Stroke in Children

Identification and treatment of the underlying risk factors for stroke reduce the potential for additional strokes; therefore, a thorough search for treatable risk factors is justified. Because some risk factors can have a cumulative effect, even children with known risk factors for stroke sometimes need to be evaluated for other conditions. Cerebral angiography is often helpful; I recommend angiography in any child with an unexplained infarction or hemorrhage. Angiography is especially important in children with intraparenchymal hemorrhage because more than one third of such children will prove to have some type of potentially treatable congenital vascular anomaly such as an arteriovenous malformation (AVM) or aneurysm. The evidence that periodic blood transfusion effectively prevents cerebral infarction due to sickle cell disease is compelling. Transfusions apparently must be continued indefinitely to maintain the reduction of stroke risk, and without iron chelation, chronic transfusion eventually results in severe iron toxicity and, most likely, death, so the decision to begin transfusion is not an easy one. Measurement of the time-averaged mean flow velocity in the large cerebral vessels with transcranial Doppler (TCD) is highly predictive of stroke risk in these children, enough to justify its routine use in screening patients with sickle cell disease for stroke risk. I believe that patients with sickle cell disease should be offered chronic transfusion after an initial large-vessel stroke or when the TCD results suggest a high risk of stroke. The family must be made aware of the serious complications of chronic transfusion and the importance of complying with chelation once it is started. There are no controlled clinical trials to guide the use of anticoagulants, antiplatelet agents, or thrombolytic agents in children, although these drugs are being used more and more often in pediatric patients. For the most part, our approach has been adapted from our experience with adults. Heparin followed by warfarin is often used for sinovenous thrombosis and for arterial dissection. I also suggest long-term anticoagulation for children with coagulopathy or a high risk of embolism due to congenital or acquired cardiac disease. It is reasonable to use a thrombolytic agent in children with an acute infarction; because few children present soon enough after the onset of symptoms, however, thrombolysis is infrequently used. Aspirin is used more than other antiplatelet agents in children, largely because of years of experience with aspirin and the lack of evidence that other agents are more effective. Despite its frequent use, there are no unequivocal indications for the use of aspirin in children. Aspirin is often started empirically in children suspected to be at substantial risk for additional ischemic stroke but whose risk is ill defined, an approach not too dissimilar from that often used in adult patients. Although the risk of Reye's syndrome in a child taking daily aspirin for stroke prevention is a common concern, I know of no published examples of children who developed Reye's syndrome while taking prophylactic aspirin. This apparently low risk must be weighed against the often-considerable risk of ischemic stroke that could be reduced by the use of daily aspirin. In situations such as vasculopathy or infarction of unknown cause, the small risk of Reye's syndrome seems acceptable.