34

© JAPI • may 2012 • VOL. 60

Original Article

Study of 63 Cases of Methyl Alcohol Poisoning (Hooch

Tragedy in Ahmedabad)
Sandip Shah*, Vikas Pandey*, Nilay Thakore**, Ilesh Mehta***

Abstract
Background : Many outbreaks of methyl alcohol poisoning have been reported from India. Early and aggressive
management with bicarbonate, ethanol and hemodialysis in patients having significant toxicity will decrease
mortality and improve patient’s outcome. Our experience of retro bulbar steroid injection indicates that it may
improve visual outcome.
Materials and Methods : Hospital based study of patients admitted to V.S. Hospital during the outbreak of
methanol poisoning in Ahmedabad. Patients were identified by history supplemented by ophthalmic examination
and biochemistry. A stepwise treatment was undertaken i.e. aggressive treatment with bicarbonate, ethanol
and institution of hemodialysis in patients who had refractory high anion gap metabolic acidosis, visual signs
and symptoms, deteriorating vital signs and serum methanol level > 50 mg/dL. Patients who were having optic
neuritis were given retrobulbar steroids.
Results : Total 63 males were admitted between 18 to 60 years. 17 patients were terminally ill with hypotension,
could not be subjected for hemodialysis and expired. Of remaining 46 patients, 20 responded to conservative
management whereas 26 underwent hemodialysis of which only 3 died.
Conclusion : Patients undergoing hemodialysis showed immediate improvement in their clinical and biochemical
parameters with rapid reductions of methyl alcohol levels below the toxic range with subsequent reduction in
morbidity and mortality. All the patients given retrobulbar corticosteroid injection showed improvement in
fundoscopic examination and perimetric charting with maximal improvement in visual acuity in hemodialysed
patients.

Introduction
M ethyl alcohol is a cheap and potent adulterant used in
manufacture of illicit liquors. Many outbreaks of methyl
alcohol poisoning have been reported from India.1,2 The present
study describes our experience in the management of patients
with methyl alcohol poisoning and emphasizes the role of early
and aggressive treatment with bicarbonate, ethanol and of
hemodialysis in patients having significant toxicity.3
Materials and Methods
This study involved 63 patients who were admitted to
Vadilal Sarabhai General Hospital during methanol poisoning
outbreak in Ahmedabad in 2009. Our present study does not
truly represent the burden of this outbreak since only a fraction
of the patients were directed to this institution. Patients were
selected according to criteria mentioned in Table 1 and managed
in a stepwise manner as mentioned in Table 2. Fomepizole, a FDA
approved drug was not available, so not used as our treatment
modality. The dose of ethanol and criteria for selection of
patients who needed dialysis is mentioned in subsequent tables.
Complete ophthalmic evaluation was undertaken and all those
who had visual toxicity, retrobulbar triamcinolone was injected
irrespective of severity of damage.
Results
Total 63 male patients between 18 to 60 years were admitted.
Most of them had consumed 150 to 250 ml of alcohol 24-48
hours back. All except one had ABGA suggestive of high
anion gap metabolic acidosis with hypokalemia. Seventeen
patients had hypotension, could not undergo hemodialysis and
died. Of remaining 46 patients, 20 responded to conservative
management, rest 26 underwent hemodialysis and only 3
died. Patients who underwent hemodialysis showed rapid
improvement in their clinical and bio chemical parameters
with rapid reduction in methyl alcohol levels to below the toxic
range with subsequent reduction in morbidity and hospital
stay. Ethyl alcohol drip was admitted in patients managed
conservatively up to one week unlike hemodialysed patients
who were administered intravenous ethyl alcohol for 3 days.
Ophthalmic examination revealed dilated pupils with sluggish
reaction to light (20%), hyperemia of disc with blurred disc
margin (55%), retinal congestion (45%) and varying degree of
vision loss (Visual blurring 60%, Below finger counting 10%).
All these patients were given retrobulbar corticosteroid. They
improved with declined retinal congestion and edema (75%).
These patients were followed up and showed improvement in
fundoscopic examination and perimetric charting. The recovery
was maximal in patients who underwent hemodialysis.

Discussion
Senior Resident, **Associate Professor, ***Head of Unit, Department of
*
Methanol, also known as wood alcohol, is a commonly used
Medicine, Sheth K.M. School of Postgraduate Medicine and Research,
Smt. N.H.L. Municipal Medical College, V.S. Hospital, Ahmedabad organic solvent, the ingestion of which has severe potential
Received: 20.07.2009; Revised: 12.09.2011; Accepted: 23.09.2011 ramifications. It is a constituent in many commercially available
© JAPI • may 2012 • VOL. 60 35

Table 1 : Criteria of diagnosing methanol toxicity industrial solvents and in poorly adulterated alcoholic beverages.
1. Documented plasma methanol concentration >20 mg/dL (>200 Toxicity usually occurs from intentional overdose or accidental
mg/L).* ingestion and results in metabolic acidosis, neurologic squeal,
2. Documented recent history of ingesting toxic amounts of and even death. Methanol toxicity remains a common problem in
methanol and osmolal gap >10 mOsm/kg.* many parts of the developing world, especially among members
3. History or strong clinical suspicion of methanol poisoning with
of lower socioeconomic classes.
at least two of the following criteria*: Methanol is readily and rapidly absorbed from all routes
A. Severe metabolic acidosis i.e. Arterial pH <7.3 of exposure (dermal, inhalation and oral), easily crosses all
B. Serum bicarbonate <20 meq/L(mmol/L) membranes, and thus is uniformly distributed to organs and
tissues. The potentially lethal dose of methanol is variable. The
C. Osmolal gap >10 mOsm/kg
lowest reported is 30 ml.[5] The peculiarity of methanol poisoning
*
Any one of the three is the latent period between the ingestion of the alcohol and the
Table 2 : Stepwise algorithm of management
@ appearance of manifestations. The latency may be related
to the concomitant ingestion of ethanol which affects the
Suspected or Confirmed Methanol Poisoning
metabolism of methanol. 6 Methanol has relatively low
toxicity. Methanol is metabolized in a sequential fashion,
Does patient meet criteriaz in Table 2? No Reconsider diagnosis and reassess principally in the liver by alcohol dehydrogenase leading to
formation of formaldehyde. The latter undergoes oxidation
Yes
to formic acid, facilitated by formaldehyde dehydrogenase.
Supportive care as needed
Administer folic acid or folinic acid (Leucovorin)
The conversion of formaldehyde to formic acid is very
rapid with a half-life of 1-2 minutes. There does not appear
No PH <7.3?
Fomepizole Available? No
to be any accumulation of formaldehyde in the blood.
Bicarbonate
Not Necessary
Formate metabolism is dependent upon the presence of
Yes Yes Administer ethanol per tetrahydrofolate to form 10-formyltetrahydrofolate that can
Table 3
be metabolized to carbon dioxide and water or alternative
Administer bicarbonate to
correct pH to >7.3
Administer dose of
15 mg/Kg
metabolic pathways. The half-life of formate is 20 hours in
humans.
pH < 7.25-7.30 Moniter
OR
Visual signs/symptoms
serum
ethanol
Nicholls7 has demonstrated that formic acid can inhibit
OR
Deteriorating vital signs despite intensive
concentration
every 1-2 cytochrome C oxidase activity in intact mitochondria, in
hourly and
supportive care
OR
adjust infu- submitochondrial particles, and in isolated cytochrome
sion rate in
Renal failure
OR
attempt to
achieve a
aa3. Formic acid binds to the sixth coordination position
Significant electrolyte disturbance unre-
sponsive to conventional therapy
target
concentration of ferric heme ion in cytochrome oxidase, preventing
OR
Serum methanol concentration ≥ 50 mg/dl*
of 100-150
mg/dl oxidative metabolism. This is due to the affinity of formic
acid for ferric iron moiety. This affinity is also thought to be
Continue until
Yes No
serum methanol
concentration is < 20
causing methemoglobinemia seen rarely in cases of severe
mg/dl methanol poisoning. The inhibition of cytochrome oxidase
Hemodialyze Fomepizole Treated? No
complex at the terminal end of the respiratory chain in the
Administer ethanol per
Table 3 No Fomepizole Treated? Yes mitochondria leads to “histotoxic hypoxia.” The binding of
Yes Maintain doses of 10 mg/kg every 12
formic acid to cytochrome oxidase is similar to that seen with
Monitor serum ethanol concentration
every 1-2 hours and adjust infusion rate
hours for 4 doses, followed by 15 mg/Kg
every 12 hours until serum methanol other toxins such as cyanide, hydrogen sulfide, and carbon
in an attempt to achieve a target concen-
tration of 100-150 mg/dl Treat accord-
concentration is < 20 mg/dl
monoxide, although formic acid is a less potent inhibitor. The
ing to Table 4
until serum inhibition of cytochrome oxidase by formic acid increases
methanol
Continue until serum methanol
concentration is <20 mg/dl
concentration
are < 20 mg/dl
with decreasing pH. This suggests that the active inhibitor
is the undissociated acid as the concentration of the latter
increases with fall in pH and as the inner membrane of the
*
Although this should be considered to be an indication for hemodialysis in ethanol treated patients, hemodialysis may be withinheld in fomepizole
treated patient with serum methanol concentration greater than 50 mg/dl, but this may result in significant prolongation of hospitalization.

These guidelines are based on the data presented in this document. Where data was insufficient to validate a specific recommendation the Committee’s
best judgment, based on the available data is presented. This algorithm should be considered to represent general guidelines. Deviations from this
mitochondria is only permeable to the undissociated acid.
algorithm may be justified in individual patients based on the clinical judgement of the treating physician.
Therefore, as the pH falls, cytochrome oxidase inhibition is
@ alaamed research/scribd potentiated and the onset of cellular injury is hastened.

Table 3 : Ethanol dosage regimens

A. Loading Dose of Ethanol
1. Intravenous : 7.6 – 10 mL/kg of a 10% solution in Dextrose 5%. Ethanol is available as 5% or 10% solutions in Dextrose 5%; the latter is
preferred.
2. Oral : 0.8 – 1 mL/kg of 95% Ethanol, administered PO in orange juice.
B. Maintenance Dose of Ethanol
  10% ethanol IV 40% ethanol PO 95% ethanol PO Hemodialysis with 10% ethanol IV
  (mL/kg/hr) (mL/kg/hr) (mL/kg/hr) (mL/kg/hr)
Moderate 1.4 0.3 0.15 2.7
Drinker        
Chronic 2 0.4 0.2 3.9
Drinker        
Nondrinker 0.8 0.2 0.1 2.7
36 © JAPI • may 2012 • VOL. 60
Table 4 : Methanol metabolism22
ADH: alcohol dehydrogenase; ALDH: aldehyde dehydrogenase
The symptoms of methanol poisoning are non-specific
except for the visual disturbances. Ocular changes consisting
of retinal edema, blurring of the disc margins, hyperemia of the
discs and optic atrophy are late squeal and are characteristic of
poisoning.8-11 The terminal event is often respiratory arrest. The
fatal period is from 6-36 hours. Metabolic acidosis is the most
striking and is probably due to the accumulation of formic
acid and lactic acid.12,13 The ocular changes correlate to the
degree of acidosis.8,10,11 Retinal damage is believed to be due
to the inhibition of retinal hexokinase by formaldehyde, an
intermediate metabolite of methanol.10
Ethyl alcohol used, delays metabolism of methyl alcohol to
its toxic metabolites by competing for alcohol dehydrogenase.14
Maintenance of serum ethanol level above 100 mg% is required.15
Folinic acid also increases metabolism of formates and prevents
complications.16 Fomepizole(4-methyl pyrazole) is a direct
alcohol dehydrogenase antagonist17 which is FDA approved for
treatment but not available in India.
Hemodialysis whenever available should be used as a
treatment modality in classified patients such as those having
persistent refractory high anion gap metabolic acidosis, visual
and mental obtundation, >30 ml of methyl alcohol ingestion or
>50mg/dl of blood levels,18,19 deteriorating vital signs despite
intensive supportive care, renal failure or significant electrolyte
disturbances unresponsive to conventional therapy.20
Intravenous or topical steroid therapy could salvage vision in
patients having retinal toxicity.21 Our experience of retrobulbar
injection of triamcinolone4 indicates that it may improve visual
outcome. Steroids are helpful in alleviating signs of retinal
inflammation. But as the retinal toxicity is due to accumulation
of toxic metabolites of methanol, treatment with Folinic acid
and Hemodialysis cause removal of these products and in our
study significant visual improvement is noted in patients who
underwent hemodialysis.14
Acknowledgement
We would like to express our respect and gratitude to our
Alma-mater ‘Sheth K.M. School of Postgraduate and Research’
for the foundation they laid in shaping our careers.
We gratefully acknowledge the contribution of Dr. Roshan
Mistry and Dr. Bhikhudan, our junior residents during this
case study.
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