INTRODUCTION

Poisoning induced by alcohols (methanol, ethanol, and ethylene glycol) may cause neurological changes ranging from confusion to deep coma, amaurosis, and death. Despite intensive treatment, morbidity and mortality continue to be very high, mainly because of the delay in diagnosis and treatment.1-6 Toxicity from methanol, ethanol, and ethylene glycol is related to the degree of metabolic acidosis and the increase in plasma osmolality induced.1-3 By inhibiting the main metabolic pathway of methanol and ethylene glycol, alcohol dehydrogenase (ADH), ethanol, and fomepizole prevent the formation of the main toxic metabolites, formic acid from methanol and glycolic and oxalic acids from ethylene glycol.7 The established treatment for severe poisoning by methanol and ethylene glycol is administration of ethanol and pre-emptive HD.1-7 Conventional HD treatment may rapidly decrease levels of methanol, ethanol, and ethylene glycol, as well as their metabolites, and also correct electrolyte and acid-base
disorders, but high-flux membranes may remove a greater amount of toxic per hour of HD, increasing its efficacy [8]. The study objective was to prospectively analyze the effectiveness of therapeutic measures, including dialysis, in cases of poisoning by these alcohols where an early treatment protocol including bicarbonate administration, ethanol infusion, HD using high-flux membranes, and a modified bath to prevent hypophosphatemia and hypokalemia was used.

MATERIALS AND METHODS

Data from 14 patients admitted to our hospital in the past 3 years for poisoning with methanol (11), ethanol (1), and ethylene glycol (2) are reported. Initial diagnosis was made based on a clinical history with sufficient evidence of intake of toxic alcohols (statements from patients themselves or witnesses, and containers brought with residues of toxics ingested), as well as the presence of metabolic acidosis with elevation of the anion and/or osmolal gaps. In addition, whenever possible, serum levels (as well as urinary and gastric juice levels in some cases) of the corresponding toxic alcohols were measured by gas chromatography (National Institute of Toxicology and Forensic Science, Ministry of Justice, Madrid). Routine procedures were used to test all other biochemical parameters such as electrolytes, osmolality, arterial blood gases, etc. on arrival to the emergency room, before the start and at the end
of dialysis treatment, and throughout the course. Anion gap was calculated using the standard formula (Na+ + K+) ¿ (Cl- + HCO3 -), and osmolal gap by subtracting from the osmolality measured (osmometer) the osmolality calculated with the standard formula. Calculated serum osmolality (mOsm/L) = 2 x Na + Urea (mg/dL)/6 + glucose (mg/dL)/18.

To correct metabolic acidosis, 100 to 300 mL of 1 M sodium bicarbonate and 1,000 mL of isotonic saline were initially infused to all patients. Repeat infusion of 1 M sodium bicarbonate was required in some cases to maintain bicarbonate levels at safe levels until HD was started. As fomepizole was not available, ethanol infusion was used to inhibit ADH in patients with methanol and ethylene glycol poisoning. Treatment was started with a loading dose of ethanol (750 mL of a 10% solution in 5% glucose) over 30 minutes. A 10% ethanol infusion at 100 mL/h was subsequently administered. During the HD session, ethanol infusion was increased to 150-200 mL/h, and in some cases the 100 mL/h infusion was continued for 8-24 hours. In patients intoxicated by methanol, folic acid was administered IV at a dose of 20 mg/8 h to accelerate formate metabolism. In cases of ethylene glycol poisoning,
pyridoxine (50 mg/6 h IM) was administered to convert glyoxylate into glycine, and thiamine (100 mg/6 h IM&