Cosmetic treatment of fever not warranted

We practice in an era of outcome based medicine. It’s not enough anymore, at least when it comes to things like blood pressure and blood sugar, just to treat the numbers (cosmetic treatment).  Why, then, in everyday practice, don’t we apply the same rigorous skepticism to the problem of fever?


A recent study in Critical Care looked at the question. Lowering of body temperature was not associated with improved outcomes and in some patients was harmful.

Don’t forget the exceptions, e.g. the better brain outcomes in cardiac arrest and stroke patients, and, of course, treatment of heat stroke and the other hyperthermia syndromes.

Dabigatran review

From the Journal of Medical Toxicology. Concerning bleeding complications:

However, no therapeutic agent has been accepted to reliably reverse the hemorrhagic complications of dabigatran. As of yet, there is no solid evidence to guide management of bleeding complications; management should start with local control of bleeding when possible and transfusion of pRBCs if needed. Transfusion of FFP would not be expected to help control bleeding. Limited and mixed data exist for transfusion of factor VIIa and prothrombin complex concentrates; these therapies should be considered as well as dialysis..

It's not just the QT interval, stupid!

Traditionally we look to the QT interval to assess the risk of Torsades des pointes ventricular tachycardia when monitoring the effects of certain drugs. Moreover, QT interval prolongation, rather than “twisting about the point” morphology, has been the defining characteristic of Tdp. But as pointed out in a recent post over at Clinical Correlations, that thinking is simplistic. Even correcting the QT interval for rate (QTc) is of limited value. While it's true that prolonged repolarization is at fault that's only part of the story, as reflected in the post and as exemplified by amiodarone, which prolongs the QTc but does not cause Tdp. In actuality the abnormal repolarization that characterizes Tdp has other components and these may better lend themselves to the subjective “eyeball test” than to a single measurement. That said, some of the references cited in the Clinical Correlations post deal with attempts at quantitative treatment of the various components.

None of this is new mind you. I blogged this very concern over two years ago and said this:

Although the traditional assessment for prolongation of repolarization is the measurement of the QT interval, that assessment is simplistic and fraught with error due to controversy about normal limits and rate corrections, poor T wave demarcation, poor distinction between the T wave and the U wave and cycle length dependency. More subjective features including pause dependency, particularly in short-long cycle sequences, splayed T waves (or TU fusion) and macroscopic T wave alternans may be more important.

Among drugs that prolong the QT interval amiodarone has a uniquely low risk of producing TdP because the prolongation of repolarization it induces is homogeneous. Heterogeneous repolarization abnormality is the more likely substrate for TdP.