The measurement of blood pressure is now firmly established as an important component of the routine pediatric physical examination. Nevertheless, blood pressure in children has been given serious attention only since the mid-1960s. The first report of the Task Force on Blood Pressure Control in Children was published in 1977. The long-term natural history of blood pressure in children is not well understood. Norms for blood pressure and definitions of hypertension were revised and strengthened by the second task force report, published in 1987, and a recent revision contains modified recommendations and norms.
The prevalence and rate of diagnosis of hypertension in children and adolescents appear to be increasing. This is due in part to the increasing prevalence of childhood obesity as well as growing awareness of this disease. There is evidence that childhood hypertension can lead to adult hypertension. Hypertension is a known risk factor for coronary artery disease (CAD) in adults, and the presence of childhood hypertension may contribute to the early development of CAD. Reports show that early development of atherosclerosis does exist in children and young adults and may be associated with childhood hypertension.
Because body size is an essential determinant of blood pressure in children, it is necessary to include the child’s height percentile to determine if blood pressure is normal. The revised childhood blood pressure tables include 50th, 90th, 95th, and 99th percentiles by sex, age, and height based on the 1999-2000 National Health and Nutrition Examination Survey data.
Dr. Sinaiko’s review of hypertension in children (Dec. 26 issue) includes a recommendation to use oral nifedipine capsules for urgent or emergency treatment of hypertension. Dr. Sinaiko states, “For rapid absorption the drug must first be removed from the capsule or the patient must bite through the capsule.” The sublingual absorption of nifedipine is negligible, whereas absorption from the gastrointestinal tract is complete. Removing the drug from the capsule is often associated with unintentional losses, such as spillage or loss from the mouth, which make the dose of the drug administered uncertain. A significant decline in blood pressure is typically observed 5 to 10 minutes after oral administration of the short-acting capsule, with the peak effect occurring between 30 and 60 minutes. The 1996 product label for Procardia states, “There is little difference in relative bioavailability when . . . capsules are given orally and either swallowed whole; bitten and swallowed; or, bitten and held sublingually.”
Furthermore, in adults with severe elevations in blood pressure, nifedipine has been reported to cause cerebral ischemia, myocardial ischemia, and symptomatic hypotension. Preexisting myocardial ischemia, hypovolemia, or coronary artery disease seems to predispose patients to these events. However, asymptomatic patients without end-organ damage have also had signs and symptoms of ischemia when treated with oral or sublingual nifedipine. In 1985 the Cardiorenal Advisory Committee of the Food and Drug Administration rejected the use of short-acting nifedipine capsules given orally or sublingually for hypertensive emergencies, because of the lack of outcome data and the possibility of adverse effects. The use of nifedipine in children was not specifically addressed in the advisory committee’s decision, but one wonders whether the very small number of children requiring urgent or emergency treatment to lower blood pressure provides a sufficient basis for making a judgment about the safety of nifedipine. The potential for harm would seem to outweigh the potential benefits, considering the proven safety and efficacy of the alternative therapies described by Sinaiko.
Patricia M. Flint, Pharm.D.
Donald B. Middleton, M.D.
St. Margaret Memorial Hospital
Pittsburgh, PA 15215
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