“Wind, water, wound, walking, wonder drugs” are described as the “Ws” of post-operative fevers (atelectasis, UTI, wound infection, DVTs, and drug fevers, respectively). As a medical student, all of these made sense to me except the mechanism by which atelectasis, something applicable to ALL patients under general anesthesia, causes a fever. Turns out that the theory was largely driven by a study… in rats… where alveolar macrophages released inflammatory cytokines (namely TNF-alpha and IL-1)… after surgical ligation of a bronchus. Ouch. Yeah, that doesn’t seem the same as studying a response to (less traumatic) atelectasis.
Two blinded but nonrandomized studies looked at patients who underwent cardiac surgery (Engoren) and abdominal surgery (Perez-Aispuro et al) – both failed to show an association between postoperative fever and atelectasis. A more recent review article in JAMA Surgery (PMID 30840058) by Crompton et al. alluded to studies with similar conclusions and randomized controlled trials showing that spirometry (a means of improving atelectasis) did not reduce the incidence of fever.
The authors refer to Matzinger’s “danger model” of immunity whereby damaged cells signal the activation of innate immune cells via damaged-associated molecular patterns (DAMPs). These include a myriad of molecules we’re used to discussing – uric acid, nucleic acids, and various peptides. DAMPs subsequently activate inflammatory pathways in a self-limiting, noninfectious phenomenon.
Drop me a comment with your thoughts, and be sure to run this literature by any trainees (and even seasoned clinicians) in healthcare. We need to stop dogmatic teachings!
