Electronic Nose Technology Fails to Sniff Out Acute Mountain Sickness

Abstract

The electronic nose technology utilized in this study could not discriminate between climbers with and without symptoms of AMS in the setting of an acute exposure to an altitude of 4554 m. At this stage, we cannot fully exclude that this technology per se is not able to discriminate for AMS. The quest for objective means to diagnose AMS thus continues.

Will an electronic nose help at high altitude?

“…Following this study by B erendsen et al [ 3 ], we believe that the use of electronic technology is very promising in remote high-altitude settings, when adapted and further developed. Electronic technology, such as an electronic nose to “sniff” AMS, may help doctors differentiate between other causes of similar symptoms and target specific treatment to such patients, including oxygen, acetazolamide or even evacuation in cases of clinical deterioration.…”

“…This study by B erendsen et al [ 3 ] may have clear practical implications. First and foremost, it adds more emphasis to the need to plan and conduct studies to test further biochemical or other instrumental ways to diagnose AMS.…”

“…In a recent study at Capanna Regina Margherita (Italy) at 4554 m above sea level, B erendsen et al. [ 3 ] tested the hypothesis that analysing the traces of exhaled volatile organic compounds (VOCs) could help distinguish between AMS + and AMS − subjects. The rationale for such an approach is based on the assumption that oxidative stress is a part of AMS pathophysiology and that AMS is accompanied by a metabolic stress, which together result in a change in VOC exhaled concentrations.…”

“…With a given device, Aeonose (The eNose Company, Zutphen, the Netherlands), and a sample size of 101 climbers, B erendsen et al [ 3 ] failed to distinguish between AMS + and AMS − subjects, since logistic regression showed no difference in the artificial neural network predicted values between the two groups. The authors listed five possible explanations for this outcome.…”

“…The rationale of the study by B erendsen et al. [ 3 ] is the fact that oxidative stress in response to hypoxia may contribute to AMS. Indeed, altered redox homeostasis has been suggested in the physiopathology of AMS with subsequent disordered cerebral autoregulation [ 6 ].…”