# Paediatric Stroke > Paediatric stroke for NEET-PG Paediatrics: arteriopathy, sickle cell transfusion, moyamoya, iron deficiency in cyanotic CHD and management notes. - Canonical URL: https://prepelephant.com/topics/neet-pg/paediatrics/paediatric-stroke - Exam / course: NEET-PG · Subject: Paediatrics - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Paediatric Stroke", PrepElephant, https://prepelephant.com/topics/neet-pg/paediatrics/paediatric-stroke ## Direct answer Stroke in children is rare — arterial ischaemic stroke affects roughly 1-2 per 100,000 children yearly, with perinatal stroke commoner near 1 in 3,000-4,000 live births — but its cause profile is nothing like the adult's: childhood stroke is driven by cerebral arteriopathy, congenital heart disease and cardioembolism, sickle cell anaemia, meningitis and varicella, dehydration and prothrombotic states, not atherosclerosis. A hemiparesis in a previously well child, or a neonate with focal seizures, is the recognisable stem. Management differs from adult practice in two exam-defining ways: thrombolysis is not standard care in children outside trials, and cause-directed therapy leads — exchange transfusion holding haemoglobin S below 30% in sickle cell, aspirin 3-5 mg/kg for most, and revascularisation for moyamoya. ## What you must remember - **Cause hierarchy:** arteriopathies (focal cerebral arteriopathy, dissection, moyamoya), cardiac disease with right-to-left shunting or post-surgery, sickle cell anaemia (stroke risk up to about 11% by age 20 without screening), infection (bacterial meningitis, post-varicella arteriopathy) and head or neck trauma with dissection. - **Sickle cell protocol:** annual transcranial Doppler screening; velocities of 200 cm/s or more in the middle cerebral artery or internal carotid trigger chronic transfusion programmes to hold haemoglobin S below 30%; an acute stroke in sickle cell is treated with exchange transfusion, not thrombolysis. - **Moyamoya associations:** progressive bilateral stenosis with collaterals ("puff of smoke" on angiography), linked with Down syndrome, neurofibromatosis type 1, sickle cell and prior cranial irradiation; treated by revascularisation surgery such as EDAS. - **Acute imaging logic:** vascular imaging (magnetic resonance or computed tomography angiography) accompanies the brain study from the outset, because arteriopathy is both common and treatable; never perform lumbar puncture before imaging in the stroke child. - **Antiplatelet rule:** aspirin 3-5 mg/kg/day for most survivors of arterial ischaemic stroke; anticoagulation reserved for cardioembolic stroke, arterial dissection and venous sinus thrombosis. - **Cyanotic paradox:** polycythaemia is blamed, but iron deficiency with microcytosis independently raises stroke and thrombosis risk in cyanotic heart disease — check indices and replete iron. - **Perinatal stroke:** presents in the first days with focal seizures or later with early hand preference and hemiparesis; most are arterial or sinovenous, and recurrence risk is low. ## Working through a hemiplegic child A three-year-old develops right-sided weakness and slurred speech six hours after a febrile illness; varicella two months earlier is remembered by the mother. The pathway: stabilise and image urgently (magnetic resonance imaging with angiography — the angiographic sequences are not optional, since a unilateral focal arteriopathy of the terminal internal carotid and proximal middle cerebral artery is what post-varicella arteriopathy looks like), and run the stroke panel in parallel — echocardiography, sickle screening, anaemia and iron studies, and inflammatory markers. Acute thrombolysis is withheld (off-label in children and unproven), and the child receives aspirin 3-5 mg/kg after haemorrhage is excluded. Rehabilitation starts on day one, and follow-up angiography at three to six months documents whether the arteriopathy stabilises or progresses toward moyamoya. The sickle child runs a different protocol: urgent exchange transfusion, hydration and oxygen for the ictus, then a long-term transfusion programme with iron chelation. ## Where students slip The commonest transplant error is adult reflexes: thrombolysis within 4.5 hours is the adult answer, and the expected paediatric answer is imaging plus vascular study, cause-directed therapy and aspirin. The second slip is the sickle cell branch: exchange transfusion (HbS under 30%) for the acute event, and the transcranial Doppler 200 cm/s threshold for primary prevention, are the scored facts. The third is the iron paradox — the cyanotic child with a stroke and mean corpuscular volume in the 60s needs iron, not phlebotomy logic. Viva examiners round off with venous sinus thrombosis: a dehydrated child or one with mastoiditis developing headache with papilloedema and seizures, imaged with magnetic resonance venography and anticoagulated — the one paediatric stroke where anticoagulation is routine. ## Frequently asked questions ### What causes arterial ischaemic stroke in children? Cerebral arteriopathy, congenital heart disease with cardioembolism, sickle cell anaemia, meningitis and post-varicella arteriopathy, dissection after trauma, and prothrombotic states — atherosclerosis is essentially absent. ### How is stroke in sickle cell disease prevented and treated? Annual transcranial Doppler with chronic transfusion for velocities of 200 cm/s or more; acute stroke receives urgent exchange transfusion holding haemoglobin S below 30%, not thrombolysis. ### Is thrombolysis used in paediatric stroke? Not as standard care; it remains unproven and off-label in children, whose management is cause-directed with aspirin 3-5 mg/kg/day for most arterial ischaemic strokes. ### What is moyamoya disease? A progressive stenosis of the terminal internal carotid arteries with collateral "puff of smoke" vessels, associated with Down syndrome, neurofibromatosis 1 and sickle cell, treated with revascularisation surgery. ### Why check iron status in a child with cyanotic heart disease and stroke? Iron-deficiency microcytosis independently increases stroke and thrombosis risk even in cyanotic children, so identifying and treating it is protective.