Treatment for brain injury

Treatment of traumatic brain injury begins at the scene of the accident. However, before transporting the patient, it is necessary to ensure airway patency and stop external bleeding. It is especially important to avoid displacement of the bony structures of the spine or other bones, which can cause damage to the spinal cord and blood vessels. Necessary immobilization of the entire spine is provided with a cervical collar and a rigid long shield until the stability of the entire spine is confirmed by appropriate examination, including imaging methods. After an initial rapid neurological examination, pain should be relieved with short-acting opioid analgesics (eg, fentanyl).

In hospital, after a quick initial examination, neurological data (GCS, pupillary response), blood pressure, pulse and body temperature should be frequently recorded for several hours, as any deterioration requires immediate action. The results of repeated CT and GCS assessments will classify the severity of the injury, which will help orient treatment in the right direction.

The cornerstone of traumatic brain injury treatment is maintaining normal gas exchange in the lungs and adequate blood supply to the brain to avoid secondary strokes. Aggressive early treatment of hypoxia, hypercapnia, arterial hypotension, and increased intracranial pressure helps prevent secondary complications. Other complications to be aware of and prevent include hyperthermia, hyponatremia, hyperglycemia, and fluid imbalance.

To maintain normal blood supply to the brain in case of bleeding from injuries (external or internal), the latter must be quickly stopped, the intravascular volume must also be quickly replenished with appropriate solutions (0.9% sodium chloride solution, sometimes blood transfusion). The introduction of hypotonic solutions (especially 5% glucose solution) is contraindicated due to the excess of free water in them. Hyperthermia must also be corrected.

Treatment of mild traumatic brain injury

Mild injuries (GCS) are observed in 80% of patients with TBI admitted to the emergency department. If loss of consciousness was brief or absent, vital signs are stable, CT scan is normal, and cognitive and neurological status are normal, such patients can be discharged home with instructions for family members to monitor the patient’s condition at home for 24 hours. Family members are advised to return the patient to the hospital if: impaired consciousness; focal neurological symptoms; worsening headache; vomiting or worsening cognitive function.

Patients with minimal or no neurologic changes but minor changes on CT should be hospitalized and should be monitored for observation and repeat CT.

Treatment of moderate to severe traumatic brain injury

Moderate-grade injuries occur in an average of 10% of patients with traumatic brain injury who present to the emergency department. They often do not require intubation and mechanical ventilation (in the absence of other injuries) or intracranial pressure monitoring. However, because of the potential for deterioration, these patients should be hospitalized and observed, even if CT scans are normal.

Severe injuries are observed in 10% of patients with traumatic brain injury admitted to the emergency department. They are hospitalized in the intensive care unit. Since protective reflexes of the respiratory tract are usually depressed and intracranial pressure is increased, such patients are intubated, while measures are taken to reduce intracranial pressure. Dynamic observation using GCS and determination of pupillary response, repeat CT are necessary.

Increased intracranial pressure

Patients with traumatic brain injury requiring airway management or mechanical ventilation are intubated orally, as nasal intubation is associated with a higher risk of increased intracranial pressure. To minimize the risk of increased intracranial pressure during intubation using this method, appropriate medications should be used, for example, some experts recommend intravenous lidocaine at a dose of 1.5 mg/kg 1-2 minutes before the administration of muscle relaxants. The muscle relaxant commonly used is suxamethonium chloride at a dose of 1 mg/kg intravenously. Etomidate is considered a good choice for induction of anesthesia, as its effect on blood pressure is minimal (the dose for adults is 0.3 mg/kg or 20 mg for an average-sized adult; in children - 0.2-0.3 mg/kg). Alternatively, if hypotension is not present and is unlikely to develop, propofol is available and is used during intubation at a dose of 0.2 to 1.5 mg/kg.

The adequacy of oxygenation and ventilation is assessed by blood gas composition and pulse oximetry (if possible, also end-tidal CO2 concentration). The goal is to maintain normal p (38-42 mm Hg). In the past, prophylactic hyperventilation was recommended (p from 25 to 35 mm Hg). However, despite the fact that low p reduces intracranial pressure due to narrowing of cerebral vessels, this, in turn, reduces intracranial blood supply and can cause ischemia. In this regard, hyperventilation is used only in the first hours to combat increased intracranial pressure that is not amenable to correction by other methods, only up to p from 30 to 35 mm Hg and for a short time.

In patients with severe traumatic brain injury who do not follow simple commands, especially those with abnormal CT scans, dynamic observation and monitoring of intracranial pressure and IVD are recommended. The main goal is to maintain intracranial pressure <20 mmHg and IVD up to 50-70 mmHg. Venous outflow from the brain (thereby decreasing intracranial pressure) can be increased by elevating the head of the bed to 30° and positioning the patient's head in the midline. If a ventricular catheter is in place, drainage of CSF will also help decrease intracranial pressure.

Prevention of agitation, excessive muscular activity (eg, in delirium), and pain will also help prevent increased intracranial pressure. Propofol is most often used for sedation in adults because of its rapid onset and remission (0.3 mg/kg/hour intravenously continuously, titrated to 3 mg/kg/hour); loading bolus administration is not necessary. Hypotension is a possible side effect. Benzodiazepines (eg, midazolam, lorazepam) are also used for sedation. Antipsychotics delay awakening and should be avoided if possible. Haloperidol may be used for several days in delirium. If delirium is prolonged, trazodone, gabapentin, valproate, or quetiapine may be used, although it is not clear why these drugs are better than haloperidol. Muscle relaxants may occasionally be needed; In such cases, adequate sedation must be provided, since it will be impossible to assess arousal clinically under these conditions. Opioid analgesics are often required for adequate analgesia.

Normal circulating blood volume and osmolarity should be maintained, although a slight increase in the latter is acceptable (target plasma osmolarity is 295 to 320 mOsm/kg). Intravenous osmotic diuretics (eg, mannitol) are given to reduce intracranial pressure and maintain plasma osmolarity. However, this measure should be reserved for patients whose condition is deteriorating and for patients with hematomas in the preoperative period. A 20% solution of mannitol is administered at a dose of 0.5-1.0 g/kg over 15-30 min, repeated at a dose of 0.25-0.5 g/kg as often as the clinical situation requires (usually up to 6 times over 8 hours). This reduces intracranial pressure for several hours. Mannitol should be used with great caution in patients with severe coronary artery disease, cardiac or renal failure, or pulmonary venous congestion, since mannitol can rapidly expand intravascular volume. Because osmotic diuretics increase fluid excretion relative to Na ⁺ ions, prolonged use of mannitol may result in water depletion and hypernatremia. Furosemide 1 mg/kg IV may also reduce total body fluid content, particularly if the transient hypervolemia associated with mannitol is to be avoided. Fluid and electrolyte balance should be monitored especially when osmotic diuretics are used. A 3% saline solution is being studied as an alternative for controlling intracranial pressure.

Hyperventilation (i.e., CO2 _p 30 to 35 mmHg) may be needed for a very short period of time when elevated intracranial _pressure does not respond to standard treatment. An alternative treatment for traumatic brain injury with intractable high intracranial pressure is decompressive craniotomy. This procedure involves removing a flap of bone from the cranial vault (which is then replaced) and performing dura mater plasty, which allows the swelling to spread beyond the skull.

Another method of treating traumatic brain injury is pentobarbital coma. Coma is induced by administering pentobarbital at a dose of 10 mg/kg for 30 minutes, then 5 mg/kg per hour for up to 3 doses, then 1 mg/kg per hour. The dose can be adjusted by slowing the surge in EEG activity, which must be constantly monitored. Arterial hypotension develops frequently; treatment consists of administering fluids or, if necessary, vasopressors.

The effectiveness of therapeutic systemic hypothermia has not been proven. Glucocorticoids for intracranial pressure control are useless. A recent international study found worse outcomes with their use.

Treatment of traumatic brain injury and convulsive syndrome

Prolonged seizures, which may worsen brain injury and increase intracranial pressure, should be prevented and treated promptly if they occur. In patients with significant structural damage (eg, large contusions or hematomas, brain injuries, depressed skull fractures) or a GCS <10, anticonvulsants may be given prophylactically. When phenytoin is used, a loading dose of 20 mg is administered intravenously (at a maximum rate of 50 mg/min to avoid adverse cardiovascular effects such as hypotension and bradycardia). The starting maintenance dose for adults is 2-2.7 mg/kg 3 times daily; children require a higher dose: up to 5 mg/kg twice daily. Plasma drug concentrations are measured to adjust the dose. The duration of treatment varies and depends on the type of injury and EEG results. If there have been no seizures for a week, anticonvulsants should be discontinued, as their value in preventing future seizures has not been established. Research into new anticonvulsant drugs is ongoing.

Treatment of traumatic brain injury with skull fracture

Closed skull fractures without displacement do not require specific treatment. In depressed fractures, surgical intervention is sometimes indicated to remove bone fragments, ligate damaged vessels of the cerebral cortex, restore the dura mater, and treat brain tissue. In open fractures, surgical treatment is indicated. The use of antibiotic prophylaxis is ambiguous due to the limited amount of data on its effectiveness and the problem of the emergence of antibiotic-resistant strains of microorganisms.

Surgical treatment of traumatic brain injury

In intracranial hematomas, the spilled blood is evacuated surgically. Rapid evacuation of the hematoma can prevent or eliminate displacement and compression of the brain. However, many hematomas do not require surgical intervention, including small intracerebral hematomas. Patients with small subdural hematomas can also often be treated non-operatively. Indications for surgical treatment include:

• displacement of the brain from the midline by more than 5 mm;
• compression of the basal cisterns;
• progression of neurological symptoms.

Chronic subdural hematoma may require surgical drainage, but its urgency is much lower than in acute cases. Large or arterial hematomas are treated surgically, while small venous epidural hematomas can be observed dynamically using CT.