To the editor: The case of a patient with severe methanol and toluene poisoning has been recently published in

Nefrología.1 We have treated a patient with severe methanol poisoning and we want to emphasize the importance of prolonged haemodialysis in its treatment.



CASE REPORT



This was a 40-year-old male patient who was brought into the Emergency Department after suffering frfom severe

headache, dizziness, irritability and incoherent language. According to the family, the patient had chronic alcoholism although he had not had any alcohol in the last 3 days. In the emergency room, there was deterioration in level of consciousness with progressive coma, so the patient was admitted to the ICU where orotracheal intubation, and mechanical ventilation was used.



Laboratory analysis on admission showed an arterial blood gas with a pH of 6.98, PO2 96, PCO2 31, and bicarbonate

4.9 mEq/l. Plasma creatinine was 1/53 mg/dl, BUN 33 mg/dl, sodium 135 mEq/l, potassium 6.2 mEq/l, chloride 102 mEq/l, haemoglobin 16 g/dl, glucose 198 mg/dl, serum osmolarity 421 mOsm/kg and lactic acid 10.5 mmol/l. A head CT did not reveal any visible parenchymal or signs of cerebral haemorrhage.



After questioning the family again, the possibility that the patient had consumed approximately half a litre of methanol was mentioned.



Treatment was initiated with pyridoxine, thiamine, nalaxone, tiapride, flumazenil, sodium bicarbonate, inotropics and intravenous ethanol. Haemodialysis began approximately 3 hours after admission to ICU. A highpermeability 2.1 m2 surface area polysulfone membrane and a bicarbonate bath for 7 hours was used with blood flow at 300 ml/min. Unfortunately, despite continuing inotropics and highdose bicarbonate, the patient suffered from severe haemodynamic instability. Due to the persistent deep coma without response to stimuli, brain CT was repeated and demonstrated cerebral oedema and signs of transtentorial herniation that did not respond to treatment. Faced with a situation of brain death, authorisation for organ donation was requested and was given.



Later, the methanol levels from before haemodialysis (1,793 mg/l) and afterwards (173.4 mg/dl) were made

available.



DISCUSSION



Acute methanol poisoning should be suspected in all patients with metabolic acidosis with an elevated anion gap, neurological deterioration or vision loss.2-4 Although methanol does not cause significant direct intoxication, it is transformed by the liver to formaldehyde and formic acid with leads to metabolic acidosis and cases damage to all levels of the brain and the optic nerve.2-4 Mortality from methanol poisoning is high. In a recent study, it has been established that it is much greater in patients with a blood pH below 7, coma upon admission, delay in seeking medical care and elevated plasma methanol levels.5,6 Treatment is based on inhibition of the alcohol dehydrogenase enzyme, correction of metabolic acidosis and elimination of toxic metabolites by dialysis. Enzyme

inhibition can be achieved with fomepizole or, when this is not immediately available, with ethanol.7 Finally,

haemodialysis with high-permeability membranes at a high flow rate for a prolonged period is capable of reducing

methanol levels as occurred in our patient.8



Unfortunately, many cases lead to brain death and are potential multiorgan donors, given that many publications

have demonstrated that the viability of the organs is adequate.9