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LETTER
Year : 2014  |  Volume : 60  |  Issue : 1  |  Page : 88

Methanol poisoning with blindness and putaminal necrosis - was metabolic acidosis missed?


Division of Medical Toxicology, Emergency Room, Hazrat Ali-Asghar (p) Hospital, Shiraz University of Medical Sciences, Shiraz, Iran

Date of Web Publication14-Mar-2014

Correspondence Address:
H Sanaei-Zadeh
Division of Medical Toxicology, Emergency Room, Hazrat Ali-Asghar (p) Hospital, Shiraz University of Medical Sciences, Shiraz
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.128828

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How to cite this article:
Sanaei-Zadeh H. Methanol poisoning with blindness and putaminal necrosis - was metabolic acidosis missed?. J Postgrad Med 2014;60:88

How to cite this URL:
Sanaei-Zadeh H. Methanol poisoning with blindness and putaminal necrosis - was metabolic acidosis missed?. J Postgrad Med [serial online] 2014 [cited 2019 Nov 15];60:88. Available from: http://www.jpgmonline.com/text.asp?2014/60/1/88/128828


Sir,

I would like to address the article by Srivastava et al. in a recent issue of your journal on methanol intoxication. [1] The authors explained a case of methanol poisoning who presented with acute-onset blindness and encephalopathy six hours post-ingestion of country liquor. Interestingly, his arterial blood gas analysis was normal at presentation. Also, the patient's brain computed tomography scan and magnetic resonance imaging showed bilateral putaminal hemorrhagic necrosis on day 30. However, a major point about this case is of concern. How can it be possible that a methanol-poisoned patient present with blindness without metabolic acidosis and then develop bilateral putaminal necrosis? To the best of my knowledge, such a case has not been reported in the literature previously. It should be mentioned that in methanol poisoning, the onset and severity of clinical and laboratory abnormalities depend largely on the generation of formic acid. [2],[3],[4],[5] There is a latent phase of 6-30 h post-ingestion or longer if the patient has co-ingested ethanol (such as in the presented case), for clinical effects of methanol poisoning to occur. [2],[3],[4],[6],[7],[8],[9] This characteristic latent period is thought to result from the slow metabolism of methanol to formic acid. [2],[4],[6],[9] Moreover, it has been stated that in cases of methanol poisoning without metabolic acidosis, visual dysfunction usually does not develop. [10] Also, it has been shown that the severity of visual abnormalities in methanol-poisoned patients is directly correlated with the severity of metabolic acidosis. [2],[3],[6] Furthermore, the most severe neurologic dysfunctions are found in methanol-poisoned patients with the most severe metabolic acidosis. [2],[11] It should be noted that a rare complication of methanol poisoning is putaminal necrosis, which presents with rigidity, tremor, masked face, and monocolonous speech. It has been attributed to reduced cerebral blood flow and/ or accumulation of formic acid in the putamen. [2] With respect to the above-mentioned points, I think that the most plausible explanation for the development of blindness, encephalopathy, and putaminal hemorrhagic necrosis in this patient is previous consumption of country liquor before the current presentation or laboratory technical error in determining acidosis at hospital presentation that has been missed.

 
 :: References Top

1.Srivastava T, Kadam N. Bilateral putaminal hemorrhagic necrosis with rapid recovery of sensorium in a patient with methanol intoxication. J Postgrad Med 2013;59:243-4.   Back to cited text no. 1
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2.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.   Back to cited text no. 2
    
3.Jacobsen D, McMartin KE. Methanol and ethylene glycol poisonings. Mechanism of toxicity, clinical course, diagnosis and treatment. Med Toxicol 1986;1:309-34.  Back to cited text no. 3
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4.Hovda KE, Hunderi OH, Rudberg N, Froyshov S, Jacobsen D. Anion and osmolal gaps in the diagnosis of methanol poisoning: clinical study in 28 patients. Intensive Care Med 2004;30:1842-6.  Back to cited text no. 4
    
5.Hovda KE, Mundal H, Urdal P, McMartin K, Jacobsen D. Extremely slow formate elimination in severe methanol poisoning: a fatal case report. Clin Toxicol (Phila) 2007;45:516-21.  Back to cited text no. 5
    
6.Hovda KE, Hunderi OH, Tafjord AB, Dunlop O, Rudberg N, Jacobsen D. Methanol outbreak in Norway 2002-2004: epidemiology, clinical features and prognostic signs. J Intern Med 2005;258:181-90.   Back to cited text no. 6
    
7.Sanaei-Zadeh H, Zamani N, Shadnia S. Outcomes of visual disturbances after methanol poisoning. Clin Toxicol (Phila) 2011;49:102-7.   Back to cited text no. 7
    
8.Bennett IL Jr, Cary FH, Mitchell GL Jr, Cooper MN. Acute methyl alcohol poisoning: a review based on experiences in an outbreak of 323 cases. Medicine (Baltimore) 1953;32:431-63.  Back to cited text no. 8
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9.Teo SK, Lo KL, Tey BH. Mass methanol poisoning: a clinico-biochemical analysis of 10 cases. Singapore Med J 1996;37:485-7.  Back to cited text no. 9
    
10.Benton CD Jr, Calhoun EP Jr. The ocular effects of methyl alcohol poisoning; Report of a catastrophe involving 320 persons. Am J Ophthalmol 1953;36:1677-85.   Back to cited text no. 10
[PUBMED]    
11.Kraut JA, Kurtz I. Toxic alcohol ingestions: Clinical features, diagnosis, and management. Clin J Am Soc Nephrol 2008;3:208-25.  Back to cited text no. 11
    



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[Pubmed] | [DOI]



 

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