-
~
Aust pp 65-68 ~ N Z- J Med ~ (1979). _ 9,_ ~
An Outbreak of Acute Methyl Alcohol Intoxication S. Naraqi*, R. F. Dethlefst, R. A. Slobodniuk! and J. S. Sairere** From the Department of Clinical Sciences Faculty of Medicine, University of Papua New Guinea Port Moresby, Papua New Guinea
Summary:
An outbreak of acute methyl alcohol intoxication. S. Naraqi, R. F. Dethlefs, R. A. Slobodniuk and J. S. Sairere, Aust. N.Z. J. Med., 1979, 9, pp. 65-68.
An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60-600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8-36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.
Outbreaks of acute methyl alcohol (methanol) intoxication occur periodically in both developed and developing countries. Since 1953. very little has been written on the clinical features of this poisoning. Most of the recent publications on this subject deal with haemodialysis as the most effective treatment.'-" Methanol, a cheap 'Lecturer in Medicine +Specialist Medical Officer, Ophthalmology :Registrar in Medicine. "Resident in Medicine. Correspondence- Dr S. Naraqi. P.O. Box 5623. Boroko, Papua New Guinea Accepted for publication. 16 October, 1978
alcohol. is used as duplicating fluid, paint remover and a s a cleaning agent and can be purchased from drug storcs in the form of mcthylated spirit. It has been suggested that there will be an increase in the number o f methanol poisoning outbreaks in the developing countries of the Pacific R e g i ~ nThis . ~ increase is thought to be the result of an interface between traditional and modern factors in rapidly changing societies of the area, as more and moi-c of these countries become independent. In most of the developing countries, extensive laboratory facilities and haemodialysis arc not available. It is therefore important for the medical practitioners who work in such countries to make themselves familiar with the clinical manifestations and diagnosis of methyl alcohol poisoning and ils management by means other than dialysis. In Papua New Guinea, two outbreaks of methyl alcohol intoxication occurred in 1977. despite extensive publicity and educational campaigns after the first accident. The first outbreak is the subject of this report. (The second outbreak occurred six months after the present one in the city of Lae. Four persons werc involved; lhree of them died and one became blind.) Report of the Outbreak Getieral Injiwniu fiori In March 1977. 32 young men attended a drinking part! in a village near Port Moresby. They drank the contents of a drum which was said to have been found near their village. A sample of the fluid was analysed latcr by gas chromatography and found to be pure methyl alcohol. Small bottles of coke or regular glasses mere filled up to a third with methanol and twice as much water, orange juice or cola beverage was added before consumption. Four persons who attended the party but did not drink the inaterial because o C its unusual odour and/or taste did not become ill. Age of the patients ranged from 17 39 years (mean: 23). Estimated amount of pure methanol consumed by each individual ranged from 60-600 ml (mean: 275). Three patients had consumed ethanol immediately prior to drinking methanol. The interval between consumption of methanol and the appearancc ofthe first symptoms of toxicity (latent period) ranged rrom X 36 hours (mean: 18).
TABLE 1 Symptoms and signs of acute methanol intoxication in 28 patients huniber of patients Ocular: Blurred vision Eye pain Conjunctival congestion Pupillary changcs Fundi changes Diminished visual acuity (counting fingers) Gastrointestinal: Abdominal pain Vomiting Nausea Epigastric tenderness Decreased bowel sounds
20 (13)* 16 (9) 21 17 21
available in seken patients before sodium bicarbonate infusion. All showed severe metabolic acidosis. pH rmgcd from 7 . 1 3 7.26. K O , from 10 29 and serum bicarbonate from 10 14 mEq I . POz was normal and serum potassium high ( 5 . 4 6 . 4 mEq,r) i n all. In three out of six paticnts who had daily blood gas analysis. acidosis persisted for 36-48 hours. TABLE 2 Summary ufthe pertinent findings in Cour fatal cases o f acute methanol intoxication Patients
II
17 ( 5 ) 17 ( 6 ) 14 10 7
Central Nervous: Headache Dizziness Lethargy Restless11ess Coma Seizures
19 (3) 13 (1) 15 7 6 (4) 4
Respiratory: Breath odour (of formalin) Kussmaul respiration
23 17
*Numbers in parenthesis indicate the frequency ofrespectivc symptoms as the chief cornplaints of the patients. .Syniptonzs und Signs The symptoms and signs observed in these patients are shown in Table 1 . Disc hyperaemia and dilated pupils with absent or sluggish light reflex were common findings. The details of ocular manifestations and complications arc reported separately.' Headache and diiziness were transient and disappeared after 24 hours. Four patients were admitted comatose and two developed coma during the hospital course. SeiLures developed within 48 hours after admission. Kussmaul (deep and rapid) respiration (respiratory rate ranged froin 28 36imin) was observed within 24 hours after admission in 15 and on the second hospital day in two patients. No one complained of respiratory difficulties. Respiratory rate was not increased in the other ten patients and remained normal throughout their hospital course. Fever, and syniptoms or signs related to renal or cardiovascular systems were notably absent.
Laborarorjz Invrstigutiuns A full scale laboratory investigation could not be done on all of the patients prior to treatment owing to the large number of patients admitted in a short period of time. shortage of staff and a state holiday. Haemoglobin, peripheral leukocyte count and differential, blood urea nitrogen, serum sodium and chloride and blood sugar performed before any treatment in half to two-thirds of the patients were all within normal limits. Serum am e level was measured in 22 patients and was elevated in 11 (ranging from 400-1320 IU /). Serum calcium level was low in six patients with pancreatitis (4 -7.8 mg?,,). Blood gas analysis was
I
Age (years) Latent period (hours) Presenting symptom Ocular changes Seizures Serum amylase ( I U ,I ) Blood pH Scrum potassium ( m E q l) Methanol level: (nip;100 mlj Amount of bicarbonate used for treatment** (mmol) Duration of acidosis (hours)
I1
111
IV
27 19 19 20 8 36 12 12 Coma ('omd Coma Coma
*
*
*
*
*
*
r
460 345 1000 1320 7 26 7 13 7 4M 1 2 3 6 4 5 4 6 4 6 1 73
233
326
4000 4000 4000
3000
48
111
36
48
36
*Present. i.Performed after bicarbonate therapy.
:Ethanol level was 123 i n patient 111. In the other three. as with patients who survived. the amount was negligible. **500 ml every 4-6 hours. Methanol unJ Etliariol Level In 15 patienti methanol and ethanol levels w r e measured retrospectively on a sample of blood drawn within the first 48 hours after admission. Methanol level ranged from 5-326 mg8'100ml. The fatal cases had the highest lcvels (Table 2). Levels above 50 mg'l00 ml were seen in two nonfatal cascs, one with severe visual impairment (66 mg) and the other with no residual complications (176 mg). A significant ethanol level n,as found only in one patient who did not survive. 7i.eutrnent
Peritoneal or haemodialysis was not available to our patients. Ethanol was not used in any of them. Pancreatitis was treated with nasogastric suctioning and intravenous fluids. Seventeen patients with acidosis, which was diagnosed either by the presence of Kussmaul respiration (ten patients) or low blood pH (seven patients). received sodium bicarbonate (4.5:" solution) infusion for the treatment of acidosis. The amount ranged from 500 4000 mmol and it was given over 4 48 hours (500,'4 ~6-hourly).usually within the first three days of hospitalization. Hospitul Cour.w and Outcome Hospital stay ranged from 2-30 days (mean: 6). Four patients died within 72 hours of admission. Clinical and laboratory findings in these patients are summarized in Table 2. Of those
bTBRU4RY __
1975)
67
M L l HYL A1 COHOL INTOXICATIO\
--
-~ ~
TABLE 3 Significant .ind non-signihcant prognostic fdctors in 28 pdlients
4 ith
ncute methanol intoticatlon
-
Patient groups Fatal With Tequctde Complete recolerq
--__
Number of patient5
Amount consumed (ml) Rdnge Medn
4 X 16
bnknomn 120 600 360 60 500 240
Latent period (hour\) Range - Mean Coma 8 36 8 23 8 36
17 15 17
4
Seimres
2
2 0
0
0
Duration of dcldo5is* (houi s) Range - Mean 36 4x 24 48 4 -24
42 25 10
*Based o n the presence of Kussmaul respiration and the continuous need for sodium bicarbonate infusion ( P< 0.01).
who recovered. 16 were free of complications and cight had disabling complications: two became totally blind; four had severe visual impairment and two had difficulty with speech (which was attributed to a pseudobulbar palsy syndrome) as well as severe visual defects. None of the patients with pancreatitis dcveloped pancreatic abscess or pscudocyst during a three month follow up period. Prognostic Fucror.5 To identify the significant prognostic factors, patients were arbitrarily divided into three groups (Table 3). The estimated amount of consumed inethanol and the length 01 latent period had no effect on the outcome. Coma. seizures and prolonged acidosis (more than 36 hours) wcre found to indicate a bad prognosis: all patients who had coma or seizures either died OT had severe residual defects after recorery; only one patient with acidosis for longer than 36 hours recovered completely. Using Wileoxon rank sum test method, it was found rhat the mean duration of acidosis &:is significantly higher in fatal cases as compared to non-fatal ones. The difference remained significant nhen the combined “fatal” and “with sequelae” groups were compared with the “complete recovery” group.
Discussion
As documented previously and confirmed in this report. acute methyl alcohol intoxication produces a distinct clinical picture: there is a latent period of several hours to scveral days between the consumption of methanol and the appearance of first symptoms of toxicity; a combination of blurred vision, abdominal pain and vomiting as well as conjuctival congestion, dilated pupils with absent or sluggish light reflex. hyperaemic discs and Kussmaul respiration are found in the majority of the patients in the first 24 hours after admission. The diagnosis of methanol poisoning should be considered in any patient who has a combination of typical ocular changes with either gastrointestinal findings or metabolic acidosis even in the absence of a history of methanol ingestion. Four distinct clinical syndromes were observed in this outbreak, visual disturbances, pancreatitis, metabolic acidosis and diffuse
encephalopathy. Visual disturbances were the most common findings. Ocular pain and conjunctival congestion have not reccived emphasis previously. Steroids, given to two of the patients. had no beneficial effect on ocular damage.6 The incidence, of pancrcatitis in this outbreak is consistent with the findings of others both based on serum amylase level and on post mortem examination.’ Abdominal pain and tenderness in patients with no rise in serum amylase level, may have been due to gastritis which has been Sound in post mortem of fatal cases of methanol intoxication.’ Metabolic acidosis was thought to be present in 60% of the patients as indicated by Kussmaul respiration. This was confirmed in one-third of the patients by studying serum bicarbonate and blood gases. Kussmaul respiration is a useful sign for the detection of acidosis but it is not a reliable index of the degree of acidosis. Furthermore, not all of the patients with acidosis have K ussmaul respiration.’ Therefore the diagnosis of metabolic acidosis: as well as monitoring of its treatment, should be based on serum bicarbonate measurement andlor blood gas analysis whenever possible. The mortality rate in this outbreak (1273 was the same as the outbreak in Georgia.’ Prolonged acidosis, coma and seizures were found to be poor prognostic factors. The identification of poor prognostic factors may be of value if the supply of sodium bicarbonate is short or dialysis Sacilities are limited. Bradycardia, another sign of a poor prognosis’, was not observed in our patients. There was no relationship between methanol intake and the prognosis. Extreme variation in the individual response to a given quantity of methanol has been reported and some of the observations in this outbreak confirmed it.”‘ One of the patients in this
68
~ _ _ _
hARAQ1 EI' AL.
VOL.
9,
NO.
1
~
outbreak who not only survived but recovcred completely, admitted to drinking the equivalent to 600 ml ofpure methanol. This is fw more than the amount reported by Bennett et d.who cite the survival of a patient after ingestion of 500 ml of 409,,, methanol.' The unavailability of dialysis in developing countries imposes special problems in the management of patients with methanol poisoning. Haemodialysis is the most effective treatment but is not available in most of these countries. A flying-in haemodialysis team would be an ideal substitute. but most of the developing countries do not have one and its importation from a nearby country may be costly and d to arrange. Peritoneal dialysis is the second choice and is available t o a limited dcgree in some o f these countries.2.3It can, and should be used in sporadic cases. In the absence of dialysis, alkalinization by sodium bicarbonate is thc cornerstone of treatment of these patients. Measurement o f serum bicarbonate level and/or blood gas analysis are the only effective means of monitoring the effcct of treatment. Hypernatraeinia, hypokalaemia and tetany are the cornplications of sodium bicarbonate therapy and should be watched for. Ethyl alcohol has been used and recommended in the treatment of methyl alcohol intoxication. Its efficacy has a sound theoretical
basis. It delays the metabolism ofmethanol in the liver and results in the excretion of unmetabolized methanol rrom the kidneys and lungs. This inay prevent or diminish the degrec of ocular damage which are thought to be caused by formaldchqde, one of the metabolites of methanol. However, only a small proportion of methanol is excreted froin lungs or kidneys and the efficacy of ethyl alcohol has not been shown clcarl!.. Acknowledgements Authors would like to thank Dr. R. D. Hornahrook for neurological evaluatiori of the patients with pseudohulhar palsy-. Ms. Margaret Johnson and Dr. John V. McGregor for their technical assistance. Dr. John H. Beard and Dr. A. Buck for pcrforining methanol and ethanol levels and anal.ising contents o f the drum and Dr. Anthony Griew for statistical analysis of the data.
1. Bazztn.l. I..J~R..C/U(Y. 1: 11.. WITI'III I I .I..Ci nndCU)pm,M. h.(lY531. Acuiemerhyl nlcohol poisonmg: Arcvicu based onexpuncncesin anouibrcak of 223 cabe~.Mrdktnr 23, 431.
2. 3.
4. 5
6.
K&krn\-LARlMRII, H and I'AVN~XBFRG. A M. (1974~: Merhanol intoxication Comparison o f penloneal dialysis and humndielysis ireatrnent, Arch brrrm. Mcd. 134. 293. III'\(PHI.KI. 1.J. (lY74J .Methanol poisoning Menagemcnt ofacidosis with combined hernodialysis and pcrironcnl dinlpis. M p d . J. Aa.w 1. X33. IiIitonal (1974): Mclhanol poi3oniny. dfid J . .Au.cr. I, R I R . P A ~ A K I - S I W N I WKI R . J ( l Y 7 6 ) Mcili-drinkers and Ioius caters: Some educniional aspel, ol'lrdnseullurdl psych!dtry in Pdpui! Urn (iuinca, Aitss,. .\'7..1. Piichioi. 10. 129. DEnIl.I.l.5. K. t . dnd \ A R A Q ~ , S (19%). Oculdr nlnlilte~tallunb and complicntiuns of nculc mclliyl alcohol rnlox!cation. M r d J. .4iar. 2, 4113.
~
Aust pp 65-68 ~ N Z- J Med ~ (1979). _ 9,_ ~
An Outbreak of Acute Methyl Alcohol Intoxication S. Naraqi*, R. F. Dethlefst, R. A. Slobodniuk! and J. S. Sairere** From the Department of Clinical Sciences Faculty of Medicine, University of Papua New Guinea Port Moresby, Papua New Guinea
Summary:
An outbreak of acute methyl alcohol intoxication. S. Naraqi, R. F. Dethlefs, R. A. Slobodniuk and J. S. Sairere, Aust. N.Z. J. Med., 1979, 9, pp. 65-68.
An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60-600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8-36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.
Outbreaks of acute methyl alcohol (methanol) intoxication occur periodically in both developed and developing countries. Since 1953. very little has been written on the clinical features of this poisoning. Most of the recent publications on this subject deal with haemodialysis as the most effective treatment.'-" Methanol, a cheap 'Lecturer in Medicine +Specialist Medical Officer, Ophthalmology :Registrar in Medicine. "Resident in Medicine. Correspondence- Dr S. Naraqi. P.O. Box 5623. Boroko, Papua New Guinea Accepted for publication. 16 October, 1978
alcohol. is used as duplicating fluid, paint remover and a s a cleaning agent and can be purchased from drug storcs in the form of mcthylated spirit. It has been suggested that there will be an increase in the number o f methanol poisoning outbreaks in the developing countries of the Pacific R e g i ~ nThis . ~ increase is thought to be the result of an interface between traditional and modern factors in rapidly changing societies of the area, as more and moi-c of these countries become independent. In most of the developing countries, extensive laboratory facilities and haemodialysis arc not available. It is therefore important for the medical practitioners who work in such countries to make themselves familiar with the clinical manifestations and diagnosis of methyl alcohol poisoning and ils management by means other than dialysis. In Papua New Guinea, two outbreaks of methyl alcohol intoxication occurred in 1977. despite extensive publicity and educational campaigns after the first accident. The first outbreak is the subject of this report. (The second outbreak occurred six months after the present one in the city of Lae. Four persons werc involved; lhree of them died and one became blind.) Report of the Outbreak Getieral Injiwniu fiori In March 1977. 32 young men attended a drinking part! in a village near Port Moresby. They drank the contents of a drum which was said to have been found near their village. A sample of the fluid was analysed latcr by gas chromatography and found to be pure methyl alcohol. Small bottles of coke or regular glasses mere filled up to a third with methanol and twice as much water, orange juice or cola beverage was added before consumption. Four persons who attended the party but did not drink the inaterial because o C its unusual odour and/or taste did not become ill. Age of the patients ranged from 17 39 years (mean: 23). Estimated amount of pure methanol consumed by each individual ranged from 60-600 ml (mean: 275). Three patients had consumed ethanol immediately prior to drinking methanol. The interval between consumption of methanol and the appearancc ofthe first symptoms of toxicity (latent period) ranged rrom X 36 hours (mean: 18).
TABLE 1 Symptoms and signs of acute methanol intoxication in 28 patients huniber of patients Ocular: Blurred vision Eye pain Conjunctival congestion Pupillary changcs Fundi changes Diminished visual acuity (counting fingers) Gastrointestinal: Abdominal pain Vomiting Nausea Epigastric tenderness Decreased bowel sounds
20 (13)* 16 (9) 21 17 21
available in seken patients before sodium bicarbonate infusion. All showed severe metabolic acidosis. pH rmgcd from 7 . 1 3 7.26. K O , from 10 29 and serum bicarbonate from 10 14 mEq I . POz was normal and serum potassium high ( 5 . 4 6 . 4 mEq,r) i n all. In three out of six paticnts who had daily blood gas analysis. acidosis persisted for 36-48 hours. TABLE 2 Summary ufthe pertinent findings in Cour fatal cases o f acute methanol intoxication Patients
II
17 ( 5 ) 17 ( 6 ) 14 10 7
Central Nervous: Headache Dizziness Lethargy Restless11ess Coma Seizures
19 (3) 13 (1) 15 7 6 (4) 4
Respiratory: Breath odour (of formalin) Kussmaul respiration
23 17
*Numbers in parenthesis indicate the frequency ofrespectivc symptoms as the chief cornplaints of the patients. .Syniptonzs und Signs The symptoms and signs observed in these patients are shown in Table 1 . Disc hyperaemia and dilated pupils with absent or sluggish light reflex were common findings. The details of ocular manifestations and complications arc reported separately.' Headache and diiziness were transient and disappeared after 24 hours. Four patients were admitted comatose and two developed coma during the hospital course. SeiLures developed within 48 hours after admission. Kussmaul (deep and rapid) respiration (respiratory rate ranged froin 28 36imin) was observed within 24 hours after admission in 15 and on the second hospital day in two patients. No one complained of respiratory difficulties. Respiratory rate was not increased in the other ten patients and remained normal throughout their hospital course. Fever, and syniptoms or signs related to renal or cardiovascular systems were notably absent.
Laborarorjz Invrstigutiuns A full scale laboratory investigation could not be done on all of the patients prior to treatment owing to the large number of patients admitted in a short period of time. shortage of staff and a state holiday. Haemoglobin, peripheral leukocyte count and differential, blood urea nitrogen, serum sodium and chloride and blood sugar performed before any treatment in half to two-thirds of the patients were all within normal limits. Serum am e level was measured in 22 patients and was elevated in 11 (ranging from 400-1320 IU /). Serum calcium level was low in six patients with pancreatitis (4 -7.8 mg?,,). Blood gas analysis was
I
Age (years) Latent period (hours) Presenting symptom Ocular changes Seizures Serum amylase ( I U ,I ) Blood pH Scrum potassium ( m E q l) Methanol level: (nip;100 mlj Amount of bicarbonate used for treatment** (mmol) Duration of acidosis (hours)
I1
111
IV
27 19 19 20 8 36 12 12 Coma ('omd Coma Coma
*
*
*
*
*
*
r
460 345 1000 1320 7 26 7 13 7 4M 1 2 3 6 4 5 4 6 4 6 1 73
233
326
4000 4000 4000
3000
48
111
36
48
36
*Present. i.Performed after bicarbonate therapy.
:Ethanol level was 123 i n patient 111. In the other three. as with patients who survived. the amount was negligible. **500 ml every 4-6 hours. Methanol unJ Etliariol Level In 15 patienti methanol and ethanol levels w r e measured retrospectively on a sample of blood drawn within the first 48 hours after admission. Methanol level ranged from 5-326 mg8'100ml. The fatal cases had the highest lcvels (Table 2). Levels above 50 mg'l00 ml were seen in two nonfatal cascs, one with severe visual impairment (66 mg) and the other with no residual complications (176 mg). A significant ethanol level n,as found only in one patient who did not survive. 7i.eutrnent
Peritoneal or haemodialysis was not available to our patients. Ethanol was not used in any of them. Pancreatitis was treated with nasogastric suctioning and intravenous fluids. Seventeen patients with acidosis, which was diagnosed either by the presence of Kussmaul respiration (ten patients) or low blood pH (seven patients). received sodium bicarbonate (4.5:" solution) infusion for the treatment of acidosis. The amount ranged from 500 4000 mmol and it was given over 4 48 hours (500,'4 ~6-hourly).usually within the first three days of hospitalization. Hospitul Cour.w and Outcome Hospital stay ranged from 2-30 days (mean: 6). Four patients died within 72 hours of admission. Clinical and laboratory findings in these patients are summarized in Table 2. Of those
bTBRU4RY __
1975)
67
M L l HYL A1 COHOL INTOXICATIO\
--
-~ ~
TABLE 3 Significant .ind non-signihcant prognostic fdctors in 28 pdlients
4 ith
ncute methanol intoticatlon
-
Patient groups Fatal With Tequctde Complete recolerq
--__
Number of patient5
Amount consumed (ml) Rdnge Medn
4 X 16
bnknomn 120 600 360 60 500 240
Latent period (hour\) Range - Mean Coma 8 36 8 23 8 36
17 15 17
4
Seimres
2
2 0
0
0
Duration of dcldo5is* (houi s) Range - Mean 36 4x 24 48 4 -24
42 25 10
*Based o n the presence of Kussmaul respiration and the continuous need for sodium bicarbonate infusion ( P< 0.01).
who recovered. 16 were free of complications and cight had disabling complications: two became totally blind; four had severe visual impairment and two had difficulty with speech (which was attributed to a pseudobulbar palsy syndrome) as well as severe visual defects. None of the patients with pancreatitis dcveloped pancreatic abscess or pscudocyst during a three month follow up period. Prognostic Fucror.5 To identify the significant prognostic factors, patients were arbitrarily divided into three groups (Table 3). The estimated amount of consumed inethanol and the length 01 latent period had no effect on the outcome. Coma. seizures and prolonged acidosis (more than 36 hours) wcre found to indicate a bad prognosis: all patients who had coma or seizures either died OT had severe residual defects after recorery; only one patient with acidosis for longer than 36 hours recovered completely. Using Wileoxon rank sum test method, it was found rhat the mean duration of acidosis &:is significantly higher in fatal cases as compared to non-fatal ones. The difference remained significant nhen the combined “fatal” and “with sequelae” groups were compared with the “complete recovery” group.
Discussion
As documented previously and confirmed in this report. acute methyl alcohol intoxication produces a distinct clinical picture: there is a latent period of several hours to scveral days between the consumption of methanol and the appearance of first symptoms of toxicity; a combination of blurred vision, abdominal pain and vomiting as well as conjuctival congestion, dilated pupils with absent or sluggish light reflex. hyperaemic discs and Kussmaul respiration are found in the majority of the patients in the first 24 hours after admission. The diagnosis of methanol poisoning should be considered in any patient who has a combination of typical ocular changes with either gastrointestinal findings or metabolic acidosis even in the absence of a history of methanol ingestion. Four distinct clinical syndromes were observed in this outbreak, visual disturbances, pancreatitis, metabolic acidosis and diffuse
encephalopathy. Visual disturbances were the most common findings. Ocular pain and conjunctival congestion have not reccived emphasis previously. Steroids, given to two of the patients. had no beneficial effect on ocular damage.6 The incidence, of pancrcatitis in this outbreak is consistent with the findings of others both based on serum amylase level and on post mortem examination.’ Abdominal pain and tenderness in patients with no rise in serum amylase level, may have been due to gastritis which has been Sound in post mortem of fatal cases of methanol intoxication.’ Metabolic acidosis was thought to be present in 60% of the patients as indicated by Kussmaul respiration. This was confirmed in one-third of the patients by studying serum bicarbonate and blood gases. Kussmaul respiration is a useful sign for the detection of acidosis but it is not a reliable index of the degree of acidosis. Furthermore, not all of the patients with acidosis have K ussmaul respiration.’ Therefore the diagnosis of metabolic acidosis: as well as monitoring of its treatment, should be based on serum bicarbonate measurement andlor blood gas analysis whenever possible. The mortality rate in this outbreak (1273 was the same as the outbreak in Georgia.’ Prolonged acidosis, coma and seizures were found to be poor prognostic factors. The identification of poor prognostic factors may be of value if the supply of sodium bicarbonate is short or dialysis Sacilities are limited. Bradycardia, another sign of a poor prognosis’, was not observed in our patients. There was no relationship between methanol intake and the prognosis. Extreme variation in the individual response to a given quantity of methanol has been reported and some of the observations in this outbreak confirmed it.”‘ One of the patients in this
68
~ _ _ _
hARAQ1 EI' AL.
VOL.
9,
NO.
1
~
outbreak who not only survived but recovcred completely, admitted to drinking the equivalent to 600 ml ofpure methanol. This is fw more than the amount reported by Bennett et d.who cite the survival of a patient after ingestion of 500 ml of 409,,, methanol.' The unavailability of dialysis in developing countries imposes special problems in the management of patients with methanol poisoning. Haemodialysis is the most effective treatment but is not available in most of these countries. A flying-in haemodialysis team would be an ideal substitute. but most of the developing countries do not have one and its importation from a nearby country may be costly and d to arrange. Peritoneal dialysis is the second choice and is available t o a limited dcgree in some o f these countries.2.3It can, and should be used in sporadic cases. In the absence of dialysis, alkalinization by sodium bicarbonate is thc cornerstone of treatment of these patients. Measurement o f serum bicarbonate level and/or blood gas analysis are the only effective means of monitoring the effcct of treatment. Hypernatraeinia, hypokalaemia and tetany are the cornplications of sodium bicarbonate therapy and should be watched for. Ethyl alcohol has been used and recommended in the treatment of methyl alcohol intoxication. Its efficacy has a sound theoretical
basis. It delays the metabolism ofmethanol in the liver and results in the excretion of unmetabolized methanol rrom the kidneys and lungs. This inay prevent or diminish the degrec of ocular damage which are thought to be caused by formaldchqde, one of the metabolites of methanol. However, only a small proportion of methanol is excreted froin lungs or kidneys and the efficacy of ethyl alcohol has not been shown clcarl!.. Acknowledgements Authors would like to thank Dr. R. D. Hornahrook for neurological evaluatiori of the patients with pseudohulhar palsy-. Ms. Margaret Johnson and Dr. John V. McGregor for their technical assistance. Dr. John H. Beard and Dr. A. Buck for pcrforining methanol and ethanol levels and anal.ising contents o f the drum and Dr. Anthony Griew for statistical analysis of the data.
1. Bazztn.l. I..J~R..C/U(Y. 1: 11.. WITI'III I I .I..Ci nndCU)pm,M. h.(lY531. Acuiemerhyl nlcohol poisonmg: Arcvicu based onexpuncncesin anouibrcak of 223 cabe~.Mrdktnr 23, 431.
2. 3.
4. 5
6.
K&krn\-LARlMRII, H and I'AVN~XBFRG. A M. (1974~: Merhanol intoxication Comparison o f penloneal dialysis and humndielysis ireatrnent, Arch brrrm. Mcd. 134. 293. III'\(PHI.KI. 1.J. (lY74J .Methanol poisoning Menagemcnt ofacidosis with combined hernodialysis and pcrironcnl dinlpis. M p d . J. Aa.w 1. X33. IiIitonal (1974): Mclhanol poi3oniny. dfid J . .Au.cr. I, R I R . P A ~ A K I - S I W N I WKI R . J ( l Y 7 6 ) Mcili-drinkers and Ioius caters: Some educniional aspel, ol'lrdnseullurdl psych!dtry in Pdpui! Urn (iuinca, Aitss,. .\'7..1. Piichioi. 10. 129. DEnIl.I.l.5. K. t . dnd \ A R A Q ~ , S (19%). Oculdr nlnlilte~tallunb and complicntiuns of nculc mclliyl alcohol rnlox!cation. M r d J. .4iar. 2, 4113.
