Methyl alcohol poisoning. (Experience of an outbreak in Bombay).
Methyl alcohol is a cheap and potent adulterant of illicit liquors. Many outbreaks of methyl alcohol poisoning have occurred in our country.,, Such outbreaks have been responsible for a heavy toll of mortality and morbidity. This paper describes our clinical experience in the management of patients with methyl alcohol poisoning emphasizing that early identification and prompt management is of prime importance in these unfortunate patients.
The outbreak of methanol poisoning described in this paper occurred in a suburban area of Bombay (in a locality between Chembur and Ghatkopar). Most of the patients were admitted to the nearby peripheral hospital, where the killer drink had already taken its heavy toll. Only 47 patients were directed to the K.E.M. Hospital, Bombay. Detailed history was taken from all the patients except two who were critically ill. All the cases were throughly examined with special attention to the eyes. Independent ophthalmic opinion was also taken in all the patients. A sample of blood was drawn for haemogram, plasma bicarbonate levels, serum electrolytes, BUN, serum creatinine, SGOT, SGPT and serum proteins. The urine was tested qualitatively for the presence of methanol and its metabolites. A standard protocol of therapy was followed in all the patients to start with. This was modified later according to individual patient's needs. The protocol consised of I.V. infusion of 7.5% sodium bicarbonate, in a loading dose of 180 meq followed by a maintenance dose of 18 meq/hr. Additionally, 2% absolute alcohol in dextrose was infused at a rate of 9 gm/hr. Massive doses of corticosteroids, Vit. B1, B6 and B12 were also given to all the patients in consultation with the ophthalmologists. The amount of I.V. sodium bicarbonate and absolute alcohol administered was guided by the clinical condition of the patient and plasma bicarbonate levels.
Despite receiving adequate sodium bicarbonate and ethyl alcohol, five patients showed persistent metabolic acidosis and further deterioration of vision and were taken up for hemodialysis. In these patients, the dose of ethyl alcohol administered was increased in order to compensate for the loss during dialysis. Oral therapy with ethanol (20%) and sodium bicarbonate was continued till the patients recovered completely. Two patients died soon after admission and were autopsied and the results of the chemical analyses were available later on.
Out of the 47 patients admitted, 46 were males and only one was female. Most of them were between 30 and 40 years of age [Table 1].
The quantity of the illicit drink consumed was known in all the cases except in one who died soon after admission. It ranged from 100-500 ml [Table 2]. The proportion of methanol to ethanol in the drink was not known.
The interval between the consumption of the drink and the appearance of symptoms varied between 8 and 60 hours. Majority of the patients had symptoms within 12-24 hours after alcohol consumption. Thirteen patients did not have any symptoms, but had sought admission out of fear. It was interesting to note that all of them had biochemical acidosis and three had definite fundal changes.
The symptoms which prompted the patients to seek medical aid are shown in [Table 3].
On detailed examination of the eyes, as many as 33 patients were found to have changes of varying severity. The changes noted were dilated pupils with or without sluggish reaction to light, hyperemia of the discs, retinal congestion and oedema, blurring of the disc margins, and later on optic atrophy and varying degrees of loss of vision. There was a good correlation between the ocular changes and the degree of acidosis [Table 4].
An interesting feature was the elevated haematocrit that these patients manifested on routine check up. As many as 35 patients had an hemoglobin value of more than 14 gm%, and PCV of more than 45%. Definite hypokalemia (serum potassium: 2.4 to 3 meq/1) was seen in as many as 8 patients before starting any form of therapy.
Response to intensive alkali and ethanol therapy was good in 30 patients. Out of the five patients who were taken up for hemodialysis, only one showed slight improvement in vision after dialysis. On the whole, fifteen patients were left with permanent visual damage of varying degree. The autopsy done on two patients who died before any form of therapy could be given, showed marked cerebral oedema with neuronal degeneration. Blood vessels showed congestion with infiltration around them. Chemical analysis revealed presence of methanol as well as ethanol in all the viscera including the stomach.
Methanol poisoning is fairly common in our country. Being cheap and potent, it is the first adulterant of illicit liquors. It goes by the names of khopadi, ladda, dalda, bewada, french polish, etc. Methanol poisoning, whether sporadic or mass poisoning is an acute medical emergency. If not recognised in time and treated on sound basis of pharmacology and toxicology of this alcohol, it can lead to considerable magnitude of morbidity as well as mortality. Our present study does not truly represent the mortality of this outbreak since only a fraction of the patients were directed to this institution and many more had already died either at home or in the nearby peripheral hospitals.
The potentially lethal dose of methanol is variable. The lowest reported is 30 ml. The peculiarity of methanol poisoning is the latent period between the ingestion of the alcohol and the appearance o manifestations. The latency may be related to the concomitant ingestion of ethanol which affects the metabolism of methanol. The symptoms of methanol poisoning are non-specific except for the visual disturbances. Ocular changes consisting of retinal oedema, blurring of the disc margins, hyperemia of the discs and optic atrophy as a late sequlae are quite characteristic of poisoning.,,, ,
The terminal event is often respiratory arrest. The fatal period is from 6-36 hours. It is the personal experience of the authors, that once the symptoms develop they progress at an alarmingly fast rate.
Metabolic acidosis is the most striking disturbance seen in methanol poisoning. It is probably due to the accumulation of formic acid and lactic acid.,,, Animal experiments (except in monkeys) are of limited value, as most animals do not develop acidosis secondary to mathanol administration., The ocular changes correlate to the degree of acid osis.,,,, Retinal damage is believed to be due to the inhibition of retinal hexokinase by formaldehyde, an intermediate metabolite of methanol.
The elevation of hematocrit seen in majority of patients included in this study has also been reported earlier. According to Swartz et al, an increase in the RBC size is probably responsible for this finding and not the hemoconcentration. 17.3% of the patients in the present study had hypokalemia initially, which is an important point to be considered while treating these patients.
The essential therapy of methanol poisoning is adequate alkalinisation and ethanol administration. Ethanol competes with methanol for the enzyme alcohol dehydrogenase in the liver, thereby preventing the accumulation of toxic metabolites of methanol in the body. The recommended dose of ethanol is 0.6 gm/kg body weight (a loading dose) followed by an infusion of 66 mg/kg/hour in nondrinkers and 154 mg/kg/hour in chronic drinkers. The idea is to maintain a blood level of ethanol at 100 mg%., Alkalinisation is the oldest form of therapy suggested to combat the acidosis and very large doses of sodium bicarbonate may be required. The recommended dose is 180 meq as the loading dose, followed by 1S meq/hour of sodium bicarbonate as an infusion.
Dialysis is recommended in those patients who have visual disturbances, blood methanol of 50 mg% or more, ingestion of more than 60 ml of methanol and severe acidosis not corrected by sodium bicarbonate administration.,,,,,
There have been several episodes of methanol poisoning in our country carrying a very high mortality rate. In 1971, 90 deaths were reported from Khopoli due to methanol poisoning and subsequently 100 deaths from Hyderabad; 20 deaths from Madras and more than 300 deaths from Bangalore have also been reported. Krishnamurthi et al, from Madras in 1967, have described 87 patient of methanol poisoning managed with intensive alkali therapy and supportive measures; 32 patients in their series died. Subsequently Divekar et al, from Bombay, described their experience in managing 45 cases of methanol poisoning from Khopoli. Their patients were also treated with intensive alkalinisation, ethanol administration and supportive measures. Out of the 45 cases, 7 died and 3 developed permanent blindness. Bade and Sapre, from Poona, have described 11 cases of methanol poisoning in 1981. In their series, 2 were brought dead and the rest died within 3 days. Hence it can be seen from the previous Indian reports that there is a high mortality associated with methanol poisoning which has been attributed to the delay in the treatment. In none of the above mentioned series, hemodialysis could be offered as a means of treatment. Our experience is different from the previous ones in the sense that the patients were treated fairly early and haemodialysis was given to some of them achieving a low mortality rate.
We thank Dr. C. K. Deshpande, Dean, Seth G.S. Medical College and K.E.M. Hospital for permitting us to publish the hospital records. We also thank the opthalmologists in the K.E.M. Hospital for the help rendered by them in managing these patients.