Background: Methemoglobinemia (MetHb) is a rare and potentially severe dyshemoglobinemia that can be induced by exposure to oxidizing agents, decreasing the functional capacity of the hemoglobin molecule to transport and release oxygen into the tissues. MetHb can originate from gases with oxidizing capacity generated by internal combustion engines, although since the universalization of catalyst converters in automobiles, a tiny proportion of MetHb poisoning is due to exposure to engine gases and fumes. Within this group, only two cases due to suicidal motivations have been reported in the last 30 years. Case presentation: Here, we expose the case of a patient with MetHb levels of 25.2% (normal 0–1.5%) who with suicidal motivations had attached and locked a hose to the exhaust pipe of her vehicle with electrical tape, becoming exposed to a sustained concentration of the vehicle’s exhaust. Upon her arrival at the emergency department, the presence of generalized greyish cyanosis with alterations of the sensorium, dissociation between saturation measured by arterial blood gas analysis and pulse oximetry (98% vs. 85%), no response to high-flow oxygen therapy, and an excellent response to intravenous methylene blue treatment were highlighted. Conclusions: This report illustrates an original case of acute toxic acquired MetHb due to inhalation of oxidizing substances originating from the bad ignition of an internal combustion engine. When evaluating a patient with suspected gas intoxication, we usually consider poisoning by the most common toxins, such as carbon monoxide or cyanide. In this context, we propose an algorithm to assist in the suspicion of this entity in patients with cyanosis in the emergency department. MetHb poisoning should be suspected, and urgent co-oximetry should be requested when there is no congruence between cyanosis intensity and oxygen saturation measured by pulse oximetry, if there is discordance between the results of oxygen saturation measured by arterial blood gas and pulse oximeter, and if there is no response to oxygen treatment. This algorithm could be useful to not delay diagnosis, improve prognosis, and limit potential sequelae.

The purpose of the study was to analyze the relationship between the high-sensitivity troponin T levels in patients with confirmed influenza virus infection and its severity determined by mortality during the care process. In addition, a high-sensitivity troponin T cut-off value was sought to allow us to a safe discharge from the emergency department. An analytical retrospective observational study was designed in which high-sensitivity troponin T is determined as an exposure factor, patients are followed until the resolution of the clinical picture, and the frequency of mortality is analyzed. We included patients ≥ 16 years old with confirmed influenza virus infection and determination of high-sensitivity troponin T. One hundred twenty-eight patients were included (96.9% survivors, 3.1% deceased). Mean and median blood levels of high-sensitivity troponin T of survivors were 26.2 ± 58.3 ng/L and 14.5 ng/L (IQR 16 ng/L), respectively, and were statistically different when compared with those of the deceased patients, 120.5 ± 170.1 ng/L and 40.5 ng/L (IQR 266.5 ng/L), respectively, p = 0.012. The Youden index using mortality as the reference method was 0.76, and the cut-off value associated with this index was 24 ng/L (sensitivity 100%, specificity 76%, NPV 100%, PPV 4%) with AUC of 88,8% (95% CI: 79.8–92.2%), p < 0.001. We conclude that high-sensitivity troponin T levels in confirmed virus influenza infection are a good predictor of mortality in our population, and this predictor is useful for safely discharging patients from the emergency department.

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