ACR Index: 8.9
Hypertension was first noted in neonates in the 1970’s. Since that time, the prevalence of hypertension in children has increased as formal diagnostic criteria have been defined by Zubrow et al (1995), and the Second Task Force (1996) of the National High Blood Pressure Education Program. Revised diagnostic criteria combined with advances in diagnostic imaging have afforded clinicians a more systematic approach in determining the precise etiology of hypertension in the pediatric population.
In general, hypertension affects an estimated 1-4.5% of children, with secondary hypertension being more common than primary hypertension. Of the children diagnosed with secondary hypertension, an estimated 3-5% have a renovascular etiology, with fibromuscular dysplasia being the most common cause. This is in stark comparison to the adult population, where primary (essential) hypertension is more common and renovascuar hypertension is most commonly due to atherosclerosis. It is paramount that all clinicians involved in the care of pediatric patients screen for, and appropriately address elevated blood pressure in order to minimize target-organ damage.
Hypertension in neonates can be the result of a diverse array of disease processes from renovascular disorders, thromboembolism from umbilical catheterization, mid-aortic coarctation, renal vein thrombosis, acquired renal parenchymal disease, renal obstruction, cerebral vascular disease, and medications, among others. Since hypertension is generally asymptomatic in a majority of cases, a thorough history, physical exam, and systematic approach to the diagnostic evaluation is needed to determine the precise etiology.
Preliminary laboratory evaluation includes a complete blood count, plasma electrolytes, calcium, BUN, creatinine, urinalysis, plasma renin activity, plasma catecholamines, two-dimensional echocardiogram, and an abdominal ultrasound and DMSA scan to provide some structural and functional evaluation of the kidneys. Other testing that can be ordered as indicated includes thyroid function studies, a cortisol level and an aldosterone level.
Further evaluation for renovascular disease would be justified if there was no evidence of an alternative explanation for the hypertension, and the laboratory evaluation was consistent with a renin-dependent hypertensive state without an obvious cause.
The most common diagnostic imaging modalities utilized in the evaluation of suspected renovascular hypertension include: Doppler ultrasonography, pre and post-captopril DMSA renography, magnetic resonance angiography, and CT angiography. Digital subtraction angiography is the gold standard for diagnosing renovascular hypertension, as the other mentioned modalities have a sensitivity that is too low to exclude renovascular hypertension. In medical settings where DSA is difficult to perform or not readily available, other methods, preferably CTA or MRA, can be used as reasonable second-line alternatives after ultrasound.
The treatment of renovascular hypertension is diverse and dependant on the precise etiology; but includes medical management, angioplasty with or without stenting, vascular grafting, and nephrectomy. In general, the long-term results of surgical intervention are good with at least 75% of the children having their high blood pressure cured or improved.
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