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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2012  |  Volume : 23  |  Issue : 1  |  Page : 37-43
Hemodialysis for methyl alcohol poisoning: A single-center experience


1 Department of Nephrology and Clinical Transplantation, Institute of Kidney Diseases and Research Center, Institute of Transplantation Sciences (IKDRC-ITS), Ahmedabad, India
2 Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, IKDRC-ITS, Ahmedabad, India

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Date of Web Publication3-Jan-2012
 

   Abstract 

Methanol is a cheap and potent adulterant of illicit liquors. Hemodialysis (HD) is the best method to rapidly remove both toxic acid metabolites and parent alcohols, and it plays a fundamental role in treating severely poisoned patients. This retrospective study was carried out on 91 patients with detectable serum methanol levels who underwent HD. Because toxic alcohol levels were not immediately available, the initial diagnosis and treatment was based on clinical history with evidence of toxic alcohol intake, presence of high anion metabolic acidosis and/or end organ damage. Patients received bicarbonate, ethanol, according to clinical features and blood gases. Patients underwent HD in the setting of known methanol ingestion with high anion gap metabolic acidosis, or evidence of end-organ damage, regardless of methanol level. HD prescription included large surface area dialyzer (≥1.5 m2), blood flow rate of 250-350 mL/min and dialysate flow rate of 500 mL/min for 4-6 h. Between 9 and 11 July 2009, 91 males with mean age 40 ± 8.5 years underwent HD, and 13 patients required a second HD session. Patients consumed 100-500 mL illicit liquors, and symptoms appeared six and 60 h later. Clinical features were gastro-intestinal symptoms (83.5%), visual disturbances (60.4%), central nervous system symptoms (59.3%) and dyspnea (43.9%). Before HD, mean pH was 7.11 ± 0.04 (range 6.70- 7.33) and mean bicarbonate levels were 8.5 ± 4.9 mmol/L (range 2-18). Three patients died due to methanol intoxication. Mortality was associated with severe metabolic acidosis (pH ≤ 6.90), ventilator requirement and coma/seizure on admission (P < 0.001). Timely HD, bicarbonate, ethanol and supportive therapy can be life-saving in methanol intoxication.

How to cite this article:
Kute VB, Godara SM, Shah PR, Gumber MR, Goplani KR, Vanikar AV, Munjappa BC, Patel HV, Trivedi HL. Hemodialysis for methyl alcohol poisoning: A single-center experience. Saudi J Kidney Dis Transpl 2012;23:37-43

How to cite this URL:
Kute VB, Godara SM, Shah PR, Gumber MR, Goplani KR, Vanikar AV, Munjappa BC, Patel HV, Trivedi HL. Hemodialysis for methyl alcohol poisoning: A single-center experience. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2018 Dec 18];23:37-43. Available from: http://www.sjkdt.org/text.asp?2012/23/1/37/91297

   Introduction Top


Methyl alcohol is a cheap and potent adulterant of illicit liquors. Many outbreaks of methanol poisoning have occurred in India. [1],[2],[3],[4] Such outbreaks have been responsible for a heavy mortality and morbidity. Hemodialysis (HD) is the best method to rapidly remove both toxic acid metabolites and parent alcohols, and it plays a fundamental role in treating severely poisoned patients. [5],[6],[7],[8] HD can be a life-saving therapy in the case of accidental or intentional overdose of methanol. Consultation with nephrology doctors and emergency HD should be immediately obtained for severely acidotic patients in whom the diagnosis appears likely, especially if accompanied by visual or renal impairment. Nephrologist's consultation and HD should not be delayed in waiting to obtain confirmatory methanol levels. Selling and consuming alcohol is a criminal offence in Gujarat, India's only dry state. This has led to a proliferation of illegal liquor dens, whose home-made brew is mostly consumed by those from low-income families who cannot afford high-priced liquors available outside the state. Many victims, mostly from the slums of Ahmedabad, die after consuming the illicit liquor containing methanol. We present a singlecenter experience of the effectiveness of HD in one of the largest outbreaks of methanol poisoning.


   Patients and Methods Top


Ninety-one patients who were referred from three peripheral hospitals for HD were included in this retrospective study. The outbreak of methanol poisoning described in this paper occurred in the city of Ahmedabad. 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. [7],[9] We administered supplemental thiamine (100 mg IV) and pyridoxine (50 mg IV) and methylcobalamin to all patients. [4] 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. [7] 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 hour) in any patient with documented recent ingestion of methanol or strong clinical suspicion of ingestion of methanol with an arterial pH <7.3, serum HCO 3 <20 mEg/L, with provision for increasing the ethanol infusion rate during HD. [10] Arterial or venous blood gas analysis was performed to determine the extent of acidosis. Metabolic acidosis due to other etiologies like diabetes mellitus, starvation and chronic kidney disease were excluded. All patients underwent immediate treatment with HD in the setting of known methanol ingestion if either of the following conditions was present: high anion gap metabolic acidosis, regardless of toxic alcohol level, pH ≤7.30, serum bicarbonate less than 15 meq/L, evidence of end-organ damage (e.g., visual changes) and deteriorating vital signs despite intensive care. [7],[11],[12] The HD prescription included a large surface area polysulfone membrane dialyzer (≥1.5 m [2] ), a blood flow rate of 250-350 mL/min and a dialysate flow rate of 500 mL/min against a 35 mEq/L bicarbonate bath with normal\enriched phosphorus and potassium to prevent hypo-phosphatemia and hypokalemia during HD. [5],[6],[7],[8],[10],[13],[14] HD was done through temporary femoral catheter for 4-6 h. Heparin-free HD was used to avoid the risk of intracranial hemorrhage, with 25-50 mL saline flushes being administered every 15-30 min into the arterial (pre-dialyzer) limb. [6],[15] HD was repeated if there was rebound toxicity, persistent metabolic acidosis and endorgan damage (visual changes). Because methanol levels were not usually known until many hours or days later, prescription of HD duration was based on the clinical course, pH and bicarbonate correction. Fingerstick glucose was monitored during HD to rule out hypoglycemia as the cause of any alteration in mental status. Electrocardiogram monitoring was done in critically ill patients requiring prolonged HD for evidence of electrolyte disturbance. Treatment with HD or ethanol were not done in asymptomatic patients with normal serum pH and normal anion gap and no evidence of end-organ damage and ingestion of small volume of methanol. If all conditions were met, patients were admitted for observation with monitoring of blood gases and electrolytes to exclude the development of a metabolic acidosis or an increasing anion gap. [5] If acidosis did not develop within 24 h of the ingestion, a toxic alcohol poisoning was excluded. Three patients died and were autopsied, and the results of the chemical analyses were available later.


   Statistical Analysis Top


Data was analyzed using SPSS-12 and t-test was used to compare the two groups. Categorical variables are compared using the chi-square test. Variables are expressed as mean ± SD, and P <0.05 was considered to be statistically significant.


   Results Top


On July 9, 10 and 11, 2009, 53, 31 and seven patients underwent HD for methanol poisoning. A total 91 patients underwent HD, of which 13 (14.2%) patients required a second session of HD. This resulted in restoration of consciousness and disappearance of visual disturbances in all patients. All patients were males, with a mean age 40 ± 8.5 years. The exact quantity of the toxic alcohol consumed was not known in all the cases but, according to the interview of the patient, relatives and peripheral hospital workers, it ranged from 100 to 500 mL. The interval between the consumption of toxic alcohol and the appearance of symptoms varied between six and 60 h. Majority of the patients had symptoms within 24 h after methanol consumption. Clinical features and treatment given to methanol-poisoned patients are shown in [Table 1]. Clinical features were gastrointestinal symptoms like nausea, vomiting and abdominal pain in 83.5% (n=76), visual disturbances like visual blurring and photophobia in 60.4% (n=55), central nervous system (CNS) symptoms like giddiness, sedation, altered sensorium, seizure and coma in 59.3% (n=54) and dyspnea in 43.9% (n=40). Five patients did not have any symptoms. None of the patients had flank pain, hematuria, oliguria, cranial nerve palsies and tetany. Before HD, mean pH was 7.11 ± 0.04 (range 6.70-7.33), mean bicarbonate levels were 8.5 ± 4.9 mmol/L (range 2-18) and mean base deficit was 18.4 mmol/L (range 2-29). Initial arterial pH was ≤6.9 in nine patients, of which six survived, and initial arterial pH was >6.9 in 82 patients, all of which survived. Arterial pH ≤6.9 was associated with significantly higher mortality (2/8, 25% vs 1/83, 1.2%, P = 0.0003, relative risk 20.7; 95% confidence interval 2.1-204). There was a significant difference in the mean pH in the first arterial blood gas of patients who subsequently died (6.81 ± 0.08) and survivors (7.17 ± 0.14) (P = 0.00007). Patients who died were admitted at a late stage (>24 h) to the hospital. As shown in [Table 2], mortality was associated with severe metabolic acidosis (pH ≤ 6.90), ventilator requirement and coma/seizure on admission (P < .001). Heparin-free HD was used, with only a 3.8% (n=4) clotting rate in the extracorporeal circuit. Aspiration pneumonia developed in five patients, of which three died, which might suggest a greater degree of methanol intoxication in these patients. In available reports, more than 50% of the patients had packed cell volume (PCV) of more than 45%. All the manifestations of methanol poisoning were reversed in survivors without any permanent sequelae (visual or CNS). Of eight patients transferred to the intensive care unit, three patients died due to methanol intoxication. The autopsy of these patients revealed marked cerebral edema and gastrointestinal tract revealed congestion and hemorrhage. 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. 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.
Table 1: Clinical features and treatment given to the methanol-poisoned patients.

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Table 2: Prognostic factors in patients with methanol poisoning.

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   Discussion Top


Acute methanol poisoning should be suspected in all patients with metabolic acidosis with an elevated anion gap, neurological deterioration or vision disturbances. [16],[17],[18] Metabolic acidosis was the most striking disturbance seen in our patients. It is probably due to the accumulation of formic acid and lactic acid. [19],[20] Rapid recognition and early treatment are crucial. It is important to emphasize that the onset of methanol toxicity is delayed when ethanol is co-ingested. The possibility of concomitant ethanol and toxic alcohol ingestion must always be considered, particularly in alcoholics, who may ingest alcohol in any form. Methanol is rapidly and completely absorbed after oral ingestion. A peak serum alcohol concentration is reached within 1-2 h. Activated charcoal, gastric lavage and syrup of ipecac have no role in the management of toxic alcohol exposures. An arterial gas served as an essential triage tool when caring simultaneously for multiple patients with poisoning when one has limited HD capability. [7],[21],[22] The American Academy of Toxicology recommends treatment with fomepizole rather than ethanol, unless fomepizole is not available or causes an allergic reaction. All alcohols have a low molecular weight, protein binding and distribution volume and may, therefore, be efficiently removed by HD. [8],[21],[22],[23],[24] Intermittent HD is the most efficient method for rapidly decreasing serum levels of toxic alcohols or for removing organic acid anions like format. [8] Because results of serum methanol analyses were not immediately available, patients received bicarbonate, ethanol and HD according to clinical features and metabolic acidosis on blood gases. Eight hours of HD is often recommended if methanol analyses are unavailable. [25] The length of HD in the present study was somewhat shorter (range 4-6 h), mainly because of the high number of patients and limited dialyzing capacity present. The plasma osmolal gap can provide important information in real time, costs little and is widely available. Clinicians need to be able to interpret this test for early treatment decision-making, pending definitive poison identification by gas chromatography. [7],[26],[27],[28] The duration of HD in hours can be estimated using the formula (-V ln (5/A)/0.06 k), where V is total body water in liters, A is the initial alcohol concentration in mmol/L and k is 80% of the dialyzer urea clearance in mL/min at the observed blood flow rate. [29],[30],[31] However, the equation requires measurements of the toxic alcohol level. Because methanol levels were not usually known until many hours or days later, HD duration was based on the clinical course, pH and bicarbonate levels. [19],[32],[33],[34],[35],[36] HD provides a clearance of 200 mL/min for methanol and 223 mL/min for formate at blood flows of 100-400 mL/min. HD significantly reduced formate elimination half-life compared with endogenous elimination and questionable role of folate. [36],[37] Peritoneal dialysis and other forms of continuous renal replacement therapy are inefficient at clearing toxic alcohols and their metabolites, and are not recommended. [5],[6],[7],[38] Observation of high hematocrit in our patients has been reported earlier. [4],[39] According to Swartz et al, [39] an increase in the RBC size is probably responsible for this finding, and not the hemoconcentration.

Many outbreaks of methanol poisoning have been reported from India. [1],[2],[4],[40],[41] Krishnamurthi et al [3] have described 87 patients of methanol poisoning treated with alkali therapy and supportive measures, with mortality in 32 patients. Divekar et al [2] have described 45 patients of methanol poisoning treated with alkali, ethanol and supportive measures, with mortality in seven patients. Bade and Sapre [1] have described 11 patients of methanol poisoning, with two having been brought dead, and the rest died within three days. Kumar et al [40] from Chennai, in 2001, have described 67 patients treated with bicarbonate, ethanol and folic acid, with mortality in 21 patients mainly due to the non-availability of arterial blood gas analysis and dialysis. 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 and lack of HD therapy. The mortality rate was low in our patients who received early and timely dialysis treatment, similar to the experience by Ravichandran et al, [4] who have described 47 patient of methanol poisoning who were treated fairly early and HD was given to some of them, achieving a low mortality rate in two patients. Rathi et al [41] reported that prompt administration of ethanol and institution of HD resulted in complete reversal of methanol manifestations.

All our patients developed a severe degree of poisoning as demonstrated by the clinical signs and the degree of metabolic acidosis before HD. One of the most important aspects of our study was that it showed a very low mortality (n=3 of 91 patients) from methanol poisoning due to timely HD along with supportive therapy, and all the manifestations of methanol poisoning were reversed without any permanent sequelae (visual or CNS). This low mortality is in contrast to high death rates reported by other studies. [1],[2],[3],[4],[40] In our study, poor prognosis was associated with severe metabolic acidosis (pH ≤6.90), ventilator requirement and coma/seizure on admission, similar to other reports. [17],[33],[34]

The limitation of our retrospective study is that it does not truly represent the mortality of this outbreak, as only a small number of the patients were directed to our institution for HD, and many more had already died either at home or in the nearby peripheral hospitals. Serum methanol concentrations were not performed near the end of HD to ascertain the adequacy of treatment. Data on methanol levels/osmolar gap were not available. Patients treated without HD were not included in the study.

Methanol poisoning should be suspected in all patients with unexplained metabolic acidosis with an elevated anion gap, vision disturbances or neurological deterioration after ingestion of illicit liquors in habitual alcohol consumers. Timely HD along with bicarbonate, ethanol and supportive therapy can be life-saving in methanol intoxication. Mortality was associated with severe metabolic acidosis (pH ≤6.90), ventilator requirement and coma/ seizure on admission.

 
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[PUBMED]    
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Correspondence Address:
Vivek B Kute
Department of Nephrology and Clinical Transplantation, Institute of Kidney Diseases & Research Centre, Dr H L Trivedi Institute of Transplantation Sciences (IKDRC-ITS), Civil Hospital Campus, Asarwa, Ahmedabad - 380 016, Gujarat
India
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    Tables

  [Table 1], [Table 2]

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