Pediatric Head Trauma Treatment & Management

The goal of medical care of patients with head trauma is to recognize and treat life-threatening conditions and to eliminate or minimize the role of secondary injury. Guidelines for the treatment of patients with head trauma have been established.^[16]

Consultation with a neurosurgeon should be obtained. A child advocacy team or child protective services should be contacted if child abuse is suspected, the mechanism of injury is unknown or unexplained, or the history is inconsistent. Guidelines for the evaluation of suspected child physical abuse have been established.^[17]

Criteria for hospitalization in patients with head trauma should be directed on an individual basis. Usual indications for admission include the following:

• Documented loss of consciousness longer than 5 minutes
• Coma, altered mental status, or seizures
• Focal neurologic deficit
• Protracted vomiting, severe and persistent headache
• Intoxication with substances such as alcohol or drugs that interfere with the neurologic examination
• Suspected child abuse
• Unreliable caregiver
• Underlying pathology such as coagulopathy or hydrocephalus

Admission to an intensive care unit (ICU) should be based on the severity of the trauma and associated injuries. Transfer to a hospital where consultation with a neurosurgeon is available may be required, especially when surgical intervention is necessary.

The results from one study note that children with minor blunt head trauma (defined by initial Pediatric Glasgow Coma Scale [PGCS] scores of 14 or 15) and normal cranial computed tomography (CT) scans are at very low risk for subsequent abnormal CT or magnetic resonance imaging (MRI) scans and are highly unlikely to require neurosurgical intervention; hospitalization of these children is generally unnecessary.^[18]

Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation secondary to the increased intracranial pressure (ICP); therefore, frequent serial assessments of neurologic status must be performed.

In all patients, tetanus immunization status should be checked and updated, especially when lacerations or contaminated wounds are present. Anticonvulsants may be needed to control or provide prophylaxis for seizure activity. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used for minor pain control. Beta-blockers can be prescribed for patients with trauma-induced migraines.

Patients with minor head injury (ie, Pediatric Glasgow Coma Scale [PGCS] score of 14-15) can be discharged with observation instructions in the care of a reliable adult.

Patients who sustained a loss of consciousness lasting less than 5 minutes and have normal findings on neurologic examination, no symptoms of increased ICP (eg, vomiting or headache), no signs of basilar skull fracture, and normal findings on CT scanning or skull radiography can also be discharged with close observation by a reliable adult.

The Brain Trauma Foundation has developed guidelines regarding the medical management of patients with severe head injury. These guidelines suggest that cardiopulmonary resuscitation should be the foundation on which treatment of intracranial hypertension must be based. They also state that, in the absence of any obvious signs of increased ICP, no prophylactic treatment should be initiated, because this may directly interfere with optimal resuscitation.

Airway management

A stable airway should be obtained to provide adequate oxygenation and ventilation. If endotracheal intubation is required, adequate sedation and paralysis must be ensured to prevent further increases in ICP. Rapid-sequence induction (RSI) and endotracheal intubation are generally recommended. Stabilization of the cervical spine should be achieved in every patient with severe head trauma. Nasal intubation or nasogastric tube placement should be avoided, especially when basilar skull fracture is suspected.

Breathing may be impaired because of neurologic or thoracic injuries. Patients with significant head injury and altered mentation should receive 100% oxygen supplementation and should be supported with positive-pressure ventilation. Endotracheal intubation should be performed in cases where the patient has difficulty maintaining the airway because of large secretions, poor gag reflex, coma, or the need for prolonged ventilatory support.

Premedication for RSI includes atropine (0.02 mg/kg for children younger than 8 y) to blunt the effect of vagal stimulation and decrease the secretions. Lidocaine (1-2 mg/kg) may be used to decrease airway stimulation during intubation and prevent an increase in ICP. Thiopental (4-7 mg/kg), etomidate (0.3 mg/kg), and midazolam (0.1 mg/kg) have been successfully used to sedate the patient for intubation.

Ketamine is contraindicated in patients with significant head and eye injuries, because it may increase ICP and intraocular pressure (IOP). Succinylcholine, a depolarizing paralytic agent, may be used in older children in doses of 1-1.5 mg/kg. It acts rapidly and has a short duration of action. Succinylcholine is contraindicated in neuromuscular disorders. Nondepolarizing agents, including rocuronium, pancuronium, and vecuronium, are commonly used in young children.

Cardiovascular management

Achieving normotension and euvolemia is the goal in cardiovascular management. Cerebral perfusion pressure (CPP), defined as mean arterial blood pressure (MAP) minus ICP (ie, CPP = MAP – ICP), is the physiologic variable that defines the pressure gradient driving cerebral blood flow (CBF) and metabolite delivery; it is therefore closely related to ischemia. Several clinical studies suggest that 70-80 mm Hg may be the critical threshold for CPP.

Adequate volume resuscitation with isotonic solutions is indicated to maintain adequate filling pressures, normal cardiac output, and ultimately normotension (MAP >90 mm Hg). Several adult and pediatric studies have found hypertonic solutions to be superior to lactated Ringer solution or isotonic sodium chloride for resuscitation. The use of hypertonic solutions is associated with improved blood pressure response, overall decreased fluid requirements, fewer interventions employed to control ICP, fewer complications, and improved survival.

Hypertension, if present, could represent a compensatory mechanism responding to the increased ICP; thus, reflex treatment of it may significantly compromise cerebral perfusion. When normotension is desired in the presence of intracranial or intracerebral hemorrhage after surgical evacuation, calcium channel blockers or beta-blockers should be given instead of direct vasodilators to prevent sudden hypotension.

Continuous cardiac monitoring should be performed because of the high incidence of ventricular dysrhythmias in patients with head trauma and patients in whom cardiac contusion is suspected.

ICP and cerebral perfusion management

Medical management of increased ICP includes elevating the head end of the bed to 30° and maintaining the head and neck in the midline position. Sedation and paralysis are used to prevent agitation and increased muscular activity, which may increase ICP. If neuromuscular blockers are used, monitoring the ICP and having an electroencephalograph (EEG) in place are necessary.

The use of loop or osmotic diuretics (eg, furosemide and mannitol) is directed mostly at decreasing cerebrospinal fluid (CSF) production and at improving cerebral compliance and CBF by reducing cerebral blood volume (CBV). The effect on the reduction of cerebral edema remains unproved. These agents are also used to maintain euvolemia.

Hyperventilation should be used carefully in the treatment of acute ICP elevations. Studies have shown that prolonged prophylactic use of hyperventilation in head trauma patients is associated with a negative outcome.

CBF is known to be diminished in the first 24 hours in patients who have sustained severe traumatic brain injury (TBI), with absolute values close to those seen in ischemia. Hyperventilation decreases CBF. It also potentially leads to the loss of autoregulation. This may cause further ischemic injury and does not produce a consistent reduction in ICP. Therefore, mild hyperventilation, with an arterial carbon dioxide tension (PaCO₂) of 30-35 mm Hg, is tolerated better over a longer period, with less deleterious effects.

Removal of CSF via extraventricular drains improves the ICP in these patients and provides continuous ICP monitoring.

Corticosteroids do not decrease the cerebral edema associated with head trauma and are not currently recommended. However, in the presence of head trauma and spinal cord injury, prompt use of methylprednisolone as a continuous infusion may improve outcome after spinal injury.

Barbiturate therapy lowers the ICP and exerts cerebral protection through 3 mechanisms:

• Alterations in vascular tone
• Inhibition of free radical–mediated lipid peroxidation
• Suppression of metabolism

By lowering metabolic demands, barbiturate therapy decreases CBF and cerebral blood volume (CBV), exerting beneficial effects on ICP and global cerebral perfusion. However, several studies have shown that in comparison with mannitol, barbiturates do not improve outcome when given as empiric coma therapy or when used as prophylactic treatment of ICP.

The only patients to respond favorably to barbiturate ICP control seem to be those in whom the autoregulatory response is preserved. Therefore, barbiturate therapy should be reserved for intractable increased ICP after all conventional medical therapies have failed. The goal should be to achieve EEG burst suppression because maximal reductions in CBF and metabolism occur at this level. The main side effects are hypotension and cardiovascular toxicity. Hence, when barbiturates are used, invasive hemodynamic monitoring is generally recommended.

Bleeding management

Disseminated intravascular coagulopathy (DIC) is present in one third of head trauma patients. Aggressive management of DIC and correction with replacement factors are required to decrease the risk of further intracranial bleeding and allow surgical intervention when necessary.

Seizure management

Posttraumatic seizures, which occur in 10% of pediatric patients with head trauma, may affect the outcome adversely by raising the ICP, increasing the metabolic demands of the brain, and causing hypoxia or hypoventilation in a spontaneously breathing patient. Benzodiazepines (eg, lorazepam and diazepam) may be used to control the seizure, and phenytoin or phenobarbital may be used for maintenance anticonvulsant therapy.

Surgical decompression is required in the presence of a rapidly expanding epidural or subdural hematoma that causes an increase in ICP and focal compression.

Craniotomy and surgical drainage of an epidural hematoma and repair of vessels should be done immediately if signs of increased ICP, altered mentation, focal neurologic signs, pupillary changes, or a midline shift are present. Conservative management with close monitoring in a pediatric ICU (PICU) is acceptable if no focal neurologic signs, altered mentation, or pressure effects with midline shift are present and if the hematoma is smaller than 2 cm.

A subdural hematoma with midline shift or altered mental status should be emergently drained. A small subdural hematoma with no midline shift or pressure effects should be managed conservatively with close monitoring. Surgical drainage of subdural hematoma is not required in most cases.

Most patients with penetrating injuries require surgical debridement and evacuation of the hematoma and receive prophylactic antibiotics, as well as anticonvulsants.

Depressed skull fractures require surgical elevation if the depth of the depression is thicker than the calvaria, if the depression is greater than 1 cm, and if bony fragments are causing the compression against the brain tissue.