Treatment of craniocerebral trauma

Treatment of craniocerebral trauma begins already at the site of the accident. But before transporting the patient, it is necessary to provide airway patency and stop external bleeding. It is especially important to avoid displacements of the bone structures of the spine or other bones, which can cause damage to the spinal cord and vessels. The necessary immobilization of the entire spine is provided by means of a cervical fixing collar and a solid long shield until the stability of the entire spine is confirmed by an appropriate examination involving visualizing methods of investigation. After the initial rapid neurological examination, pain relief should be relieved by opioid analgesics of short action (for example, fentanyl).

In a hospital after a quick initial examination within a few hours, it is often necessary to record neurological data (SHKG, pupillary response), blood pressure, pulse and body temperature, since any deterioration requires urgent action. The results of repeated CT and SCG assessment will allow us to classify the severity of the lesion, which will help orient the treatment in the right direction.

The cornerstone of the treatment of craniocerebral trauma is maintenance of normal gas exchange in the lungs and full blood supply to the brain in order to avoid secondary strokes. Active early treatment of hypoxia, hypercapnia, arterial hypotension and increased intracranial pressure helps prevent secondary complications. Other complications that should be remembered and which must be prevented include hyperthermia, hyponatremia, hyperglycemia and fluid imbalance in the body.

To maintain normal blood supply to the brain during bleeding from lesions (external or internal), the latter must be quickly stopped, 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 because of the excess of free water in them. Hyperthermia must also be corrected.

Treatment of craniocerebral trauma of mild degree

Damages of mild degree (according to GCG) are observed in 80% of patients with CCI, delivered to the emergency department. If the loss of consciousness was short or it was not, if the vital functions are stable, the norm is CT, normal cognitive and neurological status, then such patients can be discharged home with recommendations for relatives about the need for home monitoring of the condition of the victims within 24 hours. The need to return the patient to the hospital at the appearance of: impaired consciousness; focal neurologic symptoms; increased headache; vomiting or impaired cognitive function.

Patients who have minimal or no neurologic changes, but have minor changes in CT, should be hospitalized, such patients are shown with follow-up and repeated CT.

Treatment of craniocerebral trauma of moderate and severe severity

A moderate degree of damage is observed in an average of 10% of patients with craniocerebral trauma delivered to the emergency room. They often do not need intubation and artificial ventilation (in the absence of other injuries) or monitoring of intracranial pressure. However, due to the possibility of worsening, these patients should be hospitalized and observed, even in the absence of changes in CT.

Severe lesions are observed in 10% of patients with craniocerebral trauma delivered to the emergency room. They are hospitalized in the intensive care unit. Since respiratory protective reflexes are usually suppressed, and intracranial pressure is increased, these patients are intubated, while taking measures to reduce intracranial pressure. It is necessary to observe dynamically with the use of the ShCG and determine the pupillary response, repeated CT.

Increased intracranial pressure

Patients with craniocerebral trauma that need to maintain airway patency or ventilation are intubated through the mouth, as with intubation through the nose the likelihood of increased intracranial pressure is higher. To minimize the increase in intracranial pressure with intubation by this method, appropriate drugs should be used, for example, some specialists recommend intravenous lidocaine at a dose of 1.5 mg / kg for 1-2 minutes before the muscle relaxants. As a muscle relaxant, suksamethonium chloride is usually used at a dose of 1 mg / kg intravenously. A good choice for introductory anesthesia is etomidate, since its effect on blood pressure is minimal (the dose for adults is 0.3 mg / kg or 20 mg for an adult of average size, in children 0.2-0.3 mg / kg). Alternatively, if there is no arterial hypotension and its development is unlikely, propofol is available, with intubation it is used at a dose of 0.2 to 1.5 mg / kg.

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

Patients with severe craniocerebral trauma who do not perform simple commands, especially those with CT abnormalities, are recommended dynamic monitoring and control of intracranial pressure and MTD. The main goal is to maintain intracranial pressure <20 mmHg. And MTD to 50-70 mm Hg. Strengthen the venous outflow from the brain (thereby lowering the intracranial pressure) by raising the head end of the bed to 30 ° and placing the patient's head in the middle line. If a ventricular catheter is installed, CSF drainage will also help reduce intracranial pressure.

Prevention of agitation, excessive muscle activity (for example, in case of delirium) and pain will also help prevent increased intracranial pressure. For sedation, adults are more likely to use propofol, due to rapid development and rapid cessation of its effect (a dose of 0.3 mg / kg per hour continuously intravenously, titrated to 3 mg / kg per hour), loading bolus administration is not necessary. A possible side effect is arterial hypotension. For sedation, benzodiazepines are also used (eg, midazolam, lorazepam). Antipsychotic drugs slow the awakening, so, if possible, they should be avoided. In delirium, haloperidol can be used for several days. If delirium is delayed, trazodone, gabapentin, valproic acid preparations or quetiapine may be used, although it is not clear what these drugs are better than haloperidol. Sometimes muscle relaxants may be needed; in such cases it is necessary to provide adequate sedation, because in these conditions it is clinically impossible to assess the excitability. For adequate analgesia, opioid analgesics are often required.

It is necessary to maintain the normal volume of circulating blood and its osmolarity, although a slight increase in the latter is permissible (the target plasma osmolality level is from 295 to 320 mOsm / kg). Intravenous osmotic diuretics (for example, mannitol) are prescribed to reduce intracranial pressure and maintain osmolarity of the blood plasma. However, this measure should be left for patients whose condition worsens, as well as in the preoperative period to those affected with hematomas. A 20% solution of mannitol is administered at a dose of 0.5-1.0 g / kg for 15-30 minutes, repeating the dose of 0.25-0.5 g / kg as often as required by the clinical situation (usually up to 6 time for 8 hours). This reduces intracranial pressure for several hours. Mannitol should be used with great care in patients with severe coronary heart disease, cardiac and renal insufficiency, or venous congestion in the lungs, as mannitol can very quickly increase intravascular volume. Because osmotic diuretics increase the excretion of fluid relative to Na ⁺ ions , prolonged use of mannitol can lead to water depletion and hypernatremia. Furosemide at a dose of 1 mg / kg intravenously also helps to reduce the total fluid in the body, especially if it is necessary to avoid the temporary hypervolemia associated with the use of mannitol. Water and electrolyte balance should be monitored, first of all, when using osmotic diuretics. 3% saline solution is being studied as an alternative means for controlling the intraocular pressure.

Hyperventilation (ie p _a C0 ₂ 30 to 35 mm Hg) may be needed for a very short period of time when elevated intracranial pressure does not respond to standard treatment. An alternative method of treating craniocerebral trauma, which is accompanied by an unpatched high intracranial pressure, is decompression craniotomy. During this intervention, the skull flap (which is subsequently returned) is removed and the dural plasty is performed, which allows the swelling to spread beyond the skull.

Another way to treat craniocerebral trauma is pentobarbital coma. Who is induced by administration of pentobarbital at a dose of 10 mg / kg for 30 minutes, then 5 mg / kg per hour to 3 doses, followed by 1 mg / kg per hour. The dose can be controlled by slowing the burst of EEG activity, which must be constantly monitored. Arterial hypotension develops often, the treatment consists in injecting a liquid or, if necessary, vasopressors.

The effectiveness of curative systemic hypothermia has not been proven. Glucocorticoids for monitoring intra-arterial pressure are useless. In a recent international study, there was a worsening in the outcome of their use.

Treatment of craniocerebral trauma and convulsive syndrome

Prolonged convulsions, which can aggravate brain damage and increase intracranial pressure, should be prevented and, as soon as possible, suppressed at their occurrence. Patients with significant structural damage (for example, large bruises or bruises, brain wounds, crushed fractures of the skull) or <10 points according to the ShCG, anticonvulsants can be prescribed prophylactically. When using phenytoin, a loading dose of 20 mg is administered intravenously (at a maximum rate of not more than 50 mg / min to avoid side effects of cardiovascular effects such as hypotension and bradycardia). The starting maintenance dose for adults is 2-2.7 mg / kg 3 times a day; children need more: up to 5 mg / kg 2 times a day. To select a dose, measure the concentration of the drug in the blood plasma. The duration of treatment varies and depends on the type of damage and EEG results. If there were no seizures during the week, anticonvulsants should be canceled, as their importance for the prevention of seizures in the future is not established. Studies of new anticonvulsants are continuing.

Treatment of craniocerebral trauma with a skull fracture

Closed fractures of the skull without bias do not require specific treatment. With depressed fractures, surgical intervention is sometimes indicated for the removal of bone fragments, ligation of damaged vessels of the cerebral cortex, restoration of the dura mater, and treatment of brain tissue. With open fractures, surgical treatment is indicated. The use of antibiotic prophylaxis is ambiguous due to the limited amount of data on its effectiveness and in connection with the problem of the emergence of antibiotic-resistant strains of microorganisms.

Surgical treatment of craniocerebral trauma

With intracranial hematomas, the spilled blood is evacuated surgically. Rapid evacuation of the hematoma can prevent or eliminate the displacement and compression of the brain. However, many hematomas do not require surgical intervention, including intracerebral hematomas of small size. Patients with small subdural hematomas also can often be treated without surgery. Indications for surgical treatment are:

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

With chronic subdural hematoma, surgical drainage may be required, but its urgency is significantly lower than in acute subdural hematoma. Large or arterial hematomas are treated surgically, and small venous epidural hematomas can be observed dynamically with the help of CT.