Abstract
Four infants, two with omphaloceles and two with gastroschisis, developed sustained systemic hypertension following closure of their abdominal wall defects. Mean systolic blood pressure rose from a preoperative level of 70 mmHg to a peak postoperative level of 131 mmHg. Lower extremity blood pressures were not reduced. However, three infants had edema of the lower extremities. In all infants, blood urea nitrogen, serum creatinine, intravenous pyelograms, and urinalyses were normal. Catecholamine levels in two infants were normal. Three infants had normal peripheral plasma renin activity (PRA) and iodohippurate renal scans. One infant had an elevated PRA associated with evidence of utero pelvic junction obstruction by renal scan. The duration of hypertension ranged from 12 days to 180 days (mean 89.5 days). Two infants were treated with hydrochlorothiazide and hydralazine, while in two, hypertension resolved spontaneously. The etiology of the hypertension remains unclear. Possible mechanisms include: 1) compression of the renal parenchyma and/or vasculature; and 2) pressure or traction on the splanchnic and/or pelvic nerve supply. Since the incidence of abdominal wall defects is roughly 1 per 2300 live births, hypertension secondary to surgical correction of this condition may not be uncommon.
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Adelman, R., Sherman, M. NEONATAL HYPERTENSION FOLLOWING CLOSURE OF ABDOMINAL WALL DEFECTS. Pediatr Res 14, 1010 (1980). https://doi.org/10.1203/00006450-198008000-00219
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DOI: https://doi.org/10.1203/00006450-198008000-00219