Early Prophylactic Hypothermia for Patients With Severe Traumatic Injury: Premature to Close the Case

This study demonstrates that there is no role for the initiation of hypothermia during the acute phase of TBI (1, 2). However, it would be damaging to abandon the concept prematurely. Inflammation Also Paves the Way to Tissue Repair As soon as trauma occurs, the inflammatory cascade begins to take place. The deleterious role of inflammation in the secondary injury response is well-documented, hence the rationale to attempt early prophylactic hypothermia in TBI. However, inflammation also initiates tissue repair and regeneration (3–6). We now know that the secondary injury response accompanies the regenerating and healing response. Rather than considering the injury cascades and resolving phases as two sequential antagonistic processes, we now understand them as two overlapping aspects of the same dynamic process dedicated to regeneration and healing (3–5). The resolving phase is an active process intrinsic to the progression of the inflammatory response. It is triggered by several pro-inflammatory mediators such as IL-1β and TNF-α, that recruit, among others, IL-10, TGFβ, and the members of a novel superfamily of lipid mediators called specialized pro-resolving mediators (SPMs) (3–6). The members of the SPMs family that include lipoxins, resolvins (Rvs), maresins, and protectins are central to this process (3, 7). They actively terminate inflammation and promote tissue regeneration (3, 7, 8). Indeed, the temporal switch from t...
Source: Frontiers in Neurology - Category: Neurology Source Type: research