North American Journal of Medical Sciences

CASE REPORT
Year
: 2013  |  Volume : 5  |  Issue : 10  |  Page : 623--624

Bilateral putaminal hemorrhages: Serious complication of methanol intoxication


Nitipong Permpalung, Wisit Cheungpasitporn, Daych Chongnarungsin, Travis M Hodgdon 
 Department of Medicine, Bassett Medical Center, Cooperstown, New York, USA

Correspondence Address:
Wisit Cheungpasitporn
Department of Medicine, Bassett Medical Center, Cooperstown, New York - 13326
USA

Abstract

Context: Methanol intoxication is a life-threatening condition. Hallmark of clinical presentations include severe wide anion gap metabolic acidosis with very high serum osmolar gap and visual complication. Case Report: We report a case of severe methanol intoxication with bilateral putaminal hemorrhage, an uncommon serious complication. A 56-year-old man presented with altered mental status. Fundus examination showed optic disc edema. Arterial Blood Gas (ABG) revealed severe anion gap metabolic acidosis with osmolal gap. Head computed tomography (CT) showed hypodense lesions in basal ganglia bilaterally. Hemodialysis and intravenous fomepizole were initiated. Serum methanol level was significantly elevated. Unfortunately, patient was lethargic 2 weeks after discharge. Repeated CT of head demonstrated new putaminal hemorrhages. Conclusion: Bilateral putaminal hemorrhage is an uncommon but serious complication in methanol intoxication. Clinicians should have high index of suspicion for putaminal hemorrhage when patients with recent methanol intoxication present with altered mental status.



How to cite this article:
Permpalung N, Cheungpasitporn W, Chongnarungsin D, Hodgdon TM. Bilateral putaminal hemorrhages: Serious complication of methanol intoxication.North Am J Med Sci 2013;5:623-624


How to cite this URL:
Permpalung N, Cheungpasitporn W, Chongnarungsin D, Hodgdon TM. Bilateral putaminal hemorrhages: Serious complication of methanol intoxication. North Am J Med Sci [serial online] 2013 [cited 2020 Apr 9 ];5:623-624
Available from: http://www.najms.org/text.asp?2013/5/10/623/120804


Full Text

 Introduction



Methanol or wood alcohol is commonly found as a component of household products including paint removers or windshield washer fluid. Due to catastrophic consequences of methanol consumption, it cannot be used as an alcohol beverage. We report a case of middle aged man presented with confusion, severe metabolic acidosis secondary to methanol intoxication. A repeat CT scan of brain revealed bilateral putaminal hemorrhage as a late complication of methanol poisoning.

 Case Presentation



A 56-year-old man with history of episodic alcohol abuse and rectal adenocarcinoma status post-surgery and neoadjuvant chemoradiation therapy presented to emergency department with altered mental status. On admission, he was comatose with dilated pupils and minimal reaction to light. Fundus examination showed optic disc edema without evidence of retinal hemorrhage. Arterial Blood Gas (ABG) revealed severe metabolic acidosis; pH 6.89, pCO 2 13, pO 2 178, HCO 3 < 3. Blood tests also demonstrated anion gap and osmolal gap. Head computed tomography (CT) showed new hypodense lesions in basal ganglia bilaterally and old small vessel ischemia changes in periventricular matter [Figure 1]a.{Figure 1}

Emergent hemodialysis (HD) and treatment with intravenous fomepizole were initiated. Serum methanol level, obtained after hemodialysis, came back significantly elevated. Ophthalmologist was consulted for visual defect and diagnosed the patient with legal blindness without other focal neurological deficit prior to discharge. Type of alcohol, consumed by the patient, was still unknown. Unfortunately, patient developed confusion and lethargy 2 weeks after discharge. New CT of head without contrast demonstrated new hyperdensities in putaminal area compatible with the diagnosis of putaminal hemorrhages [Figure 1]b.

 Discussions



Methanol intoxication is a life-threatening condition. Bilateral putaminal hemorrhages, complication carrying very high morbidity, have been described in methanol intoxication and can be found in other diseases including inborn error metabolism, renal failure with severe metabolic acidosis, and ethylene glycol intoxication. [1],[2] The proposed underlying mechanism is acid-induced neural cell death. [3] In addition to putaminal hemorrhage, another important complication is visual loss. The mechanism is currently presumed to be formic acid-induced retinal damage from animal models. [4] There are no studies conducted in human for the pathophysiology of methanol optic neuropathy. There was one recent research demonstrating the role of intravenous erythropoietin with oral prednisolone to improve a visual acuity in the patients with optic neuropathy. [5]

Our case presentation demonstrates that even appropriate treatment, promptly initiated. The patient still developed putaminal hemorrhage. Clinicians should have high index of suspicion for putaminal hemorrhage when patients with recent methanol intoxication present with alter mental status, confusion or behavioral change.

References

1Martínez Bermejo A, Arcas J, Roche MC, López-Martín V, Royo A, Merinero B, et al. Bilateral hypodensity of the basal ganglia. Clinico-evolutionary correlation in children. Rev Neurol 2001;33:101-11.
2Corr P, Szólics M. Neuroimaging findings in acute ethylene glycol poisoning. J Med Imaging Radiat Oncol 2012;56:442-4.
3Sherwood TW, Lee KG, Gormley MG, Askwith CC. Heteromeric acid-sensing ion channels (ASICs) composed of ASIC2b and ASIC1a display novel channel properties and contribute to acidosis-induced neuronal death. J Neurosci 2011;31:9723-34.
4Chen JM, Zhu GY, Xia WT, Zhao ZQ. Proteomic analysis of rat retina after methanol intoxication. Toxicology 2012;293:89-96.
5Pakravan M, Sanjari N. Erythropoietin treatment for methanol optic neuropathy. J Neuroophthalmol 2012;32:325-8.