Craniocerebral trauma in children

Traumatic brain injury in children (TBI) is a mechanical damage to the skull and intracranial structures (brain, blood vessels, nerves, meninges).

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Epidemiology of TBI in Children

Occupying one of the leading places among the causes of death in children, traumatic brain injury often leads to severe disability with pronounced neurological and mental deficits.

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Causes of traumatic brain injury in children

The main causes of traumatic brain injury in children:

• transport injuries (most often road traffic injuries),
• falling from a height (for a young child, a dangerous height may be 30-40 cm),
• domestic injuries,
• neglect or abuse of parents,
• criminal trauma (in older children).

The last two reasons have become increasingly important in recent years.

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The mechanism of development of TBI in a child

In the pathogenesis of TBI, it is customary to distinguish several damaging mechanisms:

• Damaging mechanisms in traumatic brain injury.
• The primary damaging mechanism is direct trauma.
• Secondary damaging mechanisms are hypoxia or cerebral ischemia, arterial hypotension and to a lesser extent hypertension, hypoglycemia and hyperglycemia, hyponatremia and hypernatremia, hypocarbia and hypercarbia, hyperthermia, cerebral edema.

The variety of secondary damaging factors determines the complexity of therapy for this pathology.

Cerebral edema

The main syndrome in the development of secondary damage is increasing cerebral edema.

Causes of cerebral edema:

• disturbance of regulation of cerebral vessels (vasogenic edema),
• subsequent tissue ischemia (cytotoxic edema).

The consequences of increasing cerebral edema are an increase in ICP and impaired tissue perfusion.

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Mechanisms of development of cerebral edema

When considering the mechanisms of development of cerebral edema, it is necessary to take into account its physiological characteristics.

Physiological features of the brain: high oxygen consumption and high organ blood flow, inability of the cranium to change its volume depending on the volume of the brain, autoregulation of the MC, effect of temperature on the vital activity of the brain, effect of rheological properties of blood on oxygen delivery. High oxygen consumption and high organ blood flow. The brain is an extremely metabolically active organ with high oxygen consumption against the background of high organ blood flow. The mass of the brain does not exceed 2% of the body weight, while it utilizes about 20% of all oxygen in the body and receives up to 15% of dry matter. In children, the oxygen consumption of the brain is 5 ml per 100 g of brain tissue per minute, significantly exceeding that of adults (3-4 ml).

The MC in children (excluding newborns and infants) also exceeds the MC in adults and is 65-95 ml per 100 g of brain tissue per minute, while in adults this figure is on average 50 ml. The inability of the cranium to change its volume depending on the volume of the brain. This circumstance can cause a sharp increase in ICP with increasing brain volume, which in turn can worsen tissue perfusion, especially in the pericortical areas.

Cerebral perfusion pressure (CPP) directly depends on ICP and is calculated using the formula:

CPP = BPav - ICP, where BP is the mean BP at the level of the circle of Willis

In children, ICP normally does not exceed 10 mm Hg and depends on the volume of the main components of the cranial cavity. Brain tissue occupies up to 75% of the intracranial volume, interstitial fluid - about 10%, another 7-12% is CSF and about 8% is blood located in the vascular bed of the brain. According to the Monroe-Kelly concept, these components are incompressible by nature, therefore, a change in the volume of one of them at a constant level of ICP leads to compensatory changes in the volume of others.

The most labile components of the cranial cavity are blood and CSF; the dynamics of their redistribution serves as the main buffer for ICP when the volume and elasticity of the brain changes.

Autoregulation of MBF is one of the processes that limit the blood volume in the cerebral vessels. This process maintains the constancy of MBF with fluctuations in BPc in adults from 50 to 150 mm Hg. A decrease in BPc below 50 mm Hg is dangerous due to the development of hypoperfusion of brain tissue with the occurrence of ischemia, and exceeding 150 mm Hg can lead to cerebral edema. For children, the boundaries of autoregulation are unknown, but they are presumably proportionally lower than in adults. The mechanism of autoregulation of MBF is currently not completely clear, but probably consists of a metabolic and vasomotor component. It is known that autoregulation can be disrupted by hypoxia, ischemia, hypercarbia, head trauma, and under the influence of some general anesthetics.

Factors affecting the magnitude of MBF are the level of CO2 and pH in the vessels of the brain, blood oxygenation, and neurogenic factors. The level of CO2 and pH in the vessels of the brain is an important factor determining the magnitude of MBF. The magnitude of MBF is linearly dependent on paCO2 within the range from 20 to 80 mm Hg. A decrease in paCO2 by 1 mm Hg reduces MBF by 1-2 ml per 100 g of brain tissue per minute, and its drop to 20-40 mm Hg reduces MBF by half. Short-term hyperventilation accompanied by significant hypocarbia (paCO2 <20 mm Hg) can lead to severe ischemia of brain tissue due to vasoconstriction. With prolonged hyperventilation (more than 6-8 hours), MBF can normalize as a result of gradual correction of CSF pH due to bicarbonate retention.

Blood oxygenation (MBF depends on it to a lesser extent) In the range from 60 to 300 mm Hg, PaO2 has virtually no effect on cerebral hemodynamics, and only when PaO2 decreases below 50 mm Hg does MBF increase sharply. The mechanism of cerebral vasodilation in hypoxemia has not been fully established, but it may consist of a combination of neurogenic reactions caused by peripheral chemoreceptors, as well as the direct vasodilating effect of hypoxemic lactic acidosis. Severe hyperoxia (PaO2>300 mm Hg) leads to a moderate decrease in MBF. When breathing 100% oxygen at a pressure of 1 atm, MBF decreases by 12%.

Many of the listed mechanisms of MC regulation are realized by means of nitric oxide (NO), released from the endothelial cells of the brain vessels. Nitric oxide is one of the main local mediators of the tone of the microcirculatory bed. It causes vasodilation caused by hypercarbia, increased metabolism, the action of volatile anesthetics and nitrates (nitroglycerin and sodium nitroprusside).

Neurogenic factors also play a significant role in the regulation of MC. First of all, they affect the tone of large vessels of the brain. The adrenergic, cholinergic and serotonergic systems affect MC equally with the vasoactive peptide system. The functional significance of neurogenic mechanisms in the regulation of MC is indicated by studies of autoregulation and ischemic brain damage.

The influence of temperature on the functioning of the brain

The temperature of the brain tissues is of great importance for oxygen consumption by the brain. Hypothermia causes a significant decrease in metabolism in brain cells and leads to a secondary decrease in MC. A decrease in brain temperature by 1 °C leads to a decrease in cerebral oxygen consumption (COC) by 6-7%, and at 18 °C COC is no more than 10% of the initial normothermic values. At temperatures below 20 °C, the electrical activity of the brain disappears, and an isoline is recorded on the EEG.

Hyperthermia has an opposite effect on brain metabolism. At temperatures from 37°C to 42°C, there is a gradual increase in MC and O2 media, but with further increases, a critical decrease in oxygen utilization by brain cells occurs. This effect is associated with possible protein degradation at temperatures above 42°C.

The influence of blood rheological properties on oxygen delivery

Oxygen delivery to brain cells depends not only on the MC value, but also on blood properties. Hematocrit is the most important factor determining both the oxygen capacity of the blood and its viscosity. In anemia, cerebral vascular resistance decreases and MC increases. The positive effect of reducing blood viscosity is most obvious in cases of focal cerebral ischemia, when the best oxygen delivery occurs at a hematocrit value of 30 to 34%.

Clinical characteristics of traumatic brain injury in children

Disorders that develop in patients during the acute period of TBI affect vital organs and systems, lead to respiratory and cardiovascular failure, and indirectly affect liver and kidney function and intestinal motility, which significantly complicates treatment.

Mild TBI often does not lead to loss of consciousness. In moderate and severe brain contusions, focal symptoms are often not expressed, and depression of consciousness and autonomic disorders predominate. An early phase of increased blood filling of the brain vessels with subsequent vasogenic edema is often observed. Diffuse axonal damage occurs in children much more often than in adults.

Due to the anatomical and physiological characteristics of the child's body, the processes occurring during TBI in children have significant differences. Children are more likely to have periods of temporary recovery of consciousness after relatively mild injuries, rapid improvement in their condition is possible, and their prognosis is better than can be assumed based on the initial neurological symptoms.

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Classification of TBI

There are several principles for classifying traumatic brain injury depending on the damage to the skull, the nature of the brain damage, and the degree of severity.

Classification of TBI depending on the damage to the skull:

• Closed TBI.
• Open TBI is a combination of damage to the integrity of the skin, aponeurosis and bones of the cranial vault.

Classification of TBI by the nature of brain damage:

• Focal brain damage (cerebral contusion, epidural, subdural and intracerebral hematomas).
• Diffuse brain injury (concussion and diffuse axonal injury).

Classification of TBI by severity:

• Mild TBI (concussion and mild brain contusions).
• Moderate TBI (moderate brain contusion).
• Severe TBI (severe brain contusion, diffuse axonal injury and brain compression).

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How to recognize a traumatic brain injury in a child?

Diagnostic algorithm

According to some data, only 84% of all hematomas develop within the next 12 hours after the injury, which is why any concussion in children is considered an indication for mandatory hospitalization. Differential diagnostics are carried out with other conditions that cause CNS depression.

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Physical examination

When examining a patient with TBI, it is necessary to begin with a careful examination. First of all, the function of external respiration and the state of the cardiovascular system are assessed. Particular attention should be paid to the presence of abrasions, bruises, signs of external or internal bleeding and fractures of the ribs, pelvic bones and limbs, leakage of cerebrospinal fluid and blood from the nose and ears, bad breath.

Diagnosis of the severity of TBI consists primarily of an assessment of the depression of consciousness, neurological symptoms, and the degree of involvement of vital functions of the body in the pathological process.

Assessment of the degree of depression of consciousness

To assess the degree of depression of consciousness, it is preferable to use the most widely used Glasgow Coma Scale in the world. It is based on three clinical criteria: eye opening, verbal functions, and motor response of the patient. Each criterion is assessed using a point system, the maximum number of points on the scale is 15, the minimum is 3. Clear consciousness corresponds to 15 points, 14-10 points correspond to stupor of varying degrees, 8-10 points - to stupor, less than 7 points - to coma. The unconditional advantages of this scale include its simplicity and sufficient versatility. The main disadvantage is the impossibility of its use in intubated patients. Despite certain limitations, the Glasgow scale is very effective for dynamic assessment of the patient's level of consciousness and has a high prognostic value.

In young children (under 3-4 years old), due to insufficiently developed speech, a modified Glasgow Coma Scale can be used.

Modified Glasgow Coma Scale for Young Children

Patient's reactions	Points
Opening the eyes
Arbitrary	4
At the request of	3
For pain	2
Absent	1
Motor reactions
performing movements on command	6
movement in response to painful stimulation (repulsion)	5
withdrawal of a limb in response to painful stimulation	4
pathological flexion in response to painful irritation (decortication)	3
pathological extension in response to pain stimulation (decerebration)	2
Speech response
the child smiles, is guided by sound, follows objects, is interactive	5
a child can be calmed down when crying, interactivity is incomplete	4
when crying, he calms down, but not for long, he moans	3
does not calm down when crying, restless	2
There is no crying or interactivity.	1

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Assessment of the extent of brain stem damage

In particular, the functions of the cranial nerves are assessed, the presence of anisocoria, the pupil's reaction to light, the oculovestibular (cold water test) or oculocephalic reflexes. The actual nature of neurological disorders can only be assessed after the restoration of vital functions. The presence of respiratory and hemodynamic disorders indicates the possible involvement of stem structures in the pathological process, which is considered an indication for immediate adequate intensive care.

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Laboratory research

Patients in serious condition undergo examinations aimed at identifying concomitant disorders of body functions: a general blood test (mandatory exclusion of hemic hypoxia) and urine are examined, the electrolyte, acid-base and gas composition of the blood, serum glucose, creatinine, and bilirubin levels are determined.

Instrumental research

To diagnose TBI, X-rays of the skull and cervical spine, computed tomography and magnetic resonance imaging of the brain, neurosonography, fundus examination, and lumbar puncture are performed.

X-ray of the skull and cervical spine in two projections.

CT of the brain is the most informative examination for TBI - it allows to identify the presence of hematomas in the cranial cavity, contusion foci, displacement of the midline structures of the brain, signs of impaired cerebrospinal fluid dynamics and increased intracranial pressure, as well as damage to the bone structures of the cranial vault.

Relative contraindications to emergency CT:

• shock,
• carrying out resuscitation measures

If the severity of the patient's condition increases during the first day, a repeat CT scan is necessary due to the risk of an increase in the primary foci of hemorrhage or the formation of delayed hematomas.

Neurosonography is a fairly informative research method for identifying displacement of the midline structures of the brain (in the absence of the possibility of performing CT), especially in young children.

MRI complements CT by allowing visualization of subtle structural abnormalities in the brain that occur with diffuse axonal injury.

Fundus examination is an important auxiliary diagnostic method. However, fundus examination does not always reveal an increase in ICP, since signs of optic nerve papilla edema are present in only 25-30% of patients with proven increased ICP.

Lumbar puncture

In the context of the wider use of modern diagnostic methods, it is used less and less (despite its high information content), including due to the frequent complications of this procedure in patients with increasing cerebral edema.

• Indications: differential diagnosis with meningitis (main indication).
• Contraindications: signs of wedging and dislocation of the brain.

In addition to the mandatory diagnostic measures for TBI, patients in serious condition undergo examinations aimed at identifying concomitant injuries: ultrasound of the abdominal organs and retroperitoneal space, chest X-ray, pelvic bones and, if necessary, bones of the upper and lower extremities, and an ECG.

Treatment of traumatic brain injury in children

There are surgical and therapeutic methods of treatment.

Surgical treatment of TBI in children

Indications for neurosurgical intervention:

• compression of the brain by an epidural, subdural or intracranial hematoma,
• depressed fracture of the cranial vault bones.

A mandatory component of preoperative preparation is hemodynamic stabilization.

Therapeutic treatment of TBI in a child

All therapeutic measures can be conditionally divided into three main groups.

Groups of therapeutic measures:

• general resuscitation,
• specific,
• aggressive (if the first two are ineffective).

The goal of the therapy is to stop cerebral edema and reduce intracranial pressure. When treating patients with TBI, it is necessary to monitor brain functions, ensure adequate gas exchange, maintain stable hemodynamics, reduce the metabolic needs of the brain, normalize body temperature, and, if indicated, prescribe dehydration, anticonvulsant, and antiemetic therapy, painkillers, and provide nutritional support.

Monitoring brain functions

Rational therapy of cerebral edema is impossible without monitoring its functions. If the level of consciousness decreases below 8 points on the Glasgow scale, ICP measurement is indicated to control intracranial hypertension and calculate CPP. As in adult patients, ICP should not exceed 20 mm Hg. In infants, CPP should be maintained at 40 mm Hg, in older children - 50-65 mm Hg (depending on age).

When the BCC is normalized and blood pressure is stable, it is recommended to raise the head end of the bed by 15-20° to improve venous outflow from the patient’s head.

Ensuring adequate gas exchange

Maintaining adequate gas exchange prevents the damaging effects of hypoxia and hypercarbia on MC regulation. Breathing with a mixture enriched with oxygen up to 40% is indicated, рАО2 must be maintained at a level of at least 90-100 mm Hg.

When consciousness is suppressed and bulbar disorders occur, spontaneous breathing becomes inadequate. As a result of decreased muscle tone in the tongue and pharynx, obstruction of the upper respiratory tract develops. Patients with TBI may rapidly develop respiratory disorders, which makes it necessary to decide on tracheal intubation and switching to artificial ventilation.

Indications for switching to artificial ventilation:

• respiratory failure,
• depression of consciousness (Glasgow Coma Scale score less than 12) The earlier the transition to mechanical ventilation is performed, the less pronounced the impact of respiratory disorders on MC.

Types of tracheal intubation: nasotracheal, fiberoptic.

Nasotracheal intubation helps avoid hyperextension of the cervical spine, which is dangerous in cervical spinal trauma.

Contraindications to nasotracheal intubation: damage to the nose and paranasal sinuses

Fiberoptic intubation is indicated in cases of damage to the facial bones.

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Tracheal intubation technique

Intubation should be performed under general anesthesia using intravenous anesthetics barbiturates or propofol. These drugs significantly reduce MBF and ICP, reducing the brain's need for oxygen. However, with a deficit in circulating blood volume, these drugs significantly reduce blood pressure, so they should be administered with caution, titrating the dose. Immediately before intubation, it is necessary to preoxygenate the patient by inhaling 100% oxygen for at least 3 minutes. The high risk of aspiration of gastric contents requires sealing the patient's airways by inflating the cuff of the intubation tube.

Modes of artificial ventilation: auxiliary modes, forced artificial ventilation.

Auxiliary ventilation modes

When providing respiratory support, auxiliary ventilation modes are preferable, in particular the synchronized support ventilation mode (SSV), which allows for rapid synchronization with the device in children with severe TBI. This mode is more physiological in terms of breathing biomechanics and allows for a significant reduction in average intrathoracic pressure.

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Forced artificial ventilation of the lungs

This ventilation mode is recommended for deep coma (less than 8 points on the Glasgow scale), when the sensitivity of the respiratory center to the level of carbon dioxide in the blood decreases. Discoordination between the patient's respiratory movements and the respiratory apparatus can lead to a sharp increase in intrathoracic pressure and the occurrence of a hydraulic shock in the superior vena cava basin. With a long-term lack of synchronization, venous outflow from the head may be disrupted, which can contribute to an increase in ICP. To prevent this phenomenon, it is necessary to sedate the patient with benzodiazepine drugs. If possible, avoid the use of muscle relaxants that have a ganglionic blocking effect to varying degrees and thus reduce mean arterial pressure. The use of suxamethonium iodide is highly undesirable due to its property to increase ICP and increase MBF. In conditions of a full stomach, which is observed in almost all patients with TBI, if it is necessary to use muscle relaxants, rocuronium bromide is considered the drug of choice. ALV should be carried out in the normoventilation mode with maintaining paCO2 at a level of 36-40 mm Hg, and paO2 not lower than 150 mm Hg and with an oxygen concentration in the breathing mixture of 40-50%. Hyperventilation with preserved cerebral perfusion can lead to spasm of cerebral vessels in intact zones with an increase in the severity of ischemia. When choosing the parameters of ALV, it is necessary to avoid a high level of peak pressure in the airways in combination with a positive pressure at the end of inspiration of no more than 3-5 cm H2O.

Indications for discontinuing mechanical ventilation:

• relief of cerebral edema,
• elimination of bulbar disorders,
• restoration of consciousness (up to 12 points on the Glasgow Coma Scale).

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Maintaining stable hemodynamics

Main directions of hemodynamic maintenance:

• infusion therapy,
• inotropic support, administration of vasopressors (if necessary).

Infusion therapy

Traditionally, in TBI, it was recommended to limit the volume of infusion therapy. However, based on the need to maintain sufficient CPP and, consequently, high mean BP, such recommendations contradict clinical practice. Arterial hypertension that occurs in patients with TBI is caused by numerous compensatory factors. A decrease in BP is considered an extremely unfavorable prognostic sign; it is usually caused by severe impairment of the vasomotor center and BCC deficit.

To maintain adequate BCC, it is necessary to carry out infusion therapy in a volume close to the physiological needs of the child, taking into account all physiological and non-physiological losses.

The qualitative composition of drugs for infusion therapy requires the following requirements:

• maintaining plasma osmolality within 290-320 mOsm/kg,
• maintaining normal electrolyte levels in blood plasma (target sodium concentration not less than 145 mmol/l),
• maintaining normoglycemia.

The most acceptable solutions in these conditions are isoosmolar solutions, and if necessary, hyperosmolar crystalloid solutions can be used. The introduction of hypoosmolar solutions (Ringer's solution and 5% glucose solution) should be avoided. Considering that hyperglycemia often occurs in the early phase of TBI, the use of any glucose solutions at the initial infusion stage is not indicated.

The incidence of fatal outcomes and the severity of neurological consequences of TBI are directly related to high plasma glucose levels due to hyperosmolarity. Hyperglycemia should be corrected by intravenous administration of insulin preparations; hypertonic solutions of NaCl are recommended to prevent a decrease in plasma osmolarity. Infusion of solutions containing sodium should be carried out under the control of its serum level, since an increase in its concentration above 160 mmol/l is fraught with the development of subarachnoid hemorrhages and demyelination of nerve fibers. Correction of high osmolality values due to an increase in the sodium level is not recommended, since this can lead to the movement of fluid from the intravascular space into the interstitium of the brain.

In conditions of a disrupted BBB, maintaining the BCC with colloidal solutions may not be indicated due to the frequently observed "rebound effect". A disrupted BBB can be detected by CT with contrast. In case of a risk of dextran molecules penetrating into the interstitium of the brain tissue, inotropic therapy may be preferred to the administration of colloids to stabilize hemodynamics.

Inotropic support

Initial doses of dopamine are 5-6 mcg/(kg x min), epinephrine - 0.06-0.1 mcg/(kg x min), norepinephrine - 0.1-0.3 mcg/(kg x min). Considering that the listed drugs can promote an increase in diuresis, a corresponding increase in the volume of infusion therapy may be required.

Dehydration therapy

Osmotic and loop diuretics are now prescribed with greater caution in TBI. A mandatory condition for the introduction of loop diuretics is the correction of electrolyte disturbances. Mannitol is recommended to be prescribed in the early stages of treatment (a dose of 0.5 g per 1 kg of body weight is administered over 20-30 minutes). An overdose of mannitol can lead to an increase in plasma osmolarity above 320 mOsm/l with the risk of possible complications.

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Anticonvulsant and antiemetic therapy

If necessary, anticonvulsant and antiemetic therapy should be administered to prevent increased intrathoracic pressure with a decrease in CPP.

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Anesthesia

In case of TBI, it is not necessary to prescribe analgesics, since brain tissue does not have pain receptors. In case of multiple trauma, pain relief with narcotic analgesics should be carried out under conditions of auxiliary or forced mechanical ventilation while ensuring hemodynamic stability. Reduction of metabolic needs of the brain. In order to reduce the metabolic needs of the brain in the phase of its pronounced edema, it is rational to maintain deep drug sedation, preferably with benzodiazepines. Barbiturate coma, providing the maximum reduction in oxygen consumption by the brain, can be accompanied by an unfavorable tendency to destabilize hemodynamics. In addition, long-term use of barbiturates is dangerous due to the development of water-electrolyte disorders, leads to gastrointestinal paresis, potentiates liver enzymes, and complicates the assessment of the neurological state in dynamics.

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Normalization of body temperature

The administration of antipyretic drugs is indicated at a body temperature of at least 38.0 °C in combination with local hypothermia of the head and neck.

Glucocorticoids

The use of glucocorticoids in the treatment of cerebral edema in TBI is contraindicated. It has been established that their use in the treatment of TBI increases 14-day mortality.

Antibiotic therapy

In children with open TBI, as well as for the purpose of preventing purulent-septic complications, it is recommended to administer antibiotic therapy taking into account the sensitivity of the most likely, including hospital, bacterial strains.

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Nutritional support

A mandatory component of intensive care in children with severe TBI. In this regard, after the restoration of hemodynamic parameters, the introduction of total parenteral nutrition is indicated. Subsequently, as the gastrointestinal tract functions are restored, enteral tube nutrition takes the main place in providing the body with energy and nutrients. Early provision of patients with TBI with nutrition significantly reduces the incidence of septic complications, shortens the duration of stay in the intensive care unit and the duration of hospitalization.

To date, there are no completed randomized trials confirming the efficacy of calcium channel blockers and magnesium sulfate in the treatment of cerebral edema in children. Antioxidant therapy is a promising and pathogenetically justified method for the treatment of TBI, but it has also not been sufficiently studied.