Neonatal hypertension (NH) is an uncommon but important clinical problem in neonates. The most important non-renal association with NH is Bronchopulmonary Dysplasia (BPD). Exact mechanism of hypertension in BPD infants… Click to show full abstract
Neonatal hypertension (NH) is an uncommon but important clinical problem in neonates. The most important non-renal association with NH is Bronchopulmonary Dysplasia (BPD). Exact mechanism of hypertension in BPD infants is not known. The purpose of this case series is to describe our experience with the use of spironolactone, an aldosterone antagonist, in neonates with hypertension and BPD. Methods Retrospective case review conducted at Level II NICU in Calgary from 2013 to 2017 revealed 10 preterm infants with BPD and NH who had plasma renin and aldosterone levels done as part of their investigations for hypertension. NH was defined by blood pressure >95 th centile of the normative data. Maternal characteristics included age, smoking and drug use, history of pregnancy induced hypertension, preeclampsia, gestational diabetes, antenatal steroids and mode of delivery. Neonatal characteristics included gestational age, birth weight, sex, intrauterine growth restriction, APGAR scores, insertion of umbilical arterial catheterization and the presence of BPD. All infants had serum creatinine, electrolytes, urinalysis, plasma renin and aldosterone levels, renal ultrasound and ECHO done. Data collected also included age at diagnosis of hypertension, age at initiation of treatment, medications used, response to treatment and follow up. Results NH in all infants was diagnosed after 36 weeks GA and treatment was started at presence of persistent hypertension >99 th centile. 3 infants were initially started on amlodipine and Furosemide with no response and were changed to aldactazide. 2 infants received only Furosemide with no response. 5 of the remaining infants were started on aldactazide as a first line treatment to target hyperaldosteronism. All infants responded within 48 hours of treatment with aldactazide. All 10 infants developed mild hyponatremia which required sodium chloride supplementation until aldactazide was discounted. Hypertension was transient lasting from 3 months till 16 months post term and medications were discontinued with normal blood pressures. Conclusion Transient hyperaldosteronism is one of the possible causes for hypertension in preterm infants. Our case series demonstrates association preterm of NH with elevated aldosterone and low rennin without any other apparent cause for the hypertension. All infants responded to aldactazide, an aldosterone antagonist containing medication.
               
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