Effects of dexamethasone on blood pressure in premature infants with bronchopulmonary dysplasia,☆☆,

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Abstract

Objective: To determine the incidence and time course of blood pressure elevation in dexamethasone-treated premature infants with bronchopulmonary dysplasia.

Methods: In a prospective, self-controlled, consecutive case study, 16 ventilator-dependent very low birth weight neonates treated with dexamethasone were studied. Systolic, diastolic, and mean arterial pressure and heart rate were recorded at three specific times daily. Data were recorded from day 1 of dexamethasone treatment through the duration of therapy and up to 2 weeks after its completion. Retrospective daily data were collected for up to 14 days before therapy.

Results: The 788 daily observations (a systolic and diastolic average of the three blood pressure recordings per day) were recorded for 16 infants, a mean of 49 ± 11 daily observations each (range, 24 to 67). Systolic and diastolic blood pressures before dexamethasone therapy were correlated to corrected gestational age. At initiation of dexamethasone, blood pressures increased significantly from days 1 to 2. For all observations, mean systolic pressure was 51 ± 9.5 mm Hg before dexamethasone therapy, compared with 64 ± 10.2 mm Hg during therapy (p <0.01); diastolic pressure was 29 ± 6.7 mm Hg before therapy compared with 41 ± 8.2 mm Hg during therapy (p <0.01). After completion of dexamethasone therapy, pressures continued to increase: systolic, 67 ± 8.8 mm Hg (p <0.01); diastolic, 42 ± 6.2 mm Hg (not significant). Both systolic and diastolic pressures increased as a function of weight and age; when we controlled for these covariates, an independent effect of dexamethasone itself on the group was shown. Of the 2182 individual systolic pressure readings, 9.4% were considered in the hypertensive range. The six infants treated with hydralazine had higher mean systolic pressures before dexamethasone therapy than did infants without hydralazine (56 ± 9.4 mm Hg vs 46 ± 6.4 mm Hg; p <0.001) and were 2 weeks older at initiation of therapy.

Conclusions: Blood pressure significantly increases during dexamethasone therapy, particularly within the first 48 hours, and does not return to baseline levels after therapy. Those infants most likely to be labeled hypertensive tend to be older at initiation of therapy but do not appear to have any other significant risk factors. (J Pediatr 1997;130:594-602)

Section snippets

METHODS

Babies with a clinical diagnosis of BPD were eligible for inclusion in the study if they were treated with dexamethasone to improve pulmonary mechanics. The decision to institute steroid therapy was made by the clinical team (attending neonatologist, neonatal fellow, pediatric residents, and neonatal nurse practitioners) caring for the infant. All infants in the study were ventilator and oxygen dependent at initiation of dexamethasone and had a chest radiograph consistent with the diagnosis of

RESULTS

In the 25-month period from Jan. 1, 1991, to Feb. 3, 1993, a total of 20 neonates with ventilator-dependent chronic lung disease were treated with dexamethasone. Three of the families of these 20 eligible babies declined participation in the study. One other infant was excluded from the analysis after his early death on the fourth day of steroid therapy.

The characteristics of the 16 study infants are presented in Table I.

. Characteristics of study Infants (n = 16)

Birthweight (gm) (mean ± SD)715

DISCUSSION

There is general agreement that blood pressure increases as a function of weight and age in preterm infants.23, 24, 25, 26, 27 This study confirms this finding and, in addition, demonstrates a significant independent effect of dexamethasone on both SBP and DBP in this population of very low birth weight babies. Ours is the first such study of dexamethasone to adjust for the effects of postconceptional age and weight on blood pressure.

The prospective measurements of blood pressure allowed

Acknowledgements

We thank Majid Rasoulpour, MD, for his thoughtful review of the manuscript and the neonatal nurse practitioners and the nursing staff of the neonatal intensive care unit for their patience and assistance in collecting the blood pressure data.

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    From the Divisions of Research and Neonatology and the Neonatal Intensive Care Unit, Connecticut Children's Medical Center, and the Department of Pediatrics, University of Connecticut School of Medicine, Hartford, Connecticut.

    ☆☆

    Reprint requests: Kathleen A. Marinelli, MD, Connecticut Children's Medical Center, Division of Neonatology, 282 Washington St., Hartford, CT 06106.

    0022-3476/97/$5.00+0 9/21/78304

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