Inspection for external trauma, such as scalp or facial swelling, abrasions, laceration, or ecchymosis, can indicate TBI. Palpable step-off or depression indicates skull fracture, which may be associated with contusion of the brain, laceration of the dura or brain, and cerebrospinal
fluid (CSF) leak. Significant scalp swelling in the infant may be indicative of hemorrhage, which can cause anemia with pallor and tachycardia. A basilar skull fracture at the base of the anterior fossa causes “raccoon’s eyes,” or periorbital ecchymoses and can be associated with rhinorrhea (CSF leak from the nares). Fracture in the base of the middle fossa causes “battle sign,” or postauricular ecchymoses, and can be associated with otorrhea (leak of CSF from the ear). Hemotympanum can indicate temporal or basilar skull fracture. Otorrhea indicates disruption of the tympanic membrane related to temporal skull fracture. The cervical spine must be immobilized and protected from spinal cord injury until radiographic clearance is accomplished. The entire spine is immobilized, inspected, and palpated for deformity, swelling, tenderness, and crepitance.
Every patient assessment must begin with evaluation of adequate airway, breathing, and circulation, which are vital to sustain life. A decreased level of consciousness (LOC) after TBI can interfere with protection of the pediatric airway. Inadequate ventilation results in hypercarbia and hypoxia, which cause vasodilation and secondary ischemic brain injury. Vasodilation and resultant ischemia contribute to further increases in ICP. Vital control centers located within the brainstem regulate respiratory and cardiac functions. Brainstem pathophysiology can be identified by changes in the vital signs. The following abnormal respiratory rate and patterns indicate neurologic dysfunction secondary to progressive brainstem compression as a result of increasing ICP:
1. Cheyne-Stokes: repeated cycles of breaths that gradually increase and decrease in rate and depth, followed by a respiratory pause – indicates bilateral hemispheric or diencephalic injury.
2. Central Neurogenic Hyperventilation: increased rate and depth of respirations – indicates midbrain/ upper pons injury.
3. Apneustic: a pause at full or prolonged (slow and deep) inspiration – indicates injury to the upper pons.
4. Ataxic: no pattern in rate or depth – indicates medulla or lower brainstem dysfunction with impending herniation; injury to the respiratory centers in the medulla (also known as agonal respirations).
5. Apnea: respirations cease.

The child’s LOC, and whether it is worsening or improving, is the most important indicator of neurologic status. The neurologically intact child is awake, alert, and responsive to his/her surroundings. Level of responsiveness varies with the developmental age of the child. Infants should respond to feeding and measures to console them. Toddlers and older children should recognize and respond to their parents. Older children and adolescents should be able to follow commands. Children of all ages should respond to and withdraw from painful stimulus. After neurologic injury, pediatric head-injured victims may have alteration in LOC, first subtly, becoming restless, disoriented, and confused. Further decreases in the LOC leads to somnolence (arouses to full consciousness and resumes sleep if not stimulated), lethargy (requires vigorous stimulation to arouse to full consciousness), stupor (nearly unconscious, may moan or withdraw from pain), and finally comatose (unresponsive). A worsening LOC suggests neurologic deterioration. Any subtle change from documented baseline, including parent’s concern that child is “not acting right,” must be taken seriously and reported to the physician.