving three problems:

1. Combating threatening violations of the vital functions of the body, bleeding, shock, compression and swelling of the brain.

2. Treatment of local extracranial and cranial injuries, which begins immediately after diagnosis.

3. Early prevention of possible complications. It may include radical surgery at various times after injury, depending on the general condition of the patient and the severity of brain damage.

In case of craniofacial trauma, craniomaxillary and craniomandibular fixation is considered the most rational, which allows for sealing of the brain skull, eliminating the cause of brain compression and ensuring reliable immobilization of jaw fragments.

7. Medical and social and labor rehabilitation of patients.Fronto-facial injuries.

Frontofacial injuries are the most severe among craniofacial injuries. With this injury, in addition to a fracture of the upper jaw, a fracture of the forehead occurs.

noal bone, anterior cranial fossa, ethmoid bone, nasal bones. Contusion of the frontal lobes of the brain is possible.

The Fronto-Facial Injuries Clinic has a number of features.

Among them we can note pronounced edema not only the tissues of the face, but also the head. Due to swelling, it is sometimes impossible to examine the eyes, which is important to determine their injury, as well as to identify damage to the optic and oculomotor nerves. With such an injury, compression of the optic nerve in its canal, damage in the chiasm, as well as the formation of hematomas in the retrobulbar area are possible. These patients may have severe nosebleeds immediately after injury, which is quite difficult to stop. This occurs with a fracture of the upper jaw, ethmoid bone, or nasal bones. In this case, liquorrhea is often observed, including difficult to diagnose hidden liquorrhea. All patients with frontofacial fractures should potentially be considered as having CSF leak.

It is sometimes possible to stop bleeding from the nose, including with a fracture of the upper jaw or base of the skull, with posterior nasal tamponade.

In such patients, a tracheostomy is often applied, because Intubation through the glottis is very difficult for them. At the same time, they often have aspiration of vomit, blood, and mucus, which makes it necessary to sanitize the tracheobronchial tree through a tracheostomy.

Damage to the frontal lobes of the brain affects the patient’s behavior and determines the uniqueness of the clinical picture. Patients are disoriented in their own identity, place and time. They show negativism, resist examination, are uncritical of their condition, and are stereotypical in speech and behavior. They have bulimia, thirst, and untidiness. Possible psychomotor agitation.

Treatment. When providing first aid, it is necessary to normalize the victim’s breathing, stop the bleeding, and begin anti-shock measures. Before the patient is brought out of shock, primary surgical treatment of head and face wounds is contraindicated. Surgical interventions are performed only for health reasons. A mandatory examination by an ophthalmologist, a neurologist, and, if indicated, a neurosurgeon is required.

An X-ray examination of the skull and facial bones should be performed in two projections. If an intracranial hematoma is present, it should be removed as soon as possible. Therapeutic immobilization is carried out no earlier than 4 - 7 days after the patient is recovered from a serious condition. In case of brain contusions, permanent immobilization of the broken upper jaw is possible only after stabilization of vital functions (blood pressure, breathing, cardiac activity). This can usually be achieved within 2–4 days from the moment of injury.

From a practical point of view, traumatic brain injury combined with fractures of the facial bones (including the upper jaw) is divided into four groups (Gelman Yu.E., 1977):

Group 1 - severe TBI (severe and moderate brain contusion, intracranial hematomas) and severe fractures of the facial bones (Le Fort type I and II fracture of the upper jaw, simultaneous fracture of the upper and lower jaws). Half of these patients develop traumatic shock.

Temporary immobilization in patients of group 1 is possible immediately after they are brought out of shock. Therapeutic immobilization using conservative methods is allowed for 2–5 days from the moment of injury and recovery from shock; osteosynthesis is carried out no earlier than on the seventh day.

Group 2 - severe TBI and minor trauma to the facial bones (Le Fort III fracture of the upper jaw, unilateral fractures of the upper and lower jaws, zygomatic bones, etc.). Therapeutic immobilization in patients of group 2 can be carried out after 1-3 days.

Group 3 - mild TBI (concussion, mild brain contusion) and severe injuries to the facial bones. The severity of the patients' condition is mainly due to trauma to the facial skeleton. Therapeutic immobilization in patients of this group, including osteosynthesis, is possible already on the first day after injury.

Group 4 - non-severe TBI and minor injuries to the bones of the facial skeleton. Patient immobilization of fragments can be carried out already in the first hours after injury.

Early specialized treatment not only does not aggravate the patient’s condition, but also promotes earlier cessation of liquorrhea and reduces the risk of developing intracranial inflammatory complications.

Traumatic brain injury in the structure of combined injuries is leading both in frequency (46.9% of all victims with combined injuries) and in severity. Brain injury occurs as a result of traffic accidents (58.7%), falls from height (37%), falls on the street (3%) and blows to the head (1.3%). At the time of injury, 33% of patients (mostly men) are intoxicated. Skull fractures occur in 56.5% of victims, closed - in 44%, open - in 12.1%, fractures of the bones of the cranial vault predominate (27.7%), then - the vault and base (15.8%) and the base ( 13%). Damage to the facial skeleton is observed in 28.1% of patients (more often - the lower jaw, nasal bones, upper jaw, less often - the zygomatic bone).

Signs and symptoms of traumatic brain injury

The diagnosis of a fracture of the skull vault is made on the basis of external signs (deformation of the vault area, palpation of indentation and protrusion of fragments, open fracture). Symptoms of a fracture of the base of the skull are: hemorrhages in the eyelids (“spectacles”), mastoid process, bleeding or traces of it from the mouth, from the nasal and ear passages, leakage of cerebrospinal fluid from the nose and ears, dysfunction of the cranial nerves, and general cerebral disorder.

The clinical picture of the state of the brain in most cases is obscured by the symptoms of concomitant more severe injuries (fractures of the ribs, pelvis, limbs). It can be assumed that in case of severe injury resulting from transport accidents, as well as from a fall from a height, regardless of the location of the damage, a brain injury (usually a concussion) should be expected.

Degrees of concussion

In the clinical picture, the following degrees of concussion are distinguished:

mild degree(without pronounced focal symptoms, with short-term loss of consciousness, the presence of a skull fracture);

moderate severity(with pronounced focal symptoms - hemiparesis, paralysis, convulsions with loss of consciousness or stuporous state for many minutes or even hours);

severe degree(with multiple scattered symptoms, meningeal symptoms, secondary boulevard disorders: respiratory, swallowing, cardiovascular disorders, as well as the presence of a coma or prolonged somnolent state for several weeks).

Brain contusions, as a rule, accompany severe fractures of the base of the skull and constantly serve as the main obstacle to active orthopedic treatment of fractures of the extremity bones, even when traumatic brain injury does not dominate in severity in the clinical picture of the victims. It can be assumed that in some cases, a wait-and-see approach (“until a trend toward improvement is determined”) in relation to concomitant severe injuries to the extremities is poorly justified, as a result of which the condition of the victims may worsen due to secondary complications of the injury: intoxication, anemia, infection, etc. etc., which in themselves exclude active surgical interventions.

Diagnosis of irreversible brain damage in polytrauma is extremely difficult and is mostly determined at autopsy. The most important symptoms that make it possible to identify brain damage against the background of multiple general trauma are deep coma, severe respiratory distress, drop in blood pressure, pulmonary edema, areflexia, maximally dilated pupils without their reaction to light, hypothermia, bioelectrical “silence” of the brain. Topical diagnosis of contusion-hemorrhagic foci in brain contusions using clinical methods for combined injuries is difficult due to damage to peripheral nerves, polyfractures of the limbs, pelvis, and spine.

First aid for traumatic brain injury

The victim with symptoms of a concussion is provided with physical and mental rest, placed with his head elevated, the collar unbuttoned, cooled, the forehead with a damp towel. Transportation is carried out strictly on a stretcher to the surgical, trauma or neurological department.

In case of brain contusions, the main attention is paid to the fight against acute respiratory failure. For these purposes, the patency of the upper respiratory tract is restored, an air duct is inserted, oxygen is inhaled, if necessary, the victim is intubated and artificial ventilation of the lungs is carried out using manual respirators or portable machines.

Prevention of liquor hypertension is carried out by intravenous administration of a 40% glucose solution (40-60 ml), urea (20% solution 100-150 ml), mannitol (20% solution 300-400 ml), Lasix (1-2 ml), novocaine (0 ,25% solution 300-400 ml). In case of a hyperthermic reaction, amidopyrine (4% solution 5-10 ml) is administered intramuscularly, analgin (2 ml of 50% solution), diphenhydramine (1 ml of 1% solution) is administered intravenously. The head is cooled with ice packs and wet towels. In cases of severe shock, intensive infusion therapy is carried out: 400 ml of polyglucin (gelatinol), 500 ml of a 10% glucose solution + insulin (12 units), and a glucose-caine mixture (up to 1000 ml drip) are injected intravenously. Hydrocortisone is also administered up to 0.5 g, sodium hydroxybutyrate up to 80-100 ml of a 20% solution per day. Victims are transported in a horizontal position with their head raised.

Damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). Based on the nature of the injury, a distinction is made between closed and open, penetrating and non-penetrating TBI, as well as concussion or contusion of the brain. The clinical picture of traumatic brain injury depends on its nature and severity. The main symptoms are headache, dizziness, nausea and vomiting, loss of consciousness, memory impairment. Brain contusion and intracerebral hematoma are accompanied by focal symptoms. Diagnosis of traumatic brain injury includes medical history, neurological examination, skull x-ray, CT or MRI of the brain.

General information

Damage to the bones of the skull and/or soft tissues (meninges, brain tissue, nerves, blood vessels). The classification of TBI is based on its biomechanics, type, type, nature, shape, severity of injury, clinical phase, treatment period, and outcome of the injury.

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

• shock-anti-shock (the shock wave propagates from the site of the received blow and passes through the brain to the opposite side with rapid pressure changes);
• acceleration-deceleration (movement and rotation of the cerebral hemispheres in relation to a more fixed brain stem);
• combined (simultaneous impact of both mechanisms).

By type of damage:

• focal (characterized by local macrostructural damage to the brain matter, with the exception of areas of destruction, small and large focal hemorrhages in the area of ​​impact, counter-impact and shock wave);
• diffuse (tension and spread of primary and secondary axonal ruptures in the centrum semiovale, corpus callosum, subcortical formations, brain stem);
• combined (a combination of focal and diffuse brain damage).

According to the genesis of the lesion:

• primary lesions: focal contusions and crushes of the brain, diffuse axonal damage, primary intracranial hematomas, brainstem ruptures, multiple intracerebral hemorrhages;
• secondary lesions:

1. due to secondary intracranial factors (delayed hematomas, disturbances in cerebrospinal fluid and hemocirculation due to intraventricular or subarachnoid hemorrhage, cerebral edema, hyperemia, etc.);
2. due to secondary extracranial factors (arterial hypertension, hypercapnia, hypoxemia, anemia, etc.)

According to their type, TBIs are classified into: closed - injuries that do not violate the integrity of the skin of the head; fractures of the bones of the calvarium without damage to the adjacent soft tissues or a fracture of the base of the skull with developed liquorrhea and bleeding (from the ear or nose); open non-penetrating TBI - without damage to the dura mater and open penetrating TBI - with damage to the dura mater. In addition, isolated (absence of any extracranial damage), combined (extracranial damage as a result of mechanical energy) and combined (simultaneous exposure to various energies: mechanical and thermal/radiation/chemical) traumatic brain injury are distinguished.

Based on severity, TBI is divided into 3 degrees: mild, moderate and severe. When correlating this rubric with the Glasgow Coma Scale, mild traumatic brain injury is assessed at 13-15, moderate at 9-12, severe at 8 points or less. A mild traumatic brain injury corresponds to a mild concussion and contusion, a moderate one corresponds to a moderate brain contusion, a severe one corresponds to a severe brain contusion, diffuse axonal damage and acute compression of the brain.

According to the mechanism of occurrence of TBI, there are primary (the impact of traumatic mechanical energy on the brain is not preceded by any cerebral or extracerebral catastrophe) and secondary (the impact of traumatic mechanical energy on the brain is preceded by a cerebral or extracerebral catastrophe). TBI in the same patient can occur for the first time or repeatedly (twice, three times).

The following clinical forms of TBI are distinguished: concussion, mild brain contusion, moderate brain contusion, severe brain contusion, diffuse axonal damage, brain compression. The course of each of them is divided into 3 basic periods: acute, intermediate and long-term. The duration of the periods of traumatic brain injury varies depending on the clinical form of TBI: acute - 2-10 weeks, intermediate - 2-6 months, long-term with clinical recovery - up to 2 years.

Brain concussion

The most common injury among possible traumatic brain injuries (up to 80% of all TBIs).

Clinical picture

Depression of consciousness (to the level of stupor) during a concussion can last from several seconds to several minutes, but may be absent altogether. Retrograde, congrade and antegrade amnesia develops for a short period of time. Immediately after a traumatic brain injury, a single vomiting occurs, breathing becomes more frequent, but soon returns to normal. Blood pressure also returns to normal, except in cases where the medical history is aggravated by hypertension. Body temperature during a concussion remains normal. When the victim regains consciousness, there are complaints of dizziness, headache, general weakness, cold sweat, flushing of the face, and tinnitus. The neurological status at this stage is characterized by mild asymmetry of skin and tendon reflexes, small horizontal nystagmus in the extreme abductions of the eyes, and mild meningeal symptoms that disappear during the first week. With a concussion as a result of a traumatic brain injury, after 1.5 - 2 weeks, an improvement in the patient’s general condition is noted. It is possible that some asthenic phenomena may persist.

Diagnosis

Recognizing a concussion is not an easy task for a neurologist or traumatologist, since the main criteria for diagnosing it are the components of subjective symptoms in the absence of any objective data. It is necessary to familiarize yourself with the circumstances of the injury, using the information available to witnesses to the incident. Of great importance is an examination by an otoneurologist, with the help of which the presence of symptoms of irritation of the vestibular analyzer in the absence of signs of prolapse is determined. Due to the mild semiotics of a concussion and the possibility of a similar picture arising as a result of one of many pre-traumatic pathologies, special importance in diagnosis is given to the dynamics of clinical symptoms. The justification for the diagnosis of “concussion” is the disappearance of such symptoms 3-6 days after receiving a traumatic brain injury. With a concussion, there are no fractures of the skull bones. The composition of the cerebrospinal fluid and its pressure remain normal. CT scan of the brain does not detect intracranial spaces.

Treatment

If a victim with a traumatic brain injury has come to his senses, first of all he needs to be given a comfortable horizontal position, his head should be slightly raised. A victim with a traumatic brain injury who is in an unconscious state must be given the so-called. The “saving” position is to lay him on his right side, his face should be turned to the ground, his left arm and leg should be bent at a right angle at the elbow and knee joints (if fractures of the spine and limbs are excluded). This position promotes the free passage of air into the lungs, preventing the tongue from retracting and vomit, saliva and blood from entering the respiratory tract. Apply an aseptic bandage to bleeding wounds on the head, if any.

All victims with traumatic brain injury are necessarily transported to a hospital, where, after confirmation of the diagnosis, they are placed on bed rest for a period that depends on the clinical characteristics of the course of the disease. The absence of signs of focal brain lesions on CT and MRI of the brain, as well as the patient’s condition, which allows one to refrain from active drug treatment, allows us to resolve the issue in favor of discharging the patient for outpatient treatment.

For a concussion, overactive drug treatment is not used. Its main goals are to normalize the functional state of the brain, relieve headaches, and normalize sleep. For this purpose, analgesics and sedatives (usually in tablet forms) are used.

Brain contusion

Mild brain contusion is detected in 10-15% of victims with traumatic brain injury. A bruise of moderate severity is diagnosed in 8-10% of victims, a severe bruise - in 5-7% of victims.

Clinical picture

A mild brain contusion is characterized by loss of consciousness after injury of up to several tens of minutes. After consciousness is restored, complaints of headache, dizziness, and nausea appear. Retrograde, congrade, and anterograde amnesia are noted. Vomiting is possible, sometimes with repetitions. Vital functions are usually preserved. Moderate tachycardia or bradycardia and sometimes increased blood pressure are observed. Body temperature and respiration without significant deviations. Mild neurological symptoms regress after 2-3 weeks.

Loss of consciousness with a moderate brain contusion can last from 10-30 minutes to 5-7 hours. Retrograde, congrade and anterograde amnesia are strongly expressed. Repeated vomiting and severe headache are possible. Some vital functions are impaired. Bradycardia or tachycardia, increased blood pressure, tachypnea without respiratory distress, and increased body temperature to subfebrile are detected. The manifestation of meningeal signs, as well as stem symptoms, is possible: bilateral pyramidal signs, nystagmus, dissociation of meningeal symptoms along the body axis. Pronounced focal signs: oculomotor and pupillary disorders, paresis of the limbs, speech and sensitivity disorders. They regress after 4-5 weeks.

Severe brain contusion is accompanied by loss of consciousness from several hours to 1-2 weeks. It is often combined with fractures of the bones of the base and vault of the skull, and profuse subarachnoid hemorrhage. Disorders of vital functions are noted: respiratory rhythm disturbances, sharply increased (sometimes decreased) blood pressure, tachy- or bradyarrhythmia. Possible blockage of the airways, intense hyperthermia. Focal symptoms of hemispheric damage are often masked behind stem symptoms that come to the fore (nystagmus, gaze paresis, dysphagia, ptosis, mydriasis, decerebrate rigidity, changes in tendon reflexes, the appearance of pathological foot reflexes). Symptoms of oral automatism, paresis, focal or generalized seizures can be detected. Restoring lost functions is difficult. In most cases, gross residual motor and mental disorders remain.

Diagnosis

The method of choice for diagnosing a brain contusion is a CT scan of the brain. A CT scan reveals a limited area of ​​low density, possible fractures of the calvarial bones and subarachnoid hemorrhage. With a brain contusion of moderate severity, CT or spiral CT in most cases reveals focal changes (non-compactly located areas of low density with small areas of increased density).

In case of severe contusion, CT scan reveals areas of heterogeneous increase in density (alternating areas of increased and decreased density). Perifocal cerebral edema is severe. A hypodense track is formed in the area of ​​the nearest section of the lateral ventricle. Through it, fluid with breakdown products of blood and brain tissue is discharged.

Diffuse axonal brain injury

Diffuse axonal brain damage is typically characterized by a prolonged coma after a traumatic brain injury, as well as pronounced brain stem symptoms. Coma is accompanied by symmetrical or asymmetrical decerebration or decortication, both spontaneous and easily provoked by irritations (for example, painful ones). Changes in muscle tone are very variable (hormetonia or diffuse hypotension). A typical manifestation is pyramidal-extrapyramidal paresis of the limbs, including asymmetric tetraparesis. In addition to gross disturbances in the rhythm and frequency of breathing, autonomic disorders also appear: increased body temperature and blood pressure, hyperhidrosis, etc. A characteristic feature of the clinical course of diffuse axonal brain damage is the transformation of the patient’s condition from a prolonged coma to a transient vegetative state. The onset of this state is indicated by spontaneous opening of the eyes (with no signs of tracking or fixation of gaze).

Diagnosis

The CT picture of diffuse axonal brain damage is characterized by an increase in brain volume, as a result of which the lateral and third ventricles, subarachnoid convexital spaces, and also the cisterns of the base of the brain are under compression. The presence of small focal hemorrhages in the white matter of the cerebral hemispheres, corpus callosum, subcortical and brain stem structures is often detected.

Brain compression

Brain compression develops in more than 55% of cases of traumatic brain injury. Most often, the cause of compression of the brain is an intracranial hematoma (intracranial, epi- or subdural). Rapidly increasing focal, brainstem and cerebral symptoms pose a danger to the life of the victim. Availability and duration of the so-called the “light gap” - expanded or erased - depends on the severity of the victim’s condition.

Diagnosis

A CT scan reveals a biconvex, less often a flat-convex, limited zone of increased density, which is adjacent to the cranial vault and is localized within one or two lobes. However, if there are several sources of bleeding, the area of ​​​​increased density can be significant in size and have a crescent shape.

Treatment of traumatic brain injury

When a patient with a traumatic brain injury is admitted to the intensive care unit, the following measures must be taken:

• Examination of the victim’s body, during which abrasions, bruises, joint deformities, changes in the shape of the abdomen and chest, bleeding and/or liquor leakage from the ears and nose, bleeding from the rectum and/or urethra, and a specific odor from the mouth are detected or excluded.
• Comprehensive x-ray examination: skull in 2 projections, cervical, thoracic and lumbar spine, chest, pelvic bones, upper and lower extremities.
• Ultrasound of the chest, ultrasound of the abdominal cavity and retroperitoneal space.
• Laboratory tests: general clinical analysis of blood and urine, biochemical blood test (creatinine, urea, bilirubin, etc.), blood sugar, electrolytes. These laboratory tests must be carried out in the future, daily.
• ECG (three standard and six chest leads).
• Testing urine and blood for alcohol content. If necessary, consult a toxicologist.
• Consultations with a neurosurgeon, surgeon, traumatologist.

A mandatory method of examining victims with traumatic brain injury is computed tomography. Relative contraindications to its implementation may include hemorrhagic or traumatic shock, as well as unstable hemodynamics. Using CT, the pathological focus and its location, the number and volume of hyper- and hypodense zones, the position and degree of displacement of the midline structures of the brain, the condition and degree of damage to the brain and skull are determined. If meningitis is suspected, a lumbar puncture and dynamic examination of the cerebrospinal fluid are indicated, which allows monitoring changes in the inflammatory nature of its composition.

A neurological examination of a patient with a traumatic brain injury should be performed every 4 hours. To determine the degree of consciousness impairment, the Glasgow Coma Scale is used (state of speech, response to pain and ability to open/close eyes). In addition, the level of focal, oculomotor, pupillary and bulbar disorders is determined.

For a victim with impaired consciousness of 8 points or less on the Glasgow scale, tracheal intubation is indicated, due to which normal oxygenation is maintained. Depression of consciousness to the level of stupor or coma is an indication for auxiliary or controlled mechanical ventilation (at least 50% oxygen). With its help, optimal cerebral oxygenation is maintained. Patients with severe traumatic brain injury (hematomas, cerebral edema, etc. detected on CT) require monitoring of intracranial pressure, which must be maintained below 20 mmHg. For this purpose, mannitol, hyperventilation, and sometimes barbiturates are prescribed. To prevent septic complications, escalation or de-escalation antibacterial therapy is used. For the treatment of post-traumatic meningitis, modern antimicrobial drugs approved for endolumbar administration (vancomycin) are used.

Patients begin feeding no later than 3 days after TBI. Its volume is increased gradually and at the end of the first week following the date of the traumatic brain injury, it should provide 100% of the patient’s caloric needs. The route of nutrition can be enteral or parenteral. To relieve epileptic seizures, anticonvulsants are prescribed with minimal dose titration (levetiracetam, valproate).

The indication for surgery is an epidural hematoma with a volume of over 30 cm³. It has been proven that the method that ensures the most complete evacuation of the hematoma is transcranial removal. Acute subdural hematoma with a thickness of more than 10 mm is also subject to surgical treatment. In comatose patients, acute subdural hematoma is removed using craniotomy, maintaining or removing a bone flap. An epidural hematoma with a volume of more than 25 cm³ is also subject to mandatory surgical treatment.

Prognosis for traumatic brain injury

Concussion is a predominantly reversible clinical form of traumatic brain injury. Therefore, in more than 90% of cases of concussion, the outcome of the disease is the recovery of the victim with full restoration of ability to work. Some patients, after the acute period of concussion, experience certain manifestations of post-concussion syndrome: disturbances in cognitive functions, mood, physical well-being and behavior. 5-12 months after a traumatic brain injury, these symptoms disappear or are significantly smoothed out.

Prognostic assessment in severe traumatic brain injury is carried out using the Glasgow Outcome Scale. A decrease in the total number of points on the Glasgow scale increases the likelihood of an unfavorable outcome of the disease. Analyzing the prognostic significance of the age factor, we can conclude that it has a significant impact on both disability and mortality. The combination of hypoxia and arterial hypertension is an unfavorable prognosis factor.

Traumatic brain injuries rank first among all injuries (40%) and most often occur in people aged 15–45 years. The mortality rate among men is 3 times higher than among women. In large cities, every year out of a thousand people, seven receive traumatic brain injuries, while 10% die before reaching the hospital. In the case of a mild injury, 10% of people remain disabled, in the case of a moderate injury - 60%, severe - 100%.

Causes and types of traumatic brain injuries

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

Most often, participants in road accidents suffer from traumatic brain injuries: drivers, passengers of public transport, pedestrians hit by vehicles. In second place in terms of frequency of occurrence are household injuries: accidental falls, blows. Next come injuries sustained at work and sports.

Young people are most susceptible to injuries in the summer - these are so-called criminal injuries. Elderly people are more likely to get a TBI in the winter, and the leading cause is a fall from a height.

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

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

• by severity: light(concussion, slight bruise), average(serious injury) heavy(severe brain contusion, acute compression of the brain). The Glasgow Coma Scale is used to determine severity. The victim's condition is assessed from 3 to 15 points depending on the level of confusion, ability to open eyes, speech and motor reactions;
• type: open(there are wounds on the head) and closed(no damage to the scalp);
• by type of damage: isolated(damage affects only the skull), combined(the skull and other organs and systems are damaged), combined(the injury was not only mechanical, the body was also affected by radiation, chemical energy, etc.);
• according to the nature of the damage:
• shake(minor injury with reversible consequences, characterized by a short-term loss of consciousness - up to 15 minutes, most victims do not require hospitalization, after examination the doctor may prescribe a CT or MRI);
• injury(a disruption of brain tissue occurs due to an impact of the brain on the wall of the skull, often accompanied by hemorrhage);
• diffuse axonal brain injury(axons - the processes of nerve cells that conduct impulses - are damaged, the brain stem suffers, microscopic hemorrhages are noted in the corpus callosum of the brain; such damage most often occurs in an accident - at the time of sudden braking or acceleration);
• compression(hematomas form in the cranial cavity, the intracranial space is reduced, crush areas are observed; emergency surgical intervention is required to save a person’s life).

It is important to know
Brain injury most often occurs at the site of impact, but often damage occurs on the opposite side of the skull - in the impact zone.

The classification is based on the diagnostic principle; on its basis, a detailed diagnosis is formulated, according to which treatment is prescribed.

Symptoms of TBI

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

Diagnosis « brain concussion» diagnosed on the basis of anamnesis. Typically, the victim reports that there was a blow to the head, which was accompanied by a short-term loss of consciousness and a single vomiting. The severity of the concussion is determined by the duration of loss of consciousness - from 1 minute to 20 minutes. At the time of examination, the patient is in a clear state and may complain of a headache. No abnormalities other than pale skin are usually detected. In rare cases, the victim cannot remember the events that preceded the injury. If there was no loss of consciousness, the diagnosis is considered doubtful. Within two weeks after a concussion, weakness, increased fatigue, sweating, irritability, and sleep disturbances may occur. If these symptoms do not disappear for a long time, then it is worth reconsidering the diagnosis.

At mild brain contusion And the victim may lose consciousness for an hour, and then complain of headache, nausea, and vomiting. Eye twitching when looking to the side and asymmetry of reflexes are noted. An X-ray may show a fracture of the bones of the skull vault, and blood in the cerebrospinal fluid.

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

Moderate brain contusion severity is accompanied by loss of consciousness for several hours, the patient does not remember the events preceding the injury, the injury itself and what happened after it, complains of headache and repeated vomiting. The following may be observed: disturbances in blood pressure and pulse, fever, chills, soreness of muscles and joints, convulsions, visual disturbances, uneven pupil size, speech disturbances. Instrumental studies show fractures of the vault or base of the skull, subarachnoid hemorrhage.

At severe brain contusion the victim may lose consciousness for 1–2 weeks. At the same time, gross violations of vital functions (pulse rate, pressure level, frequency and rhythm of breathing, temperature) are detected. The movements of the eyeballs are uncoordinated, muscle tone is changed, the swallowing process is impaired, weakness in the arms and legs can reach convulsions or paralysis. As a rule, this condition is a consequence of fractures of the vault and base of the skull and intracranial hemorrhage.

It is important!
If you or your loved ones suspect that you have suffered a traumatic brain injury, you need to see a traumatologist and neurologist within a few hours and carry out the necessary diagnostic procedures. Even if it seems that you are feeling fine. After all, some symptoms (cerebral edema, hematoma) may appear after a day or even more.

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

At compression of the brain Two clinical pictures can be observed. In the first case, there is a “light period”, during which the victim regains consciousness, and then slowly enters a state of stupor, which is generally similar to stupor and numbness. In another case, the patient immediately falls into a coma. Each condition is characterized by uncontrolled eye movements, strabismus, and cross-limb paralysis.

Long-term head compression accompanied by swelling of the soft tissues, reaching a maximum 2–3 days after its release. The victim is in psycho-emotional stress, sometimes in a state of hysteria or amnesia. Swollen eyelids, impaired vision or blindness, asymmetrical swelling of the face, lack of sensitivity in the neck and back of the head. A computed tomography scan shows swelling, hematomas, skull fractures, areas of brain contusion and crush injuries.

Consequences and complications of TBI

After suffering a traumatic brain injury, many become disabled due to mental disorders, movements, speech, memory, post-traumatic epilepsy and other reasons.

Even mild TBI affects cognitive functions- the victim experiences confusion and decreased mental abilities. More severe injuries may result in amnesia, impairment of vision, hearing, speech and swallowing skills. In severe cases, speech becomes slurred or even lost completely.

Disorders of motor skills and functions of the musculoskeletal system are expressed in paresis or paralysis of the limbs, loss of sensitivity of the body, and lack of coordination. In cases of severe and moderate injuries, there is failure to close the larynx, as a result of which food accumulates in the pharynx and enters the respiratory tract.

Some TBI survivors suffer from pain syndrome- acute or chronic. Acute pain syndrome persists for a month after injury and is accompanied by dizziness, nausea, and vomiting. Chronic headache accompanies a person throughout his life after receiving a TBI. The pain can be sharp or dull, throbbing or pressing, localized or radiating, for example, to the eyes. Attacks of pain can last from several hours to several days, intensifying during moments of emotional or physical stress.

Patients have a hard time experiencing the deterioration and loss of body functions, partial or complete loss of performance, and therefore suffer from apathy, irritability, and depression.

Treatment of TBI

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

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

The neurologist examines the patient every 4 hours and assesses his condition using the Glasgow scale. If the patient's consciousness is impaired, tracheal intubation is indicated. A patient in a state of stupor or coma is prescribed artificial ventilation. Intracranial pressure is regularly measured in patients with hematomas and cerebral edema.

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

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

Prognosis of recovery for TBI of varying severity

In the case of a concussion, the prognosis is favorable provided that the victim follows the recommendations of the attending physician. Full recovery of ability to work is observed in 90% of patients with mild TBI. In 10%, cognitive functions remain impaired and there are sudden changes in mood. But these symptoms usually disappear within 6–12 months.

The prognosis for moderate and severe forms of TBI is based on the number of points on the Glasgow scale. An increase in scores indicates positive dynamics and a favorable outcome of the injury.

In victims with moderate TBI, it is also possible to achieve complete restoration of body functions. But often headaches, hydrocephalus, vegetative-vascular dysfunction, coordination problems and other neurological disorders remain.

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

Of great importance in returning the patient to an active life is the complex of rehabilitation measures provided to him after the acute phase has stopped.

Directions for rehabilitation after traumatic brain injury

World statistics show that 1 dollar invested in rehabilitation today will save 17 dollars to ensure the life of the victim tomorrow. Rehabilitation after TBI is carried out by a neurologist, rehabilitation specialist, physical therapist, occupational therapist, massage therapist, psychologist, neuropsychologist, speech therapist and other specialists. Their activities, as a rule, are aimed at returning the patient to a socially active life. The work to restore the patient’s body is largely determined by the severity of the injury. Thus, in case of severe injury, the efforts of doctors are aimed at restoring the functions of breathing and swallowing, and improving the functioning of the pelvic organs. Specialists are also working to restore higher mental functions (perception, imagination, memory, thinking, speech) that may have been lost.

Physical therapy:

• Bobath therapy involves stimulating the patient's movements by changing the positions of his body: short muscles are stretched, weak muscles are strengthened. People with mobility limitations get the opportunity to learn new movements and hone those they have learned.
• Vojta therapy helps connect brain activity and reflex movements. The physical therapist stimulates various areas of the patient's body, thereby encouraging him to perform certain movements.
• Mulligan therapy helps relieve muscle tension and pain-free movements.
• Installation "Exart" - suspension systems, with the help of which you can relieve pain and return atrophied muscles to work.
• Exercise classes. Classes are shown on cardio simulators, simulators with biofeedback, as well as on a stabilization platform - for training coordination of movements.

Occupational therapy- a direction of rehabilitation that helps a person adapt to environmental conditions. The occupational therapist teaches the patient to take care of himself in everyday life, thereby improving his quality of life, allowing him to return not only to social life, but even to work.

Kinesio taping- applying special adhesive tapes to damaged muscles and joints. Kinesitherapy helps reduce pain and swelling, without limiting movement.

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

Physiotherapy:

• Drug electrophoresis combines the introduction of drugs into the victim’s body with the influence of direct current. The method allows you to normalize the state of the nervous system, improve blood supply to tissues, and relieve inflammation.
• Laser therapy effectively combats pain, tissue swelling, and has an anti-inflammatory and reparative effect.
• Acupuncture can help reduce pain. This method is part of a complex of therapeutic measures in the treatment of paresis and has a general psychostimulating effect.

Drug therapy is aimed at preventing brain hypoxia, improving metabolic processes, restoring active mental activity, and normalizing a person’s emotional background.

After moderate and severe traumatic brain injuries, it is difficult for victims to return to their usual way of life or come to terms with forced changes. In order to reduce the risk of developing serious complications after a TBI, you need to follow simple rules: do not refuse hospitalization, even if it seems that you are feeling fine, and do not neglect various types of rehabilitation, which, with an integrated approach, can show significant results.

Which rehabilitation center after TBI can I go to?

“Unfortunately, there is no single rehabilitation program after traumatic brain injury that would allow the patient to return to his previous condition with a 100% guarantee,” says a rehabilitation center specialist. - The main thing to remember: with TBI, much depends on how quickly rehabilitation measures begin. For example, “Three Sisters” admits victims immediately after hospitalization; we even provide assistance to patients with ostomies, bedsores, and work with the youngest patients. We accept patients 24 hours a day, seven days a week, and not only from Moscow, but also from the regions. We devote 6 hours a day to rehabilitation sessions and continuously monitor the dynamics of recovery. Our center employs neurologists, cardiologists, neurourologists, physical therapists, occupational therapists, neuropsychologists, psychologists, speech therapists - all of them are experts in rehabilitation. Our task is to improve not only the physical condition of the victim, but also the psychological one. We help a person gain confidence that, even after suffering severe trauma, he can be active and happy.”

License to carry out medical activities LO-50-01-009095 dated October 12, 2017 issued by the Ministry of Health of the Moscow Region

Editorial opinion

If there is a suspicion of a TBI, then under no circumstances should you attempt to sit the victim down or lift him. You cannot leave him unattended and refuse medical care.

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Combined trauma is a pressing social and medical problem that lies at the intersection of traumatology, neurosurgery, general surgery, resuscitation and other disciplines. The share of combined trauma in the structure of transport and some other types of injuries reaches 50–70%. Its almost constant component is traumatic brain injury (up to 80%).

The need for a unified terminology and classification of combined traumatic brain injury is obvious. It is due to the fact that victims are hospitalized in various hospitals and treated by doctors of many specialties. Assessing the severity of the patient’s condition and injury is not always unambiguous, and without this it is difficult to develop adequate tactics and ensure continuity in treatment. Without a unified classification, real statistics, effective scientific development of a problem, and resolution of organizational issues are impossible.

Combined injury is simultaneous damage by one type of energy, in particular mechanical, to two or more organs or parts of the body, topographically different areas or different systems. In light of this general concept, a traumatic brain injury is combined if the mechanical energy simultaneously causes extracranial damage.
It is advisable to retain the term “combined injury” to denote simultaneous effects on the body of various types of energy (mechanical, thermal, radiation, chemical, etc.).

Other terms often used to designate injuries—“multiple trauma” or “polytrauma”—are very vague; these concepts may include multiple injuries to an organ or limb or simultaneous injury to several body systems.

Based on these premises, preference should be given to the term “combined injury”.

The appearance of the craniocerebral component in the structure of combined injury always introduces qualitatively new features into its pathogenesis, clinical picture, diagnosis and treatment.

Unlike all other variants of combined injuries of internal organs and the musculoskeletal system without a craniocerebral component, combined traumatic brain injury is characterized by a simultaneous violation of the higher regulatory (brain) and predominantly executive (internal organs, limbs, spinal cord, etc. .) body systems. At the same time, in the absence of the craniocerebral component, with combined injuries, only the executive organs suffer, with the primary preservation of the central nervous system.

The classification of combined traumatic brain injury is based on the following principles:
1. Localization of extracranial injuries.
2. Characteristics of traumatic brain and extracranial injury.
3. The ratio of cranial and extracranial injuries according to their severity.

Considering the localization of extracranial injuries, which leaves its mark on the clinical picture and surgical tactics, it is advisable to identify the following combinations of traumatic brain injury:
1. With damage to the facial skeleton.
2. With damage to the chest and its organs.
3. With damage to the abdominal organs and retroperitoneal space.
4. With damage to the spine and spinal cord.
5. With damage to the limbs and pelvis.
6. With multiple extracranial injuries.

In addition to the local factor, the features of diagnosis, therapy, as well as the outcome of the disease are largely determined by the ratio of injuries by severity. This justifies the practical need to divide each type of combined injury into 4 groups:
1. Severe traumatic brain injury and severe extracranial injuries.
2. Severe traumatic brain injury and non-severe extracranial injuries.
3. Mild traumatic brain injury and severe extracranial injuries.
4. Non-severe traumatic brain injury and non-severe extracranial injuries.

Severe traumatic brain injury includes severe brain contusions and brain compression, and also, in the context of combined trauma, moderate brain contusion.

Non-severe traumatic brain injury includes concussion and mild brain contusions.

Severe extracranial injuries include fractures of the femur, pelvis, tibia, shoulder, multiple fractures of extremity bones; fractures of the upper jaw type FOR - 2, FOR-3, bilateral fracture of the lower jaw, multiple fractures of the facial skeleton; one- and two-sided rib fractures, accompanied by respiratory failure and chest compression; fractures and dislocations of the vertebrae with damage to the spinal cord and its roots, unstable fractures of the vertebral bodies; damage to the organs of the thoracic and abdominal cavities, retroperitoneal space.

Non-severe extracranial injuries include closed fractures of the bones of the hand, foot, forearm, fibula, nose, unilateral fractures of 1-3 ribs without damage to the pleura, bruises of the torso and limbs.

Multiple extracranial injuries include cases when, along with a traumatic brain injury, there is damage to organs of two or more different systems (for example, traumatic brain injury + hip fracture + lung injury).

It is acceptable to apply the term “severe combined traumatic brain injury” to patients of groups I, II, III, i.e. when one or both components of the combined traumatic brain injury are severe. However, in these cases, it is necessary to decipher the nature of the damage. In patients with combined trauma, even with mild extracranial injuries, the disease is more severe than with isolated trauma. It should be emphasized that the gradations of severity of combined injury are to some extent arbitrary, since when assessing the severity of a patient’s condition, it is necessary to take into account not only the severity of individual cranial and extracranial injuries, but also the patient’s age, the state of his cardiovascular system, previous diseases, etc. .

In the classification structures of combined TBI, it is necessary to take into account its inherent high frequency and features of the manifestation of traumatic shock.

Victims of groups 1 and 2 are subject to treatment in neurosurgical and neurotraumatology hospitals, victims of groups III and IV are hospitalized in departments according to the profile of the dominant injury.

In a detailed diagnosis of combined injury, the currently dominant injury should be indicated in the first place, which determines the priority direction of diagnostic and surgical actions. Over time, the various components of combined traumatic brain injury can change places in terms of their predominance in the clinical picture.

We give approximate formulations of the primary diagnosis of combined traumatic brain injury.

Group I
“Severe combined injury: compression of the brain by an acute subdural hematoma in the right frontoparietal region. Closed linear fracture of the parietal and temporal bones on the right. 3 closed fracture of 4-10 ribs on the right along the mid-axillary line. Hemopneumothorax on the right. Traumatic shock of the second degree.”
“Severe combined injury: moderate brain contusion localized in the frontal and temporal lobes on the left. Subarachnoid hemorrhage. 3 closed fracture of the pubic and ischial bones, rupture of the extraperitoneal urethra. Traumatic shock of the 1st degree.”

Group II
“Severe combined traumatic brain injury: severe brain contusion, predominantly of the left hemisphere, subarachnoid hemorrhage. “closed fracture of the radius in a typical location with displacement of fragments.”

“Severe combined traumatic brain injury. Compression of the brain by an acute subdural hematoma in the right frontotemporal region against the background of a crush injury to the pole of the right frontal lobe, subarachnoid hemorrhage. Linear fracture of the right half of the frontal bone. Fracture of the nasal septum. Bruises of the soft tissues of the head and face. Alcohol intoxication."

III group
“Severe combined injury: closed transverse fracture of the left femur in the middle third with displacement, fracture of the left ilium without displacement. Mild brain contusion. Traumatic shock of the first degree.”

“Severe combined injury: closed compression fracture of the C6 vertebral body with contusion and compression of the spinal cord. Brain concussion. Alcohol intoxication."

IV group
“Combined traumatic brain injury: mild brain contusion, bruised wound in the occipital region. Fracture of the 8th rib along the scapular line on the right.”

“Combined injury: closed fracture of the lower jaw on the left without displacement. Brain concussion. Alcohol intoxication."

The final diagnosis upon discharge of the patient must be detailed. It indicates the exact location of the damage, complications, concomitant diseases, etc.

For example: “Severe combined injury: compression of the brain by a subdural hematoma of the right fronto-parietal-temporal region, a crush site of the basal parts of the frontal and temporal lobes on the right, a fracture of the right temporal bone with transition to the base of the middle cranial fossa. 3-closed pertrochanteric fracture of the right femur with displacement of fragments. Bilateral lower lobe pneumonia. Hypertension, stage I B."

A.P. Fraerman, V.V. Lebedev, L.B. Likhterman