Paediatric Stroke
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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.