Abstract
The pathophysiology of post-cardiac arrest syndrome features ischaemic/reperfusion injury and the release of high levels of inflammatory cytokines [1]. These inflammatory markers include interleukin-6 (IL-6), C-reactive protein (CRP), tumour necrosis factor, procalcitonin and pentraxin 3 [2]. Observational studies suggest that IL-6 levels appear to increase early after cardiac arrest, whereas most other markers peak at around 24–48 h [3]. The magnitude of the increase of these inflammatory markers appears to be associated with the severity of the circulatory shock, the development of organ failure and, in some studies, also neurological injury and functional outcome [4, 5]. Therefore, efforts to curb this inflammatory response are of particular interest to researchers. Other studies that have investigated the use of hydrocortisone during intensive care unit care after cardiac arrest have shown conflicting results, with no indications of decreased mortality but some hints of improved functional outcome in the survivors [6]. One problem with these previous studies is that the timing of the delivery of steroids was delayed. Nonetheless, there are also studies in which steroids were administered during cardiopulmonary resuscitation, which resulted in some changes in post-arrest haemodynamics [7]. If early reperfusion causes the release of inflammatory mediators, it would make sense to provide anti-inflammatory agents as soon as possible after the return of spontaneous circulation (ROSC).