Head Trauma in Children
Nicholas Cortolillo
John H. Kimball
Caroline R. Deyoe
Jessica L. Buicko
Head injuries account for a significant number of injuries in the pediatric population, resulting in over 300 000 pediatric hospitalizations annually.1
Almost 90% of injury-related deaths in children are associated with head trauma.
Falls and motor vehicle crashes are the two most common mechanisms for injury.2
The American Association of Neurological Surgeons defines traumatic brain injury (TBI) as a blow or jolt to the head or penetrating head injury that disrupts the normal function of the brain.1
RELEVANT ANATOMY AND PHYSIOLOGY
Primary brain injury refers to immediate physical damage as a result of shear forces.
Secondary brain injury refers to delayed endogenous cytotoxic injury to brain tissue.
Inflammatory cytokines released after structural damage induce harmful changes on the cellular level, manifesting with microvascular dysfunction leading to both cerebral edema and ischemia.
Systemic factors, such as hypotension and hypoxia, can potentiate this cascade and cause neurons to necrose.
Several anatomical factors exacerbate the severity of TBI in children.
Pediatric patients have thinner bones, larger head-to-toe ratio, less myelinated tissue, and late development of air sinuses.2
Skull fractures in a pediatric patient suggest massive transfer of energy, and TBI should be suspected.3
The brain reaches 80% of adult brain size by age 2 years; this reduces the subarachnoid space and leads to less of a fluid cushion for the brain to be suspended and protected in the skull.3
Underdeveloped neck musculature and higher relative head weight translates to increased head velocity and momentum in children.3
EPIDEMIOLOGY AND ETIOLOGY
Head injury in children occurs in a bimodal distribution; most frequent hospitalizations for TBI are in age groups 0 to 4 and 15 to 19 years, according to Centers for Disease Control and Prevention (CDC) data.4
For ages 0 to 4 years, falls represent the most common mechanism (more than 40%), followed by motor vehicle accidents (MVAs) and assault.4
This trend continues into early teen years, when MVA replaces falls as the most common mechanism of TBI, followed by assault.4
INITIAL EVALUATION: HISTORY
Includes both timing and mechanism: fall, drop, collision, blow to head, MVA.
Any delay in presentation is cause for concern and warrants evaluation to exclude nonaccidental cause of injury.
Also, discrepancies between the story and extent of injury are suspicious for abuse.
Condition immediately after injury: loss of consciousness vs immediate cry.
Condition since the injury: alertness, eating, vomiting, seizures, neurologic deficits (motor exam most crucial).
CLINICAL PRESENTATION
Patients may present with loss of consciousness or vomiting.
Younger children may show signs of irritability or lethargy.
Patients may complain of worsening headache or amnesia.
Impact seizures after injury are seen more frequently in children, and although usually self-limited, require a computed tomography (CT) of the head.
DIAGNOSTIC IMAGING
CT scan is the imaging modality of choice when imaging is indicated.
Patients with a skull fracture or other high-risk clinical findings should receive a head CT.8
High-risk clinical findings:
Focal neurologic findings; motor examination is the best indicator of prognosis
Seizure
Persistent altered mental status
Prolonged loss of consciousness
Long-term radiation risk of cranial CT scan in the pediatric population necessitates careful consideration of patient’s risk of having an intracranial injury.
MEDICAL AND SURGICAL MANAGEMENT
Rapid assessment of airway, breathing, circulation, disability, exposure (ABCDE)
Early endotracheal intubation through rapid sequence in patients who have a Glasgow coma score (GCS) of <8 (see Table 7.1), respiratory failure, or hemodynamic instability
Neurosurgical evaluation when warranted. Indications include
GCS 8 or less
Motor score 1 or 2
Multiple injuries associated with brain injuries such as major abdominal or thoracic injury and those needing major volume resuscitation
Imaging findings showing brain hemorrhage, cerebral swelling, transtentorial or cerebellar herniation3
Hyperventilation with PaCO2 <35 can induce cerebral ischemia, useful in setting of impending herniation
IV access to ensure adequate cerebral perfusion; use isotonic fluid to avoid cerebral edema9
COMMON INJURIES
Scalp injuries
The human SCALP consists of 5 layers. The Skin is the outer layer, followed by the Connective tissue, galea Aponeurotica, Loose areolar tissue, and Periosteum.5
The scalp is highly vascular and could be a source of substantial blood loss.
However, shock in a child secondary to blood loss from a scalp injury is a diagnosis of exclusion.
Subgaleal hemorrhage may produce up to 50% of blood volume loss in children and occurs due to rupture of emissary veins traversing the subgaleal space, allowing blood to dissect within the areolar plane and across cranial suture lines.5
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