Matt Harmon

69 Chapter three Chapter 3a To the editor: Should we assume that hypo- thermia is a dysfunction in sepsis? Alexandre A. Steiner, Monique T. Fonseca and Francisco G. Soriano Critical care, 2016 DOI: 10.1186/s13054-016-1584-y Wiewel et al. 1 clearly showed that development of hypothermia instead of fever in sepsis is not tied to a switch from a pro-inflammatory to an anti-inflammatory state. The authors then suggest that vascular dysfunction could play a role in hypothermia. While this hypothesis deserves attention, we urge researchers to consider that there is no hard evidence indicating that hypothermia is a dysfunction in sepsis. Not all systems fail simultaneously in sepsis, and those with preserved function are likely to launch evolutionarily conserved compensatory responses. Could thermoregulation be preserved during septic hypothermia? Could hypothermia be adaptive when the costs of fever exceed its benefits? According to evidence from rat models of systemic inflammation, the answers to these questions may be yes. First, hypothermia in endotoxemic rats is an early, transient phenomenon that is not consequential to circulatory shock. 2 Second, hypothermia in endotoxic shock is brought about by downregulation of thermogenesis when thermogenic capacity is unimpaired. 2,3 Third, rats with endotoxic shock do not attempt to restore normothermia when given the chance to select a warmer environment; on the contrary, they seek a cooler environment. 3 Last, spontaneous hypothermia has been shown to be more advantageous than fever in rats with severe forms of endotoxemia and Escherichia coli  sepsis. 2,4 There has been a complete disconnect between these experimental data and clinical studies on this subject. Recently, though, Fonseca et al. 5 published the first effort to reconcile experimental and clinical evidence on septic hypothermia.