Head Trauma

Oluwakemi B. Badaki-Makun

Joel A. Fein

INTRODUCTION

Head injury in children accounts for up to 650,000 emergency department visits, 95,000 hospitalizations, and 7,400 deaths per year. It is the most significant cause of morbidity and mortality in pediatric trauma patients. The highest injury rates are found in children <4 years. Brain injuries can be subdivided into primary and secondary injuries. Primary injuries occur as a result of a mechanical damage at the time of insult and can be from direct trauma to the brain or shear forces experienced by the neuronal axons as a result of acceleration-deceleration injury. These injuries are usually irreversible. Fatal or irreversible injury is usually a sequela of neuronal cell death and vascular disruption during the first few milliseconds of impact. Secondary brain injuries result from subsequent pathophysiologic changes such as hypoperfusion, hypoxia, edema, and metabolic derangements. The only injuries that are reversible with therapy are those with secondary effects on the brain and blood vessels, such as cerebral edema and impaired glucose and oxygen delivery to the neurons.

DIFFERENTIAL DIAGNOSIS LIST

Focal Injuries

Scalp lacerations
Hematoma (subgaleal, subdural, epidural)
Cerebral contusion
Fractures

Diffuse Injuries

Concussion syndrome
Diffuse axonal injury
Increased intracranial pressure (ICP)

DIFFERENTIAL DIAGNOSIS DISCUSSION

Scalp Lacerations

Scalp lacerations are common findings in patients with head injuries. Blood loss can be extensive, especially in infants and young children, given the high vascularity of the scalp. The physician should apply direct pressure to stop local bleeding, carefully assess the depth of the wound, and evaluate it for retained foreign bodies. In addition, the integrity of the galea aponeurotica (a tendinous sheath located just above the periosteum) should be evaluated; attention to careful reapproximation of this layer often results in better hemostasis and easier closure of the laceration. Finally, the physician should search for skull fractures or “step-offs” (dents).

Hematomas

Hematoma caused by head injury may exist outside of the confines of the skull (e.g., cephalohematoma, subgaleal hematoma) or inside the skull (e.g., epidural or subdural hematoma). Intracranial lesions may require neurosurgical intervention, whereas extracranial lesions rarely require any treatment other than supportive care.

Cephalohematoma

Newborn infants commonly incur a cephalohematoma, in which blood collects between the periosteum and the table of the skull and is therefore prevented from spreading past the midline. This type of injury is common in traumatic deliveries.

Subgaleal Hematoma

A posttraumatic, well-circumscribed “lump” on an older child’s head usually represents a subgaleal hematoma.

Epidural and Subdural Hematomas

Epidural hematomas are less often associated with underlying brain injury than are subdural hematomas (Table 37-1).

Subarachnoid Hemorrhage

Common in more severely injured patients, subarachnoid hemorrhage (SAH) results from shearing of small vessels in the pia mater. It is usually associated with other intracranial injuries. Due to the location of the bleed, SAH causes meningeal irritation and the clinical symptoms can mimic meningitis.

Cerebral Contusions and Lacerations

Cerebral contusions are bruises of the cortex and can occur as a coup injury (at the contact location) or as a contre-coup injury (rebounding, on the opposite side). Late intraparenchymal hematomas may occur.

Cerebral lacerations usually result from penetrating injury to the brain or from a depressed skull fracture. The clinical manifestations are more often a result of the associated concussion and the underlying brain injury than of the focal lesions themselves.

Skull Fractures

A significant proportion of children seen in emergency departments with head injury have skull fractures. Infants and children with trauma to the parietal area are at higher risk.

Linear Skull Fractures

Linear skull fractures comprise 75% to 90% of all skull fractures. Usually no treatment is necessary. However, if the fracture is located over a vascular structure (e.g., the middle meningeal artery), there is an increased incidence of epidural hemorrhage. Diastatic (“growing”) fractures can develop when meninges get caught between the bone edges and continue to separate them.

TABLE 37-1 Epidural Versus Acute Subdural Hematoma

	Epidural Hematoma	Subdural Hematoma
Common mechanism	Blunt direct trauma, frequently to parietal or temporal regions, lower forces	Acceleration-deceleration injury, direct trauma, higher forces
Etiology	Arterial or venous (bleed between skull and dura)	Venous (bridging veins between dura and arachnoid membranes)
Incidence	Uncommon	Common
Peak age	Usually >2 yr	Usually >1 yr, peak at 6 mo
Location	Unilateral, commonly parietal	75% Bilateral, diffuse, over cerebral hemispheres
Skull fracture	Common	Uncommon
Associated seizures	Uncommon	Common
Retinal hemorrhages	Rare	Common
Decreased level of consciousness	Common	Almost always (50% present in coma)
Mortality	Rare	Uncommon
Morbidity in survivors	Low	High, due to associated underlying brain injury
Other clinical findings	Dilated ipsilateral pupil, contralateral hemiparesis	Decreased level of consciousness
	Period of lucidity prior to acute decompensation and rapid progression to herniation (only 20%)	Headaches, irritability, emesis
Onset	Acute	Acute (within 24 hr), subacute (within 1 d to 2 wk), or chronic (after 2 wk)
Findings on computed tomography	Lentiform “lens-shaped,” usually not crossing suture lines	Lunar “crescent shaped,” often not crossing midline (due to falx cerebri)