Positive serum ethanol concentration on admission to hospital as the factor predictive of treatment outcome in acute methanol poisoning

Sergey Zakharov,Sergey Zakharov,Tomas Navratil,Tomas Navratil,Olga Nurieva,Jaromir Belacek,Daniela Pelclova,Daniela Pelclova,Katerina Kotikova

doi:10.1007/s00706-016-1846-z

Abstract

Mass methanol poisonings present a serious problem for health systems worldwide, with poor outcome associated with delayed treatment. Positive pre-hospital serum ethanol concentration may have predictive value as the prognostic factor of the treatment outcome. We studied the effect of positive serum ethanol level on admission to hospital on survival in patients treated during the Czech methanol outbreak during 2012–2014. Cross-sectional cohort study was performed in 100 hospitalized patients with confirmed methanol poisoning. Pre-hospital ethanol was administered in 42 patients (by paramedic/medical staff to 30 patients and self-administered by 12 patients before admission); 58 patients did not receive pre-hospital ethanol. Forty-two patients had detectable serum ethanol concentration on admission to hospital [median 18.3 (IQR 6.6–32.2) mmol dm−3]. Pre-hospital ethanol administration by paramedic/medical staff had a significant effect on survival without visual and CNS sequelae when adjusted for arterial blood pH on admission (OR 8.73; 95 % CI 3.57–21.34; p < 0.001). No patients receiving pre-hospital ethanol died compared with 21 not receiving (p < 0.001). Positive serum ethanol concentration on admission to hospital was a predictor for survival without health sequelae when adjusted for arterial blood pH (OR 8.10; 95 % CI 2.85–23.02; p < 0.001). The probability of visual and CNS sequelae in survivors reduced with increasing serum ethanol concentration on admission.Graphical abstract

Highlights

Mass and cluster acute methanol poisonings due to the consumption of illicit alcohol occur frequently throughout the world [1,2,3,4]
Pre-hospital ethanol administration by paramedic/medical staff had a significant effect on survival without visual and CNS sequelae when adjusted for arterial blood pH on admission
The accumulation of formic acid leads to the metabolic acidosis with anion gap increase, optic nerve and retinal nerve fibers damage, and necrosis of basal ganglia [10,11,12,13]

Summary

Introduction

Mass and cluster acute methanol poisonings due to the consumption of illicit alcohol occur frequently throughout the world [1,2,3,4]. In the absence of protective ethanol concentration in blood serum, methanol is metabolized by hepatic alcohol dehydrogenase enzyme (cytosolic ADH1) to the highly toxic formic acid, which inhibits mitochondrial respiration [8, 9]. Ethanol has 10–12 times higher affinity for ADH than methanol and its serum concentration of 22–33 mmol dm-3 is sufficient to completely block the metabolism of methanol to formaldehyde, and on the second step to formate [15, 16]. The indications for ethanol administration are either a documented plasma methanol concentration of more than 6.2 mmol dm-3, a high osmolal gap with documented the recent history of ingesting toxic amounts of methanol, or a metabolic acidosis with history or strong clinical suspicion of poisoning [17, 18]

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