Pediatric Head Trauma Treatment & Management

Updated: Apr 12, 2023
  • Author: Michael J Verive, MD, FAAP; Chief Editor: Muhammad Waseem, MBBS, MS, FAAP, FACEP, FAHA  more...
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Approach Considerations

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. [6] Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents, previously published in 2003, were updated in 2012 and provide an excellent basis for treatment decisions. [40]

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 also been established and were updated in 2015. [42]

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 scans or magnetic resonance imaging (MRI) studies and are highly unlikely to require neurosurgical intervention; hospitalization of these children is generally not necessary. [43]

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. Routine seizure prophylaxis is not recommended; prophylaxis should be provided for patients on an individual basis with consultation with neurosurgery. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used for minor pain control, but may be contraindicated with DIC or severe head trauma. 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.



Elevation of the head to 30° and maintaining midline position continues to be recommended because it improves the venous drainage and decreases the intracranial pressure without affecting the cerebral blood flow. A cervical spine collar should be used until clearance of the spine is achieved.

Athletes with concussion injuries should not be cleared to return to sports activities until all residual symptoms from their original head injury are no longer occurring. For more information, see Repetitive Head Injury Syndrome and Postconcussive Syndrome in Emergency Medicine.

The frequency of “second impact syndrome” among head-injured children participating in sporting activities has been documented. [44] Several states have now passed or are considering legislation to mandate education of youth coaches, athletes, and parents regarding how to recognize participants who have had a concussion and the importance of not letting the athlete return to play until all symptoms have resolved and (in many cases) the athlete has been cleared by appropriate medical personnel.


Resuscitation and Treatment of Life-Threatening Conditions

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 intracranial pressure (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 copious 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 years) to blunt the effect of vagal stimulation and decrease the secretions (controversial and not supported by high-level evidence). Lidocaine (1-2 mg/kg) may decrease airway stimulation during intubation and prevent an increase in ICP; however, although lidocaine has been widely used in the past to blunt transient increases in ICP during endotracheal intubation, there is no high-level evidence to support its continued use for this purpose. [45] 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 (controversial) 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, patients with penetrating eye injury, glaucoma, upper motor neuron injury, and history of malignant hyperthermia in patient or family, among other conditions. 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 unless there is evidence of increased ICP requiring supraphysiologic blood pressure to drive cerebral perfusion pressure (CPP). Cerebral perfusion pressure is defined as mean arterial blood pressure (MAP) minus ICP (ie, CPP = MAP – ICP) and is the physiologic variable that defines the pressure gradient driving cerebral blood flow (CBF) and metabolite delivery; it is therefore closely related to ischemia. CPP should be determined in a standard fashion, with ICP zeroed to the tragus (as an indicator of the foramen of Monro and midventricular level) and MAP zeroed to the right atrium with the head of the bed elevated 30°.

Several clinical studies suggest that 70-80 mm Hg may be the critical threshold for CPP in adults. Recent guidelines suggest that a CPP threshold 40-50 mm Hg may be considered in children, with age-specific thresholds with infants at the lower end and adolescents at the upper end of this range. [40]

Adequate volume resuscitation with isotonic solutions is indicated to maintain adequate filling pressures, normal cardiac output, and, ultimately, normotension (MAP >90 mm Hg in adults; pediatric values vary with age and height, but MAP for children at the 50th percentile for height can be estimated using the formula MAP = (1.5 × age in years) + 55). [46]

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

Little evidence supports any specific threshold for the treatment of intracranial hypertension in children. Pooled studies suggest that prolonged elevations of ICP greater than 20 mm Hg are associated with poorer outcomes in children with traumatic brain injury (TBI), thus a threshold of 20 mm Hg is typically used to guide medical management.

Osmotic therapy is a key component of medical management of intracranial hypertension. Hypertonic saline should be considered for the treatment of severe pediatric TBI associated with intracranial hypertension. Effective doses as a continuous infusion of 3% saline range from 0.1-1 mL/kg of body weight per hour administered on a sliding scale. The minimum dose needed to maintain ICP at less than 20 mm Hg should be used. Serum osmolarity should be maintained less than 360 mOsm/L.

Although mannitol is commonly used in the management of elevated ICP in adult and pediatric TBI, the evidence supporting its use in pediatric patients is inconclusive and did not meet the standards for inclusion in the 2012 guidelines. [40] However, hypertonic saline solution is another osmotic agent that may be used to manage high ICP.

CBF is known to be diminished in the first 24 hours in patients who have sustained severe TBI, with absolute values close to those seen in ischemia.

Hyperventilation reduces ICP by producing hypocapnia-induced cerebral vasoconstriction and a reduction in CBF and cerebral blood volume, resulting in a decrease in ICP. However, hyperventilation may decrease cerebral oxygenation and may induce brain ischemia. In addition, after TBI, the CBF response to changes in PaCO2 can be unpredictable.

Avoidance of prophylactic severe hyperventilation to a PaCO2 of less than 30 mm Hg may be considered in the initial 48 hours after injury. If hyperventilation is used in the management of refractory intracranial hypertension, advanced neuromonitoring for evaluation of cerebral ischemia may be considered. [40] The opposite, hypoventilation, must also be avoided; eucapnia should be the upper limit of the PaCO2 (partial pressure of carbon dioxide) goal.

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. [40]

Bleeding management

Disseminated intravascular coagulopathy (DIC) is present in one third of head trauma patients. Aggressive management of DIC and correction with replacement factors (including fresh frozen plasma, cryoprecipitate, and/or platelets) are required to decrease the risk of further intracranial bleeding and allow surgical intervention when necessary. The administration of recombinant factor VIIa in patients with severe coagulopathy secondary to traumatic brain injury may allow more rapid correction of DIC and may reduce mortality. [47]

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) or phenytoin/fosphenytoin may be used for initial seizure control, and phenytoin or phenobarbital may be used for maintenance anticonvulsant therapy.

While not indicated in all patients, prophylactic treatment with phenytoin or fosphenytoin may be considered to reduce the incidence of early posttraumatic seizures (PTS) in pediatric patients with severe TBI. [40]

Temperature control

In general, hyperthermia in patients with TBI and increased ICP should be avoided and treated promptly, as hyperthermia increases intracranial blood volume and pressure and is implicated in increased secondary posttraumatic injury.

However, the use of therapeutic hypothermia remains controversial. Although initial studies suggested reduced ICP in patients with TBI who had been treated with moderate hypothermia (core body temperature 32-33°C, beginning within 8 hours, and continued for up to 48 hours), the “Cool Kids” trial of hypothermia in pediatric TBI was halted secondary to futility. [40]

Analgesia, sedation, and neuromuscular blockade

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, as neuromuscular blockade eliminates the motor signs of seizures.

Etomidate may be considered to control severe intracranial hypertension; however, the risks resulting from adrenal suppression must be considered.

In the absence of outcome data, the specific indications and the choice and dosing of analgesics, sedatives, and neuromuscular-blocking agents used in the management of infants and children with severe TBI should be left to the treating physician. In addition, as stated by the Food and Drug Administration, continuous infusion of propofol for either sedation or refractory intracranial hypertension in infants and children with severe TBI is not recommended. [40]

Barbiturate therapy lowers the ICP and exerts cerebral protection through the following 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, exerting beneficial effects on ICP and global cerebral perfusion.

High-dose barbiturate therapy may be considered in hemodynamically stable patients with refractory intracranial hypertension despite maximal medical and surgical management. When high-dose barbiturate therapy is used to treat refractory intracranial hypertension, continuous arterial blood pressure monitoring and cardiovascular support to maintain adequate cerebral perfusion pressure are required. [40]

Continuous EEG (to achieve burst-suppression pattern) or bispectral index (BIS) monitoring (target range, 6-20) are required to allow titration of barbiturate therapy.


Surgical Decompression and Elevation

Surgical decompression is required in the presence of a rapidly expanding epidural or subdural hematoma that causes an increase in intracranial pressure (ICP) and focal compression. Surgical decompression should also be considered in patients with focal traumatic brain injury (TBI) and refractory intracranial hypertension with a potentially salvageable brain.

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 mental status, 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.

Decompressive craniectomy (DC) with duraplasty, leaving the bone flap out, may be considered for pediatric patients with TBI who are showing early signs of neurologic deterioration or herniation or are developing intracranial hypertension refractory to medical management during the early stages of their treatment. [40]