Hyperdehydroepiandrosterone in neonates with hypoxic ischemic encephalopathy and circulatory collapse

Circulatory collapse is a very common complication of the critical illnesses in neonates including neonates with hypoxic ischemic encephalopathy; it can be the end result and cause of death of several conditions. Often, despite treatment with fluid resuscitation and vasopressor agents, circulatory collapse persist, and blood pressure can remain critically low, compromising adequate blood flow to vital organs and brain. Low blood pressure has been associated with increased mortality.

To investigate adrenal function in newborn infants who suffer from circulatory collapse during hypoxic ischemic encephalopathy. A total of 30 infants were analyzed in the study: 15 neonates in group A (neonates had hypoxic ischemic encephalopathy with vasopressor resistant hypotension) and 15 neonates in group B (neonates with hypoxic ischemic encephalopathy without vasopressor resistant hypotension). All the studied patients were subjected to history, examinations and laboratory investigation including serum cortisol concentrations and cortisol precursor's levels.

The cortisol concentrations did not differ significantly between the two groups: (12.9 ± 4.3) μg/dL and (12.1 ± 2.4) μg/dL in group A and group B, respectively. There are highly significant differences between groups A and B regarding Dehydroepiandrosterone (342.1 ± 101.3) μg/dL, (33.4 ± 16.5) μg/dL, respectively.

In this study, we noticed that cortisol concentrations did not differ between both groups in contrast to the expectation that neonates with critical illnesses should have higher cortisol concentrations than normal neonates. However, the marked increase in dehydroepiandrosterone DHEA may cause decrease cortisol function, so those neonates having accumulation of dehydroepiandrosterone may suffer from manifestation of adrenal insufficiency and vasopressor resistant hypotension in spite of normal cortisol level.