Paediatric stroke and cerebral sinovenous thrombosis: SAQ

This boy has an acute arterial ischaemic stroke in the left middle cerebral artery territory. The sudden onset of a right hemiparesis with facial involvement and dysarthria, the recent viral illness, and the normal glucose all point to a focal cerebral arteriopathy as the likely cause, which is the commonest arteriopathy in this age group. The priority is to confirm the vascular anatomy with MRA, to exclude a haemorrhage, to start supportive care, and to initiate antithrombotic therapy. [2][7]

Question 1 (10 marks)

Outline the acute management of this boy from the moment of arrival, including the investigations you would request and the therapy you would start. [2]

I would apply the stroke alert pathway. On arrival I would assess and support the airway, breathing, and circulation, confirm the bedside glucose is normal at 5.8 millimoles per litre, and establish the exact time of onset, which was about thirty minutes ago. I would activate the stroke alert, notify the paediatric neurology and radiology teams, and perform a focused neurological examination to localise the deficit to the left middle cerebral artery territory, which the findings confirm. [3]

The imaging is the next priority. The MRI brain with diffusion-weighted imaging has already shown the acute infarct. I would request a magnetic resonance angiography to visualise the arterial tree and identify the arteriopathy, because the arteriopathy is invisible on a plain MRI and its identification is essential for the recurrence risk assessment. I would request a magnetic resonance venography to exclude a concurrent venous thrombosis, and I would ensure a haemorrhage is excluded on the diffusion and the gradient-echo sequences before starting any antithrombotic therapy. [3]

The acute therapy is supportive care with antithrombotic therapy. I would maintain normoglycaemia, normothermia, and normoxia, because fever and metabolic disturbance extend the infarct. I would treat any seizures with standard anticonvulsants and keep the child nil by mouth until the swallow is assessed. Once the haemorrhage is excluded, I would start aspirin at 1 to 5 mg per kg per day for secondary prevention, because this is the standard for most non-cardioembolic childhood arterial ischaemic strokes. I would send blood for a full blood count, coagulation studies, electrolytes, and a lipid profile, and I would request an echocardiogram and an electrocardiogram to seek a cardioembolic source. [2][12]

I would not routinely give intravenous thrombolysis, because the American Heart Association does not recommend routine intravenous alteplase for children outside a clinical trial. The Thrombolysis in Pediatric Stroke trial could not establish efficacy, and children achieve lower systemic alteplase levels than adults at the standard dose. I would admit the boy to the paediatric ward or the paediatric intensive care unit, depending on his level of consciousness and his seizure risk, and I would involve the rehabilitation team from the outset. [5][2]

Question 2 (10 marks)

Discuss the role of the arteriopathy workup and serial imaging in this boy, the evidence for the choice of antithrombotic therapy, and how you would counsel the family about the recurrence risk and the follow-up. [7]

The arteriopathy workup is central to this boy's management because the arteriopathy is both the likely cause and the strongest predictor of recurrence. The MRA on presentation would show the arterial tree, and in a boy with this presentation the likely finding is a focal cerebral arteriopathy of childhood, a unilateral narrowing of the terminal internal carotid and proximal middle cerebral artery. Fullerton and colleagues showed that focal cerebral arteriopathy is dynamic, worsening over the first days to weeks, and that a severity score predicts the outcome. I would repeat the MRA at one to two weeks and again at three to six months to track the arteriopathy, because the evolution guides the duration of the secondary prevention and the assessment of the recurrence risk. [7]

The choice of antithrombotic therapy rests on the cause. For most non-cardioembolic strokes, including this boy's, aspirin 1 to 5 mg per kg per day is the standard secondary prevention. If the echocardiogram or the workup revealed a cardioembolic source, an arterial dissection, or a documented prothrombotic condition, I would switch to anticoagulation with low-molecular-weight heparin. The secondary prevention framework reported by Darteyre and colleagues emphasises that the cause search guides the drug choice and the duration, and that every childhood stroke needs a structured follow-up plan. [12][2]

I would counsel the family in honest terms at each stage. I would explain that their son has had a stroke, which is a blockage of a blood vessel to part of the brain, that the weakness in his right arm and face came from it, and that the team has taken a picture of the blood vessels to find the cause. I would explain that the likely cause is an inflammation of the artery wall that followed his viral illness, that the medicine called aspirin will thin the stickiness of the platelets to lower the chance of another clot, and that the team will repeat the scan of the blood vessels over the coming weeks to watch the artery heal. I would state that the risk of another stroke is between fifteen and twenty-five percent, that the team will work to lower it, and that the rehabilitation will start now and continue as he recovers. I would arrange a follow-up in the paediatric neurology clinic, connect the family to the rehabilitation and educational support services, and provide a clear plan for what to do if the symptoms recur. [3][12]