| Abstract|| |
Introduction/Purpose: The outbreak of methanol poisoning described in this paper occurred in Ahmedabad, Gujarat, India in July 2009. Our intention is to share the experience of clinical features, laboratory investigations and their relation during this tragedy. Materials and Methods: Single center, retrospective study of clinical features and laboratory parameters of 178 cases of methanol toxicity treated at tertiary care hospital in Ahmedabad, Gujarat. Results: Maximum patients (39.8%, n = 45) were received in 48 h; Mean age of presentation was 41.9 ± 10.2 years. Most of them were men (175 out of 178). On presentation, 83% patients had gastro-intestinal symptoms, 46% had neurological symptoms, 73% had visual symptoms and 32% had dyspnoea. 62% had blurred vision, 10.5% had blindness. Patients with visual symptoms had high mean level of methanol (120.12 ± 23.12 vs. 55.43 ± 29.24, P = 0.014). On fundus examination 52.8% (n = 62) had bilateral hyperaemia of discs, 8.4% (n = 12) had bilateral disc pallor and 4.5% had papilledema (n = 5). Patients with hyperaemia of discs, discs pallor or papilledema, had higher mean methanol level (121.1 ± 32.2 mg% v/s 70.1 ± 23.2 mg%, P = 0.032). Mean of pH values was 7.17 ± 0.22 and bicarbonate was 12.3 ± 7.3 mmol/L. Both pH and bicarbonate levels correlated well with mortality and serum methanol level. Mean serum methanol level was 87.1 mg/dL, and correlated significantly with the mortality (53.1 ± 41 mg/dL v/s 121 ± 92 mg/dL, P value < 0.05). Conclusion: GI symptoms, neurological symptoms and breathlessness are important clue to ED physician for diagnose methanol poisoning. Visual symptoms and fundus findings correlate well with the methanol level. Arterial Blood Gas derived pH and bicarbonate levels correlate significantly with the methanol level and mortality.
Keywords: Ahmedabad, Gujarat, hooch tragedy, methanol poisoning, Shardaben hospital
|How to cite this article:|
Jarwani BS, Motiani PD, Sachdev S. Study of various clinical and laboratory parameters among 178 patients affected by hooch tragedy in Ahmedabad, Gujarat (India): A single center experience. J Emerg Trauma Shock 2013;6:73-7
|How to cite this URL:|
Jarwani BS, Motiani PD, Sachdev S. Study of various clinical and laboratory parameters among 178 patients affected by hooch tragedy in Ahmedabad, Gujarat (India): A single center experience. J Emerg Trauma Shock [serial online] 2013 [cited 2020 Sep 27];6:73-7. Available from: http://www.onlinejets.org/text.asp?2013/6/2/73/110745
| Introduction|| |
Methanol poisoning is fairly common in our country. Many outbreaks of methanol poisoning have been reported from India. ,, Being cheap and potent, it is the first adulterant of illicit liquors.
| Materials and Methods|| |
The outbreak of methanol poisoning described in this paper occurred in Ahmedabad, Gujarat, India in July 2009. Most patients were received in three Municipal Corporation run tertiary care hospitals, Government hospital and few private/corporate setups. We, at the Shardaben Hospital (municipal corporation run hospital), received 178 patients in four days.
Initial diagnosis was made based on a clinical history with sufficient evidence of intake of toxic alcohol, as well as the presence of high anion metabolic acidosis. The accidental exposure and amount of illicit liquors was confirmed by interviewing the patient, relatives and peripheral hospital workers. A brief initial screening examination, including vital signs, mental status and that of the eyes, was performed to identify immediate measures required to stabilize the patient. Airway was secured as necessary in severely intoxicated patients. Hypotension was treated with intravenous crystalloid, followed by standard vasopressors as necessary. Independent ophthalmic opinion was also taken in all the patients. The changes noted were dilated pupils with or without sluggish reaction to light, hyperemia of the discs, retinal congestion and edema, blurring of the disc margins and, later, optic atrophy and varying degrees of loss of vision. All patients were treated with cofactor therapy folinic acid (leucovorin) 50 mg IV every 6 h to accelerate formate metabolism. We administered supplemental thiamine (100 mg IV) and pyridoxine (50 mg IV) and methylcobalamin to all patients. Corticosteroid was also given to patients for visual changes in consultation with the ophthalmologists. All patients with a pH below 7.3 were treated with 1-2 meq/kg of sodium bicarbonate via IV bolus and volume expansion with isotonic saline to correct acidosis and promote diuresis. ,, A maintenance infusion was then prepared by mixing approximately 133 meq of sodium bicarbonate in 1 L of D 5 W. The infusion rate was 150-250 mL/h. The appropriate rate was adjusted in individual patients according to the initial pH, fluid status and serum sodium level. The goal of treatment was maintenance of an arterial or venous pH above 7.35, at which point the infusion was discontinued. As fomepizole was unavailable, patients were treated with ethanol (4-8 mL/kg of a 10% ethanol solution, followed by 0.5-1 mL/kg of 10% ethanol solution infused per h and 50 ml of 95% through Ryle's tube) in any patient with documented recent ingestion of methanol or strong clinical suspicion of ingestion of methanol with an arterial pH <7.3, bicarbonate <20 mEg/L, A standard protocol of therapy was initiated in all the patients to start with and was modified later according to individual patient's needs. Intervention as and when required done. But these management aspects are out of scope of this article.
All the data was collected retrospectively and analyzed.
Our intention is to share the experience of clinical features, laboratory investigations and their relation during this tragedy. Our intention is also to know the prognostic factors in this situation.
Study of treatment given, interventions and outcome is out of the purview of this study.
Data was analyzed using epi2000 and t-test was used to compare the two groups (those who survived v/s those who died after hospitalization). Whenever required ANOVA or Mann-Whitney, two sample tests were applied. Individual variables are compared using the paired t-test. Variables are expressed as mean ± SD, and P < 0.05 was considered to be statistically significant.
| Results|| |
On July 9 th , 2009 an illicit liquor incident took place. The liquor was brewed in the house of locale, who also died after consuming the liquor. More than 1000 liters of hooch containing methanol was brought to Ahmedabad. Eight people, including three women, who were responsible for supplying the spurious brew were subsequently arrested.
Patients presented with breathlessness, visual symptoms, altered mental status. Initially, we were confused about the cause but as many patients started pouring in, we realized the cause can be methanol poisoning in the light of clinical presentation and history. Local authorities also confirmed about such outbreak.
We got 2 patients 12 h after history of hooch ingestion and 1 patient after 18 h of ingestion; maximum patients (39.8%, n = 45) patients in 48 h; 22.1% (n = 21) in 72 h; 3.5% (n = 4) after 72 h, 2 pt after 96 h and 1 patient after 100 h after ingestion.
Mean age of presentation was 41.9 ± 10.2 years, median was 40 years and highest number of victims were in 30-40 years of age-group [Graph 1[Additional file 1]]. Most of them were men (175 out of 178). However, to our surprise, there were 3 female as well. One of female was herself a bootlegger. Most were poor labourer (32%); lorry driver (30%); sweepers (28%) staying in the 'Challis' (close congested localities). Most were driven in by relatives or friends; however few were carried in by Non-Government organizations (NGOs) and social workers. Hundred and eight ambulance services (108 services which was launched in Gujarat on 29 th August 2007 was proven prompt enough to bring the patients to the hospital and also pioneered inter hospital transport).
From those patients were history was possible to elicit, it was found that the mean time of presentation was 30 h and few were carried in as lately as 100 h after history of ingestion. However, those who were brought in late (n = 7) were relatively stable (normal vitals, no visual or neurological symptoms) and dropped in because of panic.
As per history (whenever possible to obtain, n = 77), average amount consumed by them was 150 ml. The proportion of methanol to ethanol in the drink was not known. The forensic science laboratory report revealed that the country-made liquor, consumed by these victims, had a large dose of methyl alcohol-four times the permissible dose-making it lethal.
Eight three percent patients had GI symptoms, 46% had neurological symptoms, 73% had visual symptoms and 32% had dyspnoea [Graph 2[Additional file 2]]. Among GI symptoms nausea 80%, n = 80), vomiting (70%, n = 64) and abdominal pain (8%, n = 12) were common. Few even had taken local treatment for that without getting diagnosed outside. Among the neurological symptoms, giddiness (33%, n = 24), sedation (42%, n = 32), altered sensorium (28%, n = 20), seizure (15%, n = 12) and coma (15%, n = 12) were common.
Among those who survived and could be followed-up, we could diagnose four patients with bilateral putaminal necrosis [Figure 1], delayed onset neuropathy and axonopathy. Two of them had bilateral 7 th and 8 th cranial nerve palsies as well.
Among the visual symptoms most had blurring of vision (62%), 10.5% had blindness. Patients with visual symptoms had high mean level of methanol against those with normal ethanol levels (120.12 ± 23.12 vs. 55.43 ± 29.24, P = 0.014).
On fundus examination, 34.3% had normal fundi examination. Among the rest, 52.8% (n = 62) had bilateral hyperaemia of discs, 8.4% (n = 12) had bilateral disc pallor and 4.5% had papilledema (n = 5) [Graph 3[Additional file 3]]. Among the patients with hyperaemia of discs, discs pallor or papilledema, mean methanol level was higher than in patients with normal fundus examination (121.1 ± 32.2 mg% v/s 70.1 ± 23.2 mg%, P = 0.032).
Mean packed cell volume (PCV) was 45.6 ± 2.1 femtoliters/cell, hemoglobin was 10.2 ± 1.1 mg%; mean potassium level was 3.2 ± 0.6 mEq/L and random blood sugar level 162.2 ± 32.8 mg/dL, mean base deficit was 18.4 mmol/L (range 2-29), anion gap of 25 mmol/L. However, these parameters were not significantly related with serum methanol level or mortality (ANOVA test, logistic regression analysis respectively).
Among the important deviation of the laboratory reports were ABG derived pH, bicarbonate level and serum methanol level. Mean of ABG derived pH values was 7.17 ± 0.22. It correlated statistically significant with the methanol level [Graph 3] (P < 0.05) and with the mortality (P < 0.01). Those who had expired had lower mean pH then those who survived (6.94 ± 0.33 v/s 7.23 ± 0.15, P < 0.01).
Mean of ABG derived bicarbonate was 12.3 ± 7.3 mmol/L. It correlated statistically significant with the serum methanol level [Graph 4[Additional file 4]] (P < 0.05). Bicarbonate also had significant correlation with mortality. Those who expired had much lower bicarbonate level then those who survived had (7.5 ± 4.1 mmol/L v/s 13.3 ± 6.7 mmol/L, P < 0.01).
Mean serum methanol level was 87.1 mg/dL, the maximum was 376 mg/dL, the minimum was 12 mg/dL. Those who expired had significantly higher serum methanol level (53.1 ± 41 mg/dL v/s 121 ± 92 mg/dL, P value < 0.05).
Mean serum ethanol level was 93 m/dL in survival group v/s 154.2 in those who expired (P value 0.39). There was no statistically significant difference of serum ethanol level v/s delay of presentation (Mann-Whitney two sample test, P value 0.16), level of acidosis (Mann-Whitney two sample test, P value 0.47) or bicarbonate level (Mann-Whitney two sample test, P value 0.55).
| Discussion|| |
Methanol poisoning is fairly common in our country. Many outbreaks of methanol poisoning have been reported from India. ,, 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. 
The mean time interval between ingestion and presentation was 30 h. This is because, upon ingestion, methanol is quickly absorbed in the gastrointestinal tract and metabolized in the liver. In the first step of degradation, methanol is transformed into formaldehyde via the enzyme alcohol dehydrogenase (ADH). This reaction is slower than the next step, the transformation of formaldehyde into formic acid via the enzyme aldehyde dehydrogenase. This may explain the reason for the latency of symptoms between ingestion and effect.
Mean age of presentation was 41.9 ± 10.2 years, which signifies alcohol consumption is very common in this particular age group where most of them are earning members of the families. Male are commonly affected, consistent with the Indian culture, where female are less frequently consuming alcohol. However, three female in our study says, few female even in lower socio-economic strata are also consuming such alcohol. Notably, one of the female herself was bootlegger.
In our study the time interval between poisoning and ED presentation in deceased do not correlate statistically significant with mortality. However in some studies, it is shown as even the prognostic factor of mortality. , It may be because of various confounding factors like initial outside treatment, amount of methanol consumed, co-morbid conditions, facilities at the receiving hospital and authorities and administrative commitments.
GI symptoms predominates in such tragedy, few are even brought-in because of such symptoms.  Neurological symptoms in such back-ground clinch the diagnosis.  Most common neurological presentation is with giddiness and altered mental status. However, seizure and coma are the late presenting symptoms.
Visual symptoms are an important clincher in difficult to diagnose cases of methanol intoxication. Detailed visual symptoms history and thorough fundus examination are important in such cases. Fundus findings also correlate well with serum methanol levels.
Ocular changes consisting of disc oedema, blurring of the disc margins, hyperaemia of the discs and optic atrophy as a late squeal, are quite characteristic of methanol poisoning. 
Optic nerve demyelination has been reported to be due to formic acid destruction of myelin. The major damage occurs at the retrolaminar optic nerve, with intra-axonal swelling and organelle destruction. ,
Methanol is rapidly and completely absorbed after oral ingestion. A peak serum alcohol concentration is reached within 1-2 h. An arterial blood gas serves as an essential triage tool when caring simultaneously for multiple patients with poisoning. 
Metabolic acidosis was the most striking disturbance seen in our patients. Metabolic acidosis is probably due to the accumulation of formic acid and lactic acid.  Arterial blood gas derived pH value and bicarbonate levels correlate significantly with the serum methanol level and are also good prognostic factors in methanol poisoning. 
In our study the serum ethanol level did not show significant correlation with mortality, pH or Bicarbonate levels. This may because of possibility of concomitant ethanol ingestion in different forms. It is important to emphasize that the onset of methanol toxicity is delayed when ethanol is co-ingested. Hence, the possibility of concomitant ethanol and toxic alcohol ingestion must always be considered, particularly in alcoholics, who may ingest alcohol in any form.  Ethanol was given for treatment purpose through Ryle's tube and intra-venous route to all victims and the timing of sample collection was also variable. Hence the correlation of blood ethanol level and morbidity and mortality needs to study further.
Increased PCV level, elevated RBS and hypokalemia were found in this study, but did not correlate significantly with the serum methanol level or mortality. These variables are needed to be studied further.  However, these variables should be taken into consideration while treating these patients. According to Swartz et al. an increase in the RBC size is probably responsible for this finding and not the hemoconcentration. 
| Conclusion|| |
GI symptoms, neurological symptoms and breathlessness are important clue to ED physician for diagnose methanol poisoning. Visual symptoms and fundus findings correlate well with the methanol level. Increased PCV, blood sugar, hypokalemia are important associations to be taken into consideration while treating these patients. ABG derived pH and bicarbonate levels correlate significantly with the methanol level. Methanol level takes time to be available or not possible in some settings and mortality. Hence, pH and bicarbonate level helps to manage such patients and predict the mortality risk as well.
Limitations of the study
The limitation of our retrospective study is that we have limited history about the amount of hooch consumption, exact time of consumption, co-ingestions, treatment taken from outside set-ups initially. We are not analyzing or taking into consideration the outcome in different treatment groups.
GI symptoms, neurological symptoms and breathlessness are important clue to ED physician for diagnose methanol poisoning. Visual symptoms and fundus finding correlate well with the methanol level. Increased PCV, blood sugar, hypokalemia are important associations to be taken into consideration while treating these patients. ABG derived pH and bicarbonate levels correlate significantly with the methanol level and mortality.
| Acknowledgment|| |
I would like to thank my Head of Department, Dr. Subha Desai; head of the Unit Dr. I. K. Ramnani and residents, who helped to treat these patients and put together these data for analysis.
| References|| |
|1.||Ravichandran R, Dudani RA, Almeida AF, Chawla KP, Acharya VN. Methyl alcohol poisoning.(Experience of an outbreak in Bombay). J Postgrad Med 1984;30:69-74. |
|2.||Krishnamurthi MV, Natarajan AR, Shanmugasundaram K, Padmanabhan K, Nityanandan K. Acute methyl alcohol poisoning. (A review of an outbreak of 89 cases). J Assoc Physicians India 1968;16:801-5. |
|3.||Divekar MV, Mamnani KV, Tendolkar UR, Bilimoria FR. Acute methanol poisoning: Report on a recent outbreak in Maharashtra. J Assoc Phys India 1974;22:477-83. |
|4.||Kumar SS, Seerala Boopathy K, Bhaskar ME. Methanol poisoning-A Chennai experience. J Assoc Physicians India 2003;51:425-6. |
|5.||Kute VB, Godara SM, Shah PR, Gumber MR, Goplani KR, Vanikar AV, et al. Hemodialysis for methyl alcohol poisoning: A single-center experience. Saudi J Kidney Dis Transpl 2012;23:37-43. |
|6.||Hassanian-Moghaddam H, Pajoumand A, Dadgar SM, Shadnia Sh. Prognostic factors in methanol poisoning. Hum Exp Toxicol 2007;26:583-6. |
|7.||Martin-Amat G, McMartin KE, Hayreh SS, Hayreh MS, Tephly TR. Methanol poisoning: Ocular toxicity produced by formate. Toxicol Appl Pharmacol 1978;45:201-8. |
|8.||McMartin KE, Ambre JJ, Tephly TR. Methanol poisoning in human subjects. Role for formic acid accumulation in the metabolic acidosis. Am J Med 1980;68:414-8. |
|9.||Berger JR, Ayyar DR. Neurological complications of ethylene glycol intoxication. Report of a case. Arch Neurol 1981;38:724-6. |
|10.||Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA, American Academy of Clinical Toxicology Ad Hoc Committee on the Treatment Guidelines for Methanol Poisoning. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol 2002;40:415-46. |
|11.||Sanaei-Zadeh H, Esfeh SK, Zamani N, Jamshidi F, Shadnia S. Hyperglycemia is a strong prognostic factor of lethality in methanol poisoning. J Med Toxicol 2011;7:189-94. |
|12.||Swartz RD, Millman RP, Billi JE, Bondar NP, Migdal SD, Simonian SK, et al. Epidemic methanol poisoning: Clinical and biochemical analysis of a recent episode. Medicine (Baltimore) 1981;60:373-82. |
Bhavesh S Jarwani
Department of Medicine and Emergency Medicine, Smt. NHL Municipal Medical College, VS General Hospital, Ahmedabad, Gujarat
Source of Support: None, Conflict of Interest: None