11.1 Traumatic Brain Injury & Intracranial Hemorrhage

Why Pediatric TBI Is Different

Traumatic brain injury (TBI) remains a leading cause of death and acquired disability in children. Mechanisms differ by age: falls and non-accidental trauma dominate in infants and toddlers; motor-vehicle collisions, bicycle injuries, and sports predominate in school-age children and adolescents. The pediatric skull is thinner, the head-to-body ratio is larger, and myelination is incomplete, so the same impact energy produces more deformation and more diffuse axonal injury than in adults. Open fontanelles and unfused cranial sutures allow limited volume buffering, which can delay classic adult herniation signs — but that buffering is not protective. Infants can accumulate substantial intracranial volume before decompensation, then deteriorate abruptly.

On the AACN CCRN Pediatric exam, items almost always test secondary injury prevention: avoid hypoxia, hypotension, hypercarbia, fever, seizures, and uncontrolled intracranial hypertension. Primary injury has already occurred; nursing actions determine how much secondary ischemic and cytotoxic damage follows.

Severity Grading and Airway Thresholds

Severity is graded with the Glasgow Coma Scale (GCS):

A GCS of 8 or less is the classic cue to secure a definitive airway (less than eight, intubate), because protective airway reflexes are unreliable and hypoventilation rapidly raises PaCO2 and cerebral blood volume. Use age-appropriate GCS modifications for preverbal children (eye, verbal/grimace, motor). Document the best motor response carefully — it drives both GCS and prognosis discussions.

ICP Physiology and Age-Specific Signs

The Monro-Kellie relationship still applies: intracranial volume is shared among brain, blood, and cerebrospinal fluid (CSF). An expanding hematoma or edema raises intracranial pressure (ICP) once compensatory CSF and venous shifts are exhausted. Normal pediatric ICP is often cited near 3–15 mmHg; sustained elevations above approximately 20 mmHg are commonly treated, guided by institutional protocol and neurosurgery.

Cerebral perfusion pressure remains:

CPP = MAP − ICP

Targets are age-dependent. Broad exam-level ranges: infants often aim for CPP near ≥40–50 mmHg, younger children ≥50–60 mmHg, and adolescents nearer adult ≥60 mmHg. Chasing adult CPP numbers in an infant with aggressive fluids and vasopressors can cause pulmonary edema without improving outcome.

Cushing’s triad — hypertension with widening pulse pressure, bradycardia, and irregular respirations — is a late herniation warning in every age group. Do not wait for it to escalate care. A unilaterally dilated, poorly reactive pupil with declining motor exam is an emergency requiring immediate notification, airway security, and ICP-lowering measures per protocol.

Intracranial Hemorrhage Patterns

Recognizing hemorrhage type guides urgency and differential diagnosis:

Epidural hematoma can look deceptively well after injury (lucid interval) before arterial bleeding expands and consciousness collapses — serial exams matter as much as the first GCS. Acute subdural hematoma in an infant without a clear high-energy mechanism should trigger a careful, protocolized evaluation for abusive head trauma, including retinal exam and skeletal survey when indicated by the team — nursing’s role is meticulous documentation of history inconsistencies, bruise patterns, and neuro changes, not making the legal diagnosis alone.

Nursing Interventions That Prevent Secondary Injury

Position the child with head of bed elevated about 15–30 degrees and the neck midline to promote venous drainage; avoid jugular compression from tight ties or extreme rotation. Maintain normoxia and avoid both hypoxia and unnecessary hyperoxia. Target normocapnia for most patients; brief controlled hyperventilation is reserved for acute herniation rescue, not routine care, because hypocapnia vasoconstricts and can worsen ischemia. Support blood pressure to meet age-appropriate CPP goals — hypotension is independently linked to worse TBI outcomes.

Osmotherapy (mannitol or hypertonic saline per order) reduces brain water and can buy time for imaging or operative decompression. Watch for hypotension after mannitol diuresis and for rising sodium with hypertonic saline. Treat fever aggressively; each degree of hyperthermia increases cerebral metabolic demand. Control pain and agitation without oversedation that masks the exam — coordinate sedation holidays with the team when ICP is stable. Seizure prophylaxis decisions are neurosurgery- and protocol-driven; untreated clinical or electrographic seizures raise metabolic demand and ICP.

When an external ventricular drain (EVD) is present, maintain the prescribed leveling landmark, keep the system patent, and never arbitrarily flush or change height without an order. CSF drainage is both a diagnostic ICP tool and a therapy. Continuous or frequent neuro checks, paired with ICP/CPP trends when monitored, let you detect plateau waves and herniation early enough to intervene.

Putting It Together for the Exam

Expect scenario items that combine an age-specific sign (bulging fontanelle in a 6-month-old) with a physiology question (CPP calculation) or a hemorrhage pattern (lucid interval → epidural). Prioritize airway, oxygenation, perfusion, and venous drainage before advanced pharmacologic ICP therapy. Document trends — a falling GCS motor score or a newly asymmetric pupil is more actionable than a single static number.