Sequelae of Methanol Poisoning in Humans and Experimental Animals

The minimal lethal dose of methanol in humans has not been determined. It has been suggested that about I g kg can cause death if the patient is untreated and has not consumed ethanol.43 In some clinical cases, the blood methanol content is low in the last phase of the poisoning. In three such cases blood methanol concentration was 0.275,_0.277. and 0.194 gi , respectively. On the assumption that the body water in diffusion equilibrium with the blood represents about 709 of the body weight, it has been calculated that 0.19, 0.19, and 0.14 g kg, respectively, was present in the body. Data on the rate of methanol oxidation in humans probab.y do not exist. In rhesus monkeys given I gkg of methanol, Makar et al.26 showed that 37 mgkg; hr was oxidized. Provided that the rate of methanol oxidation is the same in man, the amount of methanol oxidized during 18 hr the average time needed for development of severe acidosis in clinical cases would beO.666g: kg. It seems reasonable stil! to regard I gkg Qf methanol as the approximate minimal lethal dose in man. The severe s mptoms appearing after about 18 hr are well known: vomiting, Kusmauls respiration, pain in the back and the extrerities, and often exceedingly ifent abdominal pains. Simultaneously, or shortly after the onset of severe symptoms. amblyopia appears which may develop rapidly into amaurosis. The pupils are dilated and do not react to light. Sopor and coma follow. The next alarming symptom is a reddish-cyanotic color of the skin. Now the cessation of respiration is not far away. Vhen respiratory arrest occurs it seems too late to save the patient.4"3'44 By ophthalmoscopy, a slight injection of the optic discoccurs in rnan cases, dth or without some blurring of the disc margins. Extensive retinal edemas ere not seen in our cases.3944 Those patients who have regained full vision i.e., V 66 with no central relative scotoma in the course ofa week after treatment, retain it. In patients whose vision partly returns, a decline is observed in the course of some weeks or a fe months. The first clinical sign of optic nerve atrophy, the pale papilla, is seen from 4 to 6 weell aj.Le poisoning. A very marked Post-mortem examination shows some large and ma,y small hemorrhages in the brain and both ganglion cells and glia cells are degenerated. Degeneration of retinal ganglion lls …