Introduction Only mild therapeutic hypothermia (MTH) is shown to improve outcome after return of spontaneous circulation, post out of hospital cardiac arrest (OHCA), though its mechanism remains unknown. We hypothesise that the benefit of MTH is mediated through modulation of the inflammatory response.
Methods During our prospective observational study from Aug 2008 to October 2009, 196 OHCA patients were enrolled. 173 were eligible for inclusion; 115 died in Emergency Department (ED), 38 died in intensive care unit (ICU) and 20 survived to discharge. Patients had blood sampled on arrival in the ED and at 24 h, 72 h and 5 days. A small subgroup of patients had blood sampled prehospital during the initial resuscitation phase. Serum levels of cytokines important in the regulation of inflammation (interleukin 6 (IL-6), IL-8, IL-10) were measured along with markers of neutrophil activation (elastase and CD 11b). All patients who reached the ICU had MTH induced and were maintained at 32–34° for 24 h.
Results Levels of the pro-inflammatory cytokine IL-8 were significantly higher at 24 h after return of spontaneous circulation in patients who died in ICU, compared to those who survived to discharge (478.1 pg/ml (CI 171.1 to 831.1) cf 108.0 pg/ml (CI 44.8 to 171.1) p=0.03). Serum levels of the ‘anti’-inflammatory cytokine IL-10 were also much higher in non-survivors (CI 80.9 pg/ml (22.3 to 139.4) cf CI 10.2pg/ml (3.6 to 16.8) p=0.002). IL-10 predicted survival 24 h with an area under the Receiver Operating Characteristic of 0.91 (CI 0.77 to 1.0, p<0.001), and a sensitivity of 100%, specificity 75% at a cut off of 32 pg/ml, LR 4.0. Indicators of neutrophil activation, were markedly elevated in all patients on arrival in the ED.
Discussion OHCA is associated with massive systemic inflammation. We have shown that this begins much earlier than previously described, and that levels of both the classically pro-inflammatory and counterregulatory chemokines predict survival. Our findings are consistent with the hypothesis that MTH works, at least in part, by modulating the inflammation.
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