12.2 Stroke, Brain Death & Space-Occupying Lesions

Pediatric Stroke: Arterial, Venous, and Hemorrhagic

Stroke in children is uncommon but under-recognized, and delayed diagnosis worsens outcomes. Unlike adults, pediatric arterial ischemic stroke (AIS) is rarely driven by atherosclerosis. High-yield etiologies include congenital or acquired heart disease with emboli, cerebral arteriopathy (including focal cerebral arteriopathy after infection), sickle cell disease, prothrombotic states, dissection after trauma, and meningitis/vasculitis. Children may present with sudden hemiparesis, facial droop, aphasia/dysarthria, seizure at onset, severe headache, or unexplained altered consciousness. Seizure at stroke onset is far more common in children than in adults and can mask the focal deficit.

Cerebral venous sinus thrombosis (CVST) presents with headache, papilledema, seizures, and encephalopathy, often in the setting of dehydration, infection (mastoiditis/otitis), or thrombophilia. Hemorrhagic stroke may result from arteriovenous malformation, aneurysm, coagulopathy, or tumor bleed and presents with sudden headache, vomiting, coma, or focal signs.

Acute PICU response

Treat pediatric stroke as a time-sensitive emergency. Priorities are airway protection, oxygenation, euthermia, glucose control, and blood pressure support within ordered parameters. Obtain urgent neuroimaging (CT to exclude hemorrhage, then MRI/MRA or institutional stroke protocol imaging). Activate the pediatric stroke team early. In sickle cell disease, exchange transfusion pathways may be indicated for AIS. Antithrombotic decisions are specialist-driven; nursing focuses on neurologic trend detection, aspiration prevention, DVT prophylaxis when appropriate, and family support through a terrifying diagnosis.

Secondary prevention depends on cause: cardiology evaluation, sickle cell disease-modifying therapy, anticoagulation for selected venous events, and rehabilitation starting in the PICU.

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Brain Death Determination: The PICU Nurse’s Role

Death by neurologic criteria (brain death) is the irreversible loss of all functions of the entire brain, including the brainstem. Pediatric determination follows consensus guidelines with age-specific observation intervals and two separate examinations by qualified physicians. Nursing does not declare brain death, but nursing care makes a valid exam possible and protects family trust.

Prerequisites the nurse helps verify

Before any brain death exam, reverse or exclude confounders:

• Normalize core temperature (hypothermia falsely depresses brainstem responses).
• Correct severe hypotension and ensure adequate perfusion.
• Clear sedatives, neuromuscular blockers, and metabolic toxins as much as possible; confirm train-of-four return after paralytics.
• Treat severe electrolyte, acid-base, and endocrine derangements that could mimic coma.

The clinical exam documents coma, absence of brainstem reflexes (pupils, corneal, oculocephalic/oculovestibular as appropriate, gag/cough), and apnea. Apnea testing requires preoxygenation, continuous monitoring, and observation for any respiratory effort while PaCO2 rises to the protocol threshold. Abort the test for instability (desaturation, hypotension, arrhythmia) and restore ventilation. Ancillary tests (EEG, cerebral blood flow studies) are used when the clinical exam cannot be completed fully.

Nursing responsibilities include meticulous documentation, coordination of exam timing, advocacy for quiet respectful care, preparation for organ donation conversations led by trained requestors, and ongoing family presence support. Use clear, consistent language with the care team. Avoid implying uncertainty once criteria are met, and avoid rushing families through decision points.

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Brain Tumors and Other Space-Occupying Lesions

Pediatric brain tumors differ from adult patterns. Posterior fossa tumors (medulloblastoma, cerebellar astrocytoma, ependymoma) are common in children and can obstruct CSF flow at the fourth ventricle, producing acute hydrocephalus. Brainstem gliomas cause cranial nerve deficits and long-tract signs. Supratentorial masses may present with seizures, hemiparesis, or personality change. Any expanding mass — tumor, abscess, hematoma, or severe edema — creates mass effect: midline shift, cranial nerve compression, and herniation syndromes.

Classic warning signs of rising ICP or impending herniation include declining consciousness, Cushing triad (hypertension, bradycardia, irregular respirations), unilateral or bilateral pupil changes, posturing, and sudden vomiting. Infratentorial masses may decompensate with little warning because of limited posterior fossa compliance.

PICU management themes

• Protect airway early if Glasgow Coma Scale falls or bulbar function is impaired.
• Elevate head of bed as ordered, keep neck midline, and avoid jugular compression.
• Administer osmotic therapy, CSF diversion, and steroids per tumor/edema protocols.
• Prepare for operative resection, biopsy, or emergency EVD for obstructive hydrocephalus.
• After resection, watch for posterior fossa syndrome (mutism, emotional lability, hypotonia), CSF leak, infection, diabetes insipidus or other endocrine injury (especially after sellar/suprasellar surgery), and seizures.

Family teaching should address that personality or speech changes after posterior fossa surgery may be temporary but require structured rehab. Coordinate oncology, neurosurgery, endocrinology, and child life early.

Mass effect at the bedside

Think in terms of compliance and compensation. Children may look relatively stable until they suddenly are not. A new anisocoria, bradycardia with rising blood pressure, or extensor posturing is an emergency — call for help, support ventilation and blood pressure, and prepare for hyperosmolar therapy and operative intervention while continuing serial exams.