Damage to the central nervous system. Organic lesion of the central nervous system Injuries of the central nervous system treatment

Trauma to the nervous system is one of the most common human pathologies. Distinguish between traumatic brain injury and spinal cord injury.

Traumatic brain injury accounts for 25-45% of all cases of traumatic injuries. This is due to the high level of injuries in car accidents or transport accidents.

Traumatic brain injuries are closed (CTBI), when the integrity of the skin and dura mater is preserved, or there are soft tissue wounds without damage to the aponeurosis (broad ligament covering the skull). Traumatic brain injuries with damage to the bones, but with the preservation of the integrity of the skin and aponeurosis, are also classified as closed. Open traumatic brain injury (TBI) occurs when the aponeurosis is damaged. Injuries in which the outflow of cerebrospinal fluid occurs are classified as open in any case. Open craniocerebral injuries are divided into penetrating, when the dura mater is damaged, and non-penetrating, when the dura mater remains intact.

Classification of closed craniocerebral injuries:

1. Bruises and injuries of the soft tissues of the skull without concussion and contusion of the brain.

2. Actually closed brain injuries:

 Concussion (commotio cerebri).

 Brain contusion (contusio cerebri) mild, moderate and severe

3. Traumatic intracranial hemorrhage (brain compression – compressio):

 Extradural (epidural).

 Subdural.

 Subarachnoid.

 Intracerebral.

 Intraventricular.

4. Combined damage to the skull and brain:

 Bruises and injuries of the soft tissues of the skull in combination with trauma to the brain and its membranes.

 Closed fractures of the bones of the cranial vault in combination with damage to the brain (contusion, concussion), its membranes and blood vessels.

 Fractures of the bones of the base of the skull in combination with damage to the brain, membranes, blood vessels and cranial nerves.

5. Combined injuries when mechanical, thermal, radiation or chemical effects occur.

6. Diffuse axonal damage to the brain.

7. Compression of the head.

The most common type of injury is brain concussion . This is the mildest type of brain damage. It is characterized by the development of mild and reversible changes in the activity of the nervous system. At the time of injury, as a rule, there is a loss of consciousness for a few seconds or minutes. Perhaps the development of the so-called retrograde amnesia for events that preceded the moment of injury. There is vomiting.

After the restoration of consciousness, the following complaints are most characteristic:

 Headache.

 General weakness.

 Noise in the ears.

 Noise in the head.

 Flushing of the face.

 Sweating of palms.

 Sleep disturbance.

 Pain when moving the eyeballs.

In the neurological status, labile non-rough asymmetry of tendon reflexes, small-caliber nystagmus are detected, there may be a slight stiffness of the occipital muscles. The condition is completely stopped within 1-2 weeks. In children, concussion can occur in three forms: mild, moderate, severe. With a mild form, loss of consciousness occurs for a few seconds. If there is no loss of consciousness, then adynamia, drowsiness may occur. Nausea, vomiting, headache persist for days after the injury. Concussion of moderate severity is manifested by loss of consciousness for up to 30 minutes, retrograde amnesia, vomiting, nausea, and headache within a week. Severe concussion is characterized by prolonged loss of consciousness (from 30 minutes to several days). Then there is a state of stupor, lethargy, drowsiness. Headache persists for 2-3 weeks after injury. In the neurological status, transient damage to the abducens nerve, horizontal nystagmus, increased tendon reflexes, and congestion in the fundus are revealed. The pressure of the cerebrospinal fluid rises to 300 mm of water st.

brain contusion Unlike a concussion, it is characterized by brain damage of varying severity.

In adults, a mild cerebral contusion is characterized by a loss of consciousness after an injury from several minutes to an hour. After regaining consciousness, the victim complains of headache, dizziness, nausea, and retrograde amnesia occurs. In the neurological status, different pupil sizes, nystagmus, pyramidal insufficiency, and meningeal symptoms are revealed. Symptoms regress in 2-3 weeks.

A brain contusion of moderate severity is accompanied by loss of consciousness for several hours. There is retrograde and antegrade amnesia. Headaches are usually severe. Vomiting is repeated. Blood pressure either rises or falls. In the neurological status, there is a pronounced shell syndrome and distinct neurological symptoms in the form of nystagmus, changes in muscle tone, the appearance of paresis, pathological reflexes, and sensitivity disorders. Possible fractures of the skull bones, subarachnoid hemorrhages. CSF pressure increased to 210-300 mm of water st. Symptoms regress within 3-5 weeks.

A severe brain contusion is characterized by loss of consciousness for a period of several hours to several weeks. Severe violations of the vital functions of the body develop. Bradycardia less than 40 beats per 1 minute, arterial hypertension more than 180 mm Hg, possibly tachypnea more than 40 per 1 minute. There may be an increase in body temperature.

There are severe neurological symptoms:

 Floating movements of the eyeballs.

 Paresis of upward gaze.

 Tonic nystagmus.

 Miosis or mydriasis.

 Strabismus.

 Violation of swallowing.

 Change in muscle tone.

 Decerebrate rigidity.

 Increase or suppression of tendon or skin reflexes.

 Tonic convulsions.

 Reflexes of oral automatism.

 Paresis, paralysis.

 Seizures.

In severe bruises, as a rule, there are fractures of the bones of the vault and base of the skull, massive subarachnoid hemorrhages. Focal symptoms regress very slowly. The cerebrospinal fluid pressure rises to 250-400 mm of water st. As a rule, a motor or mental defect remains.

In childhood, brain injury is much less common. It is accompanied by persistent focal symptoms with impaired movements, sensitivity, visual, coordinating disorders against the background of severe cerebral symptoms. Often, focal symptoms are clearly indicated only for 2-3 days against the background of a gradual decrease in cerebral symptoms.

If a brain contusion is accompanied by subarachnoid hemorrhage, then the meningeal syndrome is clearly manifested in the clinical picture. Depending on the place of accumulation of the spilled blood, either psychomotor disorders (excitation, delirium, hallucinations, motor disinhibition), or hypothalamic disorders (thirst, hyperthermia, oliguria), or hypertension syndrome occur. If a subarachnoid hemorrhage is suspected, a lumbar puncture is indicated. At the same time, the cerebrospinal fluid is of a hemorrhagic nature, or the color of meat slops.

Brain compression occurs during the formation of intracranial hematomas, depressed skull fractures. The development of a hematoma leads to a gradual deterioration of the patient's condition and an increase in signs of focal brain damage. There are three periods in the development of hematomas:

spicy with a traumatic effect on the skull and brain;

latent- "light" gap after injury. It is most characteristic of epidural hematomas and depends on the background against which the hematoma is formed: concussion or brain contusion.

AND actual compression period or formed hematoma.

The most characteristic of a hematoma is the expansion of the pupil on the side of the lesion and hemiparesis on the opposite side (Knapp's syndrome).

Other symptoms of brain damage during brain compression include the following:

 Loss of consciousness.

 Headache.

 Repeated vomiting.

 Psychomotor agitation.

 Hemiparesis.

 Focal epileptic seizures.

 Bradycardia.

Among other causes of brain compression can be called hydroma. Its formation occurs during the formation of a small subdural hematoma, the hemorrhage into which stops, but it is gradually replenished with fluid from the cerebrospinal fluid. As a result, it increases in volume, and the symptoms increase according to the pseudotumor type. It may take several weeks from the moment of injury. Often with the formation of a hematoma, subarachnoid hemorrhage occurs.

In children, the clinical picture of intracranial hematomas is somewhat different. The severity of the first phase may be minimal. The duration of the light interval depends on the intensity of bleeding. The first signs of a hematoma appear when its volume is 50-70 ml. This is due to the elasticity of the child's brain tissue, their greater ability to stretch, and the wide pathways of the cerebrospinal fluid and venous circulation. Brain tissue has a great ability to compress and compress.

Diagnostics craniocerebral injuries includes a set of methods:

 Thorough neurological examination.

 Radiography of the bones of the skull reveals fractures, depressions of the bones.

 Examination of the cerebrospinal fluid allows us to speak about the presence of subarachnoid hemorrhage. Its implementation is contraindicated in hematomas, because. the substance of the brain may be wedged into the foramen magnum or into the notch of the cerebellum.

 Electroencephalography allows to detect local or diffuse changes in the bioelectrical activity of the brain, the degree of depth of their change.

 Echo-encephalometry is the number one examination method for suspected brain hematoma, tumor or abscess.

 CT and MRI are the most informative modern research methods that allow studying the structure of the brain without opening the bones of the skull.

 The study of biochemical parameters is of secondary importance, because any traumatic effect on the body will be accompanied by the activation of the sympathetic-adrenal system. This will be manifested by an increase in the release of metabolites of adrenaline and catecholamines in the acute period of injury. By the end of the acute period, the activity of the sympathetic-adrenal system is reduced, it often comes to a normal level only 12 or 18 months after the traumatic brain injury.

Long-term effects of TBI include:

 Hydrocephalus.

 Traumatic encephalopathy.

 Traumatic epilepsy.

 Paresis.

 Paralysis.

 Hypothalamic disorders.

The emerging vegetative dystonia is a symptom of the current traumatic process, and not a consequence of a traumatic brain injury.

Treatment of CTBI

In the presence of a depressed fracture or hematomas, the patient is subject to immediate neurosurgical treatment.

In other cases, treatment is conservative. Bed rest is indicated. Symptomatic therapy is carried out: analgesics, dehydration, with vomiting - eglonil, cerucal. For sleep disorders - sleeping pills. With psychomotor agitation - tranquilizers, barbiturates, neuroleptics. With severe intracranial hypertension, diuretics are prescribed (lasix, mannitol, glycerin mixture). With subarachnoid hemorrhages, repeated lumbar punctures are indicated.

In severe brain injuries, resuscitation measures, control of the activity of the pelvic organs and prevention of complications are indicated.

During the recovery period, physiotherapy exercises, physiotherapy, massage, restorative drugs, classes with a speech therapist, psychologist are shown.

Open traumatic brain injury are divided into penetrating and non-penetrating, depending on the damage to the dura mater. Injuries with damage to the dura mater are much more severe, because. there are opportunities for infection to enter the cranial cavity and develop meningitis, encephalitis and abscess. An unconditional sign of an open penetrating craniocerebral injury is the outflow of cerebrospinal fluid from the nose and ear.

The cause of open penetrating brain injuries are car accidents and gunshot wounds. The latter are especially dangerous because a blind wound channel with a high degree of infection is formed. This further aggravates the condition of the patients.

In the clinic of open craniocerebral injuries, the following manifestations may be:

 Severe cerebral phenomena with headache, vomiting, dizziness.

 Shell symptoms.

 Focal signs of damage to the substance of the brain.

 "Symptom of glasses" develops when the bones of the base of the skull are fractured.

 Bleeding from wounds.

 Liquorrhea.

 When the walls of the ventricles of the brain are injured, purulent ependymatitis occurs with an extremely severe course.

Diagnostics carried out in the same way as in the case of TCHMT. There are inflammatory changes in the blood. Liquor pressure is increased. On the fundus characteristic stagnation.

Treatment open traumatic brain injury is performed surgically. Crushed brain tissue, bone fragments, blood clots are removed. Subsequently, plastic surgery of the bone defect of the skull is performed. Drug treatment involves the appointment of antibiotics, anti-inflammatory drugs, diuretics. Anticonvulsant drugs, exercise therapy, massage, physiotherapy are prescribed.

Injuries of the spine and spinal cord

Vertebral-spinal injuries are closed - without damage to the skin and adjacent soft tissues, open - with damage to them. Penetrating vertebral-spinal injuries occur when the integrity of the walls of the spinal canal is violated and infection becomes possible. Damage to the spine without disruption of the function of the spinal cord, disruption of the activity of the spinal cord without damage to the spine, and combined injuries are possible.

Spinal injuries include:

 Fractures.

 Dislocations of the vertebrae.

 Sprains and ruptures of the ligamentous apparatus.

 Violation of the integrity of the intervertebral discs.

Spinal cord injury occurs as:

 Concussion.

 Gap.

 Hematomyelia occurs when there is bleeding in the spinal cord. In this case, the gray matter of the brain suffers to a greater extent.

 Shell spinal hemorrhages (hematorachis) occur when blood enters above or below the dura mater, subarachnoid hemorrhage occurs when blood enters under the arachnoid membrane.

Among the causes of vertebral and spinal cord injuries, transport (car injuries) and falls from a height are in the first place.

Clinical picture spinal cord injury includes the following symptoms:

 Local pain.

 Muscle tension.

 Concussion of the spinal cord in the acute stage often occurs with the phenomena of transverse lesions of the spinal cord, which are reversed. This phenomenon is called diaschisis, or diffuse inhibition in the spinal cord, or spinal shock. It proceeds with inhibition of the functions of the spinal cord below the level of the lesion, dysfunction of the pelvic organs. The duration of this state varies within different limits. Restoration of spinal cord functions occurs over a period of several weeks to 1 month.

 Contusion of the spinal cord (contusion) causes destructive changes in the substance of the brain. The diaschisis stage takes longer, recovery is slower and incomplete. There may be bedsores. The development of complications in the form of pyelonephritis, urosepsis.

 Injuries to the spine do not correspond to the level of damage to the spinal cord. This is due to the peculiarities of the blood supply to the brain. To determine the level of damage to the spine, spondylography is of exceptional importance - X-ray of the spine.

Treatment in case of spinal injuries, it implies immobilization of the patient, position on the shield, traction, control of the activity of the pelvic organs, prevention of bedsores.

If compression of the spinal cord is detected, surgical treatment is necessary. Drug therapy is carried out symptomatically. In the period of restoration of functions, sanatorium treatment and mud therapy are of particular importance.

Injuries of the peripheral nervous system occur with craniocerebral injuries, fractures of the clavicle, limbs, with gunshot, stab wounds.

A traumatic nerve tear is called neurothemesis. In this case, there is a violation of the motor, sensory and trophic functions provided by this nerve.

Reversible damage is possible with a concussion or bruise of the nerve. In this case, there may be phenomena of neuropraxia, when the axon of the nerve remains intact, changes occur at the level of microtubules and cell membranes. Axotemesis implies a rupture of the axon with the preservation of Schwann cells, epi-, peri-, endoneurium. The distal segment of the nerve, when the axon is ruptured, undergoes Wallerian degeneration, the central segment begins to regenerate.

Restoration of nerve function occurs after 2-3 weeks when it is concussed or bruised; with axotemesis, recovery occurs in parallel with nerve regeneration. The nerve growth rate is 1 mm/day. When the ends of a severed nerve diverge, recovery does not occur completely. To do this, they resort to the operation of neurorhaphy - the stitching of the nerve. It is carried out in cases where there is no restoration of nerve function within 2-3 months. If surgery is not performed, a neuroma forms at the end of the severed nerve, which can cause phantom pain. The presence of a large number of autonomic fibers in the damaged nerve determines the presence of causalgic burning pains. The patient is relieved by immersing the limbs in cold water or wrapping them in rags soaked in water.

Treatment nerve injuries include surgical treatment in the acute period according to indications. Anti-inflammatory, anticholinesterase, analgesic drugs. Physiotherapy, massage. After 1.5-2 months, mud therapy, balneotherapy, spa treatment are recommended.

Nervous system trauma

Parameter name	Meaning
Article subject:	Nervous system trauma
Rubric (thematic category)	Psychology

Trauma to the nervous system is one of the most common human pathologies. Distinguish between traumatic brain injury and spinal cord injury.

Traumatic brain injury accounts for 25-45% of all cases of traumatic injuries. This is due to the high level of injuries in car accidents or transport accidents.

Classification of closed craniocerebral injuries:

1. Bruises and injuries of the soft tissues of the skull without concussion and contusion of the brain.

2. Actually closed brain injuries:

Concussion (commotio cerebri).

Contusion of the brain (contusio cerebri) mild, moderate and severe

3. Traumatic intracranial hemorrhage (brain compression – compressio):

Extradural (epidural).

Subdural.

Subarachnoid.

Intracerebral.

Intraventricular.

4. Combined damage to the skull and brain:

· Bruises and injuries of the soft tissues of the skull in combination with trauma to the brain and its membranes.

Closed fractures of the bones of the cranial vault in combination with damage to the brain (contusion, concussion), its membranes and blood vessels.

· Fractures of the bones of the base of the skull in combination with damage to the brain, membranes, blood vessels and cranial nerves.

5. Combined injuries when mechanical, thermal, radiation or chemical effects occur.

6. Diffuse axonal damage to the brain.

7. Compression of the head.

The most common type of injury is brain concussion . This is the mildest type of brain damage. It is characterized by the development of mild and reversible changes in the activity of the nervous system. At the time of injury, as a rule, there is a loss of consciousness for a few seconds or minutes. Perhaps the development of the so-called retrograde amnesia for events that preceded the moment of injury. There is vomiting.

After the restoration of consciousness, the following complaints are most characteristic:

· Headache.

general weakness.

· Noise in ears.

Noise in the head.

· Congestion of blood to the face.

· Sweaty palms.

· Sleep disturbance.

· Pain when moving the eyeballs.

In the neurological status, labile non-rough asymmetry of tendon reflexes, small-caliber nystagmus are detected, there should be a slight stiffness of the occipital muscles. The condition is completely stopped within 1-2 weeks. In children, concussion can occur in three forms: mild, moderate, severe. With a mild form, loss of consciousness occurs for a few seconds. If there is no loss of consciousness, then adynamia, drowsiness may occur. Nausea ͵ vomiting ͵ headache persist for a day after the injury. Concussion of moderate severity is manifested by loss of consciousness for a period of up to 30 minutes, retrograde amnesia, vomiting, nausea, and headache within a week. Severe concussion is characterized by prolonged loss of consciousness (from 30 minutes to several days). Then there is a state of stupor, lethargy, drowsiness. Headache persists for 2-3 weeks after injury. In the neurological status, transient damage to the abducens nerve, horizontal nystagmus, increased tendon reflexes, and congestion in the fundus are revealed. The pressure of the cerebrospinal fluid rises to 300 mm of water st.

brain contusion Unlike a concussion, it is characterized by brain damage of varying severity.

There are severe neurological symptoms:

Floating movements of the eyeballs.

Upward gaze paresis.

Tonic nystagmus.

Miosis or mydriasis.

· Strabismus.

· Violation of swallowing.

Change in muscle tone.

Decerebrate rigidity.

Increase or suppression of tendon or skin reflexes.

· Tonic convulsions.

Reflexes of oral automatism.

· Paresis, paralysis.

· Seizures.

If a brain contusion is accompanied by subarachnoid hemorrhage, then meningeal syndrome is clearly manifested in the clinical picture. Considering the dependence of the place of accumulation of the spilled blood, either psychomotor disorders (excitation, delirium, hallucinations, motor disinhibition), or hypothalamic disorders (thirst, hyperthermia, oliguria), or hypertension syndrome occur. If a subarachnoid hemorrhage is suspected, a lumbar puncture is indicated. At the same time, the cerebrospinal fluid is of a hemorrhagic nature, or the color of meat slops.

spicy with a traumatic effect on the skull and brain;

latent– ʼʼlightʼʼ gap after injury. It is most characteristic of epidural hematomas and depends on the background against which the hematoma is formed: concussion or brain contusion.

AND actual compression period or formed hematoma.

The most characteristic of a hematoma is the expansion of the pupil on the side of the lesion and hemiparesis on the opposite side (Knapp's syndrome).

Other symptoms of brain damage during brain compression include the following:

Disturbance of consciousness.

· Headache.

· Repeated vomiting.

· Psychomotor agitation.

Hemiparesis.

Focal epileptic seizures.

· Bradycardia.

In children, the clinical picture of intracranial hematomas is somewhat different. The severity of the first phase should be minimal. The duration of the light interval depends on the intensity of bleeding. The first signs of a hematoma appear when its volume is 50-70 ml. This is due to the elasticity of the child's brain tissue, their greater ability to stretch, and the wide pathways of the cerebrospinal fluid and venous circulation. Brain tissue has a great ability to compress and compress.

Diagnostics craniocerebral injuries includes a set of methods:

Thorough neurological examination.

X-ray of the bones of the skull reveals fractures, depressions of the bones.

Investigation of the cerebrospinal fluid allows us to speak about the presence of subarachnoid hemorrhage. Its implementation is contraindicated in hematomas, because. the substance of the brain may be wedged into the foramen magnum or into the notch of the cerebellum.

· Electroencephalography allows you to identify local or diffuse changes in the bioelectrical activity of the brain, the degree of depth of their change.

Echo-encephalometry is the number one research method for suspected hematoma, tumor or brain abscess.

· CT and MRI are the most informative modern research methods that allow studying the structure of the brain without opening the bones of the skull.

· The study of biochemical parameters is of secondary importance, because any traumatic effect on the body will be accompanied by the activation of the sympathetic-adrenal system. This will be manifested by an increase in the release of metabolites of adrenaline and catecholamines in the acute period of injury. By the end of the acute period, the activity of the sympathetic-adrenal system is reduced, it often comes to a normal level only 12 or 18 months after the traumatic brain injury.

Long-term effects of TBI include:

· Hydrocephalus.

Traumatic encephalopathy.

· Traumatic epilepsy.

Paresis.

· Paralysis.

· Hypothalamic disorders.

The emerging vegetative dystonia is a symptom of the current traumatic process, and not a consequence of a traumatic brain injury.

Treatment of CTBI

In the presence of a depressed fracture or hematomas, the patient is subject to immediate neurosurgical treatment.

In severe brain injuries, resuscitation measures, control of the activity of the pelvic organs and prevention of complications are indicated.

During the recovery period, physiotherapy exercises, physiotherapy, massage, restorative drugs, classes with a speech therapist, psychologist are shown.

Open traumatic brain injury are divided into penetrating and non-penetrating based on damage to the dura mater. Injuries with damage to the dura mater are much more severe, because there are opportunities for infection to enter the cranial cavity and the development of meningitis, encephalitis and abscess. An unconditional sign of an open penetrating craniocerebral injury is the outflow of cerebrospinal fluid from the nose and ear.

In the clinic of open craniocerebral injuries, there are the following manifestations:

Pronounced cerebral phenomena with headache, vomiting, dizziness.

Shell symptoms.

Focal signs of damage to the substance of the brain.

· ʼʼSymptom glassesʼʼ develops with a fracture of the bones of the base of the skull.

Bleeding from wounds.

Liquorrhea.

When the walls of the ventricles of the brain are injured, purulent ependymatitis occurs with an extremely severe course.

Diagnostics carried out in the same way as in CTBI. There are inflammatory changes in the blood. Liquor pressure is increased. On the fundus characteristic stagnation.

Injuries of the nervous system - concept and types. Classification and features of the category "Injuries of the nervous system" 2017, 2018.

Trauma to the nervous system is one of the most common human pathologies. Distinguish between traumatic brain injury and spinal cord injury.

Traumatic brain injury accounts for 25-45% of all cases of traumatic injuries. This is due to the high level of injuries in car accidents or transport accidents.

Classification of closed craniocerebral injuries:

1. Bruises and injuries of the soft tissues of the skull without concussion and contusion of the brain.

2. Actually closed brain injuries:

Concussion (commotio cerebri).

Brain contusion (contusio cerebri) mild, moderate and severe

3. Traumatic intracranial hemorrhage (brain compression - compressio):

Extradural (epidural).

Subdural.

Subarachnoid.

Intracerebral.

Intraventricular.

4. Combined damage to the skull and brain:

Bruises and injuries of the soft tissues of the skull in combination with trauma to the brain and its membranes.

Closed fractures of the bones of the cranial vault in combination with damage to the brain (contusion, concussion), its membranes and blood vessels.

Fractures of the bones of the base of the skull in combination with damage to the brain, membranes, blood vessels and cranial nerves.

5. Combined injuries when mechanical, thermal, radiation or chemical effects occur.

6. Diffuse axonal damage to the brain.

7. Compression of the head.

The most common type of injury is a concussion. This is the mildest type of brain damage. It is characterized by the development of mild and reversible changes in the activity of the nervous system. At the time of injury, as a rule, there is a loss of consciousness for a few seconds or minutes. Perhaps the development of the so-called retrograde amnesia for events that preceded the moment of injury. There is vomiting.

After the restoration of consciousness, the following complaints are most characteristic:

Headache.

General weakness.

Noise in ears.

Noise in the head.

Rush of blood to the face.

Sweaty palms.

Sleep disturbance.

Pain on moving the eyeballs.

Brain contusion, in contrast to concussion, is characterized by brain damage of varying severity.

There are severe neurological symptoms:

Floating movements of the eyeballs.

Paresis of upward gaze.

Tonic nystagmus.

Miosis or mydriasis.

Strabismus.

Swallowing disorder.

Change in muscle tone.

Decerebrate rigidity.

Increase or inhibition of tendon or skin reflexes.

Tonic convulsions.

Reflexes of oral automatism.

Paresis, paralysis.

Convulsive seizures.

Compression of the brain occurs during the formation of intracranial hematomas, depressed skull fractures. The development of a hematoma leads to a gradual deterioration of the patient's condition and an increase in signs of focal brain damage. There are three periods in the development of hematomas:

Acute with traumatic effects on the skull and brain;

Latent - a "light" gap after an injury. It is most characteristic of epidural hematomas and depends on the background against which the hematoma is formed: concussion or brain contusion.

And actually the period of compression or formed hematoma.

The most characteristic of a hematoma is the expansion of the pupil on the side of the lesion and hemiparesis on the opposite side (Knapp's syndrome).

Other symptoms of brain damage during brain compression include the following:

Violation of consciousness.

Headache.

Repeated vomiting.

Psychomotor agitation.

Hemiparesis.

Focal epileptic seizures.

Bradycardia.

Diagnosis of craniocerebral injuries includes a set of methods:

Thorough neurological examination.

X-ray of the bones of the skull reveals fractures, depressions of the bones.

The study of cerebrospinal fluid allows us to speak about the presence of subarachnoid hemorrhage. Its implementation is contraindicated in hematomas, because. the substance of the brain may be wedged into the foramen magnum or into the notch of the cerebellum.

Electroencephalography allows you to identify local or diffuse changes in the bioelectrical activity of the brain, the degree of depth of their change.

Echo-encephalometry is the number one research method for suspected hematoma, tumor or brain abscess.

CT and MRI are the most informative modern research methods that allow studying the structure of the brain without opening the bones of the skull.

The study of biochemical parameters is of secondary importance, because. any traumatic effect on the body will be accompanied by the activation of the sympathetic-adrenal system. This will be manifested by an increase in the release of metabolites of adrenaline and catecholamines in the acute period of injury. By the end of the acute period, the activity of the sympathetic-adrenal system is reduced, it often comes to a normal level only 12 or 18 months after the traumatic brain injury.

Long-term effects of TBI include:

Hydrocephalus.

Traumatic encephalopathy.

Traumatic epilepsy.

Paresis.

Paralysis.

hypothalamic disorders.

The emerging vegetative dystonia is a symptom of the current traumatic process, and not a consequence of a traumatic brain injury.

Treatment of CTBI

In the presence of a depressed fracture or hematomas, the patient is subject to immediate neurosurgical treatment.

In severe brain injuries, resuscitation measures, control of the activity of the pelvic organs and prevention of complications are indicated.

During the recovery period, physiotherapy exercises, physiotherapy, massage, restorative drugs, classes with a speech therapist, psychologist are shown.

Open craniocerebral injuries are divided into penetrating and non-penetrating, depending on the damage to the dura mater. Injuries with damage to the dura mater are much more severe, because. there are opportunities for infection to enter the cranial cavity and develop meningitis, encephalitis and abscess. An unconditional sign of an open penetrating craniocerebral injury is the outflow of cerebrospinal fluid from the nose and ear.

In the clinic of open craniocerebral injuries, the following manifestations may be:

Pronounced cerebral phenomena with headache, vomiting, dizziness.

Shell symptoms.

Focal signs of damage to the substance of the brain.

"Symptom of glasses" develops with a fracture of the bones of the base of the skull.

Bleeding from wounds.

Liquorrhea.

When the walls of the ventricles of the brain are injured, purulent ependymatitis occurs with an extremely severe course.

Diagnosis is carried out in the same way as with CTBI. There are inflammatory changes in the blood. Liquor pressure is increased. On the fundus characteristic stagnation.

Treatment of open craniocerebral injuries is carried out surgically. Crushed brain tissue, bone fragments, blood clots are removed. Subsequently, plastic surgery of the bone defect of the skull is performed. Drug treatment involves the appointment of antibiotics, anti-inflammatory drugs, diuretics. Anticonvulsant drugs, exercise therapy, massage, physiotherapy are prescribed.

SKULL AND BRAIN INJURIES

Epidemiology

Patients with skull and brain injuries make up the largest part of neurosurgical patients. Every day, an ambulance doctor examines and decides on the hospitalization of victims with skull and brain injuries. Up to 50% of visits to the trauma center are for patients with traumatic brain injury. Statistical data show that with the development of industry and transport, the number and severity of craniocerebral injuries increase. The number of combined injuries of the head with the musculoskeletal system, organs of the abdominal cavity and chest is growing.

Despite significant advances in neurotraumatology, neuroanesthesiology and resuscitation, mortality among victims with severe traumatic brain injury is up to 70-85%. A favorable outcome largely depends on emergency diagnosis and timely surgical treatment of patients with cerebral compression.

In this regard, knowledge of the clinical picture of craniocerebral injuries, symptoms of brain compression and the main pathogenetic mechanisms of their development, as well as the ability to diagnose the severity of craniocerebral injury and intracranial hematomas, prescribe the necessary therapeutic measures and identify indications for emergency surgical operations aimed at to eliminate cerebral compression, are mandatory for a doctor of any specialty.

Classification

To select treatment tactics, a clear knowledge of the classification of injuries of the skull and brain is necessary. Distinguish isolated,

combined (the action of mechanical energy causes additional extracranial damage) and combined (cumulative impact of mechanical energy and other factors - temperature exposure, radiation, chemical damage, etc.) craniocerebral injuries.

Traumatic brain injury (TBI) can be closed (there is no direct connection between the cranial cavity and the external environment) and open (there is a connection between the cranial cavity and the external environment). Open TBI, in turn, are non-penetrating and penetrating. With a penetrating open TBI, there is damage to all integuments, including the dura mater, bone, soft tissues in a limited area (gunshot wounds, open depressed fractures, etc.). In a non-penetrating injury, there is no damage to the meninges. An open craniocerebral injury should include fractures of the base of the skull without visible damage to the soft tissues, accompanied by the outflow of cerebrospinal fluid from the nasal passages (nasorrhea) or the external auditory canal (otorrhea).

Depending on the severity of brain damage, concussion, contusion of varying severity (mild, moderate, severe) and compression by compressive factors (hematoma, hydroma, crush focus, depressed fracture, pneumocephalus, foreign body) are distinguished. In recent years, the concept of diffuse axonal damage to the brain has been distinguished.

There are three degrees of TBI according to severity:

Light (concussion and contusion of the brain of a mild degree);

Moderate severity (brain injury of moderate degree);

Severe (severe brain contusion, compression and diffuse axonal damage to the brain).

Forms of severe brain injury:

Extrapyramidal;

diencephalic;

mesencephalic;

Mesencephalobulbar;

Cerebrospinal. Brain compression:

intracranial hematoma;

subdural hydroma;

Foci of crushing of the brain;

Depressed fracture of the bones of the skull;

pneumocephalus;

Edema (swelling) of the brain.

Examination plan for a patient with traumatic brain injury

The main determining moment for establishing the correct diagnosis and developing adequate treatment tactics is a clinical examination, which begins with clarifying the anamnesis, the type and nature of the impact of the traumatic agent. It should be remembered that the medical records of such patients are most often needed as a legal document by forensic agencies and law enforcement agencies. Finding out the details of the events of the injury, it is necessary to note the independent behavior of the victim (who was nearby, whether he got up, got out of the car, how he was transported to a medical facility, etc.). It is on the basis of the story about the circumstances of the injury and the details of the actions of the victim himself that the doctor makes a conclusion about the state of consciousness in the first minutes of the injury. To a direct question: “Was there a loss of consciousness?” - the victim often replies: "It was not" due to amnesia. In the absence of contact with the patient, this information can be obtained from relatives, witnesses, medical workers. Important information will be the duration of the loss of consciousness, the presence of a convulsive syndrome, the behavior of the victim after the restoration of consciousness. To assess the level of impaired consciousness in a patient, the Glasgow Coma Scale is used (Table 8-1).

Table 8-1. Glasgow Coma Scale

■ Light TBI. Consciousness clear or moderate stunning (13-15 points):

Brain concussion;

Mild brain injury.

■ TBI of moderate severity. Deep stunning, stupor (8-12 points):

Moderate brain injury.

■ Severe TBI. Coma 1 (4-7 points):

Severe brain injury;

Diffuse axonal damage;

Acute compression of the brain.

Next, they proceed to an external examination to determine the nature of local changes and exclude associated injuries (presence of subcutaneous and subaponeurotic hematomas, abrasions, wounds, skull deformities, determination of liquorrhea, damage to the facial skeleton, chest, abdominal organs, musculoskeletal system, etc. .). After assessing the state of vital functions and their dynamics (heart rate, blood pressure, adequacy of external respiration and its rhythm), a thorough neurological examination is started. Examination of the patient is advisable to carry out by groups of neurological symptoms: cerebral, focal, meningeal. Particular attention should be paid to identifying dislocation symptoms (degree of impaired consciousness, oculomotor disorders, anisocoria, pupillary response to light, severity of corneal reflexes, hemiparesis, bilateral pathological foot signs, bradycardia, arterial hypertension). Further, to clarify the diagnosis, additional methods of examination are resorted to. The necessary minimum is craniography (mandatory in two projections, and, if necessary, anterior or posterior semi-axial images) and echoencephaloscopy (to determine the lateral displacement of the median structures of the brain by intracranial hematomas, crush foci, etc.).

Currently, the most informative methods for examining neurotraumatological patients are CT and MRI. In 96%, these methods are used to determine the type and lobar localization of intracranial lesions, the state of the ventricular system, basal cisterns, edema, ischemia, etc. The EEG method for diagnosing the severity of brain damage in the acute period of TBI has significantly less diagnostic capabilities and is not necessary for patients.

An informative diagnostic method is PET, however, due to the high cost of the study and the lack of a sufficient number of devices, its use is extremely limited in patients in the acute period of TBI.

BRAIN CONCUSSION

Concussion is the most common form of TBI; it is characterized by functionally reversible changes in the brain that developed immediately after exposure to a traumatic factor. Clinically, concussion is a single form without division into degrees.

In the pathogenesis of the ongoing disorders in the brain in this form, the phenomena of dysfunction and dyscirculation are presented. Approximately after 2-3 weeks, subject to the patient regimen, these disorders disappear, and the normal functioning of the brain is restored.

Clinical picture

Patients with this severity of injury are characterized by loss of consciousness from a few seconds to several minutes. Upon recovery of consciousness, patients present the main complaints of nausea, headache, dizziness, general weakness, loss of appetite. In some cases, there are no complaints. It is often possible to lose memory for a short period of events during, before and after trauma (control, retro, anterograde amnesia). Vegetative disturbances are possible in the form of sweating, a feeling of a rush of blood to the head, a feeling of palpitations, lability of the pulse and blood pressure. In the neurological status, small-scale nystagmus is often determined when looking to the sides, weakness of convergence, slight deviation of the tongue to the side, slight asymmetry of deep reflexes, and coordination disorders. All these focal manifestations, as a rule, with a concussion of the brain should disappear by the beginning of the second day.

Data from additional examination methods (craniography, echoencephaloscopy, spinal puncture, CT) do not reveal pathological changes. It should be noted that patients with fractures of the bones of the facial skeleton (bones of the nose, zygomatic bone, upper and lower jaws) should be diagnosed with concussion, even in the absence of a clear clinical picture of the disease.

Patients with concussion are hospitalized, but the need for inpatient treatment in neurosurgical

there is no com or neurotraumatology department, since the treatment of this group of victims is symptomatic and in the vast majority of cases does not require neurosurgical manipulations.

Treatment

It is necessary to comply with bed rest for 5-7 days; the appointment of analgesics, sedatives, antihistamines and, of course, anticonvulsants. Dehydration therapy is prescribed in cases of increased CSF pressure, which is diagnosed after spinal puncture in a hospital. Patients are shown intravenous administration and subsequent intake of nootropic and vasodilator drugs in the form of a course of treatment.

Flow

During the first week, patients experience a complete regression of neurological symptoms, an improvement in their general condition. The terms of inpatient treatment are variable (usually 7-14 days) and depend on the age of the patients, concomitant pathology, wounds of the soft tissues of the head, combined injuries. Full recovery of working capacity occurs within 3-4 weeks from the moment of injury. However, residual vegetative manifestations are possible for another 1 month. It is advisable to monitor the condition of patients by a neurologist for the period from discharge from the hospital to going to work. As a rule, no consequences are noted in patients with a reliably established diagnosis of concussion, the implementation of a protective regimen, diet and adequate treatment.

BRAIN INJURY

Clinical picture

Functional (reversible) and morphological (irreversible) changes are characteristic. The massiveness and prevalence of morphological lesions determine the degree of injury. So, with mild brain contusion, morphological damage

are small in size, limited to the superficial sections of one or more convolutions. With moderate bruising, areas of damage are localized not only in the cortex, but also in the white matter of two, and sometimes three, lobes of the brain. Severe brain contusion, unlike the previous two, is characterized by damage to almost all parts of the brain, including the trunk. Depending on the level of damage to the trunk, the following forms are distinguished: extrapyramidal, diencephalic, mesencephalic, mesencephalobulbar and cerebrospinal.

Mild brain injury

A mild brain contusion is similar in clinical manifestations to the symptoms characteristic of a concussion. However, patients often experience loss of consciousness, vomiting, autonomic disorders, tachycardia, arterial hypertension. Neurological symptoms are represented by mild, rapidly passing clonic nystagmus, flattening of the nasolabial fold, anisoreflexia, sometimes unilateral pathological foot signs, coordination disorders, and mild meningeal symptoms. In contrast to the concussion of the brain during spinal puncture, more than half of the patients have increased cerebrospinal fluid pressure (up to 200 mm of water column), the rest have normotension or even severe hypotension. A slight admixture of blood in the cerebrospinal fluid (subarachnoid hemorrhage) is possible. On craniograms, linear fractures are found in 10-15% of patients, more often in the frontal, temporal or parietal bones (Fig. 8-1). CT scan often determines the zones of local edema, narrowing of the CSF spaces.

Patients are necessarily hospitalized (preferably in the neurosurgical department), and in the presence of subarachnoid hemorrhage and / or fracture of the cranial vault - necessarily in the neurosurgical department for a period of about 2 weeks. To the previously described drug treatment, nootropic drugs (piracetam), vascular agents (vinpocetine, nicergoline, cinnarizine), diuretics (only with an increase in cerebrospinal fluid pressure, according to spinal puncture), sedatives, small tranquilizers, anticonvulsants are added. The latter are prescribed for the night. Clinical improvement usually occurs within the first 7-10 days. However, for a long time in some patients with neurological

Rice. 8-1. Computed tomogram (in the bone window). A fracture of the right parietal bone is seen. Subaponeurotic hematoma above the fracture line

Physical examination may reveal mild focal symptoms. Recovery usually occurs within 2 months after injury.

Moderate brain injury

Moderate brain contusion is characterized by more pronounced local destructive changes in the brain, especially in the pole-basal regions of the frontal and temporal lobes, involving not only the cortex, but also the white matter.

In patients, prolonged loss of consciousness (up to several hours), amnesia, repeated vomiting, severe headache, lethargy, lethargy, low-grade fever are detected. Focal neurological symptoms have a clear dependence on the lobar localization of the prevailing destructive changes. The most common are mental disorders, epileptic seizures, oculomotor disorders, pyramidal and extrapyramidal insufficiency, up to hyperkinesis, speech disorders, changes in muscle tone. On craniograms, half of the patients have fractures of the bones of the vault and base of the skull. With echoencephaloscopy, a displacement of the median M-echo by 3-4 mm may occur, which

due to the presence of a contusion focus and perifocal edema. In most patients with moderate brain contusion, spinal puncture reveals traumatic subarachnoid hemorrhage of varying severity. CT data indicate a local lesion in the form of alternating zones of small-focal hemorrhages with edema of the brain tissue. Sometimes areas of hemorrhage are not visualized.

The victims are necessarily hospitalized in the neurosurgical department for pathogenetic treatment. From the first day, parenteral administration of nootropic drugs, vascular and detoxifying drugs, as well as drugs that improve blood rheology are prescribed. With an open TBI, antibiotics are added, which are administered before the sanitation of the cerebrospinal fluid. Depending on the severity of subarachnoid hemorrhage, repeated (after 2-3 days) spinal punctures are performed until the cerebrospinal fluid is cleared. Prescribe drugs that improve metabolism and reparative processes [choline alfoscerate (gliatilin*), cerebrolysin*, actovegin*, solcoseryl*]. As a preventive measure, to reduce the likelihood of developing post-traumatic epilepsy, patients should receive anticonvulsant drugs under the control of EEG. The terms of inpatient treatment of patients with moderate brain contusion are usually limited to three weeks, followed by rehabilitation treatment under the supervision of a neurologist. In the presence of zones of local hemorrhage, repeated CT is indicated. It is possible to fully restore working capacity, however, the victims, employed in hazardous industries and working on night shifts, are transferred to lighter working conditions for a period of 6 months to 1 year.

Severe brain injury

Severe cerebral contusion is characterized by gross massive destructive changes in the cerebral hemispheres and obligatory damage to the brainstem. This causes a prolonged loss of consciousness after injury, the predominance of stem symptoms, overlapping focal hemispheric symptoms. As a rule, the condition of patients is severe or extremely severe. Violation of vital functions is noted, requiring immediate resuscitation and, first of all, external respiration. The victims are in a soporous or comatose state. To the signs

trunk lesions include floating movements of the eyeballs, divergent strabismus, vertical separation of the eyeballs (Hertwig-Magendie symptom), impaired muscle tone up to hormetonia, bilateral pathological foot signs, paresis, paralysis and generalized epileptic seizures. Practically in all supervision define the expressed meningeal symptoms. In the absence of signs of dislocation syndrome, a lumbar puncture is performed, in which, as a rule, a massive subarachnoid hemorrhage and often an increase in CSF pressure are detected. On craniograms, fractures of the bones of the vault and base of the skull are found in most patients.

A CT scan is of great help in determining the lobar localization and severity of destructive changes, which makes it possible to identify focal lesions of the brain in the form of a zone of non-uniform increase in density (fresh blood clots and areas of edematous or crushed tissue in the same zone). The greatest changes are most often found in the pole-basal regions of the frontal and temporal lobes. Often, multiple foci of destruction are found (Fig. 8-2).

Almost all patients are hospitalized in the intensive care unit, where, from the first minutes of admission, intensive therapy is carried out (ensuring adequate breathing up to tracheal intubation and mechanical ventilation, fighting acidosis, maintaining the volume of circulating blood, microcirculation, administration of antibiotics, protolytic enzymes, dehydration drugs). The victims need dynamic monitoring by a neurosurgeon, since the presence of crush foci is an important factor contributing to the development of hypertensive-dislocation syndrome, which requires emergency surgical intervention.

In the medical treatment of severe brain contusion, a slow regression of focal symptoms is characteristic. However, patients often have varying degrees of hemiparesis, aphasia, and post-traumatic epilepsy often occurs. With CT, in dynamics, a gradual resorption of pathological zones is noted with the formation of atrophic changes in the brain and cysts in their place. After the end of inpatient specialized treatment (usually 30-40 days), a course is indicated.

Rice. 8-2. Computed tomogram of the brain. One can see a convexital subarachnoid hemorrhage over the frontal and parietal lobes on the right with moderate edema of the right hemisphere in a patient with signs of premorbid encephalopathy (there is an expansion of the ventricular system of the brain and subarachnoid fissures)

rehabilitation in recovery centers. As a rule, patients who have suffered a severe brain contusion are transferred to disability.

Diffuse axonal brain injury

In recent years, the concept of diffuse axonal damage to the brain has begun to be distinguished, which is based on tension and ruptures of axons in the white matter and brainstem. This type of craniocerebral injury is more common in children and young people who have been injured in a traffic accident, when falling from a great height (catatrauma). Patients for a long time stay in a coma that arose immediately after the injury. The neurological status is characterized by a clear predominance of stem symptoms: the absence of an oculocephalic reflex, corneal reflexes, tetraparesis, decerebrate rigidity and hormetonia, which can easily be provoked by pain.

irritation, meningeal syndrome. Often there are vegetative disorders in the form of persistent hyperthermia, hypersalivation, hyperhidrosis. A characteristic feature in cases of survival of patients is the transition from coma to a stable vegetative state, which is a sign of functional or anatomical dissociation of the cerebral hemispheres and subcortical-stem structures of the brain. CT scan does not show visible focal lesions. There may be signs of increased intracranial pressure (narrowing or complete disappearance of the third ventricle, lack of visualization of the basal cisterns). A study in dynamics shows the early development of a diffuse atrophic process in the brain. The prognosis for this group of victims is usually unfavorable and depends on the duration and depth of the coma and the developed vegetative state. Lethal outcomes are more often caused by complications (pneumonia, ascending urinary infection, bedsores, cachexia).

Brain compression

Brain compression is an emergency neurosurgical pathology requiring surgical intervention. The compression syndrome in TBI implies the presence of an additional intracranial tissue volume (blood clots, foci of crushing of the brain substance, bone fragments of a depressed fracture, limited subdural accumulation of cerebrospinal fluid, etc.), which leads to a mechanical displacement of the brain structures in relation to the bone formations of the skull and outgrowths of the dura mater shells. In this case, not only compression of the brain itself occurs, but also gross secondary disorders of liquor circulation and blood circulation, especially in the venous system. The swollen brain is displaced along the axis (axially) or to the side (under the sickle of the brain) and is infringed in the natural openings. Infringement of the brain can occur in the notch of the cerebellum, in the foramen magnum, and under the falciform process. If the latter type of displacement is effectively treated conservatively, then the first two almost always require surgical treatment. Clinically, these processes are manifested by an increase in the hypertensive-dislocation syndrome. Depending on the type of brain compression, hypertensive-dislocation syndrome has features of neurological manifestations and a different rate of development. The most characteristic common features of this syndrome are:

Deepening of the disorder of consciousness (stunning-sopor-coma);

Psychomotor agitation;

Increased headache;

Repeated frequent vomiting;

Stem symptoms (bradycardia, arterial hypertension, upward gaze restriction, anisocoria, nystagmus, bilateral pathological foot signs, etc.);

Deepening of focal symptoms (aphasia, hemiparesis, mnestic disorders).

Often, the development of hypertensive-dislocation syndrome is preceded by the so-called luminous gap, which occurs some time after the impact of the injury. The main sign of the gap is the restoration of consciousness between the initial and its repeated loss. The duration and severity of the light interval are determined not only by the type of brain compression, but also by the degree of direct primary brain damage (the smaller the damage, the more pronounced the light gap), the anatomical features of the structure and the reactivity of the victim's body.

An analysis of the clinical symptoms of developing compression of the brain stem made it possible to identify five pathognomonic symptoms.

■ Light gap (in 1/3 of patients).

■ Anisocoria (in 69% of cases, and in 85% of patients - on the side of the hematoma, in 15% - on the side opposite to the hematoma).

■ Development or increase in the severity of hemiparesis with hemihypesthesia.

■ The presence or appearance of epileptic, often primary generalized seizures.

■ Increasing hemodynamic disorders:

Stage 1 - bradycardia and hypertension;

Stage 2 - tachycardia and hypotension.

Identification of at least one of these symptoms is the basis for surgical intervention.

Intracranial hematomas (epidural, subdural, intracerebral, intraventricular) are the most common causes of cerebral compression in TBI, followed by crush foci, depressed fractures, subdural hydromas, and rarely pneumocephalus.

Before proceeding to the characterization of various hematomas, it is necessary to pay attention to the fact that intracranial

hematomas, regardless of their type and source of bleeding, are formed in their main volume up to 3 hours after the injury, possibly within the first minutes or an hour. A hematoma is considered a hemorrhage having a volume of 25-30 ml.

Epidural hematomas are found in 0.5-0.8% of all TBIs, they are characterized by the accumulation of blood between the inner surface of the skull bones and the dura mater. The most "favorite" localization of epidural hematomas is the temporal and adjacent areas. Their development occurs at the site of application of a traumatic agent (hit with a stick, bottle, stone, or when falling on an immovable object), when the vessels of the dura mater are injured by bone fragments. Most often, the middle sheath artery suffers, especially the area passing in the bone canal and its branches, veins and sinuses are less often damaged (Fig. 8-3). Rupture of the vessel wall leads to a rapid local accumulation of blood (usually 80-150 ml) in the epidural space. Given the fusion of the dura mater with the bones of the skull, especially in the places of cranial sutures, the epidural hematoma acquires a lenticular shape with a maximum thickness of up to 4 cm in the center. This leads to local compression of the brain, and then to a bright clinic of hypertensive dislo-

Rice. 8-3. Epidural hematoma in the occipital region and posterior cranial fossa, formed when the transverse sinus is damaged: 1 - dura mater; 2 - fracture of the occipital bone; 3 - hematoma; 4 - damage to the transverse sinus

cationic syndrome. Quite often, patients with epidural hematomas have a light interval, during which only moderate headache, weakness, dizziness are noted. As the compression of the brain increases, the patient's condition often suddenly and rapidly worsens. Often there are episodes of psychomotor agitation, repeated vomiting, unbearable headache, followed by secondary depression of consciousness from deafness to coma. It should be noted that patients with epidural hematoma are characterized by the rapid development of cerebral compression syndrome, so a coma can occur within a few tens of minutes after the victim is relatively well. Bradycardia appears and increases up to 40-50 per minute, arterial hypertension, oculomotor disorders, anisocoria occur, focal symptoms deepen. Craniograms reveal fractures of the temporal bone (moreover, the fracture line crosses the groove from the middle meningeal artery, sometimes located above the projection of the sagittal and transverse sinuses - with fractures of the occipital, parietal and frontal bones). With echoencephaloscopy, a lateral displacement of the median structures up to 10 mm and even more is noticeable.

CT scan data (if the severity of the patient's condition allows examination) indicate the presence of a lenticular hyperdense zone adjacent to the bone and pushing back the dura mater (Fig. 8-4).

Carotid angiography makes it possible to diagnose cerebral compression in 84% of cases. Angiographic symptoms of brain compression include displacement of A 2 -A 3 segments of the anterior cerebral artery in the opposite direction from the location of the hematoma. The presence of a "vascular area" above the compressed hemisphere of the brain (Fig. 8-5).

When establishing the diagnosis of epidural hematoma, emergency surgical intervention is indicated. It should be noted that in patients with a rapidly growing hypertensive-dislocation syndrome, surgery should be performed as soon as possible, before the development of severe post-dislocation circulatory disorders in the brain stem.

With an anesthetic benefit, it is impossible to correct arterial hypertension with medication until the hematoma is removed, since this increase in blood pressure is a compensatory defense mechanism of the brain against ischemia in conditions of intracranial

Rice. 8-4. TO computed tomography of the brain. Multiple epidural hematomas are seen in the form of a hyperdense lenticular zone adjacent to the bone above the right parietal lobe with signs of dislocation of the ventricular system (compression of the right lateral ventricle, displacement of the crescent of the brain to the left). Two small epidural hematomas are defined above the left frontal lobe

Rice. 8-5. Carotid angiography. Displacement (2) of the anterior cerebral artery beyond the midline in the opposite direction from the hematoma. "Avascular zone" (1) over the compressed hemisphere of the brain

hypertension and cerebral compression syndrome. In such cases, a decrease in systemic arterial pressure to “normal” will lead to aggravation of hypoxia and ischemia of the brain tissue, especially in the brain stem.

Currently, preference should be given to the osteoplastic variant of craniotomy, however, in case of multi-comminuted fractures, a bone resection is performed with the formation of a trepanation window sufficient to adequately remove the hematoma and search for the source of bleeding (usually 6-10 cm in diameter). It must be remembered that the identification of the source of bleeding, which is the cause of the formation of a hematoma, significantly reduces the risk of repeated hematomas in the surgical area. After removal of blood clots and its liquid part, reliable hemostasis is performed using coagulation, hydrogen peroxide, hemostatic sponge and wax. Sometimes the dura mater is sutured to the periosteum along the edges of the trepanation window. With a verified isolated epidural hematoma, when there is no dislocation syndrome, there is no need to open the dura mater. The bone flap is placed in place and fixed with periosteal sutures, leaving epidural drainage for 1-2 days. In cases of emergency craniotomy due to the severity of the patient's condition caused by hypertensive-dislocation syndrome, after removal of the epidural hematoma, a linear incision of the dura mater 2-3 cm long is made and the subdural space is examined to identify concomitant hematomas, foci of crushing of the brain. The dura mater in patients of this group is not sutured in order to create decompression. With timely and adequate surgical intervention in the postoperative period, patients notice a rapid regression of cerebral, focal and dislocation symptoms. When operating on patients with acute epidural hematoma against the background of severe dislocation syndrome, the outcomes are much worse, mortality reaches 40% due to irreversible ischemic post-dislocation changes in the brain stem. Thus, there is a clear relationship between the results of treatment of patients with epidural hematomas and the timing of surgery.

Quite rarely, subacute and chronic epidural hematomas occur, when the duration of the light interval is several

days or more. In such victims, the hypertensive-dislocation syndrome develops slowly, a characteristically undulating course of a traumatic disease due to an improvement in the condition after moderate dehydration. In these cases, it is almost always possible to conduct a full-fledged neurosurgical examination, including CT, MRI, angiography, the data of which make it possible to clearly determine the location and size of the hematoma. These victims are shown surgical treatment - osteoplastic trepanation of the skull, removal of an epidural hematoma.

Subdural hematomas are the most common form of intracranial hematomas, accounting for 0.4–2% of all TBIs. Subdural hematomas are located between the dura mater and the arachnoid mater (Fig. 8-6). The sources of bleeding in these cases are the superficial cerebral veins at the point of their confluence with the sinuses. The frequency of formation of these hematomas is approximately the same both in the area of application of the traumatic agent and in the type of counterblow, which often causes their development on both sides. Unlike epidural hematomas, subdural hematomas, as a rule, spread freely through the subdural space and have a larger area. In most cases, the volume of subdural hematomas is 80–200 ml (sometimes it reaches 250–300 ml). The classic variant of the course with a light gap occurs extremely rarely due to significant damage to the medulla compared with epidural hematomas. By the time of development of the dislocation

Rice. 8-6. Subdural hematoma in the region of the left parietal lobe: 1 - dura mater; 2 - hematoma; 3 - brain (parietal lobe)

syndrome with compression of the trunk distinguish between acute, subacute and chronic subdural hematomas. In acute subdural hematoma, the picture of hypertensive-dislocation syndrome develops more often within 2-3 days. Oppression of consciousness to stupor and coma is observed, hemiparesis increases, bilateral foot signs, epileptic seizures, anisocoria, bradycardia, arterial hypertension, and respiratory disorders occur. In the absence of treatment, hormetonia, decerebrate rigidity, bilateral mydriasis later join; spontaneous breathing is absent. Craniograms do not always show damage to the bones of the vault and base of the skull. Echoencephaloscopy data will be positive only with laterally located isolated subdural hematomas. A CT scan reveals a crescent-shaped hyperdense zone, usually spreading over two or three lobes of the brain, compressing the ventricular system, primarily the lateral ventricle of the same hemisphere (Fig. 8-7). Should

Rice. 8-7. Computed tomogram of the brain. A subdural hematoma of the left fronto-parietal localization is visible (a sickle-shaped hyperdense zone above the brain surface from the anterior frontal to the posterior parts of the parietal lobe of the left hemisphere, a significant displacement of the lateral ventricles in the opposite direction). In the right parietal region, signs of craniotomy are visible

It should be noted that the absence of a hyperdense zone, according to CT data, does not always exclude subdural hematoma, since during its evolution there is a phase when the density of the hematoma and the brain are the same (isodense zone). Most often this happens by the tenth day after the injury. In this phase, the presence of a hematoma can be judged only indirectly by the displacement of the ventricular system or based on the results of an MRI study. Patients with verified subdural hematomas need emergency surgical treatment - osteoplastic craniotomy, removal of the hematoma, revision of the brain. After the bone flap is folded back, a cyanotic, tense, non-transmitting pulsation of the brain dura mater is revealed. It is advisable to make a horseshoe-shaped incision with the last base to the sagittal sinus, which will provide adequate access, reduce the likelihood of a rough cicatricial adhesive process in the trepanation zone in the postoperative and long-term periods. After identifying the hematoma, they begin to remove it by washing the clots and gentle aspiration. If the source of hematoma formation is identified, then it is coagulated and a small fragment of the hemostatic sponge is placed at the site of bleeding. Perform reliable hemostasis and revision of the brain, especially the pole-basal parts of the frontal and temporal lobes (the most common location of crush foci). Usually, with isolated subdural hematomas, in cases of timely surgical intervention, before the development of a pronounced hypertensive-dislocation syndrome, after the removal of clots, the appearance of a distinct pulsation of the brain and its expansion (a good diagnostic sign) are noted. In hospitals where there are no special neuro-intensive care units and there is no possibility of dynamic CT examination, removal of the bone flap with its subsequent preservation in a formalin solution or implantation in the subcutaneous tissue of the abdomen, anterolateral surface of the thigh is indicated. This tactic of creating external decompression makes it possible to reduce the compressive effect of cerebral edema-swelling, which increases in the first 4-5 days after surgery. The bone flap should always be removed if concomitant foci of brain crushing, intracerebral hematomas are detected, hemispheric edema persists after removal of the subdural hematoma and its bulging into a trepanation defect. These patients are shown internal decompression due to the imposition of external ventricular drainage according to Arendt for up to 5-7 days. In the postoperative

During the rational period, until the condition stabilizes, patients are in the intensive care unit, where they receive complex treatment. An elevated position of the head end (Fowler's position), ensuring adequate breathing and oxygenation (up to prolonged artificial ventilation of the lungs) are advisable. In cases of rapid regression of neurological symptoms, early autocranioplasty is possible, more often 3 weeks after the primary operation, in the absence of brain protrusions. Outcomes in subdural hematomas largely depend on the timing and adequacy of surgical intervention, the severity of brain damage, age, and the presence of concomitant pathology. With an unfavorable course, belated surgical intervention, the mortality rate reaches 50-60% and there is a large percentage of profound disability of the survivors.

Subdural hematomas quite often (compared to epidural hematomas) can have a subacute and chronic course. For subacute subdural hematomas, a relatively favorable condition of patients is characteristic for up to 2 weeks from the moment of injury. During this period, the main complaint in patients is persistent headache; focal neurological symptoms come to the fore, and only when the compensatory reactions of the brain are suppressed, stem and dislocation symptoms appear. Victims with chronic subdural hematoma are usually able to work after a "minor" head injury. However, they are concerned about periodic headache, weakness, fatigue, drowsiness. After 1 month or more, focal symptoms may appear, which is often regarded as a circulatory disorder of the ischemic type (since chronic hematomas often occur in people over 50 years of age). Patients are prescribed pathogenetic treatment, which, as a rule, is unsuccessful. Only after additional examination methods (CT, MRI, echoencephaloscopy, etc.) are performed, the correct diagnosis is established (Fig. 8-8). If subacute or chronic subdural hematomas are detected, surgical treatment is prescribed in an accelerated manner. Currently, in addition to classical osteoplastic trepanation, there is also endoscopic removal of hematomas through a burr hole, which significantly reduces surgical trauma with good treatment results.

Intracerebral hematomas occur in approximately 0.5% of TBIs and are characterized by traumatic cerebral hemorrhage with a blood-filled cavity (possibly with cerebral detritus).

Rice. 8-8. Chronic subdural hematoma. The arrows indicate the avascular zone in the form of a biconvex lens. The anterior cerebral artery is displaced to the left

Most often, the formation of intracerebral hematomas occurs when the brain is damaged by the type of counterblow due to rupture of intracerebral vessels. Hematomas are localized mainly in the temporal and frontal lobes, often at the junction with the parietal lobes. In the occipital lobe, they almost do not occur, which is explained by the anatomical features of the structure - the shock-absorbing role of the cerebellum. The volume of intracerebral hematomas is 30-150 ml, the hematoma cavity has a rounded shape. Traumatic hematomas are located in the white matter of the hemispheres, usually subcortically (in contrast to intracerebral hematomas of vascular origin, often located centrally). It is possible to form an intracerebral hematoma with the unfavorable development of a confluent crush lesion (Fig. 8-9).

Clinical neurological manifestations of intracerebral hematomas are different and depend on their location, volume, rate of development of hypertensive-dislocation syndrome and the severity of concomitant brain damage. Their main feature is the presence of gross neurological symptoms. The light gap is usually blurred. Often there are psychomotor agitation, paresis of facial muscles, hemianopsia, hemihypesthesia, paresis and paralysis, more represented in the hand, aphasia, sometimes thalamic pain in opposite limbs. With the localization of the hematoma in the pole of the frontal lobe, focal symptoms are minimal, and with an increase in the compression syndrome (usually axial) on the front

Rice. 8-9. Intracerebral hematoma of the left cerebral hemisphere

stem symptoms and a rapidly growing depression of consciousness up to coma come out on the first plan.

An informative diagnostic method for the localization of an intracerebral hematoma in the temporal lobe is echoencephaloscopy, in which a lateral displacement of the median structures is detected, sometimes a signal from the hematoma is visualized. However, currently the leading research method is CT. The tomograms show a zone of homogeneously increased density of a rounded shape with smooth edges and a zone of perifocal edema (Fig. 8-10). With the development of a hematoma in the area of the focus of crushing, its edges have uneven contours. Cerebral angiography is very valuable in terms of diagnosing the severity and prevalence of angiospasm, as well as to exclude arterial aneurysms and AVMs, which often lead to the formation of intracerebral hematomas in case of vascular wall ruptures. Often, patients have a combination of intracerebral and meningeal hematomas, as well as foci of crushing.

The main method of treatment of intracerebral hematomas is osteoplastic trepanation followed by encephalotomy over the hematoma detected by brain cannula puncture, hematoma evacuation, aspiration and washing. Drug treatment of this pathology is possible with a hematoma diameter of less than 3 cm, the absence of gross hypertensive-dislocation symptoms, and the possibility of dynamic CT examination. With a favorable course against the background of ongoing drug treatment, regression of cerebral and meningeal symptoms is noted, and on

On computed tomograms, an isodense zone appears at the site of the hematoma and compression of the brain ventricles decreases. The most formidable complication in the clinical development of intracerebral hematomas is the breakthrough of the latter into the ventricular system. The prognosis for this form of TBI depends on many factors (the size and location of the hematoma, the severity of the lesion of the stem sections, the age of the patients, the presence of concomitant meningeal hematomas and crush foci, etc.). A number of patients may have a good social recovery after removal of isolated intracerebral hematomas.

Foci of crushing of the brain are characterized by the destruction of the medulla and pia mater with the formation of detritus. Rarely there are isolated foci of crushing, more often they are combined with intracranial hematomas. Foci of crushing develop according to the type of counterblow, they are localized mainly in the pole-basal regions of the frontal and temporal lobes (due to the anatomical features of the structure of the bones

Rice. 8-10. Computed tomogram of the brain. The emerging intracerebral hematoma is visible at the site of the basal lesion of crushing of the right frontal lobe (the mechanism of damage by the type of counterblow is a fall onto the left occipital region from a height of growth)

base of the skull). Most often, damage to the temporal lobe occurs (61%), one frontal lobe is damaged 2 times less often than adjacent intact bones. There are single and multiple foci of crushing of the brain. With a single focus, one of the lobes is damaged. With multiple foci, damage to two or more lobes of the brain occurs. In the vast majority of cases, damage to the frontal and temporal lobes is noted, the parietal lobe is damaged in 1/4 of the cases. Foci of crush injuries can be formed by the mechanism of counter-shock and at the site of application of the traumatic factor (Fig. 8-11).

In the first hours and days after injury, the clinical manifestations of crush foci are determined by the volume of intracranial hematoma and are mainly represented by cerebral and dislocation symptoms.

If one of the frontal lobes is damaged, psychomotor agitation occurs (in 62% of cases), muscle tone changes, reflexes of oral automatism are detected, and sometimes motor aphasia occurs. Damage to the temporal lobe develops aphasic disorders, limb paresis, and anisoreflexia. Such symptom complexes are found in most patients.

The increase in cerebral and dislocation symptoms in patients with crush foci is explained by pathophysiological processes leading to the expansion of the brain damage zone. Among

Rice. 8-11. Bruising-crushing of the right temporal lobe. Wedging of the mediobasal parts of the left temporal lobe into the foramen of the cerebellum

These processes are dominated by significant hemodynamic disturbances caused by edema, vasospasm, microthrombosis, and endogenous intoxication. All this leads to necrosis of the medulla with hemorrhagic impregnation (hemorrhagic infarction).

Diagnosis of brain crush foci includes an analysis of the nature of the injury, the clinical picture, craniography data, echoencephaloscopy, EEG, ophthalmological examination, cerebral angiography, CT and MRI.

The most informative and accessible method for diagnosing crush foci is CT, which reveals zones of alternating hemorrhages and edema, which have a "mosaic" pattern. With an unfavorable course, crush foci are transformed into intracerebral hematomas.

The neurosurgeon detects crush foci during surgery after removal of the hematoma in cases where they are located in the area of the trepanation defect. An indirect sign of the presence of crush foci in the other hemisphere may be the persistence of edema and prolapse of the brain into a trepanation defect after removal of the hematoma and revision of the brain in the surgical area.

Studies conducted in recent years have shown the need for radical removal of crush foci during surgery in order to prevent further expansion of the area of damage to the medulla. The introduction of this tactic made it possible to reduce mortality in patients with severe TBI by almost 25%. Surgical intervention for small isolated foci of brain crush, especially with concomitant subdural hematoma up to 30 ml, should be carried out immediately in the absence of the effect of drug treatment, the appearance and growth of a dislocation syndrome, and the transformation of the lesion into an intracerebral hematoma. Usually these periods of observation and drug treatment should be no more than 4-6 days. Preference is given to decompression osteoplastic trepanation with preservation of the bone flap. In the presence of crush foci and intracranial hematomas in both hemispheres, bilateral craniotomy is performed. Indications for bone flap removal:

Severe condition of the patient with the presence of dislocation manifestations before surgery;

The presence of foci of crushing and cerebral edema, detected during the operation;

Severe brain contusion, regardless of the presence or absence of protrusion of the brain into a trepanation defect.

In the postoperative period, in addition to the introduction of vascular, nootropic drugs, hyperbaric oxygenation, intracarotid infusion of medicinal substances are indicated to prevent secondary vascular disorders and inflammatory manifestations in the brain.

Among patients with multiple extensive crush foci, a high percentage of deaths and disability is characteristic. However, with a timely operation performed in the proper volume before the development of a gross dislocation syndrome, and with a positive clinical effect from drug treatment, the victims note a good and satisfactory functional recovery. According to CT-study, in the long term, cystic cavities are formed at the site of crush foci. To prevent the development of post-traumatic epilepsy, such patients are prescribed long-term anticonvulsant treatment under electrophysiological control (EEG). Closure of the defect of the skull bones can be carried out within 3 months from the time of injury.

Depressed fractures of the skull bones are fractures in which bone fragments are displaced below the surface of the adjacent part of the cranial vault. There are impression (bone fragments are connected with the preserved areas of the cranial vault and are located at an angle to the surface of these areas) and depression fractures (the edges of bone fragments are located below the surface of the intact bone and lose contact with them). Depressed fractures occur when a blow is applied to the head with an object with a limited surface (axe, hammer, stick, etc.). Diagnosis of a depressed fracture does not cause difficulties in the revision of the wound during its primary surgical treatment. In all other cases, craniography helps. Neurological symptoms often correspond to the localization of the depression. However, with parasagittal localizations, as a result of the development of circulatory disorders (especially venous), symptoms of prolapse often occur at a distance. A depressed fracture is an indication for urgent surgical intervention, since bone fragments locally irritate the cortex

brain and create its compression. The urgency of the operation is even more relevant for open depressed skull fractures, since foreign bodies and hair get into the wound, which can lead to the development of purulent-septic complications.

The method of choice for surgical intervention for depressed fractures should be resection of depressed fragments from the superimposed burr hole. Removing bone fragments by extracting them is very dangerous, traumatic, since it excludes visual control over the actions of the surgeon. Particular care must be taken when treating fractures above the sinuses and in the parasagittal region due to frequent damage to sinuses, lacunae and large veins by bone fragments. In case of damage to the dura mater, an audit of the subdural space is carried out, foreign bodies, bone fragments, hair, and crushed areas of the brain are removed. The surgical wound is abundantly washed with a solution of nitrofuran (furacillin *). During the operation, 1-2 g of ceftriaxone (rocefin *) or another cephalosporin antibiotic is administered intravenously, followed by continuation of the course of treatment with this antibiotic in the postoperative period. With open TBI, cranioplasty should be performed only in the late post-traumatic period. The issue of cranioplasty is decided individually. In closed depressed fractures, primary cranioplasty is performed using allobone or polyacrylates. Many patients with depressed fractures report good functional recovery.

Subdural hydroma is a delimited accumulation of CSF in the subdural space as a result of a rupture of the arachnoid membrane of the basal cisterns, which causes compression of the brain. Subdural hydromas can develop in traumatic brain injury both in isolation and in combination with intracranial hematomas, crush foci. This circumstance determines the polymorphism of clinical manifestations. The clinical picture of isolated subdural hydromas is similar to that of subdural hematoma, only with them the hypertensive-dislocation syndrome develops more slowly and there are no gross stem disorders. Echoencephaloscopy often reveals a moderate shift of the median echo in the opposite direction from the localization of the hydroma. CT-study allows to verify it by the characteristic hypodense zone.

Isolated subdural hydromas leading to brain compression are subject to surgical treatment. The nature of the surgical intervention depends on the severity of the patient's condition and the severity of the hypertensive-dislocation syndrome. It is often enough to evacuate the hydroma through the burr hole, and to prevent recurrence, install active drainage of the subdural space for 2-3 days.

Pneumocephalus is the penetration of air into the cranial cavity, most often as a result of the valvular mechanism in case of damage to the membranes and the ethmoid bone. The diagnosis is clarified with the help of craniograms (profile image) and with a CT scan. In most cases, a small amount of air in the subdural space is resorbed, but cerebral compression syndrome may develop. In such cases, resort to osteoplastic trepanation and closure of the defect of the dura mater. The main danger in pneumocephalus is inflammatory complications in the form of meningitis and meningoencephalitis, which dictates the need for antibiotics from the first day. The prognosis is usually favorable.

When treating patients with severe traumatic brain injury, which is always accompanied by traumatic intracranial hemorrhage, it is necessary to take into account the factors of secondary brain damage that are not directly related to the mechanism of the primary lesion, but always affect the course of the post-traumatic period and outcome. First of all, this is secondary hypoxic-ischemic damage to the medulla due to extracranial (arterial hypotension, hypoxia and hypercapnia as a result of airway obstruction, hyperthermia, hyponatremia, carbohydrate metabolism disorders) and intracranial (intracranial hypertension due to meningeal, intracerebral and intraventricular hematomas, traumatic subarachnoid hemorrhage, epileptic seizures, intracranial infection) factors. All therapeutic measures should be aimed at eliminating these causes of secondary brain damage. If a patient develops a clinical picture of hypertensive-dislocation syndrome caused by compression of the brain by an intracranial hematoma, surgery should be performed as soon as possible before the development of irreversible post-dislocation ischemic disorders in the brain stem. In cases where there is no compression

these brain meningeal, intracerebral hematomas, crush foci conduct intensive therapy under conditions of monitor control of intracranial pressure. In hospitals where there is no possibility of round-the-clock monitoring and dynamic CT, control of the adequacy of treatment is based on an assessment of the dynamics of the neurological status (state of consciousness, breathing, physical activity, reflex sphere, changes in pupils, movement of the eyeballs). Intensive care tactics:

Endotracheal intubation with artificial lung ventilation under normoventilation (PaCO 2 = 35 mm Hg);

Restoration of normal blood pressure (ideally, mean blood pressure is maintained above 90 mm Hg, which ensures adequate perfusion pressure above 70 mm Hg);

Restoration of normal oxygenation;

Improvement of venous outflow with the help of an elevated position of the head (at an angle of 15-30%), exclusion of an increase in intra-abdominal and intrathoracic pressure (during sanitation of the trachea, coughing, convulsions, desynchronization with the apparatus) by deepening sedation up to the introduction of muscle relaxants;

Restoration of circulating blood volume, maintenance of normovolemia;

The introduction of osmotic diuretics (mannitol) at an initial dosage of 1 g/kg of body weight, a maintenance dose of 0.25 g/kg with an interval of 4-6 hours (with a plasma osmolarity of more than 340 mosmol/l, hypovolemia, arterial hypotension, the administration of osmotic diuretics is contraindicated);

Creation of hypothermia (temperature should not exceed 37.5 ° C);

External ventricular drainage (especially in cases of compression of the Sylvian aqueduct or obstruction of the cerebrospinal fluid outflow tract by blood clots) for a period of 5-10 days.

In recent years, the calcium antagonist nimodipine (Nimotop*) has been used to combat post-traumatic cerebral vasospasm and subsequent cerebral ischemia. The drug is administered intravenously at 0.5-1.0 mg / h, with good tolerance, the dose is increased to 2 mg / h (orally through a probe, 60 mg every 4 hours).

The use of hyperventilation to reduce intracranial hypertension is not indicated, since a decrease in PaCO 2 to 25 mm Hg.

leads to the development of vasoconstriction and a significant decrease in cerebral blood flow, which aggravates secondary total cerebral ischemia.

The use of these therapeutic measures can reduce mortality and reduce the percentage of disability in patients with severe traumatic brain injury.

ABSCESSES OF THE BRAIN

A brain abscess is a limited accumulation of pus in the brain, surrounded by a pyogenic membrane. An abscess differs from suppuration of the wound channel in that the latter does not have a pyogenic membrane. Origin of abscesses:

Contact;

Metastatic;

traumatic;

Cryptogenic.

Contact abscesses of the brain in peacetime account for 2/3 of all abscesses. They often occur in chronic suppurative otitis media. Usually, epitympanitis or mesotympanitis are the causes of abscess formation in the temporal lobe. Mastoiditis give abscesses in the cerebellum. The penetration of infection from the otogenic focus into the brain can occur from the sigmoid sinus affected by thrombophlebitis. In this case, the abscess is localized in the cerebellum.

Inflammatory processes of the frontal sinuses, ethmoid bones can lead to abscesses in the frontal lobes.

Metastatic abscesses most often occur during inflammatory processes in the bronchi (bronchiectasis), in the lungs (with empyema, abscesses), boils, carbuncles, septicopyemia. With these purulent diseases, as well as with inflammatory processes of the frontal sinuses and ethmoid bones, abscesses often occur in the frontal lobes. It is possible for the infection to spread into the cranial cavity and into the brain through the venous plexuses of the spine. In these cases, abscesses have the most aggressive course, since they suppress the ability to encapsulate. Metastatic abscesses are mostly multiple and often have a rhinogenic nature. Traumatic metastases are usually formed with an open craniocerebral injury, with gunshot wounds. Abscesses

are formed in the period of "late complications" and in the residual period. They arise along the wound channel or from a festering hematoma.

The causative agents of a brain abscess are more often Staphylococcus aureus, hemolytic and other streptococci (pneumococcus, Proteus vulgaris, Escherichia coli, meningococcus). Rarely, an abscess of the brain is caused by an anaerobic infection, a tubercle bacillus, various types of fungi, and a dysenteric amoeba. Sometimes sowing of pus is sterile.

Pathomorphology

The pathomorphological picture of the development of a brain abscess undergoes the following changes in stages.

■ Stage I - initial. With an open craniocerebral injury or when an infection enters the brain, a focus of meningoencephalitis (contact route of infection) or encephalitis (metastasis) occurs. At the beginning, encephalitis has the character of serous or hemorrhagic inflammation, which, under the influence of antibiotics, is eliminated or passes into the focus of purulent encephalitis. Usually this period lasts about 3 weeks.

■ II stage - latent. During this period, purulent fusion of the area of the affected brain occurs and the formation of a granulation shaft - a pyogenic membrane. The abscess capsule consists of several layers. In the center - pus, it washes the inner wall, consisting of necrotic tissue. The second layer is represented by argerophilic fibers, the third - by collagen. This layer contains thick-walled vessels. The fourth layer is the zone of encephalitic melting. Thanks to the last zone, the abscess can be removed from the brain. Through the vessels of the capsule, the abscess is in constant interaction with the body. With a favorable course, the encephalolytic zone decreases in volume. The capsule thickens and, in extremely rare cases, self-healing may occur due to scarring and calcification of the abscess. The duration of the latent period is usually 2-3 weeks. The course of an abscess goes, as a rule, along the path of a temporary compaction of the capsule, followed by an outbreak of the inflammatory process. The wall of the capsule loosens again, part of it undergoes purulent fusion with the formation of child abscesses.

■ III stage - manifest (explicit). It occurs after an increase in the abscess cavity. The main manifestations in this period are considered

melt focal symptoms from the impact of the abscess on the adjacent brain structures and dislocation syndrome. ■ IV stage - terminal. At this time, the abscess extends to the surface of the brain and its membranes. There is a breakthrough of pus into the ventricles of the brain or into the subarachnoid space, resulting in ventriculitis or meningoencephalitis, in most cases fatal. The time required for the maturation of a sufficiently dense capsule varies from 10–17 days to several months. Most authors believe that after 3 weeks a dense capsule is already formed.

Clinical picture

The clinical picture of a brain abscess consists of symptoms of infection, intracranial hypertension, and focal symptoms. The initial stage with otogenic abscesses is most often represented by purulent meningitis or meningoencephalitis. With metastatic abscesses, the initial stage is characterized by a short period of general malaise, colds, chills, subfebrile condition, and headaches. With open wounds of the skull and brain, this period corresponds to the injury itself (wound). In the latent period, all phenomena disappear and within 2-3 weeks, patients experience imaginary well-being, during which, as a rule, they do not seek medical help. In cases of open wounds, pus from the wound ceases to be released and a “plug” forms in the wound. The patient gradually becomes lethargic, sluggishly makes contact, sleeps most of the day, loses appetite (anorexia). Sometimes there is delirium, hallucinations, breathing can be rapid, the pulse is tense, bradycardia is characteristic. There are no meningeal symptoms. Body temperature is normal or more often subfebrile. There are no changes in the blood, an increase in the erythrocyte sedimentation rate is possible, a slight leukocytosis with a shift to the left; cerebrospinal fluid is not changed or the amount of protein is slightly increased. The transition to the manifest stage is acute or gradual, it is accompanied by an increase in intracranial pressure and the occurrence of focal symptoms. These include severe headaches, vomiting (in about half of the patients), bradycardia (75%), mental disorders - stupor, exhaustion, disorientation, motor and speech excitement, hallucinations. In the study of the fundus reveal

congestive optic discs. Body temperature is elevated (from subfebrile to 39 ° C) and remains constant or fluctuates periodically. In the blood - leukocytosis with a shift of the leukocyte formula to the left, in the cerebrospinal fluid - pleocytosis from tens to hundreds and thousands of cells per 1 mm 3 with an increase in protein from 1 g / l to 2 g / l, increased pressure of the cerebrospinal fluid. CSF culture is often sterile.

The terminal stage is the outcome of stage III. The clinical picture of the resulting ventriculitis is characterized by a sudden onset of unbearable headache, vomiting, dilated pupils, facial flushing, sweating, tachycardia, rapid breathing, motor excitation, followed by stunning. Body temperature rises to 39-40 °C. 12-36 hours after the breakthrough of the abscess, a soporous or coma occurs, as well as clonic-tonic convulsions.

Flow

Schematically, three forms of the course of brain abscesses are distinguished.

■ Typical shape:

The clinical picture goes through all four stages (duration - from several weeks to several months);

The abscess capsule is dense.

■ Sharp shape:

Acute onset;

Further course according to the type of encephalitis;

Duration within 1 month;

The outcome is unfavorable;

The capsule is weakly expressed.

■ Chronic form:

Slow onset of symptoms;

Increased intracranial pressure without inflammatory manifestations;

The forecast is more favorable in comparison with the previous forms.

Diagnostics

Diagnosis of a brain abscess consists of a thorough analysis of anamnestic data, an analysis of clinical manifestations, laboratory data, additional research methods.

niya: carotid angiography (dislocation and deformation of vessels, avascular zones, contrasting of the abscess capsule), CT and MRI (reveal brain abscesses; Fig. 8-12), abscessography with air or positive contrast.

Rice. 8-12. CT scan. Abscess of the left temporal lobe

Differential diagnosis should be carried out with encephalitis and brain tumor.

Treatment

Therapeutic tactics for brain abscesses involves the appointment of large doses of broad-spectrum antibiotics, preferably the latest generation, well penetrating the blood-brain barrier. In the first and second periods of development of brain abscesses, especially with their metastatic nature, the intracarotid route of antibiotic administration is indicated. Endolumbar administration [kanamycin, chloramphenicol (levomycetin succinate *) at a dose of 200,000-250,000 IU per day] can mainly be recommended at stage I (encephalitic) abscess formation, in the absence of congestion in the fundus. Along with this, it is necessary to administer other antibiotics intravenously and intramuscularly. As a rule, 2-4 types of antibiotics are used simultaneously. The entire period of drug treatment is controlled

yut dynamics of abscess development with the help of CT or MRI. Identification of a clear pyogenic capsule is the basis for open transcranial surgery. Osteoplastic trepanation is performed, a brain abscess is found and it is completely removed in the capsule. In cases of breakthrough of pus into the ventricles, an abscess is removed and a tidal system is installed with nitrofural [furatsilin *] or an isotonic solution of sodium chloride and an antibiotic (kanamycin, chloramphenicol) up to 10-12 days.

With an otogenic abscess, surgery is best done in conjunction with an otosurgeon.

In advanced cases or old age, stereotaxic surgical treatment is possible.

INJURIES OF THE SPINE AND SPINAL CORD

Epidemiology

In peacetime conditions, injuries of the spine and spinal cord account for 1-4% of the total number of all injuries, and in relation to damage to the bones of the skeleton - 6-9%. The severity of spinal cord injury and a high percentage of disability make it possible to classify these injuries as the most severe and socially significant. In St. Petersburg, annually 300-320 people get spinal cord injuries (6-7 cases per 100,000 inhabitants).

Classification

All injuries of the spine and spinal cord are divided into closed (without violation of the integrity of the skin and underlying soft tissues) and open (with violation of the integrity of the skin and underlying soft tissues: there is a risk of infection of the spine and spinal cord). Open penetrating - these are injuries with a violation of the integrity of the dura mater. There are uncomplicated (without dysfunction of the spinal cord or its roots) and complicated (with dysfunction of the spinal cord and its roots) closed spinal injuries.

According to the mechanism of impact of traumatic force, closed injuries of the spine can be the result of:

Flexion;

Combinations of flexion with rotation;

Compression along the long axis;

Extension.

According to the nature of closed injuries of the spine, there are:

Stretching and rupture of the ligamentous apparatus;

Damage to the intervertebral discs;

Subluxations and dislocations;

Fractures (vertebral bodies, posterior half-ring without damage to the bodies, combined fractures of the bodies, arches, articular and transverse processes, isolated fractures of the transverse and spinous processes);

Fracture-dislocations, in which, along with a displacement in the area of a fracture of the vertebral body, a true displacement of the articular processes occurs;

Multiple damage.

In the treatment and methodological terms, the concept of stability and instability of the damaged spine (vertebral motor segment) is of great importance. The stability of the damaged vertebral bodies and the prevention of secondary displacement in case of wedge-compression and fragmentation-compression fractures of the bodies of the lumbar and cervical vertebrae are ensured by the preservation of intact elements of the posterior support complex (supraspinous, interspinous, yellow ligaments, joints of the articular processes). Instability of the spine occurs when the posterior support complex is damaged, which is observed in all types of dislocations and fracture-dislocations. Such injuries are dangerous by the development of secondary displacements of fragments and vertebral segments with compression of the spinal cord, especially at the cervical level.

The role of the vascular factor in the development of pathomorphological changes in the spinal cord in spinal cord injury should be emphasized. As a result of compression of the functioning radicular (radiculomedullary) artery, an infarction of many segments of the spinal cord occurs.

In the acute period of traumatic lesions of the spinal cord, a "spinal shock" occurs due to a violation of tonic

corticospinal influences on the cells of the anterior horns of the spinal cord and the development of parabiosis in them. The duration of the stage of spinal shock is from several hours to a month; this is characterized by sluggish para-, tetraplegia (depending on the level of damage to the spinal cord), conduction anesthesia of all types of sensitivity below the level of the lesion, dysfunction of the pelvic organs (in particular, acute urinary retention).

Clinical syndromes of traumatic lesions of the spinal cord: concussion, contusion, crush and compression.

A concussion of the spinal cord is understood as a reversible violation of its functions in the absence of visible morphological changes in the structure. Regression of neurological deficit occurs in the first hours, days after injury without residual disorders.

With bruising and crushing of the spinal cord, gross morphological changes in the brain with foci of hemorrhages, rupture of the pathways up to a complete anatomical break are revealed. Spinal cord injury often accompanies the clinical manifestations of spinal shock. In this regard, during a neurological examination in the next few hours after the injury, it is necessary first of all to find out whether the patient has a picture of a complete transverse lesion of the spinal cord or only a partial one with an incomplete loss of its functions. The preservation of any elements of motor activity or sensitivity below the level of damage indicates a partial lesion of the spinal cord. Prolonged priapism and early trophic disorders are usually characteristic of irreversible brain damage. If, in the clinical picture of a complete transverse lesion, even slight signs of recovery are not noticeable in the next hours or days after the injury, this is a poor prognostic sign. After recovery from the clinical state of spinal shock, spinal reflex activity increases with the appearance of spastic phenomena of spinal automatism. Restoration of reflex activity begins distal to the level of the lesion, rising higher. With the addition of severe infectious-septic complications (bronchopneumonia, urosepsis, intoxication due to bedsores, etc.), spinal reflex activity can again be replaced by areflexia, resembling the clinical symptoms of spinal shock. In the case of a favorable course of the post-traumatic period in the final stage of the disease, residual effects of dysfunction of the spinal cord are observed.

Compression of the spinal cord, especially prolonged, is accompanied by ischemia, and then the death of nerve conductors. Clinical signs of it can occur at the time of injury (acute compression), a few hours after it (early compression), or after several months and even years (late compression). Acute compression, as a rule, occurs under the action of the bone edges of the vertebrae or their fragments, a dropped disc; related to the mechanism of injury. Early compression of the spinal cord occurs due to the formation of sheath (epi-, subdural) or intraspinal cord (hematomyelia) hematoma or secondary displacement of bone fragments during transportation, examination. Late compression of the spinal cord is the result of a cicatricial adhesive process and a secondary violation of the spinal circulation. With fractures, dislocations or fracture-dislocations in victims at the time of injury, a neurological picture of a complete violation of the conduction of the spinal cord most often occurs. Much less often, motor (with anterior compression) or sensory (with posterior compression) disorders predominate. Acute formation of a posterior median hernia of the intervertebral disc entails a syndrome of anterior compression of the spinal cord with the development of paresis, paralysis, hyperesthesia at the level of the lesion and with the preservation of deep and vibrational sensitivity. Percussion along the spinous processes is painful at the level of the hernia, movements in the spine are painful or impossible due to reflex bilateral tension of the back muscles. With lateral displacement of the discs, radicular pain often occurs, scoliosis towards the hernia, increased pain when coughing, sneezing. Rarely, a half spinal cord lesion occurs, the clinical manifestation of this is Brown-Séquard syndrome. Manifestations of compression of the spinal cord by an epidural hematoma as a result of damage to the epidural veins usually occur after a light gap. Characteristic features: an increase in sensory, movement disorders, dysfunction of the pelvic organs, radicular pain, reflex tension of the paravertebral muscles, shell symptoms. Intramedullary hematoma, destroying the gray matter and squeezing the lateral cords of the spinal cord, causes the development of segmental and conduction disorders, dissociated sensitivity disorders.

Clinical picture

at various levels of spinal cord injury

Establishing the level of spinal cord injury is based on determining the boundaries of violations of superficial and deep sensitivity, localization of radicular pain, the nature of motor and reflex disorders. In general, the clinical picture in spinal cord injury consists of peripheral paresis of the myotomes corresponding to the level of injury, segmental-radicular disorders of sensitivity and conduction movement disorders (spastic paresis), dysfunctions of the pelvic organs and autonomic-trophic disorders below the injured segments of the spinal cord.

From a neurosurgical point of view, it is important to determine both the level of damage to the segments of the spinal cord and the vertebrae, taking into account their mismatch (Fig. 8-13).

The clinical picture in case of damage to the upper cervical segments of the spinal cord at the level C 1 -C 1y (trauma of the upper cervical vertebrae, Fig. 8-14):

spastic tetraparesis (tetraplegia);

paralysis or irritation of the diaphragm (hiccups, shortness of breath); loss of all types of sensitivity according to the conductive type; central urination disorders (delay, periodic incontinence); bulbar symptoms (swallowing disorders, dizziness, nystagmus, bradycardia, diplopia, etc.);

Rice. 8-13. Correlation between segments of the spinal cord and vertebrae

Rice. 8-14. Magnetic resonance imaging. Vertebral fracture C p

Possible radicular pain with irradiation in the neck, neck, face.

The clinical picture in case of damage to the cervicothoracic spinal cord (cervical enlargement - C V -D I):

Upper flaccid paraplegia;

Lower spastic paraplegia;

Loss of all types of sensitivity from the level of damage downwards according to the conductive type;

Radicular pain in the arms;

Bernard-Horner syndrome (due to violation of the ciliospinal center).

In addition, damage to the cervical spinal cord often complicates traumatic shock with a sharp decrease in arterial and venous pressure, early central hyperthermia with a distortion of the usual ratios of axillary and rectal temperatures, and impaired consciousness. Often such a clinical picture is observed with a diver's injury (Fig. 8-15).

Clinical picture in trauma of the thoracic spinal cord - D II -D XII (fractures of the lower thoracic or upper lumbar vertebrae; Fig. 8-16):

Central paresis of the legs (lower paraplegia);

Loss of abdominal reflexes;

Segmental and conduction disorders of sensitivity;

Girdle radicular pain in the chest or abdomen;

Disorders of urination of the central type.

Rice. 8-15. Magnetic resonance imaging. Vertebral fracture C Vp with compression of the spinal cord

Rice. 8-16. Magnetic resonance imaging. Vertebral fracture Th XII

In case of damage to the lumbar thickening (L I -S II), located at the level of the X-XII thoracic vertebrae, there are:

Peripheral paralysis of the legs with the disappearance of the knee (L II - L), Achilles (S I -S II), cremasteric (L I -L II) reflexes;

Loss of sensation from the level of the inguinal fold, in the perineum;

Retention of urination and defecation. MRI is informative in this case (Fig. 8-17). Manifestations of compression of the cone of the spinal cord (S III -S IV -segments,

located at the level of the vertebrae L I -L II):

Flaccid lower paraparesis;

Pain and loss of sensation in the legs (due to concomitant compression of the roots of the cauda equina at this level);

Pain and loss of sensation in the perineum;

Peripheral urination disorder (true urinary incontinence).

Clinical picture for cauda equina injury:

Peripheral paralysis of the legs;

Rice. 8-17. Magnetic resonance imaging. Vertebral fracture L II

Loss of sensation in the legs and in the perineum;

Radicular pain in the legs;

Disorders of urination by the type of retention or true urinary incontinence.

Incomplete damage to the cauda equina is characterized by asymmetry of symptoms.

To determine the extent of the lesion (compression) of the spinal cord, the upper and lower boundaries are found along the length and the degree of damage to the spinal cord is determined along the diameter. The upper limit is determined by the peripheral paresis of the myotome, the level of radicular pain, hyperesthesia, conduction hypo-, anesthesia. At the same time, the level of spinal cord injury is located 1-2 segments above the upper limit of sensory disorders. The lower limit of spinal cord injury is determined by the presence of skin, deep, protective reflexes, by the level of preservation of reflex dermographism and pilomotor reflexes.

When a neurological picture of spinal cord injury is detected, additional research methods help to resolve issues of treatment tactics, in particular, to choose a method of surgical intervention.

At present, the most common method of additional examination of patients with spinal cord injury is spondylography, which allows assessing various traumatic changes in the spine: stable and unstable fractures, fracture-dislocations, dislocations of the vertebrae (Fig. 8-18). It is advisable to perform spondylography in two projections to clarify the degree of deformation of the spinal canal. In a neurosurgical hospital, a therapeutic and diagnostic lumbar puncture is widely used to determine subarachnoid hemorrhage (hematorachis) and check the patency of the subarachnoid space using liquorodynamic tests (Queckenstedt, Pussepp, Stukei). Low initial CSF pressure (below 100 mm of water column) may be one of the signs of impaired patency of the subarachnoid space. A more complete picture of the patency of the subarachnoid space, the level and degree of compression of the spinal cord can be obtained with positive myelography using non-ionic radiopaque agents [iohexol (omnipak*), iopromide (ultravist*)]. To clarify post-traumatic disorders of the spinal circulation, it is possible to use

Rice. 8-18. CT scan. Vertebral body fracture Th X

selective spinal angiography. Important additional diagnostic methods for examining patients with spinal cord injury in a modern neurosurgical clinic are computer and especially MRI, which allow non-invasively clarifying the nature of not only bone damage, but also the degree of spinal cord suffering, the type of compression within 15-30 minutes.

Treatment of spinal cord injury

Therapeutic measures for spinal cord injury have their own characteristics. At the scene of the incident, others should not provide any assistance to the patient until the arrival of medical personnel, since even slight flexion or extension of the spine can lead to displacement of fragments or damaged segments in unstable fractures, especially dangerous at the cervical level. Transportation to the hospital must be carried out on a rigid stretcher, boards, shield. In case of injury of the cervical spinal cord, the adequacy of breathing is monitored.

Moving the patient in the hospital during the examination is carried out sparingly so as not to increase the dislocation of the damaged parts of the spine.

Treatment of patients with concussion or contusion of the spinal cord in the absence of clinical and instrumental data indicating the presence of compression is conservative. Painkillers, dehydration, vitamins of group B are prescribed. In severe spinal cord injury up to 8 hours after the injury, the introduction of glucocorticoids on the first day is indicated (30 mg / kg at once, followed by the introduction of 5.4 mg / kg per hour for a period up to 24 hours after injury). Treatment of patients with dislocation or fracture-dislocation of the cervical vertebrae and spinal cord injury should be comprehensive. In the first hours after the injury, skeletal traction is applied behind the parietal tubercles with a metal clip or behind the zygomatic arches with lavsan. Initially, the mass of the load is 8-12 kg, within 12 hours (in the absence of reduction) it is increased to 16 kg. After reduction (about 90% of patients), the load is reduced to 4-6 kg, followed by prolonged immobilization for 3-5 months. In the absence of reduction, an open reposition with fusion is indicated.

In cases of diagnosed spinal cord compression, early surgical intervention is indicated to eliminate the compression, and stabilizing operations are performed. The most complete restoration of the spinal cord functions is possible during surgery 4-6 hours after the injury, which helps prevent the development of post-traumatic spinal cord edema and reduce vascular disorders resulting from compression of the vessels supplying the spinal cord. There are three main approaches to the area of spinal cord compression:

Anterior (through the vertebral body or intervertebral disc);

Posterior (through the arch of the vertebra);

Combined side.

The posterior access is carried out by decompressive laminectomy (the arches of 2-5 vertebrae are resected). This access is indicated at all levels in cases where compression is caused by a comminuted fracture of the vertebral arches, with the reduction of dislocations and fracture-dislocations. The main disadvantage of laminectomy is the difficulty of adequate fusion, which leads to the development of instability, especially in the cervicothoracic and lumbothoracic spine.

Anterior access is carried out through a destroyed vertebral body or intervertebral disc with anterior compression of the spinal cord, especially at the cervical level. After removal of the destroyed intervertebral disc, an instrumental stretching of the intervertebral fissure is performed under conditions of anesthesia and muscle relaxation. For more complete decompression of the spinal cord and revision of the wound, adjacent segments of the vertebral bodies are resected with a crown cutter and other instruments. With significant destruction of the vertebral bodies, removal of all fragments with adjacent discs and subsequent anterior corporodesis with bone autografts (ribs, iliac crest, fibula) or allografts is indicated. For dislocations and fracture-dislocations, an anterior transoral approach is recommended. The anterior approach to the bodies Th III -Th X is rarely used, since it is associated with the need to open the pleural cavity, requires special tools, and is traumatic.

Lateral access in the acute period of injury has its advantages over laminectomy at the thoracic level:

Direct visual control of the state of the spine and spinal cord during the reduction of fracture-dislocations;

Possibility of complete removal of bone and disc fragments in the anterior chamber of the spinal canal;

The possibility of double fixation of the spinal column by the type of combined fusion.

When choosing a surgical approach in each specific case of spinal cord injury, maximum decompression of the spinal cord and the most complete stabilization of the area of the damaged spinal segments should be achieved.

In the postoperative period, treatment is carried out taking into account the presence of motor and trophic disorders in the patient, respiratory and circulatory disorders. Particular attention should be paid to the prevention of the development or deepening of trophic disorders, inflammatory local and general complications. For this purpose, broad-spectrum antibiotics are used parenterally and endolumbally (kanamycin), a systematic change in body position, anti-decubitus mattresses, bladder drainage (catheterization, epicystostomy, Monroe's tidal system). To improve the conduction functions of the spinal cord, neostigmine methyl sulfate (prozerin *) is used,

galantamine, bendazol (dibazol *), B vitamins, therapeutic exercises, limb massage. In order to reduce spasticity, tolperisone (mydocalm *), tizanidin (sirdalud *), thermal procedures, and massage are used. At a later date, according to indications, a frontal myelotomy or intersection of the anterior spinal roots is performed to transfer spastic paraplegia to flaccid one, in which it is easier to carry out prosthetics and use technical devices to move the patient.

Outcomes of treatment of patients with spinal cord injury depend on the degree of primary spinal cord injury, the severity of secondary ischemic disorders, the timeliness and adequacy of surgical intervention, and the course of the postoperative period. It should be noted that even with an anatomical interruption of the spinal cord after its surgical decompression, there is a decrease in trophic disorders, healing of bedsores, and restoration of urination by an automatic type. Elimination of compression of the spinal cord also contributes to the normalization of the relationship between the spinal cord and the brain.

PERIPHERAL NERVE INJURIES

Classification

There are closed and open injuries of peripheral nerves.

■ Concussion.

■ Pressure.

■ Anatomic break:

Partial;

Intra-barrel.

By the nature of the damage:

Chopped, cut, chopped, bruised, by the type of compression, traction;

Chemical;

Burn;

Radiation.

The structure of the nerves

Human peripheral nerves are a continuation of the spinal roots. The composition of the nerves includes the axons of the motor cells of the horns of the spinal cord, the dendrites of the sensory cells of the spinal nodes and the fibers of autonomic neurons. Outside, the nerve is covered with epineurium. In the lumen of the nerve are fibers covered with endoneurium. These fibers can be combined into groups. Endoneurium separates fibers and their groups from each other. The third sheath involved in the structure of the nerve is the perineurium. Perineurium is a connective tissue that surrounds bundles of nerve fibers, vessels and performs a fixing function (Fig. 8-19). Perineural sheaths along the nerve can separate, join and divide again, forming the fascicular plexus of the nerve. The number and relative position of the bundles in the nerve trunk change every 1-2 cm, since the course of the nerve fibers is not straight. Arterial branches approach large nerves every 2-10 cm. Veins are located in the epi-, endo- and perineurium. Fibers in the peripheral nerve are pulpy and non-pulmonic. Myelin is present in the fleshy ones, but not in the non-fleshy ones. The speed of impulse conduction along the pulpy fiber is 2-4 times faster (60-70 m/s) than in the non-fleshy one. In the pulpy nerve fiber, the axon is located in the center. On its surface are Schwann cells, inside of which myelin is located. Interceptions

Rice. 8-19. The structure of the peripheral nerve (cross section): 1 - adipose tissue; 2 - blood vessel; 3 - unmyelinated fibers, mostly vegetative; 4 - myelin segmented fibers, sensory or motor; 5 - endoneural membrane; 6 - perineural membrane; 7 - epineural membrane

between them are called interceptions of Ranvier. Fiber nutrition occurs mainly in these locations.

The nerve cell in the process of its development and differentiation eventually loses the ability to regenerate, but can restore its lost processes or peripheral endings. This restoration of the morphological structure of the nerve cell can occur if its body retains its viability, and there are no insurmountable obstacles to the growth of the regenerating axon in the way of the damaged nerve germination.

When a peripheral nerve is damaged, changes occur both in its proximal segment and in the distal one. In the proximal direction, this area captures from a few millimeters to 2-3 cm from the site of damage, and in the distal direction, the entire peripheral segment of the damaged nerve and nerve endings (motor plates, bodies of Vater-Pacini, Meissner, Dogel) are involved in the process. The processes of degeneration and regeneration in the damaged nerve occur in parallel, with degenerative changes predominating in the initial period of this process, and regenerative changes begin to increase after the elimination of the acute period. Degenerative manifestations can be detected 3 hours after injury, they are represented by fragmentation of axial cylinders, axon and myelin. Granules are formed, the continuity of the axial cylinders is lost. The duration of this period is 4-7 days in the pulpy fibers and 1-2 days more - in the non-fleshy ones. Schwann cells begin to divide rapidly, their number increases, they capture grains, clumps of decaying myelin, axons and subject them to resorption. During this process, hypotrophic changes occur in the peripheral segment of the nerve. Its cross section is reduced by 15-20%. In the same period, degenerative changes occur not only in the peripheral, but also in the central part of the peripheral nerve. By the end of 3 weeks, the peripheral segment of the nerve is a tunnel of Schwann cells, called Büngner's band. Damaged axons of the proximal segment of the peripheral nerve thicken, outgrowths of the axoplasm appear, having a different direction. Those that penetrate into the lumen of the peripheral end of the damaged nerve (into the Büngner's tape) remain viable and grow further to the periphery. Those that could not get into the peripheral end of the damaged nerve are absorbed.

After the outgrowths of the axoplasm have grown to the peripheral endings, the latter are created again. At the same time, Schwann cells of the peripheral and central ends of the nerve are regenerated. Under ideal conditions, the rate of axon germination along the nerve is 1 mm per day.

In cases where the axoplasm cannot grow into the peripheral end of the damaged nerve due to obstacles (hematoma, scar, foreign body, large divergence of the ends of the damaged nerve), a flask-shaped thickening (neuroma) occurs at its central end. Tapping on it is often very painful. Usually the pain radiates to the zone of innervation of the damaged nerve. It has been established that after suture of the nerve, 35-60% of the fibers grow into the peripheral segment in 3 months, 40-85% in 6 months, and about 100% in a year. The restoration of nerve function depends on the restoration of the previous thickness of the axon, the required amount of myelin in Schwann cells and the formation of peripheral nerve endings. Regenerating axons do not have the ability to sprout exactly where they were before damage. In this regard, the regeneration of nerve fibers occurs heterotopically. Axons do not grow exactly where they were before and do not fit into the areas of skin and muscles that they innervated before. Heterogeneous regeneration means that sensitive conductors grow in place of the motor ones and vice versa. Until the above conditions are met, the restoration of conduction along the damaged nerve does not occur. The control of the regeneration of the damaged nerve can be carried out by studying the electrical conductivity along it. Up to 3 weeks after the injury, there is no electrical activity of the affected muscles. That is why it is not advisable to investigate it before this period. Electrical potentials of reinnervation are detected 2-4 months before the appearance of clinical signs of their recovery.

The clinical picture of lesions of individual nerves

The clinical picture of damage to individual nerves consists of motor, sensory, vasomotor, secretory, trophic disorders. The following syndromes of peripheral nerve damage are distinguished.

■ Syndrome of complete violation of nerve conduction. Occurs immediately after injury. The patient's nerve function is disturbed, motor and sensory disorders develop, disappear

reflexes, vasomotor disturbances occur. Pain is absent. After 2-3 weeks, it is possible to identify atrophy and atony of the muscles of the limb, trophic disorders.

■ Syndrome of partial conduction disturbance along the damaged nerve. Sensitivity disorders of varying severity are noted (anesthesia, hyperpathia, hypesthesia, paresthesia). Some time after the injury, malnutrition and hypotonia of the muscles may occur. Deep reflexes are lost or reduced. Pain may be severe or absent. Signs of trophic or vegetative disorders are presented moderately.

■ Syndrome of irritation. This syndrome is characteristic of various stages of damage to the peripheral nerve. There are pains of varying intensity, vegetative and trophic disorders.

Symptoms of a brachial plexus injury

With an injury to the primary trunks of the brachial plexus, weakness of the proximal parts of the arm occurs (Erb-Duchenne palsy). It develops with damage to the roots of C V and C. The axillary, musculocutaneous, partially radial, scapular and median nerves suffer. In this case, it is impossible to abduct the shoulder, its rotation, the function of flexion of the forearm drops out. The hand hangs like a whip. Frustrated superficial sensitivity on the outer surface of the shoulder and forearm. The defeat of C Vsh -D p-roots leads to paresis of the distal parts of the hand (Dejerine-Klumpke paralysis). The function of the ulnar, internal cutaneous nerves of the shoulder, forearm and partially median is impaired. The syndrome is characterized by paralysis of small muscles, flexors of the hand and fingers. There are sensitivity disorders along the inner edge of the shoulder, forearm, hand. Bernard-Horner syndrome is often identified.

Symptoms of damage to the axillary (axillary) nerve

It is impossible to raise the shoulder in the frontal plane to the horizontal level. Atrophy and atony of the deltoid muscle are revealed. Impaired sensitivity on the skin of the outer area of the shoulder (Fig. 8-20).

Symptoms of damage to the musculocutaneous nerve

Violated flexion of the forearm. Reveal atrophy and atony of the biceps of the shoulder, anesthesia on the outer surface of the forearm. There is no reflex from the tendon of this muscle.

Rice. 8-20. Zones of sensory impairment in case of damage to the nerves of the brachial plexus

Symptoms of damage to the radial nerve (upper third of the forearm)

The hand has a “hanging” appearance - the functions of extension of the hand, fingers, supination of the hand, abduction of the first finger are impaired, atrophy and atony of the extensors of the hand and fingers, anesthesia on the dorsal surface of the forearm, partially on the hand (I, II and half of the III finger) are revealed.

Symptoms of damage to the ulnar nerve

The hand has a "clawed" appearance - there is no palmar flexion of the hand, IV, V and partly III fingers, adduction of the first finger. Atrophy and atony of the ulnar flexors of the hand, IV, V fingers, interosseous and vermiform (III and IV interosseous spaces) muscles, hypothenar muscles, anesthesia of the ulnar edge of the hand, V and medial half of the IV fingers are noted.

Symptoms of damage to the median nerve

The hand has the shape of a "monkey" - pronation of the hand, palmar flexion of the hand and fingers, dilution of I-III fingers are disturbed. Atrophy and atony of the flexors of the hand, fingers, thenar eminence, interosseous and vermiform muscles of I-III interdigital muscles are noted.

intervals, anesthesia on the palmar surface of I-III and half of the IV fingers. There are pronounced trophic disorders on the hand, especially in the area of the second finger.

Symptoms of a femoral nerve injury

It is impossible to extend the lower leg, atrophy of the quadriceps femoris muscle is characteristic, the knee reflex is lost, anesthesia is detected on the lower third of the anterior surface of the thigh and the anterior inner surface of the lower leg (Fig. 8-21).

Obturator nerve symptoms

Difficulty adducting the leg and turning it outward. Characterized by anesthesia on the inner surface of the thigh, atrophy of the muscles of the inner surface of the thigh.

Rice. 8-21. Zones of sensory impairment in case of damage to the nerves of the lumbosacral plexus

Symptoms of damage to the sciatic nerve

Paralysis of the foot and fingers, atrophy and atony of the muscles of the foot and lower leg are characteristic, the Achilles reflex disappears. There is anesthesia on almost the entire lower leg and foot, except for the anterointernal surface of the lower leg. Characterized by severe pain in the leg.

Symptoms of damage to the peroneal nerve

Reveal the "hanging" foot. It is impossible to extend the foot and fingers, as well as turn the foot outward. The muscles of the peroneal group are atrophied, they are atonic. Anesthesia is typical on the anterolateral surface of the lower leg and the back of the foot. The patient cannot walk on his heels.

Symptoms of a tibial nerve injury

Reveal the "heel" foot. The fingers are sharply bent. Characterized by paralysis of the muscles of the flexors of the foot and fingers, the Achilles reflex is lost, atrophy and atony of the muscles of the posterior surface of the lower leg and the plantar surface of the foot. Anesthesia on the back of the leg and plantar surface of the foot. Characterized by intense pain.

Treatment of peripheral nerve injuries

Upon admission of a patient with suspected damage to the peripheral nerve, he needs a thorough examination, including an analysis of the injury, identification of motor, sensory, trophic disorders. Much attention is paid to inspection, palpation of injury sites on the neck and limbs. It is possible to use electromyography and electrodiagnostics. The latest research methods are usually used in specialized institutions. With open injuries during the primary surgical treatment, the wound should be carefully examined. When detecting violations of motor and sensory functions, attention is paid to the correspondence of the wound and the projection of the location of the peripheral nerve. With arterial or massive venous bleeding, a careful examination of the tissues in the wound area is necessary. When excising the edges of the wound, the course of the peripheral nerve is taken into account. If a damaged nerve is found in the wound, the imposition of a primary suture of the nerve is possible only in the following cases:

No infection of the wound;

Acquaintance of the surgeon with the technique of applying an epineural suture;

Availability of microsurgical instruments and suture material 5/00-6/00 and 9/00-10/00.

The presence of an assistant and good lighting of the surgical wound;

Possibility of leisurely work.

There are primary and delayed surgical interventions for damage to peripheral nerves. The latter are early (from 3 weeks to 3 months) and late (after 3 months).

Types of operations: neurolysis, nerve suture. Neurolysis is understood as the isolation of the nerve from the surrounding scars or calluses, causing its compression and clinically manifested by loss of functions and symptoms of nerve irritation.

Approaches to the damaged nerve can be projection, non-projection, roundabout and angular on the folds. As a rule, surgical incisions should be large, allowing you to find the central and peripheral ends of the damaged nerve outside the area of its damage. Going down or up along the detected nerve, the surgeon selects it from the surrounding tissues and approaches the site of its injury. In this case, it is necessary to pay special attention to the preservation of the muscle branches extending from the nerve, damage to which is strictly prohibited. After highlighting the central and peripheral ends of the affected nerve, they are excised to the level of scar-unaltered bundles. The cut of the nerve must be carried out in one plane perpendicular to its axis. To achieve such an incision, it is necessary to place a gauze ball under the nerve, and take the upper part of the epineurium on a clamp and pull it down. There are two types of nerve suture: epineural and interfascicular. The latter is performed with a thread 10-11/00 under a large (15-20 times) increase. To overcome the existing diastasis between the ends of the damaged nerve, the following techniques are used:

Flexion of the limb in the joints;

Mobilization of the ends of the damaged nerve;

Stage seam;

Nerve movement;

Bone resection;

Use of inserts from cutaneous nerves.

As a rule, it is first necessary to suture the ends of the nerve opposite in diameter, and then gradually suturing them first on the outer surface of the nerve, and then, after turning it over, on the back. Usually 4-6 stitches are applied on each side.

us. The sutures are applied until the peripheral and central ends of the nerve slightly touch, achieving tightness (Fig. 8-22).

Rice. 8-22. Nerve suture: a - sutures were placed on an atraumatic needle from the lateral and medial sides of the nerve trunk; b - location of injections and injections across the nerve; in - additional seams are imposed; d - rotation of the nerve along the axis for additional sutures on the posterior surface of the nerve trunk

The limb must be immobilized with a plaster splint for 3 weeks with 2-3 dressings after the operation. After removing the splints, a course of paraffin therapy, careful physical therapy, electrical stimulation, nootropic drugs, and vitamins are administered.

Traumatic brain injury (TBI) is one of the most common causes of disability and mortality in the population. In the United States, about 50,000 people die each year as a result of TBI. The frequency of TBI in Russia is approximately 4:1000 of the population, or 400 thousand victims annually, while about 10% of them die and the same number become disabled.
In peacetime, the main causes of TBI are road traffic accidents and household injuries.
The term "traumatic brain injury" means combined damage to the skull and brain. However, severe brain injury is often possible without concomitant damage to the bones of the skull. The opposite situation occurs, when skull fractures are accompanied by minimal brain injury.
Biomechanics of traumatic brain injury. The mechanisms of damage to the bones of the skull are more or less obvious. With local impact (hitting with a heavy object, falling on asphalt, etc.), deformation of the bones of the cranial vault and their deflection occur. Due to the low elasticity of the bones of the skull (especially in adults and the elderly), cracking occurs first in the inner bone plate, then in the bones of the vault throughout the entire thickness, cracks form. When struck with great force, bone fragments are formed, which can be displaced into the cranial cavity, often damaging the brain and its membranes. From the point of application of force, cracks can spread to a considerable distance, including to the base of the skull.
Fractures of the base of the skull are a common component of severe traumatic brain injury. Despite the massiveness of the bone structures of the base, they do not differ in strength, since they are extremely heterogeneous: powerful bone formations - the pyramid of the temporal bone, the crest of the wings of the sphenoid bone alternate with areas where the bone sharply becomes thinner or there are holes and crevices in its thickness through which blood vessels and cranial nerves (upper and lower orbital fissures, oval, round holes, canals and cavities in the pyramid of the temporal bone, etc.). With various types of injury (falling on the back of the head, falling from a height onto the legs, etc.), mechanical effects are transmitted to the bones of the base, causing them to crack in many areas. Fissures can pass through the roof of the orbit, the optic nerve canal, the paranasal sinuses, the pyramid of the temporal bone, the foramen magnum. In this case, along the course of the crack, defects can occur in the dura mater and mucous membrane of the paranasal sinuses, i.e. the integrity of the structures separating the brain from the external environment is violated.
Mechanisms of brain damage in traumatic brain injury. The mechanisms of action on the brain in traumatic brain injury are diverse and not yet fully understood. Let's focus on the most obvious ones.
With a direct impact of a damaging force on the brain, for example, when struck by a heavy object, the impact is only partially absorbed by the bones of the skull, so local damage to the brain may occur at the site of application of the force. These injuries are more significant if bone fragments are formed that penetrate the brain, if a wounding weapon or projectile penetrates the brain, causing the destruction of its structures.
Acceleration and deceleration, which occur with all types of mechanical influences that lead to a rapid movement of the head or a rapid cessation of its movement, can cause severe and multiple brain damage. But even with a fixed, motionless head, the traumatic effect of these forces is important, since the brain, due to a certain mobility, can be displaced in the cranial cavity.
Let us consider the case when, under the influence of a traumatic force, a patient's head rapidly moves, followed by rapid deceleration (hit by a heavy object, falling on a stone floor, asphalt, etc.). Directly under the influence of a traumatic force, damage (contusion) of the brain occurs on the side of the blow. At the moment of collision with an obstacle, acquiring a certain inertia, the brain hits the inner surface of the fornix, resulting in the formation of a focus of brain contusion on the opposite side (contre coup). It should be noted that damage to the brain on the side opposite to the place of application of force is one of the most frequent manifestations of traumatic brain injury. This must be constantly remembered. So, in a victim who has fallen on the back of the head, in addition to damage to the posterior parts of the brain, one should also expect joint damage to the frontal lobes.
The movement of the brain in the cranial cavity, resulting from trauma, in itself can cause multiple damage to its various departments, primarily the trunk and the intermediate pier.
So, bruises of the brainstem on the edges of the large occipital and tentorial foramen are possible. An obstacle to the displacement of the brain is the crescent of the brain, along its edge, rupture of brain structures, such as fibers of the corpus callosum, is possible. Severe damage can occur in the hypothalamus, which is fixed by the pituitary stalk to the Turkish saddle, where the pituitary gland itself is located. The bark of the lower surface of the frontal and especially the temporal lobes can be seriously damaged due to bruising on the multiple bony protrusions of the base of the skull: the crest of the wings of the sphenoid bone, the pyramid of the temporal bone, the walls of the Turkish saddle.
Due to the heterogeneity of the internal structure of the brain, the forces of acceleration and deceleration act on it unevenly, and therefore internal damage to brain structures, rupture of axons of cells that cannot withstand the deformation that occurs during trauma, are possible. Such damage to the pathways passing through the brain is multiple and can become the most significant link in a number of other brain damage (diffuse axonal damage).
Particular attention should be paid to the mechanisms of brain damage in trauma that occurs due to the rapid movement of the head in the anteroposterior direction, for example, when the unfixed head of a person in a car suddenly tilts back when a car is struck from behind. In this case, movement of the brain in an anteroposterior direction can lead to a sharp tension and rupture of the veins flowing into the sagittal sinus.
Among the mechanisms affecting the brain in traumatic brain injury, the role of uneven distribution of pressure in its various structures is undeniable. The movement of the brain in a closed cavity of the dura mater filled with cerebrospinal fluid leads to the appearance of zones of a sharp decrease in pressure with the phenomenon of cavitation (similar to what happens in a pump when its piston is moved). Along with this, there are zones where the pressure is sharply increased. As a result of these physical processes, pressure gradient waves arise in the cranial cavity, leading to structural changes in the brain.
The mechanical effect in traumatic brain injury is also transmitted to the brain ventricles filled with cerebrospinal fluid, resulting in “liquor waves” that can injure brain structures adjacent to the ventricles (hydrodynamic impact mechanism).
In severe traumatic brain injury, the brain usually experiences the combined effect of the above factors, which ultimately determines the picture of its multiple damage.
Pathological manifestations of traumatic brain injury. Pathological manifestations of the impact of trauma on the brain can be very diverse. With a mild injury (concussion), changes occur at the level of cells and synapses and are detected only with special research methods (electron microscopy). With a more intense local impact on the brain - a bruise - there are pronounced changes in the structure of the brain with the death of cellular elements, damage to blood vessels and hemorrhages in the bruised area. These changes reach the greatest extent when the brain is crushed.
With some types of traumatic impact, structural changes occur in the medulla itself, leading to rupture of axons (diffuse axonal damage). At the site of the rupture, the contents of the cell - the axoplasm pours out and accumulates in the form of small bubbles (the so-called axonal containers).
Traumatic brain injury often results in damage to the vessels of the brain itself, its membranes and the skull. These vascular changes can be extremely variable in nature and severity.
With diffuse brain damage, multiple petechial hemorrhages are observed, localized in the white matter of the hemispheres, often paraventricularly. Such hemorrhages can be in the brain stem, which poses a threat to the life of the patient.
Due to crushing of the brain, rupture of its vessels, the outflowing blood can enter the subarachnoid space, and so-called subarachnoid hemorrhages occur.
The same mechanisms underlie the more rare intracerebral and ventricular hemorrhages. Shell hematomas are of particular importance in traumatic brain injury, which are divided into 2 main groups: epidural and subdural hematomas.
Epidural hematomas are located between the bone and the dura mater
Subdural hematomas are located in the space between the dura mater and the brain.
Classification of traumatic brain injury. Traumatic brain injuries are divided into open and closed.
With an open craniocerebral injury, there is damage to the soft tissues (skin, periosteum). With a hidden injury, these changes are absent or there are minor superficial injuries.
The purpose of such a subdivision is that with an open craniocerebral injury, the risk of infectious complications is much higher.
In the group of open craniocerebral injuries, penetrating injuries are distinguished, in which all soft tissues, bone and dura mater are damaged. The danger of infection in these cases is great, especially if a wounding projectile penetrates into the cranial cavity.
Penetrating craniocerebral injuries should also include fractures of the base of the skull, combined with a fracture of the walls of the paranasal sinuses, or the pyramid of the temporal bone (structures of the inner ear, auditory, Eustachian tube), if the crowbar damages the dura mater and mucous membranes. One of the characteristic manifestations of such injuries is the outflow of cerebrospinal fluid - nasal and ear liquorrhea.
A special group is made up of gunshot wounds, many of which are penetrating. The isolation of this group of craniocerebral injuries is due to the variety of modern firearms (including the variety of injuring projectiles - shrapnel, tumbling and explosive bullets, needles, etc.). These damages require special lighting.

16.1.1. Closed craniocerebral injury

There are three main forms of closed craniocerebral injuries: concussion (commotio), bruise (contusio) and compression of the brain (compressio cerebri). This classification has existed for more than 200 years and has undergone only some minor changes.
Recently, in addition to the mentioned forms, a diffuse axonal lesion has also been distinguished, which is caused by rotation of the head with a sharp acceleration and deceleration.
Depending on the nature and severity of the injury, the total effect on the brain can be complex, and diffuse brain damage (concussion, axonal damage) can be combined with bruises of varying severity.
In this regard, in the classification of a closed craniocerebral injury adopted in our country, depending on the predominance of one or another damaging mechanism, the following forms are distinguished.
Brain concussion. This is the most common form of closed craniocerebral injury (70-80%). It is characterized by a short-term (for several minutes) loss of consciousness, impaired memory for events preceding the injury (retrograde amnesia) or events that occurred during the injury itself or after it (con- and anterograde amnesia). Vomiting, headache, dizziness, short-term oculomotor disturbances, fluctuations in blood pressure, changes in pulse and a number of other quickly passing symptoms can be observed.
Changes in the brain are determined only by microscopic examination in the form of disturbances in the structure of neurons. Electron microscopy reveals changes in cell membranes, mitochondria and other organelles.
Loss of consciousness and the appearance of a number of neurological symptoms are largely due to a violation of the interaction of the cerebral cortex with other brain structures, a general disintegration of nervous activity. The role of the reticular formation is undoubted, the function of which, in all likelihood, is one of the first to be disturbed during concussion.
Brain injury. Depending on the nature and severity of the injury, local brain damage, bruises can be extremely diverse: from relatively mild to multiple, affecting vital structures. Morphological changes in the bruised area are also extremely variable: from pinpoint hemorrhages, death of individual cell groups, local edema to gross extensive changes with complete destruction of the brain tissue (crush). rupture of blood vessels, hemorrhages in the destroyed tissue, pronounced edema, spreading to large areas of the brain, sometimes to the entire brain. Changes in volumetric intracranial relationships often lead to dislocation of the brain, wedging and infringement of the brain stem in the tentorial and large occipital foramen.
Morphological changes are also accompanied by various functional disorders, such as damage to the mechanisms of self-regulation of cerebral circulation, disruption of metabolic processes (the processes of anaerobic glycolysis begin to predominate over aerobic oxidation typical of normal brain function), and intracranial pressure can sharply increase. With bruises of the hypothalamic region and the trunk, the central mechanisms of regulation of water-salt, protein, carbohydrate and other types of metabolism are damaged; central disorders of respiration and cardiovascular activity develop, which can lead to the death of the patient. There is a violation of the functions of other organs: lungs, nights, liver, etc.
The neurological symptoms that can be observed with brain contusions are also polymorphic to the same extent. This is primarily a violation of consciousness lasting from several minutes to prolonged coma.
With mild and moderate hemispheric injuries, weakness in opposite limbs, impaired sensitivity, aphatic disorders, and epileptic seizures can be detected.
With basal bruises, often accompanying a fracture of the base of the skull, there are symptoms of damage to the cranial nerves: optic - with fractures passing through the optic nerve canal. When the pyramid is fractured, deafness and paralysis of the VII pair of cranial nerves may develop.
The most dangerous bruises of the trunk and subcortical structures, which can be manifested by paralysis of the limbs, hormetonic convulsions, decerebrate rigidity in combination with life-threatening vegetative disorders.
The picture revealed by computed tomography and magnetic resonance imaging is also variable: from small local areas of reduced density of the brain tissue to multiple foci with signs of contusion, with concomitant changes characteristic of brain compression.
Depending on the severity of the injury, bruises are mild, moderate and severe.
A brain contusion of mild severity is clinically characterized by a loss of consciousness after an injury from several minutes to 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 usually without significant impairment. Moderate bradycardia or tachycardia may occur, sometimes arterial hypertension. Respiration and body temperature without significant deviations. Neurological symptoms are usually minor (nystagmus, anisocoria, signs of pyramidal insufficiency, meningeal symptoms, etc.) and regress on the 2-3rd week. 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 hours. Pronounced con-, retro-, anterograde amnesia. The headache is often severe. There may be repeated vomiting. There are mental disorders. Possible transient disorders of vital functions, 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 noted: nystagmus, dissociation of meningeal symptoms, muscle tone and tendon reflexes along the axis of the body, bilateral pathological reflexes. Focal symptoms are clearly manifested, determined by the localization of the brain injury: pupillary and oculomotor disorders, paresis of the extremities, disorders of sensitivity, speech, etc. These focal symptoms gradually (within 2-5 weeks) are smoothed out, but they can also last for a longer time. Often there are fractures of the bones of the vault and base of the skull, as well as significant subarachnoid hemorrhage.
A severe brain contusion is clinically characterized by loss of consciousness after an injury lasting from several hours to several weeks. Motor excitation is often expressed. Severe threatening violations of vital functions are observed; stem neurological symptoms often dominate (floating movements of the eyeballs, gaze paresis, multiple nystagmus, swallowing disorders, bilateral mydriasis or miosis, eye divergence along the vertical or horizontal axis, changing muscle tone, hormegonia, bilateral pathological foot reflexes, etc.), which in the first hours or days block 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 sometimes noted. Focal symptoms regress slowly: gross residual effects are frequent, primarily a violation of the motor and mental spheres. Severe brain contusion is often accompanied by fractures of the vault and base of the skull, as well as massive subarachnoid hemorrhage.
Subarachnoid hemorrhages occur as a result of rupture of the vessels of the pia mater, veins flowing into the sinuses, and intracortical vessels, especially with brain contusions, less often due to rupture of the vessels and sinuses of the dura mater. Their symptoms are varied. The early period is characterized by phenomena of irritation of the cerebral cortex (epileptic seizures, psychomotor agitation: patients scream, try to get up, wave their arms), meningeal and radicular symptoms. The clinical picture develops acutely or gradually. In the latter case, patients complain of headache, back pain. Their localization depends on the location of the lesion of the membranes: most often pain in the occipital or parietal region prevails, less often in the cervical-occipital region with irradiation to the eyes: often there are radicular pain in the spine. Dizziness, tinnitus, flashing points before the eyes are noted. More often, subarachnoid hemorrhage manifests itself acutely, without precursors, immediately after an injury: a sudden sharp headache occurs, meningeal symptoms appear early, psychomotor agitation, delirium, orientation disorder in time and space, euphoria. Excitement is replaced by stupor. The reaction to irritation in an unconscious patient is preserved. With subarachnoid hemorrhage, localized at the base of the brain, ptosis, strabismus, double vision appear; pupillary response to light is often reduced. Tendon reflexes are initially brisk, later reduced. The pulse is slow. There is hyperthermia. The pressure of the cerebrospinal fluid is usually increased, it contains an admixture of blood. Acute meningeal phenomena are expressed within a few days and gradually decrease. The course is favorable if the bleeding can be stopped.
Diffuse axonal damage. It is usually characterized by prolonged loss of consciousness, a variety of symptoms of severe brain damage, paresis of the limbs, impaired tone, decerebration phenomena, oculomotor disorders, respiratory and cardiovascular disorders. Computed tomography reveals diffuse changes characteristic of an increase in brain volume - compression of the ventricles, subarachnoid cisterns. Against this background, small focal hemorrhages in the white matter of the brain can be detected.
Brain compression. It is noted in 3-5% of victims with traumatic brain injury. It is characterized by a rapid increase in the symptoms of brain damage, primarily its stem sections, and poses a direct threat to the life of the patient. Most often, compression of the brain is due to the formation of intracranial hematomas: meningeal (epi- and subdural) and intracerebral. Other causes of brain compression can be cerebral edema, acute violation of the outflow of cerebrospinal fluid from the ventricles of the brain, subdural hygromas, depressed fracture, and some others.
With the development of the brain compression syndrome, early recognition and emergency, as a rule, surgical intervention are necessary.
In this regard, the main types of brain compression will be discussed in the section on surgical treatment.
The assessment of the condition of a patient who has suffered a traumatic brain injury is of great importance for determining the outcome and possible consequences.
The most significant integral symptom reflecting the severity of brain damage is impaired consciousness. It may be clear in patients who have had a mild injury. With more severe damage, stun (moderate or deep) is observed; stupor (the patient reacts only to strong pain stimuli) and coma (complete loss of consciousness), which in turn can be moderate, deep and terminal (all signs of reflex activity are absent).
The Glasgow Coma Scale is widely used to assess the severity of the patient's condition. It gives an assessment in points of a number of the most significant symptoms. The greater the total score, the better the patient's condition: 15 points corresponds to a clear consciousness and good orientation of the patient in space and time, 7 points or less - a severe form of traumatic brain injury.
Diagnostics. To recognize the nature of the lesion in traumatic brain injury, it is necessary to use a set of methods. At the same time, the most important is the observance of the principle of dynamic monitoring of the patient. The condition of a patient who has suffered a traumatic brain injury, especially a severe one, can change rapidly, primarily with the development of symptoms of brain compression. A constant neurological assessment of the patient's condition in these cases is of decisive importance.
Of the modern research methods, computer and magnetic resonance imaging have undoubted advantages. These methods make it possible to obtain complete information about the state of the brain (the presence of foci of contusion, intracranial hemorrhage, signs of brain dislocation, the state of the ventricular system, etc.).
Craniography has not lost its diagnostic value, which allows to detect fractures of the skull bones, metallic foreign bodies.
Under certain conditions, especially when it is not possible to perform computed tomography, methods such as echoencephalography (determining the mixing of the median echo) and the imposition of search burr holes are of great importance.
Lumbar puncture is of some importance, which makes it possible to recognize subarachnoid hemorrhages and judge intracranial hypertension. However, it should be noted that lumbar puncture is contraindicated in patients with intracranial volumetric processes causing compression and dislocation of the brain.
In severe traumatic brain injury, it is important to control intracranial pressure for targeted appropriate therapy and prevention of the most dangerous complications. For this purpose, special sensors are used to measure pressure, which are installed in the epidural space by applying burr holes. For the same purpose, catheterization of the lateral ventricles of the brain is performed.
Before a doctor examining a patient with a traumatic brain injury, the task is to determine the type of injury (closed, open, penetrating) and the nature of the brain lesion (concussion, bruise, compression, diffuse axonal lesion), clarify the cause of compression (hematoma, depressed fracture), determine the severity of the patient's condition; assess the nature of bone damage.
Treatment. The first measures in providing first aid to patients with traumatic brain injury at the accident site should be aimed at normalizing breathing and preventing aspiration of vomit and blood, which usually occurs in patients who are unconscious. To do this, put the victim on his side or linden down. The task of the ambulance service is to clear the airways of mucus, blood, vomit, if necessary, intubate, and in case of respiratory failure, ensure adequate ventilation of the lungs. At the same time, measures are taken to stop bleeding (if any) and maintain cardiovascular activity. A patient with a severe traumatic brain injury with appropriate immobilization should be urgently delivered to a specialized hospital.
Principles of conservative treatment of traumatic brain injury. The volume and nature of therapeutic measures is determined by the clinical form and severity of the patient's condition with TBI. the severity of cerebral edema and intracranial hypertension, disorders of cerebral circulation and cerebrospinal fluid circulation, as well as concomitant complications and vegetative-visceral reactions, the age of the victim, premorbid and other factors.
With a concussion, conservative treatment is carried out, which includes analgesics, sedatives and hypnotics; bed rest is recommended for 2-5 days. With mild to moderate brain contusions, along with this, moderate dehydration therapy (furosemide, lasix, diacarb), antihistamines (suprastin, tavegil) are prescribed. With subarachnoid hemorrhage, hemostatic therapy is performed (gluconate or calcium chloride, dicynone, ascorutin). Lumbar puncture for therapeutic purposes (for sanitation of cerebrospinal fluid is used only when there are no signs of compression and dislocation of the brain.
The duration of bed rest with mild brain injury is 5-7 days, with moderate injury - up to 2 weeks. depending on the clinical course and the results of instrumental studies.
With an open craniocerebral injury and the development of purulent-inflammatory complications, antibiotics are used that penetrate the blood-brain barrier (semi-synthetic analogues of penicillin, cephalosporins, fluoroquinolones, aminoglycosides, lincomycin, etc.). With lacerated wounds of the soft tissues of the head, primary chemical treatment and mandatory prophylaxis of tetanus are necessary (tetanus toxoid, tetanus toxoid are administered). Brain compression in case of epidural, subdural or intracerebral hematoma, subdural hygroma, as well as depressed skull fractures are indications for surgical intervention - osteoplastic or decompressive craniotomy and removal of the substrate compressing the brain.
Resuscitation measures for severe traumatic brain injury, accompanied by a violation of vital functions, begin at the prehospital stage and continue in a hospital setting. In order to normalize breathing, they provide free patency of the upper respiratory tract (release them from blood, mucus, vomit, introduce an air duct, tracheal intubation, tracheostomy), use inhalation of an oxygen-air mixture, and, if necessary, artificial ventilation of the lungs.
With psychomotor agitation, convulsive reactions, sedative and anticonvulsant drugs (seduxen, barbiturates, etc.) are used. In case of shock, it is necessary to eliminate pain reactions, compensate for the lack of circulating blood volume, etc. Treatment and diagnostic manipulations, including in patients in a state of coma, should be carried out under conditions of blockade of pain (nociceptive) reactions, since they cause an increase in cerebral volumetric blood flow and intracranial pressure.
With cerebral edema and intracranial hypertension, saluretics, osmotic and colloid-osmotic drugs, artificial lung ventilation in hyperventilation mode, etc. are used. hypokalemia enter panangin, potassium chloride). With the development of a clinical picture of increasing intracranial hypertension, dislocation and compression of the brain due to its edema, osmotic diuretics (beckons, glycerin) are used at a dose of 0.25-1 g / kg. Repeated or prolonged use of saluretics and osmotic diuretics requires careful monitoring and normalization of water and electrolyte balance. The attitude to the use of corticosteroids as a decongestant therapy is very restrained, including due to the threat of internal bleeding and other complications in their use. The decrease in intracranial pressure is facilitated by artificial ventilation of the lungs in the mode of hyperventilation with an oxygen-air mixture, which also ensures the prevention and treatment of cerebral hypoxia and its consequences. To improve venous outflow from the cranial cavity and reduce intracranial pressure, it is advisable to place the patient in a position with a raised head. In cases where these methods do not eliminate intracranial hypertension, persistent convulsive and severe vegetative-visceral reactions, and the results of clinical and instrumental studies make it possible to exclude the presence of intracranial hematomas, barbiturates or sodium oxybutyrate are used in intensive care units of specialized hospitals against the background of mechanical ventilation with careful control of intracranial and arterial pressure.
In case of severe bruises and crush injuries of the brain with its pronounced edema, anti-enzymatic drugs are used - protease inhibitors (kontrykal, gordox, etc.). It is also advisable to use antioxidants - inhibitors of lipid peroxidation (alpha-tocopherol, emoxipin, etc.). In case of severe and moderate traumatic brain injury, according to indications, vasoactive drugs (eufillin, cavinton, sermion, etc.) are prescribed. Intensive therapy also includes maintaining metabolic processes using enteral (tube) and parenteral nutrition, correction of acid-base and water-electrolyte imbalances, normalization of osmotic and colloid pressure, hemostasis, microcirculation, thermoregulation, prevention and treatment of inflammatory and trophic complications.
In order to normalize and restore the functional activity of the brain, psychotropic drugs are prescribed, including nootropics and GABAergic substances (piracetam, gammalon, pyriditol, pantogam, etc.), as well as cerebrolysin and drugs that normalize the metabolism of neurotransmitters (galantamine, levodopa, nakom, madopar, etc.). ).
Measures for the care of patients with traumatic brain injury include the prevention of bedsores, hypostatic pneumonia (systematic turning of the patient, cupping, massage, skin toilet, etc.), passive gymnastics to prevent the formation of contractures in the joints of paretic extremities. In patients with depression of consciousness to stupor or coma, impaired swallowing, decreased cough reflex, it is necessary to carefully monitor the patency of the respiratory tract, use suction to free the oral cavity from saliva or mucus, and in case of tracheal intubation or tracheostomy, sanitize the lumen of the tracheobronchial tree, exercise careful control for physiological administration, take the necessary measures to protect the cornea from drying out in comatose patients (instill vaseline oil into the eyes, close the eyelids with adhesive tape, etc.). It is important to regularly carry out the toilet of the oral cavity.
Patients with traumatic brain injury are subject to long-term dispensary observation. According to indications, rehabilitation treatment is carried out. Along with the methods of physical therapy, physiotherapy and occupational therapy, metabolic (piracetam, gammalon, pyriditol, cerebrolysin, etc.), vasoactive (cavinton, sermion, stugeron, etc.) drugs, biostimulants (aloe, vitreous body. FiBS), lidase, vitamins (B1, B6, B15, C, E, etc.).
For the treatment of epileptic seizures resulting from TBI. therapy is selected individually, taking into account the nature and frequency of epileptic paroxysms, their dynamics, age, premorbidity and the general condition of the patient. In case of traumatic brain injury (taking into account its severity, features of brain damage and EEG data), prophylactic administration of antiepileptic drugs may be indicated.
Surgery. Surgical treatment of patients with traumatic brain injury includes primary surgical treatment for open injuries, stopping bleeding, eliminating brain compression, and eliminating liquorrhea. Surgical intervention is also used for the consequences of a traumatic brain injury: suppuration of a brain wound and abscesses, traumatic hydrocephalus, epileptic syndrome, extensive bone defects, vascular complications (carotid-cavernous anastomosis) and a number of others.

16.1. 1. 1. Traumatic intracranial hemorrhages

Epidural hematomas. The cause of epidural hematomas is most often a rupture of the branches of the middle meningeal artery, which, after exiting the spinous foramen, is located in a deep groove or canal in the thickness of the temporal bone. With cracks passing through this channel, the artery ruptures. The blood flowing from the artery exfoliates the dura mater from the bone and forms a hematoma, which can lead to dislocation of the brain and wedging it into the tentorial foramen within a few hours after the injury.
Epidural hematomas can be caused by bleeding from the sinuses of the dura mater when its outer wall is damaged.
It is also possible the formation of epidural hematomas due to bleeding from diploic vessels with extensive damage to the bones of the skull. Most epidural hematomas are located in the temporal region.
Clinical manifestations. It is important to note that in a significant percentage of cases, epidural hematomas occur as a result of blows of relatively low force. In this regard, many patients do not lose consciousness at all, or they note a relatively short loss of consciousness - for several minutes, usually less than an hour (in approximately 40% of cases). After the return of consciousness, a light interval sets in, and only after some time the patient's condition begins to worsen again. Stupefaction, drowsiness appear, followed by stupor and coma. There are signs of wedging of the brain into the tentorial foramen, one of the first signs of which is the expansion of the pupil, usually on the side of the lesion; paresis of opposite limbs may develop. Later, signs of decerebration appear. There are violations of cardiovascular activity - bradycardia, increased blood pressure. If the victims are not provided with emergency assistance, they die with increasing symptoms of compression of the brain stem and increased intracranial pressure.
When evaluating clinical symptoms, it should be taken into account that due to the dislocation of the brain, compression of the brain stem on the opposite edge of the tentorial foramen may occur, as a result of which hemiparesis may occur on the side of the hematoma.
In case of primary severe brain injury (brain contusion with prolonged loss of consciousness), there is no clear gap; the patient has a steadily progressive deterioration with increasing signs of brainstem compression.
Diagnostics. The characteristic sequence of development of symptoms, the presence of a light gap allow us to assume with a significant degree of probability the development of an epidural hematoma in a patient
To clarify the diagnosis, a craniographic study is of great importance: the detection of cracks in the temporal bone, corresponding to the projection of the middle meningeal artery and its things, confirms the assumption of an epidural hematoma.
Computed tomography and MRI study reveal a typical picture of an epidural hematoma, which has a characteristic lenticular shape. At the same time, these studies make it possible to reveal the degree of brain dislocation and signs of tentorial herniation. If it is impossible to use computed tomography for diagnosis, valuable information can be obtained by ultrasound examination of the brain: the mixing of the M-echo allows us to determine the side of the lesion.
Treatment. Since assistance to a patient who is suspected of having an epidural hematoma should be provided under any conditions, the imposition of search burr holes has not lost its significance, primarily in the basal parts of the temporofrontal region, according to the projections of the middle meningeal artery
Technique for removal of epidural hematomas. To perform the operation, a direct incision of soft tissues in the anterior parts of the temporal region and resection of the scales of the temporal bone by expanding the burr hole can be used. If before the operation the location and size of the hematoma are determined using computed tomography or magnetic resonance imaging, osteoplastic trepanation with a horseshoe-shaped soft tissue incision is preferable. Removal of the hematoma itself is not difficult: clots are aspirated by suction, removed with tweezers, washed with isotonic sodium chloride solution. It is important to find the source of bleeding. The damaged meningeal artery is coagulated or ligated by suturing the dura mater at the site of the artery. Sinus bleeding is stopped in the manner described earlier (see section 9.2). When bleeding from diploic veins, the edges of bone fragments are smeared with wax. After removal of the hematoma, the volume of which often reaches 70-100 ml, the brain straightens out, its pulsation appears. With osteoplastic trepanation, after stopping the bleeding, the bone is placed in place and the wound is sutured in layers.
Subdural hematomas. Subdural hematomas are located between the dura mater and the surface of the brain. The source of their formation can be veins, more often in the parasagittal region, damaged as a result of trauma, bleeding from the sinuses and vessels of the brain during contusion and softening.
There are acute, subacute and chronic subdural hematomas.
Acute subdural hematoma. Usually occurs with severe traumatic brain injury, accompanied by bruising and crushing of the brain. Acute subdural hematoma is clinically manifested within the first three days. Bleeding occurs from damaged cerebral vessels in the bruised area and from broken veins. More often, hematomas are located on the convex surface of the brain. In 10-20% of cases they can be bilateral.
The most significant is that acute subdural hematoma is one of the manifestations of severe brain injury. It develops against the background of loss of consciousness and other symptoms of massive brain damage. In this regard, the light gap, so characteristic of epidural hematomas, is often not detected. Clinically, the formation of an acute subdural hematoma can be suspected on the basis of an increase in symptoms of dislocation and compression of the brain.
As with epidural hematomas, computed X-ray or magnetic resonance imaging of the brain is crucial for the diagnosis of subdural hematomas.
Important information can be obtained using carotid angiography, which reveals a large lenticular avascular zone and a sharp displacement of cerebral vessels.
Depending on the situation, echoencephalography and the imposition of search burr holes can be used to recognize hematomas.
Identification of a subdural hematoma justifies the indications for surgical intervention, since the removal of a hematoma is a necessary condition for eliminating life-threatening dislocation and compression of the brain. At the same time, it is always necessary to take into account concomitant brain damage, the severity of which can be decisive for the prognosis, which in acute subdural hematomas is often unfavorable, mortality reaches 40-50%.
Immediately after injury, when the content of the hematoma consists mainly of liquid blood, it can be emptied through the burr holes. Osteoplastic trepanation provides a great opportunity to remove both the liquid and organized part of the hematoma, as well as revision of concomitant brain damage. When it is crushed, it is advisable to aspirate the dead brain tissue and stop bleeding.
Despite the removal of the hematoma, the pressure in the cranial cavity may remain high, the brain begins to prolapse into the wound, and therefore it is not possible to put the bone flap in place. In this case, it is important to make a plastic sheath and carefully close the wound.
Subacute subdural hematoma develops within 4-14 days after injury, is caused by less intense bleeding and is often accompanied by injuries of lesser severity. For subacute subdural hematoma, symptoms of increasing compression of the brain are characteristic already at a time when acute manifestations of traumatic brain injury begin to subside, the patient's consciousness clears up and focal symptoms begin to disappear. The prognosis for subacute subdural hematomas is more favorable and mortality is 15-20%. When recognizing them using computed tomography, it must be remembered that the density of a hematoma may not differ from the density of the brain, and only a shift in the median structures indirectly indicates the presence of a hematoma.
Chronic subdural hematomas differ from acute and subacute by the presence of a restrictive capsule, which determines the features of their clinical course. They are diagnosed weeks, months, or (rarely) years after the injury. Often they occur after minor injuries that go unnoticed by the patient. This is a kind of pathology. In the pathogenesis of chronic subdural hematomas, age-related changes, concomitant vascular pathology, alcoholism, and diabetes mellitus are of great importance. More often chronic hematomas occur in elderly people (60 years and older).
Chronic subdural hematomas are manifested by headaches, mental disorders, manifested by a change in character, memory impairment, inappropriate behavior. The appearance of these symptoms is often the reason for the hospitalization of patients with chronic subdural hematomas in psychiatric institutions. Symptoms of local brain damage can be detected: hemiparesis, aphatic disorders. The undulating course of the disease is characteristic.
Chronic subdural hematomas usually have a well-formed capsule with its own vasculature. Pathological vessels of the capsule can be a source of repeated bleeding into the hematoma cavity and lead to an exacerbation of the disease. The volume of the hematoma can be changed by fluid filtration through the semi-permeable wall of the hematoma.
Chronic hematomas often reach enormous sizes, covering most of the convexital surface from the forehead to the back of the head. Their thickness can reach several centimeters, and the total volume exceeds 200 ml. An increase in the volume of the hematoma can lead to dislocation of the brain and its wedging into the tentorial foramen.
In 10-20% of cases bilateral chronic subdural hematomas are observed.
Computed tomography and magnetic resonance imaging are the best methods used to recognize chronic subdural hematomas.
Surgery. Since most chronic subdural hematomas contain liquid lysed blood, it is advisable to empty them through burr holes. The gentle technique is also justified by the large volume of hematoma and the advanced age of the patients. Radical removal of the hematoma along with the capsule is more dangerous.
To empty the hematoma, it is advisable to use catheters with containers hermetically connected to them, where the contents of the hematoma are collected.
A catheter should be inserted into the hematoma through a small incision in the capsule to avoid air entering the hematoma cavity. The contents of the hematoma itself should flow into the drainage system as the brain expands. Forced emptying of a hematoma can provoke a brain retraction, rupture of blood vessels and the development of intracranial hemorrhages.
In some cases, it is advisable to wash the contents of the hematoma. This is best done through two burr holes, using one catheter to inject the solution into the hematoma cavity, the other to empty it.
Special care is needed to avoid infection of the hematoma.
With bilateral hematomas, drainage must be carried out simultaneously so as not to cause abrupt dislocation of the brain.
If the above precautions are observed, the emptying of hematomas in most cases leads to the recovery of patients.
Subdural hematomas in newborns. More often associated with head trauma during childbirth, especially during extraction of the fetus with forceps. They are manifested by the anxiety of the child, vomiting, a rapid increase in the size of the head. The fontanel is tense. Emptying of the hematoma is carried out either by puncture through the fontanel, or by craniotomy with radical removal of the hematoma along with the capsule.
Intracerebral hematomas. With severe bruises of the brain, causing arrosion of blood vessels, the formation of hematomas in the thickness of the brain is possible. Their occurrence exacerbates focal and cerebral symptoms caused by bruising. Their recognition is possible mainly with the help of computed and magnetic resonance imaging.
Their removal is carried out by craniotomy, which allows not only to remove the blood accumulated in the thickness of the brain, but also to revise the site of brain contusion and detect the source of bleeding.
Subdural hygromas. The cause of cerebral compression may be an acute accumulation of cerebrospinal fluid over the cerebral hemisphere due to rupture of the arachnoid membrane. The manifestations of such hygromas differ little from the signs of subdural hematomas.
Treatment consists in opening the hygroma capsule (thickened arachnoid membrane) and emptying it.
In some cases, the brain compression syndrome may be due to the accumulation of air in the subarachnoid space (pneumocephaly).

16.1.2. Skull fractures

It is advisable to subdivide skull fractures into convexital and basal ones, while it must be remembered that in severe traumatic brain injury, cracks that begin in the region of the cranial vault can also spread to its base.
Depending on the nature of the fracture, there are cracks, comminuted fractures, fractures with a bone defect - perforated fractures.
With a traumatic brain injury, there may be a divergence of the sutures, which is essentially not a fracture. Cranial fractures do not require special treatment. Within a few weeks, the defects in the area of the crack are filled with connective, and later with bone tissue.
With comminuted bone injuries, indications for surgery arise if there is a deformation of the skull with a displacement of the fragments into its cavity - a depressed fracture.
With depressed fractures, there is often concomitant damage to the dura mater and brain. The operation is indicated in almost all cases, even if there are no neurological symptoms. To eliminate a depressed fracture, a skin incision is made in such a way as to widely expose the fracture site and maintain a good blood supply to the bone flap. If the fragments lie loose, they can be lifted with an elevator. In some cases, a burr hole is placed near the fracture site through which a lift can be inserted to mobilize the depressed bone fragments.
With a rupture of the dura and concomitant damage to the brain, the defect in the membrane expands to a size that allows revision of the brain. Removed blood clots, brain detritus. Careful hemostasis is carried out. If the brain does not bulge into the wound, the dura mater must be sewn up tightly (defects in it can be closed with aponeurosis). The bone fragments are placed in place and fixed to each other and to the edges of the bone defect with wire (or strong ligature) sutures.
If, due to high intracranial pressure, the brain begins to prolapse into the wound, it is not possible to sew up the dura mater. In these cases, it is advisable to perform its plastic surgery using a periosteal-aponeurotic flap, a wide fascia of the thigh, or artificial substitutes for the dura mater. Bone fragments are removed To prevent possible liquorrhea, soft tissues must be carefully sutured in layers.
If the wound is contaminated, it is advisable to remove bone fragments because of the risk of osteomyelitis and perform cranioplasty in a few months.
With chronic depressed fractures, it is impossible to eliminate the deformation of the skull by the described method due to the strong fusion of fragments between themselves and with the edges of the bone defect. In these cases, it is advisable to perform osteoplastic trepanation along the edge of the fracture, separate the fragments, give them a normal position and then rigidly fix them with bone sutures.
Fractures of the base of the skull. Fractures of the bones of the base of the skull, as noted earlier, are usually accompanied by bruising of the basal parts of the brain, the trunk, and symptoms of damage to the cranial nerves.
Fractures of the base of the skull usually have the form of cracks, often passing through the paranasal sinuses, the Turkish saddle, the pyramid of the temporal bone. If, simultaneously with the bone, the membrane and mucous membrane of the paranasal sinuses are damaged, then there is a danger of infection of the brain, since there is a communication between the cerebrospinal fluid spaces and the paranasal air areas (such damage is regarded as penetrating).
Clinical manifestations. The picture of a fracture of the bones of the base of the skull includes cerebral symptoms, signs of stem disorders, lesions of the cranial nerves, bleeding and liquorrhea from the ears, nose, mouth, nasopharynx, as well as meningeal symptoms. Often there is bleeding from the external auditory meatus (with a fracture of the pyramid of the temporal bone in combination with a rupture of the tympanic membrane), nose (with a fracture of the ethmoid bone), mouth and nasopharynx (with a fracture of the sphenoid bone). Liquorrhea or the outflow of blood containing cerebrospinal fluid indicates the presence, in addition to ruptures of the mucous membranes and a fracture of the bones of the base of the skull, damage to the dura mater. Bleeding from the nose and ears acquires diagnostic value only in those cases when it is combined with neurological symptoms and if it is possible to exclude rupture of the mucous membranes during a bruise or eardrum under the influence of a blast wave as a causative factor. Such bleeding is minor and easily stopped. Heavy and prolonged bleeding usually indicates a fracture.
With fractures in the region of the anterior cranial fossa, bruising often occurs in the eyelids and periorbital tissue (“glasses”). It can also be a bruise with a local bruise of the soft tissues. A pronounced and symmetrical nature of bruising in the form of "glasses" is typical for a fracture of the bones of the base of the skull, sometimes with their late development and exophthalmos. With fractures in the region of the middle cranial fossa, a hematoma may form under the temporal muscle, which is determined by palpation in the form of a test tumor. Bruising in the area of the mastoid process can occur with fractures in the region of the posterior cranial fossa.
A feature of the clinical manifestations of fractures of the base of the skull is the defeat of the cranial nerves. More often there is a lesion of the facial and auditory nerves, less often - oculomotor, abducent and block, as well as olfactory, visual and trigeminal. In rare cases, with fractures in the posterior cranial fossa, damage to the roots of the glossopharyngeal, vagus, and hypoglossal nerves is observed. The most common combination is damage to the facial and auditory nerves.
course and outcome. Fractures of the base of the skull, if they are accompanied by gross injuries of the basal parts of the brain, can lead to death immediately after the injury or in the near future. Some patients are in a serious condition for a long time (disordered breathing and cardiac activity, confused consciousness), often restless, anxious. A dangerous complication of the early period in violation of the integrity of the dura mater is purulent meningitis. Persistent headaches (due to hydrocephalus, cicatricial changes in the membranes), damage to the cranial nerves, and pyramidal symptoms persist as persistent consequences.
The main complications of such fractures of the bones of the base of the skull are the outflow of cerebrospinal fluid (liquorrhea) and pneumocephalus.
There are nasal and ear liquorrhea. Nasal liquorrhea develops as a result of damage to the frontal sinus, the upper wall of the ethmoid labyrinth (in the region of the perforated plate), with cracks passing through the Turkish saddle and the sphenoid sinus.
If the pyramid of the temporal bone is damaged, cerebrospinal fluid can flow through the external auditory canal or through the auditory (Eustachian) tube into the nasopharynx (ear liquorrhea).
In the acute stage of traumatic brain injury, cerebrospinal fluid may leak with a large admixture of blood, and therefore liquorrhea may not be immediately detected.
Treatment. In the acute stage, treatment is usually conservative. It consists in repeated lumbar punctures (or lumbar drainage), dehydration therapy, prophylactic antibiotics. In a significant number of cases, in this way it is possible to cope with liquorrhea.
However, in some patients, the outflow of cerebrospinal fluid continues weeks and months after the injury and may cause recurrent meningitis. In these cases, there are indications for the surgical removal of CSF fistulas. Before the operation, the location of the fistula must be accurately determined. This can be done by radioisotope research with the introduction of radioactive drugs into the cerebrospinal fluid or by using computed and magnetic resonance imaging, especially if these studies are combined with the introduction of special contrast agents into the cerebrospinal fluid.
With nasal liquorrhea, trepanation of the frontal region is usually used. The approach to the location of the CSF fistula can be carried out both extra- and intradurally. It is necessary to carefully close the defect of the dura mater by suturing or plastics with aponeurosis or fascia.
The bone defect is usually closed with a piece of muscle.
If the source of liquorrhea is damage to the wall of the sphenoid sinus, a transnasal approach with sinus tamponade with muscle and a hemostatic sponge is usually used.
With cracks in the bones of the base of the skull, passing through the air cavities, in addition to the outflow of cerebrospinal fluid, air may enter the cranial cavity. This phenomenon is called pneumocephalus. The reason is the emergence of a kind of valve mechanism: with each breath, a certain amount of air enters the cranial cavity from the paranasal sinuses, it cannot go back, because when exhaling, the sheets of the torn mucosa or dura mater stick together. As a result, a huge amount of air can accumulate in the skull above the cerebral hemispheres, symptoms of increased intracranial pressure and brain dislocation appear, with a rapid deterioration in the patient's condition. The air accumulated in the skull can be removed by puncture through the burr hole. In rare cases, there is a need for surgical closure of the fistula in the same way as it is done with liquorrhea.
With fractures of the base of the skull passing through the canal of the optic nerve, blindness may occur due to bruising or compression of the nerve by a hematoma. In these cases, intracranial intervention with opening of the canal and decompression of the optic nerve may be justified.
Cranioplasty. The consequences of a craniocerebral injury can be various, often extensive defects of the skull. They result from comminuted fractures; when it is impossible to save the bone flap due to high intracranial pressure and prolapse of the brain into the surgical wound. The cause of bone defects can be osteomyelitis in case of infection of the wound.
Patients with large bone defects respond to changes in atmospheric pressure. The development of a cicatricial adhesive process along the edges of a bone defect can cause pain syndromes. In addition, there is always a risk of damage to areas of the brain that are not protected by bone. Cosmetic factors are also important, especially in frontobasal defects.
These reasons justify the indications for cranioplasty.
Defects in the convexital parts of the skull can be closed using prostheses made of fast-hardening plastic - styracryl, galakost. While this polymer is in a semi-liquid state, a plate corresponding to the skull defect is formed from it. To avoid the accumulation of blood and exudate between the dura mater and the plastic plate, several holes are made in the latter. The graft is firmly fixed with sutures to the edges of the defect. Tantalum plates and mesh are also used to close bone defects.
Recently, the bone of the patient himself has been used for cranioplasty. For this purpose, a symmetrical section of the skull is exposed and a bone fragment is sawn out, corresponding in size to the bone defect. With the help of special oscillating saws, the bone flap is stratified into two plates. One of them is placed in place, the other is used to close the bone defect.
A good cosmetic effect can be obtained by using a specially processed cadaveric bone for cranioplasty, but recently this method has been refrained from using because of the risk of infection with the virus of slow infections.
The most difficult cranioplasty for parabasal injuries, including the frontal sinuses, the walls of the orbit. In these cases, a complex operation to reconstruct the skull is necessary. Before surgery, the extent and configuration of bone lesions should be carefully examined. Volumetric reconstruction of the skull and soft tissues of the head using computed and magnetic resonance imaging can be of great help in this case. To restore the normal configuration of the skull in these cases, the own bones of the skull and plastic materials are used.

16.1.3. Open traumatic brain injury.

In an open craniocerebral injury, the same damaging factors act on the brain as in a closed injury. The difference lies in the risk of infection, especially with penetrating wounds.
Treatment. The tactics of treating patients with open injuries is primarily determined by the task of preventing infection of the wound.
Primary surgical treatment. After determining the nature of the damage using the previously mentioned diagnostic studies, the patient's head is shaved and the skin is thoroughly disinfected. Crushed, non-viable areas of soft tissues are excised. The skin wound, if necessary, expands in order to expose the damaged areas of the skull. Loose bone fragments and foreign bodies are carefully removed. Crushed areas of the bone are resected with nippers. If the dura mater is intact and there are no signs of intracranial hematoma, it is better not to open it. The wound is sutured tightly in layers. If the shell is damaged, its edges are excised for 1-2 mm. It is opened with additional incisions to expose the brain. Bone fragments, hair, foreign bodies are carefully removed along with brain detritus and blood clots, the wound is thoroughly washed with isotonic sodium chloride solution and disinfectant solutions (furacilin, dioxidine). A hemostatic fibrin sponge containing an antibiotic can be used to stop bleeding.
If conditions permit (there is no prolapse of the brain), it is necessary to seal the membrane hermetically. Soft tissues are carefully sutured in layers. With significant bone defects, primary cranioplasty can be performed.
When the medulla bulges, it is necessary to perform a dura mater plastic surgery, using the aponeurosis or periosteum for this. Closure of the membrane defect in these cases prevents further swelling of the brain and its infringement in the bone hole. Local and parenteral administration of broad-spectrum antibiotics is shown. Primary surgical treatment of the wound is performed during the first three days (early surgical treatment).
If, for some reason, assistance to the victims was not provided within these terms, the so-called delayed primary treatment (3-6 days after the injury) is justified.
Consequences and complications of traumatic brain injury. Many patients who have suffered a severe traumatic brain injury remain severely disabled due to mental disorders, memory loss, movement disorders, speech disorders, post-traumatic epilepsy and other causes.
Complications in the form of amnesia, decreased performance, persistent headaches, vegetative and endocrine disorders can be observed in a large number of patients who have had mild to moderate traumatic brain injury.
These symptoms may be based on atrophic processes in the brain, inflammatory changes in its membranes, impaired liquor circulation and blood circulation, and a number of others.
Some consequences of craniocerebral injuries require surgical treatment: post-traumatic purulent complications (abscesses, empyema), aresorptive hydrocephalus, severe epileptic syndrome, carotid-cavernous fistulas and a number of others,
The abscess of the brain is punctured through the burr hole, then, with the help of a catheter inserted into the abscess, pus is removed, its cavity is washed, and antibiotics are introduced. Drainage of the abscess is carried out for several days under the control of repeated CT studies until the discharge of the discharge from its cavity stops. Encapsulated abscesses can be removed entirely, along with the capsule.
The cause of hydrocephalus in patients with traumatic brain injury is often a violation of the resorption of cerebrospinal fluid. If severe ventriculomegaly is accompanied by periventricular edema, there may be indications for bypass surgery to divert cerebrospinal fluid into the abdominal cavity (lumbo- or ventriculoperitoneal drainage) or into the atrium (ventriculoatriostomy).
One of the dangerous complications of a fracture of the bones of the base of the skull can be an injury to the carotid artery.
With cracks passing through the wall of the sphenoid sinus, in the event of a rupture of the carotid artery, extremely dangerous recurrent nosebleeds can occur.
If the patient is not provided with urgent assistance, he may die from acute blood loss. Treatment consists of occlusion of the carotid artery at the site of rupture using an occlusive balloon.
If a rupture of the carotid artery occurs at the point where it passes through the cavernous sinus, characteristic symptoms of a carotid-cavernous anastomosis appear. Surgical treatment - endovasal occlusion of the cavernous sinus or carotid artery.
Employability. Clinical and labor prognosis for traumatic brain injury to a certain extent depends on the correct solution of the issue of examination of temporary disability. With a concussion of the brain, inpatient treatment lasts an average of 5-7 days, temporary disability - within 2-3 weeks; with mild brain injury - 10-14 days and 4-5 weeks, respectively; with moderate brain injury - 2-3 weeks and 1.5-2 months; with a severe brain contusion, often with a skull fracture, brain compression, massive subarachnoid hemorrhage, the duration of inpatient treatment can be 1-2 months, and sometimes much more.
With a likely favorable clinical prognosis, post-treatment of patients with an extension of the period of temporary disability is practiced.
Victims who, despite the complex of therapeutic and rehabilitation and social and preventive measures, have unfavorable clinical and labor prognosis, are subject to referral for a medical and labor examination for disability registration: persistent pronounced dysfunctions, remitting or progressive course of a traumatic disease.
The criteria for establishing disability group III are moderately pronounced vegetative-vascular, vestibular, liquorodynamic, epileptic, diencephalic, somatic disorders, mental disorders, motor and speech disorders in stationary or slowly progressive and remitting course with rare exacerbations and long periods of stable compensation in combination with social factors in each case.
The criterion for establishing disability group II is a progressive or relapsing course of a traumatic brain disease with frequent and long periods of decompensation, pronounced organic changes, mental disorders, vestibular, liquorodynamic, vegetative-vascular, metabolic and endocrine disorders, impaired motor function and speech, vision, with parkinsonism and other severe clinical manifestations
The criteria for establishing group I disability are persistent pronounced disorders of the motor function of the limbs (hemiplegia, gross hemiparesis), speech (total, sensory, motor aphasia), psyche (traumatic dementia), coordinating disorders that impede movement, epileptic convulsive syndrome with frequent seizures, prolonged twilight states of consciousness, psycho-organic syndrome and pronounced intellectual-mnestic disorders, pronounced manifestations of parkinsonism, depriving patients of the possibility of self-care.
One of the important links in the complex system of rehabilitation of disabled people who have suffered a traumatic brain injury is professional rehabilitation, which consists of the psychological orientation of a disabled person to work, shown to him for health reasons, labor recommendations for a rational employment arrangement, vocational training and retraining.

16.2. Trauma of the spine and spinal cord. Surgery

Damage to the spinal cord and its roots is the most dangerous complication of spinal cord injury. It is observed in 10-15% of those who have undergone spinal injury: 30-50% of victims die from complications caused by spinal cord injury. Most survivors become disabled with severe movement disorders, dysfunction of the pelvic organs, pain syndromes that persist for many years, often for life. Injuries of the spine and spinal cord are divided into open, in which the integrity of the skin and underlying soft tissues is violated, and closed, in which these injuries are absent. In peacetime, closed trauma is the predominant type of injury to the spine and spinal cord.
Injuries of the spine, accompanied by damage to the spinal cord and its roots, are called complicated.

16.2.1. Closed injuries of the spine and spinal cord

Spinal injuries. Closed injuries of the spine occur under the influence of flexion, rotation, extension and compression along the axis. In some cases, a combination of these effects is possible (for example, with the so-called whiplash injury of the cervical spine, when, after flexion of the spine, its extension occurs).
As a result of the impact of these mechanical forces, various changes in the spine are possible:
- stretching and rupture of ligaments;
– damage to the intervertebral discs;
- subluxations, dislocations of the vertebrae;
- fractures of the vertebrae;
- dislocation fractures.
There are the following types of vertebral fractures:
- fractures of the vertebral bodies (compression, comminuted, explosive);
- fractures of the posterior half ring;
- combined with simultaneous fracture of bodies, arches, articular and transverse processes;
- isolated fractures of the transverse and spinous processes.
Of particular importance is the state of stability of the spine. Its instability is characterized by pathological mobility of its individual elements. Instability of the spine can cause additional serious injury to the spinal cord and its roots.
It is easier to understand the causes of spinal instability if we turn to the concept of Denis, who distinguishes 3 support systems (pillars) of the spine: the anterior support complex (pillar) includes the anterior longitudinal ligament and the anterior segment of the vertebral body; the middle column unites the posterior longitudinal ligament and the posterior segment of the vertebral body, and the posterior column - articular processes, arches with yellow ligaments and spinous processes with their ligamentous apparatus. Violation of the integrity of two of the mentioned support complexes (pillars), as a rule, leads to instability of the spine.
Spinal cord injury. The causes of spinal cord injury in spinal cord injury are varied. They can be trauma to the spinal cord and its roots with a bone fragment, a vertebra displaced as a result of dislocation, a prolapsed intervertebral disc, a hematoma formed at the fracture site, etc.
A rupture of the dura mater and direct injury of the spinal cord by a bone fragment can be a consequence of the injury.
Similarly to traumatic brain injury in traumatic spinal cord injury, concussion, bruise and compression are distinguished. The most severe form of local lesions of the spinal cord is its complete anatomical break with diastasis of the ends at the site of injury.
Pathomorphology. In the pathogenesis of spinal cord injury, circulatory disorders that occur during injury are of great importance. This may be ischemia of significant areas of the spinal cord due to compression or rupture of the radicular arteries, the anterior artery of the spinal cord. Hemorrhages into the substance of the spinal cord itself (hematomyelia) or the formation of meningeal hematomas are possible.
Swelling is a common and dangerous consequence of spinal cord injury. An increase in the volume of the spinal cord as a result of edema can lead to an increase in its compression, secondary circulatory disorders, a vicious circle of pathological reactions occurs that can lead to irreversible damage along the entire diameter of the spinal cord.
In addition to the listed morphological structural changes. there are also pronounced functional disorders, which in the acute stage of injury can lead to a complete cessation of motor activity and reflex activity, loss of sensitivity - spinal shock.
Symptoms of spinal shock can persist for weeks or even months.
Clinical manifestations of spinal cord injury in spinal cord injury. The clinical symptoms of a complicated spinal fracture are determined by a number of reasons, primarily the level and degree of spinal cord injury.
There are syndromes of complete and partial transverse lesions of the spinal cord.
In the syndrome of complete transverse lesions of the spinal cord, all voluntary movements are absent downward from the level of the lesion, flaccid paralysis is observed, tendon and skin reflexes are not caused, all types of sensitivity are absent, control over the functions of the pelvic organs is lost (involuntary urination, impaired defecation, priapism), autonomic innervation suffers (sweating, temperature regulation are disturbed). Over time, flaccid paralysis of the muscles can be replaced by their spasticity, hyperreflexia, automatisms of the functions of the pelvic organs are often formed.
Features of clinical manifestations of spinal cord injury depend on the level of injury. In case of damage to the upper cervical part of the spinal cord (CI-IV at the level of I-IV cervical vertebrae), tetraparesis or tetraplegia of a spastic nature develops with the loss of all types of sensitivity from the corresponding level. If there is concomitant damage to the brain stem, then bulbar disorders appear (dysphagia, aphonia, respiratory and cardiovascular disorders).
Damage to the cervical thickening of the spinal cord (CV - ThI - at the level of V-VII cervical vertebrae) leads to peripheral paraparesis of the upper limbs and spastic paraplegia of the lower ones. There are conduction disorders of all types of sensitivity below the level of the lesion. Possible radicular pain in the hands. The defeat of the ciliospinal center causes the appearance of the Bernard-Horner symptom, a decrease in blood pressure, and a slowing of the pulse.
Injury to the thoracic part of the spinal cord (ThII-XII at the level of I-IX thoracic vertebrae) leads to lower spastic paraplegia with the absence of all types of sensitivity, loss of abdominal reflexes: upper (ThVII - ThVIII), middle (ThIX - ThX) and lower (ThXI - ThXII).
When the lumbar thickening is damaged (LI-SII at the level of X-XP of the thoracic and I lumbar vertebrae), peripheral paralysis of the lower extremities occurs, anesthesia of the perineum and legs downwards from the inguinal (pupart) ligament, and the cremaster reflex falls out.
With an injury to the cone of the spinal cord (SIII-V at the level of I-II lumbar vertebrae), there is a "saddle" anesthesia in the perineum.
Damage to the cauda equina is characterized by peripheral paralysis of the lower extremities, anesthesia of all kinds in the perineum and legs, and sharp radicular pain in them.
Spinal cord injuries at all levels are accompanied by disorders of urination, defecation and sexual function. With a transverse lesion of the spinal cord in the cervical and thoracic parts, dysfunctions of the pelvic organs occur according to the type of syndrome of "hyperreflex neurogenic bladder". In the first time after the injury, urinary retention occurs, which can be observed for a very long time (months). The sensitivity of the bladder is lost. Then, as the segmental apparatus of the spinal cord is disinhibited, urinary retention is replaced by spinal automatism of urination. With a hyperreflex bladder, involuntary urination occurs with a slight accumulation of urine in it. With damage to the cone of the spinal cord and the roots of the cauda equina, the segmental apparatus of the spinal cord suffers and the syndrome of "hyporeflex neurogenic bladder" develops. It is characterized by urinary retention with symptoms of paradoxical ischuria. Defecation disorders in the form of stool retention or fecal incontinence usually develop in parallel with urination disorders.
Damage to the spinal cord in any part is accompanied by bedsores that occur in areas with impaired innervation, where bone protrusions (sacrum, iliac crests, heels) are located under the soft tissues. Bedsores develop especially early and rapidly with gross (transverse) spinal cord injury at the level of the cervical and thoracic regions. Bedsores quickly become infected and cause sepsis.
When determining the level of damage to the spinal cord, it is necessary to take into account the relative position of the vertebrae and spinal segments. It is easier to compare the location of the segments of the spinal cord with the spinous processes of the vertebrae (with the exception of the lower thoracic region). To determine the segment, 2 must be added to the vertebra number (for example, at the level of the spinous process of the III thoracic vertebra, the V thoracic segment will be located).
This pattern disappears in the lower thoracic and upper lumbar regions, where 11 segments of the spinal cord (5 lumbar, 5 sacral and 1 coccygeal) are located at the level of ThXI-XII - LI.
There are several syndromes of partial damage to the spinal cord.
Half spinal cord syndrome (Brown-Sequard syndrome) - paralysis of the limbs and a violation of deep types of sensitivity on the side of the lesion with a loss of pain and temperature sensitivity on the opposite side. It should be emphasized that this syndrome in its "pure" form is rare, usually its individual elements are detected.
Anterior spinal syndrome - bilateral paraplegia in combination with a decrease in pain and temperature sensitivity. The reason for the development of this syndrome is a violation of blood flow in the anterior spinal artery, which is injured by a bone fragment or a prolapsed disc.
Central spinal cord syndrome (more often occurs with a sharp hyperextension of the spine). It is characterized mainly by paresis of the arms, weakness in the legs is less pronounced, there are varying degrees of sensitivity disturbance below the level of the lesion, urinary retention.
In some cases, mainly with an injury accompanied by a sharp flexion of the spine, a syndrome of damage to the posterior cords of the spinal cord may develop - loss of deep types of sensitivity.
Damage to the spinal cord (especially with complete damage to its diameter) is characterized by dysregulation of the functions of various internal organs: respiratory disorders in cervical lesions, intestinal paresis, dysfunction of the pelvic organs, trophic disorders with the rapid development of bedsores.
In the acute stage of injury, there are often violations of cardiovascular activity, a drop in blood pressure. With a vertebral fracture, an external examination of the patient and the identification of such changes as concomitant soft tissue injuries, reflex muscle tension, sharp pain when pressing on the vertebrae, and finally, external deformity of the spine (for example, kyphosis with a compression fracture in the thoracic region) may have a certain value in its recognition. ).
Concussion of the spinal cord. It is characterized by damage to the spinal cord of a functional type in the absence of obvious structural damage. Macro- and microscopically, edema of the substance of the brain and its membranes, single point hemorrhages are usually detected. Clinical manifestations are due to neurodynamic changes, transient disorders of hemo-and liquorodynamics. There are short-term, mildly expressed paresis, paresthesia, sensory disturbances, disorders of the functions of the pelvic organs. Cerebrospinal fluid is not changed, the patency of the subarachnoid space is not impaired. Spinal concussion is rare. A much more common and serious injury is spinal cord injury.
Spinal injury. The most common type of lesion in closed and non-penetrating spinal cord injuries. A bruise occurs when a vertebra is fractured with its displacement, intervertebral disc prolapse, or vertebral subluxation. When the spinal cord is injured, structural changes always occur in the substance of the brain, roots, membranes, vessels (focal necrosis, softening, hemorrhages). Damage to brain tissue is accompanied by spinal shock. The nature of motor and sensory disorders is determined by the location and extent of the injury. As a result of a spinal cord injury, paralysis, sensory disturbances, pelvic organs and vegetative functions develop. Trauma often leads to the occurrence of not one, but several foci of bruising. Secondary circulatory phenomena can cause the development of myelomalacia foci hours or even days after injury. Spinal cord injuries are often accompanied by subarachnoid hemorrhage. In the cerebrospinal fluid, an admixture of blood is found. The patency of the subarachnoid space is usually not disturbed.
Depending on the severity of the bruise, the restoration of impaired functions occurs within 3-8 weeks. However, in severe bruises with a complete anatomical interruption of the spinal cord, lost functions are not restored.
Spinal cord compression. Occurs with a fracture of the vertebrae with a mixture of fragments or with a dislocation, a hernia of the intervertebral disc. The clinical picture of spinal cord compression can occur immediately after injury or be dynamic (increasing with spinal movements) with its instability and the presence of mobile bone fragments.
Allocate the so-called hyperextension injury of the cervical spine (whiplash), which occurs in car accidents, diving, falling from a height. The mechanism of this spinal cord injury is a sharp hyperextension of the neck, which exceeds the anatomical and functional capabilities of this section and leads to a sharp narrowing of the spinal canal with the development of ischemia or spinal cord compression. Clinically, hyperextension injury is manifested by syndromes of spinal cord injury of varying severity - radicular, partial dysfunction of the spinal cord, complete transverse injury, anterior spinal artery syndrome.
Hemorrhage in the spinal cord. Most often, hemorrhage occurs when blood vessels rupture in the region of the central canal and posterior horns at the level of the lumbar and cervical thickenings. Clinical manifestations of hematomyelia are due to compression of the posterior horns of the spinal cord by outflowing blood, spreading to 3-4 segments. In accordance with this, segmental dissociated sensory disturbances (temperature and pain) acutely occur, located on the body in the form of a jacket or half jacket. With the spread of blood to the region of the anterior horns, peripheral flaccid paresis with atrophy is revealed. With the defeat of the lateral horns, vegetative-trophic disorders are noted. Very often in the acute period, not only segmental disorders are observed, but also conduction disorders of sensitivity, pyramidal symptoms due to pressure on the lateral cords of the spinal cord. With extensive hemorrhages, a picture of a complete transverse lesion of the spinal cord develops. The cerebrospinal fluid may contain blood.
Hematomyelia is characterized by a regressive course. Neurological symptoms begin to decrease after 7-10 days. Recovery of impaired functions can be complete, but neurological disorders often remain.
Hemorrhage into the spaces surrounding the spinal cord. It can be either epidural or subarachnoid. As a result of epidural hemorrhages (from the venous plexuses), an epidural hematoma is formed, gradually compressing the spinal cord. Epidural hematomas are rare.
Clinical manifestations. Epidural hematomas are characterized by an asymptomatic interval after injury. A few hours after it, radicular pain occurs with different irradiation, depending on the location of the hematoma. Then symptoms of transverse compression of the spinal cord appear and begin to increase.
The clinical picture of intrathecal (subarachnoid) hemorrhage in spinal cord injury is characterized by an acute development of symptoms of irritation of the membranes and spinal roots. There are intense pains in the back, limbs, stiff neck muscles, symptoms of Kernig and Brudzinsky. Very often, these symptoms are accompanied by paresis of the extremities, conduction disturbances of sensitivity and pelvic disorders due to damage or compression of the spinal cord by outflowing blood. The diagnosis of hematorrhachis is verified by lumbar puncture: the cerebrospinal fluid is intensely stained with blood or xanthochromic. The course of hematorrhachis is regressive, often complete recovery occurs. However, hemorrhage in the region of the cauda equina may be complicated by the development of adhesive or cystic arachnoiditis.
Diagnostics. X-ray research methods, including computed tomography and magnetic resonance imaging, are of decisive importance for determining the nature of the injury to the spine and spinal cord and choosing an adequate treatment method. These studies must be carried out with some care so as not to cause additional injury to the spinal cord.
If a fracture of the 1st and 2nd vertebrae is suspected, pictures are taken with a special positioning of the patient - pictures through the mouth.
To detect instability of the spine, a series of images is taken with its gradual (by 5-10°) flexion and extension, which makes it possible to identify the initial signs of instability and not cause a deterioration in the patient's condition.
Computed tomography, accurately performed at the level of the alleged damage, provides more complete information about damage to bone structures, intervertebral discs, the state of the spinal cord and its roots.
In some cases, myelography with water-soluble contrast is used, which makes it possible to clarify the nature of the lesion of the spinal cord and its roots, to determine the presence of a block in the subarachnoid space. In the acute stage of injury, this study should be done with great care, since the introduction of contrast may increase the compression of the spinal cord in the area of the block.
In these cases, it is preferable to use magnetic resonance imaging, which provides the most complete information about the state of the spinal cord and structures of the spine.
Treatment. All severely traumatized victims should be treated as if they had a possible injury to the spinal cord and spine, especially in cases of impaired consciousness. if there are signs of respiratory distress or characteristic symptoms of spinal lesions (paresis of the limbs, sensory disturbances, priapism, spinal deformity, etc.).
First aid at the scene of the incident consists primarily in the immobilization of the spine: cervical collar, shield. Special care is required when shifting and transporting the patient.
In case of severe injuries, a complex of intensive care measures is carried out aimed at maintaining blood pressure and normalizing breathing (if necessary, artificial ventilation of the lungs).
Patients with injuries of the spine and spinal cord should, if possible, be hospitalized in specialized institutions.
In the hospital, intensive antishock therapy continues. Until the nature of the lesion is clarified and an adequate method of treatment is chosen, immobilization is maintained.
The variety of pathophysiological mechanisms, clinical manifestations of spinal cord injury determines the approach to drug therapy, which depends on the nature and level of damage.
The acute period may be accompanied (in addition to symptoms of spinal cord injury) by shock reactions with a drop in blood pressure and impaired microcirculation, which requires anti-shock therapy under the control of electrolytes, hemoglobin, hematocrit, and blood proteins.
To prevent secondary changes in the spinal cord caused by the development of edema and circulatory disorders in the acute period, some authors consider it reasonable to use large doses of glucocorticoid hormones (dexamethasone, methylprednisolone).
Damage to the spinal cord at the level of segments ThII - ThVII can cause arrhythmia of cardiac activity, a decrease in the functional ability of the myocardium, and ECG changes. In these cases, the appointment of cardiac glycosides is indicated.
To improve microcirculation, prevent thrombosis, reduce vascular permeability, angioprotectors, anticoagulants, and vasodilators are prescribed.
With violations of protein metabolism, cachexia, poor wound healing, the use of anabolic hormones is indicated. All victims are shown the appointment of nootropics, especially in the acute period of injury.
Prevention and treatment of inflammatory complications is carried out by the introduction of antibacterial agents, taking into account the sensitivity of the microflora.
Both in the acute and in subsequent periods, patients need to prescribe sedative, tranquilizing and neuroleptic drugs.
Prevention of complications. Dysfunction of the gas organs is one of the most frequent complications of spinal cord injury.
With a complete transverse lesion of the spinal cord in the acute period (in conditions of the development of spinal shock), paralysis of the detrusor, spasm of the sphincter of the bladder, and the absence of its reflex activity are noted. The consequence of this is urinary retention (atony and overdistension of the bladder).
To prevent dysfunction of the pelvic organs from the first hours of hospital stay, it is necessary to clearly determine the state of urination and establish adequate urine output. In the first weeks after injury, the introduction of an indwelling catheter is necessary. Subsequently, a 4-time periodic catheterization of the bladder is performed with its simultaneous washing with aseptic solutions. Manipulations must be accompanied by the strictest observance of the rules of asepsis and antisepsis.
When the phenomena of spinal shock pass, the reflex activity of the bladder is restored: it is automatically emptied at a certain filling.
More severe urination disorders with the absence or suppression of its reflex activity and urinary incontinence can be observed with damage to the spinal centers of the pelvic organs (ThXII - LI) or damage to the roots of the cauda equina. In these cases, in the presence of a large amount of residual urine, periodic bladder catheterization is indicated.
One of the main tasks in the treatment of patients with spinal cord injury is the development of reflex mechanisms that ensure automatic emptying of the bladder when it is filled. The achievement of this goal can be facilitated by the use of electrical stimulation of the bladder.
Disorder of the act of defecation, which always develops with a spinal cord injury, can be the cause of subfebrile temperature and intoxication. To restore the function of the rectum, it is recommended to prescribe a diet, various laxatives, suppositories, and in some cases a cleansing enema.
For the timely and successful rehabilitation of patients, the prevention of bedsores in the sacrum, ischial tuberosities, large trochanters of the femur, and heels is of paramount importance. It is necessary to choose a rational position of the patient using the position on the stomach, sides. Indispensable conditions are the hygienic maintenance of the bed, gentle turning (every 2 hours), wiping the skin with ethyl, camphor or salicylic alcohol. Special mattresses are effective. providing automatic redistribution of pressure on the surface of the body. Suitable various pads that allow you to give a physiological or necessary in a particular case, the position of the torso and limbs.
For the prevention of contractures of the limbs, paraarticular and paraossal ossifications, the correct laying of the limbs, massage and therapeutic exercises are of great importance.
In the acute and early periods, especially with lesions of the cervical spinal cord, prevention of inflammatory pulmonary complications is of great importance. It is necessary to normalize the functions of external respiration, to aspirate discharge from the respiratory tract. Aerosol inhalations of medicines, active and passive gymnastics are useful. In the absence of trauma to the chest and lung, banks, mustard plasters are recommended. Vibromassage, ultraviolet irradiation, electrical stimulation of the diaphragm are prescribed.
For the prevention of bedsores, ultraviolet radiation of the lower back, sacrum, buttocks and heels is used in suberythemal doses.
In the presence of pain syndrome, diadynamic currents (DDT), sinusoidally modulated currents (SMT), ozocerite or mud applications are used in combination with electrophoresis of analgesic drugs, exercise therapy, and massage.
Treatment of patients with trauma to the spine and spinal cord or its consequences should always be comprehensive. Important conditions for increasing the effectiveness of the treatment of these patients are adequate rehabilitation and spa treatment.
Treatment for complicated spinal fractures. The main goals pursued in providing care to patients with a complicated fracture of the spine are the elimination of compression of the spinal cord and its roots and stabilization of the spine.
Depending on the nature of the injury, this goal can be achieved in different ways:
surgical method;
using external immobilization and reposition of the spine (traction, cervical collars, corsets, special fixing devices).
Immobilization of the spine. Prevents possible dislocation of the vertebrae and additional damage to the spinal cord; creates conditions for the elimination of the existing deformation of the spine and the fusion of damaged tissues in a position close to normal.
One of the main methods for immobilizing the spine and eliminating its deformity is traction, which is most effective in case of trauma to the cervical spine.
Traction is carried out using a special device, consisting of a bracket fixed to the skull, and a system of blocks that carry out traction.
The Cratchfield bracket is fixed with two screws with sharp ends to the parietal tubercles. Traction with the help of weights is carried out along the axis of the spine. Traction usually starts with a small load (3-4 kg) and gradually increases to 8-12 kg (more in some cases). The change in spinal deformity under the influence of traction is monitored by repeated x-rays.
In case of damage to the cervical spine, immobilization of the spine can be carried out using a special device consisting of a special corset such as a vest, a metal hoop rigidly fixed to the patient's head, and rods connecting the hoop to the vest (halo vest). In cases where complete immobilization is not required for injuries of the cervical spine, soft and hard collars are used. Corsets of a special design are also used for fractures of the thoracic and lumbar spine.
When using external immobilization methods (traction, corsets), it takes a long time (months) to eliminate spinal deformity and heal damaged structures in the required position.
In many cases, this method of treatment is unacceptable, especially when it is necessary to immediately eliminate the compression of the spinal cord. In such a situation, there is a need for surgical intervention.
The purpose of the operation is to eliminate compression of the spinal cord, correct spinal deformity and its reliable stabilization.
Surgery. Various types of operations are used: approaching the spinal cord from behind through laminectomy, from the side or from the front with resection of the vertebral bodies. A variety of metal plates, bone screws, wires are used to stabilize the spine. The resected fragments of the vertebrae are replaced with bone fragments taken from the patient's ilium or tibia, special metal and ceramic prostheses, and bone taken from a corpse.
Indications for surgical intervention in trauma of the spine and spinal cord.
When determining surgical indications, it must be taken into account that the most dangerous spinal cord injuries occur immediately at the moment of injury, and many of these injuries are irreversible. So, if the victim immediately after the injury has a clinical picture of a complete transverse lesion of the spinal cord, then there is practically no hope for an urgent operation that can change the situation. In this regard, many surgeons consider surgical intervention in these cases unreasonable.
An exception may be the presence of symptoms of a complete rupture of the roots of the spinal cord. Despite the severity of the damage, in these cases, a surgical operation is justified primarily due to the fact that it is possible to restore conduction along the damaged roots, and if they rupture, which is rare, a positive result can be obtained by microsurgical suturing of the ends of the damaged roots.
If there are even the slightest signs of the preservation of part of the functions of the spinal cord (slight movement of the fingers, the ability to determine a change in the position of the limb, the perception of strong pain stimuli) and at the same time there are signs of compression of the spinal cord (the presence of a block, displacement of the vertebrae, bone fragments in the spinal canal, etc.) , the operation is shown.
In the late period of injury, surgery is justified if compression of the spinal cord persists and the symptoms of its damage progress.
The operation is also indicated for gross deformity and instability of the spine, even in cases of complete transverse lesions of the spinal cord. The purpose of the operation in this case is the normalization of the supporting function of the spine, which is an important condition for a more successful rehabilitation of the patient.
The choice of the most adequate method of treatment - traction, external fixation, surgical intervention, the combination of these methods is largely determined by the location and nature of the injury.
In this regard, it is advisable to separately consider the most characteristic variants of spinal and spinal cord injuries.
Trauma of the cervical spine. The cervical spine is the most susceptible to damage and the most vulnerable. About 40-60% of all spinal injuries occur in the cervical region, especially often in children, which can be explained by weakness of the neck muscles, significant ligament extensibility, and large head size.
It should be noted that trauma to the cervical vertebrae is more often than other parts of the spine accompanied by damage to the spinal cord (40-60% of cases).
Damage to the cervical spine leads to the most severe complications and, more often than with trauma to other parts of the spine, to the death of the patient: 25-40% of victims with injury localized at the level of the upper three cervical vertebrae die at the scene.
The peculiarity of the structure and functional significance of the I and II cervical vertebrae make it necessary to separately consider their injuries. I cervical vertebra (atlas) can be damaged in isolation or together with the II vertebra (40% of cases). Most often, as a result of trauma, the ring of the atlas ruptures in its various links. Damage to the second cervical vertebra (epistrophy) usually results in a fracture and displacement of the odontoid process. A peculiar fracture of the II vertebra at the level of the articular processes is observed in hanged men ("fracture of the executioner").
CV-ThI vertebrae account for more than 70% of injuries - fractures and fracture-dislocations with concomitant severe, often irreversible spinal cord injuries.
For fractures of the 1st cervical vertebra, traction is usually successfully applied by rigid external stabilization with a halo vest, followed by the use of cervical collars. In case of combined fractures of the I and II cervical vertebrae, in addition to these methods, surgical stabilization of the vertebrae is used, which can be achieved by tightening the arches and spinous processes of the first three vertebrae with wire or fixing them with screws in the area of the articular processes.
In some cases, anterior access through the oral cavity can be used to eliminate compression of the spinal cord and medulla oblongata by a broken tooth of the II cervical vertebra.
Surgical fixation is indicated for fracture-dislocation of CIII-ThI vertebrae. Depending on the characteristics of the damage, it can be performed by a posterior approach with fixation of the vertebrae using wire or other metal structures for the arches and spinous processes. In case of anterior compression of the spinal cord by fragments of a crushed vertebra, a prolapsed disc, or a hematoma, it is advisable to use an anterior approach with resection of the bodies of the affected vertebra and stabilization of the spine with a bone graft. The technique of the operation is similar to that used for prolapsed median cervical discs.
Trauma of the thoracic and lumbar spine. With injuries of the thoracic and lumbar spine, compression fractures often occur with the formation of the Urban wedge. More often, these fractures are not accompanied by spinal instability and do not require surgical intervention.
With comminuted fractures, compression of the spinal cord and its roots is possible. This may lead to indications for surgery. Complicated lateral and anterolateral approaches, including transpleural approaches, may be required to eliminate compression and stabilize the spine.
Treatment of patients with sequelae of spinal cord injury. One of the frequent consequences of spinal cord injury is a sharp increase in tone in the muscles of the legs and trunk, which often complicates rehabilitation treatment.
To eliminate muscle spasticity with the ineffectiveness of drug treatment, in some cases it is necessary to perform an operation on the spinal cord (myelotomy), the purpose of which is to uncouple the anterior and posterior horns of the spinal cord at the level of segments LI - SI (myelotomy according to Bischoff, Rothballer, etc.).
With persistent pain syndromes, which often occur when the roots are damaged, and the development of the adhesive process, there may be indications for surgery on the pathways of pain afferentation.
When bedsores occur, dead tissues are excised, drugs are used that promote rapid cleansing and healing of the wound (Solcoseryl). Local ultraviolet or laser irradiation is effective.
Employability. Clinical and labor prognosis depends on the level and degree of spinal cord injury. Thus, all surviving patients with a complete anatomical interruption of the spinal cord at any level are disabled of group I, but sometimes they can work in individually created conditions. With a concussion of the spinal cord, mental workers are determined by temporary disability for 3-4 weeks. Persons engaged in physical labor need to be released from work for at least 5-8 weeks, followed by release from heavy lifting for up to 3 months. The latter is due to the fact that spinal cord injury occurs in most cases when the vertebrae are displaced, and this involves rupture or stretching of the ligamentous apparatus.
With a slight injury to the spinal cord, the sick leave is extended until the restoration of functions, less often it is advisable to transfer the patient to disability group III.
With a moderate bruise, it is desirable to prolong temporary disability, and then transfer to disability group III, but not to II, since this will not stimulate the clinical and labor rehabilitation of the patient.
With severe bruises, compression and hematomyelia, ischemic necrosis of the spinal cord, it is more rational to transfer patients to disability and continue treatment and rehabilitation, followed by re-examination, taking into account neurological deficits.
Of particular importance are the problems of medical and social rehabilitation. The doctor's task is to teach the patient to make the most of the remaining motor abilities to compensate for the defects developed after the injury. For example, you can use the system of training the muscles of the trunk, shoulder girdle in patients with lower paraparesis. Many patients need the supervision of psychologists who help them find new stimuli in life. A difficult task is the return of patients to work: this usually requires the retraining of patients, the creation of special conditions for them, and the support of society.