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Craniocerebral injury in children
Last reviewed: 23.04.2024
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Causes of craniocerebral trauma in children
The main causes of craniocerebral injuries in children:
- transport injuries (most often road),
- fall from height (for a child of early age, the dangerous height can be 30-40 cm),
- household injuries,
- negligent or cruel treatment of parents,
- criminal traumatism (in older children).
The last two reasons have become increasingly important in recent years.
The mechanism of development of head injury in children
In the pathogenesis of TBI it is common to distinguish several damaging mechanisms:
- Damage mechanisms in cases of head injury.
- The primary damaging mechanism is the injury itself.
- 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 in this pathology.
Edema of the brain
The main syndrome in the development of secondary lesions is an increasing cerebral edema.
Causes of cerebral edema:
- violation of the regulation of cerebral vessels (vasogenic edema),
- subsequent tissue ischemia (cytotoxic edema).
The consequences of an increasing edema of the brain - an increase in ICP and a violation of tissue perfusion.
Mechanisms of edema of the brain
Considering the mechanisms of the development of edema of the brain, it is necessary to take into account its physiological characteristics.
Physiological features of the brain large consumption of oxygen and high organ blood flow, the inability of the cranium to change its volume depending on the volume of the brain, autoregulation of MC, the effect of temperature on the vital activity of the brain, the effect of rheological properties of blood on the delivery of oxygen. High oxygen consumption and high organ blood flow. The brain is an extremely metabolically active organ with a large intake of oxygen 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 the whole body oxygen and receives up to 15% of the CB. In children, the amount of oxygen consumption by the brain is 5 ml per 100 g of brain tissue per minute, far exceeding that of adults (3-4 ml).
MK in children (excluding newborns and infants) also exceeds MK in adults and is 65-95 ml per 100 g of brain tissue per minute, while in adults it is 50 ml on average. 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 an increasing volume of the brain, which in turn can worsen tissue perfusion, especially in the pericortical areas.
Cerebral perfusion pressure (CPD) directly depends on ICP, it is calculated by the formula:
CPR = ADP - ICP, where AD is the mean BP at the level of the Willis circle
ICP is normal in children not exceeding 10 mm Hg and depends on the volume of the main components of the cranial cavity. The brain tissue takes up to 75% of the intracranial volume, the interstitial fluid is about 10%, another 7-12% is CSF, and about 8% is occupied by the blood located in the cerebral vascular bed. According to the Monro-Kelly concept, the named components are incompressible in nature, therefore, a change in the volume of one of them at a constant ICP level leads to compensatory changes in the volume of the 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 change.
Autoregulation MK - one of the processes that limit the amount of blood in the vessels of the brain. This process maintains the constancy of MC in the oscillations of ADP in adults from 50 to 150 mm. Gt; Art. Decrease in ADP below 50 mmHg is dangerous by the development of hypoperfusion of brain tissues with the onset of ischemia, and exceeding 150 mmHg can lead to edema of the brain. For children, the boundaries of autoregulation are unknown, but presumably they are proportionally lower than in adults. The mechanism of MC autoregulation is not completely clear to the end, but it probably consists of a metabolic and a vasomotor component. It is known that autoregulation can be disturbed by hypoxia, ischemia, hypercarbia, head trauma, under the influence of some general anesthetics.
Factors affecting the MK level of CO2 and pH in the vessels of the brain, blood oxygenation, neurogenic factors. The level of CO2 and pH in the vessels of the brain is an important factor determining the magnitude of MC. The value of MC is linearly dependent on paCO2 in the range from 20 to 80 mm. Gt; Art. A decrease in pCOO2 by 1 mmHg reduces the MC by 1-2 ml per 100 g of brain tissue per minute, and its fall to 20-40 mm. Gt; Art. Reduces MC twice. Short-term hyperventilation, accompanied by a significant hypocarbia (paCO2 <20 mm Hg), can lead to severe cerebral ischemia as a result of vasoconstriction. With prolonged hyperventilation (more than 6-8 hours), the MC can normalize as a result of a gradual correction of the CSF pH by delaying the bicarbonate.
Oxygenation of blood (MC depends on it to a lesser extent) Within the range of 60 to 300 mm. Gt; Art. PaO2 practically does not affect cerebral hemodynamics, and only when the paO2 decreases below 50 mm Hg there is a sharp increase in MC. The mechanism of cerebral vasodilation in hypoxemia is not fully established, but it can consist of a set of neurogenic reactions caused by peripheral chemoreceptors, as well as a direct vasodilating effect of hypoxemic lactic acidosis. The pronounced hyperoxia (pao> 300 mm Hg) leads to a moderate decrease in MC. When breathing 100% oxygen at a pressure of 1 atm, the MC decreases by 12%.
Many of the above mechanisms of MC regulation are realized by means of nitric oxide (NO) released from the endothelial cells of the cerebral vessels. Nitric oxide is one of the main local mediators of the microcirculatory bed tone. It determines the vasodilation caused by hypercarbia, increased metabolism, the effect of volatile anesthetics and nitrates (nitroglycerin and sodium nitroprusside).
Neurogenic factors also take a significant part in the regulation of MC. First of all, they affect the tone of large vessels of the brain. Adrenergic, cholinergic and serotonergic systems affect the MC on a par with the system of vasoactive peptides. The functional significance of neurogenic mechanisms in the regulation of MC is evidenced by studies of autoregulation and ischemic brain damage.
Influence of temperature on vital activity of the brain
The great importance for the consumption of oxygen by the brain is the temperature of its tissues. Hypothermia causes a significant decrease in metabolism in the brain cells and leads to a secondary decrease in MC. Reduction of the temperature of the brain by 1 ° C leads to a decrease in cerebral oxygen consumption (O2 media) by 6-7%, and at 18 ° C the O2 mass media makes up no more than 10% of the initial normothermic values. At a temperature below 20 ° C, the electrical activity of the brain disappears, and an isoline is recorded on the EEG.
Hyperthermia has the opposite effect on brain metabolism. At a temperature of 37 ° C to 42 ° C there is a gradual increase in MC and O2 media, but with a further increase in it, a critical decrease in the utilization of oxygen by brain cells occurs. This effect is associated with the possible degradation of proteins at a temperature above 42 ° C.
Influence of the rheological properties of blood on the delivery of oxygen
Delivery of oxygen to cells of the brain depends not only on the magnitude of MC, but also on the properties of blood. Hematocrit is the most important factor determining both the oxygen capacity of the blood and its viscosity. With anemia, the resistance of the cerebral vessels decreases, the MC increases. The positive effect of reducing blood viscosity is most evident in cases of focal cerebral ischemia, when the best oxygen delivery occurs at a hematocrit value of 30 to 34%.
Clinical characteristics of craniocerebral trauma in children
Disturbances that develop in patients in acute TBI, affect vital organs and systems, lead to respiratory and cardiovascular insufficiency, indirectly affect liver and kidney function, intestinal motility, which greatly complicates the treatment.
Lightweight TBI often does not lead to a loss of consciousness. With moderate and severe brain contusions, focal symptomatology is often not expressed, but oppression of consciousness and vegetative disorders predominate. An early phase of high blood filling of cerebral vessels with subsequent vasogenic edema is often observed. Diffuse axonal lesion occurs in children much more often than in adults.
In connection with the anatomical and physiological features of the child's organism, the processes occurring in children with CCI are significantly different. Children are more likely to have periods of temporary recovery of consciousness after relatively minor injuries, possibly a rapid improvement in the condition, in addition, they have a better prognosis than can be assumed on the basis of the initial neurologic symptoms.
Classification of TBI
There are several principles for the classification of craniocerebral trauma, depending on the damage to the skull, the nature of brain damage, and the degree of severity.
Classification of craniocerebral trauma in relation to cranial injury:
- Closed CCT.
- An open CTB is a combination of a violation of the integrity of the skin, aponeurosis and bones of the cranial vault.
Classification of TBI by the nature of brain damage:
- Focal damage of the brain (brain contusion, epidural, subdural and intracerebral hematomas).
- Diffuse brain damage (concussion of the brain and diffuse axonal lesion).
Classification of CCT by severity:
- BMS of mild degree (concussion and light bruises of the brain).
- CWT of medium degree (brain contusion of medium degree).
- TBT severe (cerebral contusion of a severe degree, diffuse axonal damage and compression of the brain).
How to recognize a traumatic brain injury in a child?
Diagnostic algorithm
According to some reports, only 84% of all hematomas develop within the next 12 hours after injury, and therefore any brain concussion in children is considered an indication for mandatory hospitalization. Differential diagnosis is performed with other conditions that cause CNS depression.
Fsical examination
When examining a patient with CCT, it is necessary to begin with a close inspection. First of all, the function of external respiration and the state of the cardiovascular system are evaluated. Particular attention should be given to the presence of abrasions, bruising, signs of external or internal bleeding and fractures of the ribs, pelvic bones and extremities, the outflow of liquor and blood from the nose and ears, odor from the mouth.
Diagnosis of the severity of TBI consists primarily of assessing the oppression of consciousness, neurological symptoms and the degree of involvement in the pathological process of vital body functions.
Assessment of the degree of inhibition of consciousness
To assess the degree of oppression of consciousness, it is preferable to use the most common Glasgow coma scale in the world. It is based on three clinical criteria for opening the eyes, verbal functions and the motor reaction of the patient. Each criterion is assessed on a point system, the maximum score on the scale is 15, the minimum is 3. The clear consciousness corresponds to 15 points, 14-10 points correspond to the stunning of different degrees, 8-10 to the comparison, less than 7 to the coma. The unconditional advantages of this scale include its simplicity and sufficient versatility. The main disadvantage is that it can not be used in intubated patients. Despite certain limitations, the Glasgow scale is very effective for dynamically assessing the patient's level of consciousness and has a high predictive value.
In young children (under 3-4 years of age), due to insufficiently formed speech, a modified Glasgow coma scale can be used.
Modified Glasgow Coma Scale for Young Children
Reactions of the patient |
Points |
Opening the eyes |
|
Arbitrary |
4 |
By request |
3 |
For pain |
2 |
Absent |
1 |
Motor reactions |
|
execution of movements on command |
6th
|
movement in response to painful irritation (repulsion) |
5
|
limb withdrawal in response to pain stimulation |
4
|
pathological flexion in response to painful irritation (decortication) |
3
|
pathological extension in response to painful irritation (decerebriation) |
2
|
Speech response | |
the child smiles, focuses on sound, monitors objects, is interactive |
5 |
child with crying can calm down the interactivity of the defective |
4 |
when crying calms down, but not for long, moans |
3 |
does not calm down when crying is restless |
2 |
Crying and interactivity are absent |
1 |
[37], [38], [39], [40], [41], [42], [43], [44],
Evaluation of the degree of lesion of the brainstem
In particular, the functions of the cranial nerves are evaluated by the presence of anisocoria, the pupil's response to light, oculo- vestibular (cold water test), or oculocephalic reflexes. The actual nature of neurological disturbances can only be assessed after recovery of vital functions. The presence of respiratory and hemodynamic disorders testifies to the possible involvement of stem structures in the pathological process, which is considered an indication for the immediate conduct of adequate intensive therapy.
Laboratory research
Patients who are in serious condition perform examinations aimed at revealing accompanying violations of the body's functions. They examine the general blood test (mandatory exclusion of hemic hypoxia) and urine, determine electrolyte, acid-base and gas composition of blood, serum glucose, creatinine, bilirubin.
Instrumental research
For CTB diagnosis, radiographs of the skull and cervical spine, computed tomography and magnetic resonance imaging of the brain, neurosonography, eye fundus examination, lumbar puncture are performed.
Radiography of the skull and cervical spine in two projections.
CT scan of the brain - the most informative study with CCT - allows to detect the presence of hematomas in the cranial cavity, foci of bruises, displacement of the median structures of the brain, signs of disturbance of liquorodynamics and growth of ICP, as well as damage to the bone structures of the cranial vault.
Relative contraindications for emergency CT:
- shock,
- resuscitation
If during the first day the severity of the patient's condition increases, it is necessary to re-perform CT because of the risk of an increase in primary foci of hemorrhage or the formation of delayed hematomas.
Neurosonography is a fairly informative research method for detecting the displacement of the median structures of the brain (in the absence of the possibility of performing CT), especially in young children.
MRI supplements CT, allowing visualization of subtle brain structure disorders that occur with diffuse axonal lesion.
Investigation of the fundus is an important auxiliary diagnostic method. Nevertheless, the examination of the fundus can not always reveal the growth of ICP, since signs of edema of the nipple of the optic nerve are present only in 25-30% of patients with a proven increase in ICP.
Lumbar puncture
In conditions of wider use of modern diagnostic methods, it is used less and less (in spite of high informativeness), including because of frequent complications of this procedure in patients with progressive edema of the brain.
- Indications - differential diagnosis with meningitis (main indication).
- Contraindications are signs of wedging and dislocation of the brain.
Patients who are in serious condition, in addition to mandatory for CCT and diagnostic activities, perform examinations aimed at identifying concomitant injuries of ultrasound of the abdominal cavity and retroperitoneal space, chest x-ray, pelvic bones and, if necessary, upper and lower extremity bones, write 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 epidural, subdural or intracranial hematoma,
- depressed fracture of the bones of the cranial vault.
A mandatory component of preoperative preparation is the stabilization of hemodynamics.
Therapeutic treatment of TBI in children
All therapeutic measures can be divided into three main groups.
Groups of therapeutic measures:
- obshcherereanimatsionnye,
- specific,
- aggressive (if the first two are ineffective).
The goal of the therapy is to stop edema of the brain and decrease the ICP. In the treatment of patients with CCI, it is necessary to monitor brain functions, provide adequate gas exchange, maintain stable hemodynamics, reduce metabolic needs of the brain, normalize body temperature, prescribe dehydration, anticonvulsant and antiemetic therapy, pain medication, and nutritional support.
Monitoring the functions of the brain
Rational therapy of cerebral edema is impossible without monitoring its functions. With a decrease in the level of consciousness below 8 points on the Glasgow scale, measurement of ICP is indicated for the purpose of controlling intracranial hypertension and calculating CPR. As in adult patients, ICP should not exceed 20 mm. Gt; Art. In infants, the CPD should be maintained at 40 mm Hg, in older children 50-65 mm Hg (depending on the age).
With normalization of bcc and stable blood pressure to improve venous outflow from the patient's head, it is recommended to raise the head end of the bed by 15-20 °.
Ensuring adequate gas exchange
Maintaining adequate gas exchange prevents the damaging effects of hypoxia and hypercarbia on the regulation of MC. Showing the breathing of a mixture enriched with oxygen to 40%, pO2 should be maintained at a level of at least 90-100 mm. Gt; Art.
When oppression of consciousness, the occurrence of bulbar disorders, independent breathing becomes inadequate. As a result of a decrease in the tone of the muscles of the tongue and pharynx, obstruction of the upper respiratory tract develops. In patients with TBI, external respiratory distress can quickly develop, which makes it necessary to decide on the intubation of the trachea and the transition to mechanical ventilation.
Indications for switching to mechanical ventilation:
- respiratory insufficiency,
- oppression of consciousness (Glasgow coma score less than 12) The earlier the transition to IVL, the less pronounced the effect of respiratory disorders on MK.
Types of intubation of the trachea: nasotracheal, fibrooptic.
Nasotracheal intubation avoids overextension in the cervical spine, which is dangerous for cervical spinal trauma.
Contraindications to nasotracheal intubation: damage to the nose and paranasal sinuses
Fibrooptic intubation is indicated for damage to the bones of the facial skull.
Technique of intubation of the trachea
Intubation should be performed under general anesthesia using intravenous anesthetics of barbiturates or propofol. These drugs significantly reduce MK and ICP, reducing the need for the brain in oxygen. However, in case of deficiency of BCC, these drugs significantly reduce BP, therefore they should be administered with caution, titrating the dose. Immediately before intubation, it is necessary to pre-oxygenate the patient by inhaling 100% oxygen for at least 3 minutes. The high risk of aspiration of gastric contents requires airway sealing of the patient by inflating the cuff of the intubation tube.
Modes of mechanical ventilation, auxiliary regimens, forced ventilation.
Auxiliary ventilation modes
When providing respiratory support, auxiliary ventilation modes are preferable, in particular, the synchronized maintenance ventilation (BSMU) mode, which in children with severe TBT allows quick synchronization with the device. This regime is more physiological in relation to the biomechanics of respiration and allows to significantly reduce the mean intrathoracic pressure.
[50],
Forced ventilation of lungs
This mode of ventilation is recommended for deep coma (the number of points on the Glasgow scale is less than 8), when the sensitivity of the respiratory center to the level of carbon dioxide in the blood decreases. Discordination between respiratory movements of the patient and the respiratory apparatus can lead to a sharp increase in intrathoracic pressure and the occurrence of a hydraulic shock in the basin of the superior vena cava. With prolonged absence of synchronization, venous outflow from the head can be disturbed, which may contribute to an increase in ICP. To prevent this phenomenon, it is necessary to sedate the patient with benzodiazepine-type drugs. It should be avoided whenever possible the use of muscle relaxants, to some extent possessing a ganglion-blocking effect and thus reducing the average blood pressure. The use of suxamethonium iodide is highly undesirable due to its ability to increase ICP and increase MC. In the conditions of the filled stomach, which is observed practically in all patients with CCT, if it is necessary to use muscle relaxants, the choice drug is rocuronium bromide IVL should be performed in a mode of ventilator ventilation, with maintaining pACO2 at a level of 36-40 mm. Gt; and paO2 is not less than 150 mm. Gt; Art. And with a concentration of oxygen in the respiratory mixture of 40-50%. Hyperventilation with preserved perfusion of the brain can lead to spasm of cerebral vessels in intact zones with an increase in the severity of ischemia. When choosing the parameters of ventilation, a high level of peak pressure in the airways should be avoided in combination with positive pressure at the end of the inspiration not more than 3-5 cm of water. Art.
Indication for discontinuation of mechanical ventilation:
- relief of cerebral edema,
- elimination of bulbar disorders,
- restoration of consciousness (up to 12 points on the coma scale of Glasgow).
Maintaining stable hemodynamics
Main directions of hemodynamics maintenance:
- infusion therapy,
- inotropic support, the appointment of vasopressors (if necessary).
Infusion therapy
Traditionally, with CCT, it was recommended to limit the amount of infusion therapy. However, based on the need to maintain a sufficient CPR and therefore a high average BP, such recommendations conflict with clinical practice. Arterial hypertension, which occurs in patients with CCT, is due to numerous compensatory factors. Decrease in blood pressure is considered an extremely unfavorable prognostic sign, as a rule, it is caused by severe disruption of the vasomotor center and deficit of BCC.
To maintain adequate BCC, infusion therapy should be carried out in a volume close to the physiological needs of the child, taking into account all physiological and non-physiological losses.
The qualitative composition of preparations for infusion therapy involves the following requirements:
- maintenance of plasma osmolality in the range of 290-320 mOsm / kg,
- maintenance of the normal content of electrolytes in blood plasma (the target concentration of sodium is not lower than 145 mmol / l),
- maintenance of normoglycemia.
The solutions most acceptable under these conditions are iso-osmolar, and, if necessary, hyperosmolar solutions of crystalloids can also be used. Avoid hypo-osmolar solutions (Ringer's solution and 5% glucose solution). Given that hypertension often occurs in early TBI, no glucose solutions are used during the initial infusion phase.
The frequency of deaths and the severity of neurological consequences of TBI are directly related to high blood glucose levels due to hyperosmolarity. Hyperglycemia should be corrected by intravenous administration of insulin preparations, to prevent the decrease of plasma osmolality, it is recommended to inject hypertonic NaCl solutions. Infusion of solutions containing sodium should be done under the control of its serum level, as increasing its concentration above 160 mmol / l is fraught with the development of subarachnoid hemorrhages and demyelination of nerve fibers. Correction of high osmolality due to increased sodium levels is not recommended, as this can lead to the movement of fluid from the intravascular space into the interstices of the brain.
In conditions of disturbed GEB, the maintenance of bcc with the help of colloidal solutions may not be indicated because of the often observed "recoil effect". Violation of the integrity of BBB can be detected with CT with contrast. With the threat of the penetration of dextran molecules into the interstitial tissues of the brain, the introduction of colloids to stabilize hemodynamics may be favored by inotropic therapy.
Inotropic support
The initial doses of dopamine are 5-6 μg / (kghmin), epinephrine - 0.06-0.1 μg / (kghmin), norepinephrine - 0.1-0.3 μg / (kghmine). Given that these medicines can help increase diuresis, a corresponding increase in the volume of infusion therapy may be required.
Dehydration therapy
To the appointment of osmotic and loop diuretics with CCT are currently treated with greater caution. A prerequisite for the introduction of loop diuretics is the correction of electrolyte disturbances. Mannitol is recommended to be prescribed in the early stages of treatment (within 20-30 minutes, a dose of 0.5 g per 1 kg of body weight is administered). Overdose of mannitol can lead to an increase in plasma osmolality above 320 mOsm / l with the threat of possible complications.
Anticonvulsant and anti-emetic therapy
If necessary, anticonvulsant and antiemetic therapy should be used to prevent an increase in intrathoracic pressure with a decrease in CPR.
[56], [57], [58], [59], [60], [61], [62], [63], [64], [65]
Anesthesia
With TBT, prescribing analgesics is not necessary, since brain tissue does not have pain receptors. When polytrauma analgesia with narcotic analgesics should be performed in conditions of auxiliary or forced ventilation while ensuring hemodynamic stability. Decreased metabolic needs of the brain. In order to reduce the metabolic needs of the brain in the phase of its edema, it is rational to maintain a deep medication sedation, preferably benzodiazepines. Barbituric coma, providing the maximum reduction in the consumption of oxygen by the brain, can be accompanied by an unfavorable tendency to destabilize hemodynamics. In addition, the long-term use of barbiturates is dangerous by the development of water-electrolyte disorders, leads to paresis of the gastrointestinal tract, potentiates liver enzymes, makes it difficult to assess the neurological state in dynamics.
[66], [67], [68], [69], [70], [71], [72], [73], [74], [75], [76], [77]
Normalization of body temperature
The introduction of antipyretics is indicated at body temperature of at least 38.0 ° C in combination with local hypothermia of the head and neck.
Glucocorticoids
The appointment of glucocorticoids in the therapy of cerebral edema with TBI is contraindicated. It is established that their purpose in the treatment of CCT increases the 14-day lethality.
Antibiotic therapy
In children with open TBI, as well as with the goal of preventing purulent-septic complications, it is recommended to perform antibiotic therapy taking into account the sensitivity of the most probable, including hospital, strains of bacteria.
[78], [79], [80], [81], [82], [83], [84], [85], [86]
Nutritional support
The mandatory component of intensive care in children with severe head injury In this regard, after the restoration of hemodynamic parameters, the introduction of complete parenteral nutrition is indicated. In the future, as the functions of the gastrointestinal tract are restored, the main place in the provision of the body's need for energy and nutrients is taken by probe enteral nutrition. Early provision of patients with TBT nutrition significantly reduces the incidence of septic complications, shortens the length of stay in the intensive care unit and the timing of hospitalization.
To date, there are no completed randomized studies that confirm the effectiveness 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 treating TBI, but it is also not well understood.