Re: An unusual migratory polycyclic eruption after administration of prostaglandin E in a neonate.

To the Editor: In the September 2016 issue of JAAD Case Reports, Young et al reported a case of a rapidly migratory polycyclic eruption after prostaglandin E1 (PGE1) infusion in a newborn on extracorporeal membrane oxygenation (ECMO). Shortly after its publication, we encountered a very similar case that corroborates many of their findings and adds further evidence to a potential role for hypoxia in the development of this eruption.

The patient was a 2-month-old Hispanic boy born at 28 weeks with complex congenital heart defects awaiting a heart transplant on veno-arterial ECMO. One day before dermatology consultation, the rate of his PGE1 infusion had been increased, and he was noted to have generalized rapidly migratory erythematous patches (Fig 1). Particularly striking was the sharp demarcation of erythema at the distal tips of the fingers and toes. There was initial concern for a reaction to vancomycin, which was held. He subsequently continued to have new patches, however, so the dermatology department was consulted, with concern for PGE1 being the causative agent. The patient had been cannulated 2 days before consultation, and per EMCO protocol had a head ultrasound scan the morning of ECMO initiation and the following morning, both of which were normal. Around noon on the day after cannulation, which was 1 day before consultation, the patient had clinical seizures, with a head computed tomography performed that evening showing new hypodensities concerning for ischemic injury. After the onset of seizures, the eruption was initially noted. This case has similar features to those discussed by Young et al and may help further define this eruption. First, the temporal association with PGE1 lends support to its etiologic role. Second, as discussed by Young et al, hypoxia may play a role. PGE1 is primarily metabolized in the lungs, with 70% to 80% being metabolized in the first pass, which is an oxygen-dependent process. When a patient is on veno-arterial ECMO, like our patient was, there is decreased pulmonary blood flow, which in turn, affects the metabolism of PGE1. As Young et al point out, hypoxia is hypothesized to contribute to harlequin color change, although the exact mechanism remains unknown. With ECMO, there is also a larger circulating blood volume leading to a larger volume of distribution for medications, which may also account for the need for increased dosing of certain medications while on ECMO to achieve the desired clinical effect. Our patient's PGE1 infusion was increased from 0.02 μg/kg/min to 0.05 μg/kg/min on the day the eruption appeared because of concern that the ductus arteriosus was closing, which may have been contributing to worsening hypoxia. The patient had been on PGE1 for almost 2 months, but interestingly the eruption did not appear until the dose was increased after the patient had severe hypoxia and was placed on veno-arterial ECMO; it disappeared a week later when the patient was decannulated. As such, recognition of this eruption should reassure clinicians that no intervention may be necessary in patients that are otherwise stable.

Fig 1

Rapidly migratory erythematous patches in a neonate on ECMO.