Hyperglycemia, Infarct Size Impact Outcomes in Pediatric Stroke

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Hyperglycemia, Infarct Size Impact Outcomes in Pediatric Stroke
Hyperglycemia, Infarct Size Impact Outcomes in Pediatric Stroke

Both hyperglycemia and infarct size are linked to poor neurological outcomes in pediatric patients with acute ischemic stroke, according to data published in JAMA Neurology1.

“Most physicians believe that hypertension and hyperglycemia are very uncommon in children and aren't important.  However, in my experience as a pediatric stroke neurologist, abnormal vital signs are actually very common after stroke in children,” Lori Jordan, MD, PhD, of the Department of Pediatric Neurology at Vanderbilt University Medical Center in Nashville, TN, told Neurology Advisor.

There is currently a lack of evidenced-based guidelines for temperature, blood glucose, and blood pressure management in pediatric patients with acute arterial ischemic stroke (AIS). To explore the prevalence of abnormal vital signs in pediatric patients with AIS and their potential impact on outcome, Dr Jordan and colleagues conducted a retrospective review at Vanderbilt Children's Hospital from 2009 to 2013. Measurements were collected for the 5 days following the AIS event and mortality and morbidity were documented at 3 months.

The study included 98 children with a median age of 6 years. In total, 11.2% (n=11) of participants died during the study (3 after discharge and 8 during the hospital stay). No deaths were primarily attributed to AIS. Stroke risk factors identified in the cohort included cardiac disease (51%), oncologic and hematologic diagnoses (25.5%), and systemic acute illness (19.4%).

Based on the stringent definition of hypertension applied in the study, 65.3% (n=64) of the participants had hypertension within the 5 days after AIS. Antihypertensives were required in 18 participants acutely and 29.9% (26/87) were discharged on antihypertensive medications.

Hypotension was common, with 68.4% (n=67) developing hypotension during hospitalization. Univariable analysis revealed an association between hypotension that required treatment and poor neurological outcome.

With the exception of one patient with type 1 diabetes who was excluded, hyperglycemia was observed in 18.1% of the participants with 3.2% requiring insulin treatment. Treatment with steroids was documented in 8 of the 17 patients with hyperglycemia. Fever was documented in 37.8% of the participants and treated in most cases. Overall, hypertension and fever were not found to be significantly associated with death, poor outcome, or infarct size. However, hyperglycemia was independently associated with worse neurological outcome (OR 3.9, 95% CI: 1.2-12.4, P=.02). Likewise, an infarct size of 4% or greater of the brain volume was associated with worse neurological outcome (OR 5.6, 95% CI: 2.0-15.4, P=.001).

“Further study is needed with a larger sample size and prospective and systematic measurement of blood sugar, blood pressure, and temperature,” Dr Jordan said. “If modification of these parameters does improve outcome, it would certainly be a straightforward treatment applicable to a large group of pediatric stroke patients.”

In an accompanying editorial2, Lauren Beslow, MD, MSCE, of the Department of Pediatrics and Neurology at Yale School of Medicine in New Haven, CT, pointed out that the American Heart Association's management recommendations for fever, hypertension, and glucose in pediatric AIS patients are based on expert opinion. With that being said, Dr Beslow recognized that the results suggest that abnormal vital signs in pediatric AIS may be more common than previously believed and echoed the need for prospective research.

References

  1. Grelli KN, Gindville MC, Walker C, Jordan LC. Association of Blood Pressure, Blood Glucose, and Temperature With Neurological Outcome After Childhood Stroke. JAMA Neurol. 2016; doi:10.1001/jamaneurol.2016.0992.
  2. Beslow LA. Back to Basics—Vital Sign and Blood Glucose Abnormalities and Outcome in Childhood Arterial Ischemic Stroke. JAMA Neurol. 2016; doi:10.1001/jamaneurol.2016.1054.
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