Cortisol and 17-a-hydroxy-progesterone levels in infants with refractory hypotension born at 30 weeks of gestation or less

Abstract

Refractory hypotension is frequent in very low-birth weight infants, whose hypothalamic-pituitary-adrenal axis has been suggested to be immature. The objective of the present study was to evaluate basal cortisol and 17-α-OH-progesterone in the first 36 h of life in preterm infants with and without refractory hypotension (mean arterial blood pressure below the lower limit for gestational age throughout the study despite aggressive volume expansion and use of vasopressors). Thirtyfive infants with ≤30 weeks of gestation and a birth weight ≤1250 g, with no postnatal use of corticosteroid or death in the first 48 h were studied. Mean arterial pressure was measured every 4 h during the first 48 h. Cortisol and 17-α-OH-progesterone were determined at 12 and 36 h and patients were divided into refractory hypotensive (N = 15) and control (N = 20) groups. The groups were not different regarding type of delivery, use of prenatal corticosteroid, requirement of mechanical ventilation, use of vasopressor drugs, morphine, fentanyl, prophylactic indomethacin, and mean sample timing. Although refractory hypotensive newborns were more immature, were smaller, suffered more deaths after 48 h of life and had a higher SNAPPE-2 score, their cortisol and 17-α-OH-progesterone levels were not different from controls at 12 h and at 36 h. The increase of cortisol in newborns with refractory hypotension 36 h after birth was significantly higher than in controls. Despite the fact that refractory hypotensive very low-birth weight neonates were submitted to a very stressful condition, their cortisol and 17-α-OH-progesterone levels were similar to controls.

Variations in CRHR1 are associated with persistent pulmonary hypertension of the newborn

“…Transient adrenal insufficiency, marked by low cortisol despite increased physiologic demand due to stress, has been described in both preterm (43, 44) and term infants (45–47) and is associated with increased hemodynamic instability, poor outcomes and longer illnesses (48, 49). Studies have found that infants with severe lung disease requiring ventilation had lower rates of cortisol in the first seven days of life and that early treatment with corticosteroids can decrease pulmonary oxidative stress and increased pulmonary arterial response to vasodilators (50–52).…”

Population Pharmacokinetics of Unbound Hydrocortisone in Critically Ill Neonates and Infants With Vasopressor-Resistant Hypotension

“…Conditions in the perinatal period that may further contribute to morbidity and mortality include sepsis, chorioamnionitis, respiratory distress, and chronic lung disease all of which are characterized by an underlying inflammatory process (5-8). In addition, systemic hypotension is common in this patient population and has been associated with cardiovascular instability and death (1, 2, 9). …”