Severe Methanol Poisoning Managed Using Bicarbonate Therapy and Hemodialysis in the Absence of an Available Antidote

Introduction  

Methanol poisoning constitutes a life-threatening medical emergency in critical care, particularly in developing countries where unregulated or illicitly produced alcohol is commonly consumed. While methanol itself is relatively non-toxic, its hepatic metabolism leads to the generation of formic acid—the principal agent responsible for high-anion-gap metabolic acidosis and optic nerve injury. In many low-resource settings, frontline hospitals often lack access to fomepizole or intravenous ethanol, the standard antidotes. The present case exemplifies the classical clinical presentation and offers important clinical insights into managing severe toxic alcohol exposure under resource-constrained conditions. 

Case presentation  

A 45-year-old male with a long-standing history of alcohol use disorder—specifically daily ingestion of unregulated white liquor from informal sources—presented to the emergency department with progressively worsening bilateral blurred vision over two days, accompanied by a dull frontal headache. He denied fever, vomiting, trauma, or recent illness. He reported ingesting a large volume of unbranded white alcohol approximately 48 hours prior to symptom onset. 

On examination, the patient was alert and hemodynamically stable. He described his vision as “foggy,” although formal Snellen testing was unavailable. There was no photophobia or diplopia. Neurological examination revealed no focal deficits. An ophthalmologic consultation was obtained; fundoscopy showed mild bilateral optic disc edema, consistent with toxic optic neuropathy. A non-contrast head CT was unremarkable—no basal ganglia injury or cerebral edema was seen. 

Laboratory investigations revealed the following: 

• Arterial pH: 6.90 

• Serum bicarbonate (HCO₃⁻): 4.9 mmol/L 

• Base excess: –30.2 mmol/L 

• Sodium: 132 mmol/L 

• Potassium: 5.07 mmol/L 

• Chloride: 100 mmol/L 

• Calculated anion gap: 32.17 mEq/L 

• Serum methanol: >100 mg/dL 

• Serum ethanol: 0.43 g/L 

• Serum creatinine: 146 µmol/L; eGFR: 43 mL/min/1.73m² 

• Serum urea: 6.4 mmol/L 

As fomepizole and IV ethanol were unavailable, the patient was treated with intravenous sodium bicarbonate and underwent two emergent hemodialysis sessions within the first 24 hours.  

Following 7 days of supportive care, the patient's acid-base status normalized. He remained alert, with corrected electrolyte imbalances. Creatinine decreased to 100 µmol/L, and eGFR improved to 67 mL/min/1.73m². Visual acuity partially recovered; the patient reported persistent mild central blurring but regained orientation and could identify objects at short distance. 

DISCUSSION  

The patient was diagnosed with acute methanol poisoning. As neither fomepizole nor intravenous ethanol was available, he was treated with intravenous sodium bicarbonate and emergent hemodialysis. The patient met all major criteria for emergent hemodialysis, including serum methanol >100 mg/dL, severe metabolic acidosis (pH <7.0), and visual symptoms, per international toxicology guidelines. Two consecutive dialysis sessions were performed within the first 24 hours. 

After 7 days of treatment, his metabolic acidosis had markedly improved: the patient was alert, electrolytes were corrected, and both pH and bicarbonate levels had normalized. Renal function also showed significant recovery, with creatinine decreasing to 100 µmol/L and eGFR increasing to 67 mL/min/1.73m². Visual acuity partially recovered, though the patient still reported mild central blurring. 

Methanol poisoning remains a life-threatening toxicological emergency, particularly in low- and middle-income countries where unregulated or illicit alcohol is commonly consumed.^1,2 Methanol itself is not directly toxic; however, once metabolized by hepatic alcohol dehydrogenase (ADH), it is converted to formaldehyde and subsequently to formic acid—the principal toxic metabolite responsible for both high-anion-gap metabolic acidosis and selective injury to the optic nerve.³ Formic acid disrupts mitochondrial oxidative phosphorylation by inhibiting cytochrome c oxidase, leading to tissue hypoxia, particularly in metabolically active structures such as the retina, optic nerves, and basal ganglia. 

This case illustrates the classic clinical triad of methanol poisoning: progressive bilateral visual impairment, severe high-anion-gap metabolic acidosis, and a recent history of ingestion of unregulated alcohol.⁴ The patient presented with a serum methanol concentration >100 mg/dL and an arterial pH of 6.90—a constellation strongly associated with poor outcomes including permanent blindness and death if not treated promptly. 

Standard management involves three pillars: inhibition of methanol metabolism using fomepizole or intravenous ethanol; correction of acidosis via sodium bicarbonate infusion; and enhanced elimination of methanol and its metabolites through hemodialysis.⁵ In this case, the unavailability of antidotal therapy posed a critical challenge. However, early recognition, prompt initiation of bicarbonate therapy, and urgent hemodialysis within the first 24 hours led to metabolic recovery, partial visual improvement, and renal function stabilization. This approach aligns with best-practice guidelines for methanol toxicity management in resource-limited settings.⁶ 

The blurring of optic disc margins observed on fundoscopy provided early objective evidence of optic neuropathy. Partial visual recovery following dialysis reinforces the importance of early intervention even in the absence of antidotes. Clinicians should maintain a high index of suspicion for toxic alcohol ingestion in patients presenting with visual disturbances, severe metabolic acidosis, and a compatible exposure history.⁷ 

Continuous ICU monitoring of acid–base status, osmolality, and neurologic changes is essential, as deterioration can be abrupt despite initial stability. 

​​From a critical care and toxicology perspective, arterial blood gas (ABG) analysis revealed severe metabolic acidosis with a markedly low pH (6.90), bicarbonate depletion (4.9 mmol/L), and a base excess of −30.2 mmol/L. This profile is typical of high-anion-gap acidosis due to formic acid accumulation. The profound acidosis contributes to tissue hypoperfusion, myocardial depression, and exacerbation of neurotoxicity. Electrolyte disturbances were notable, with initial mild hyponatremia (Na​⁺ 132 mmol/L), hyperkalemia (K⁺ 5.07 mmol/L), and normal chloride. The hyperkalemia likely resulted from transcellular potassium shifts secondary to acidosis and formate-induced cellular dysfunction. Following correction of acidosis with bicarbonate and hemodialysis, potassium dropped to 3.02 mmol/L, necessitating close electrolyte monitoring to prevent arrhythmias. 

Renal impairment on admission (creatinine 146 µmol/L, eGFR 43 mL/min/1.73m²) was likely functional, secondary to hypoperfusion and systemic toxicity. Renal function improved after metabolic stabilization and toxin clearance (creatinine decreased to 100 µmol/L, eGFR increased to 67 mL/min/1.73m²), underscoring the reversibility of early renal involvement. 

In the context of bilateral visual blurring accompanied by severe metabolic acidosis, several differential diagnoses must be considered:⁸ 

Ethylene glycol poisoning typically causes acute kidney injury with rapid elevation in serum creatinine and may present with coma and seizures. Calcium oxalate crystals in the urine are a hallmark feature—absent in this case. Furthermore, the patient had no known exposure to antifreeze, industrial solvents, or products containing ethylene glycol. 

Alcoholic ketoacidosis is seen in chronic alcohol users, often following reduced oral intake or episodes of vomiting. However, the acidosis is usually less severe (pH rarely <7.0), the anion gap is lower, and urinary or serum ketones are strongly positive. In this patient, there was no ketonuria, no vomiting, and the pH was profoundly low—making this diagnosis unlikely.⁹ 

Lactic acidosis due to sepsis or shock was not supported clinically. There were no signs of infection (no fever, no leukocytosis) or shock (no hypotension, no lactate elevation). Additionally, no clear source of infection was identified, and the overall clinical picture was inconsistent with systemic inflammatory response.¹⁰ 

Optic neuritis generally presents with unilateral vision loss, progressive over days, often associated with painful eye movements. In this case, the patient had bilateral vision loss, no pain on ocular movement, bilateral optic disc edema, and a history of ingesting unregulated alcohol—favoring a toxic etiology over inflammatory causes. 

Central nervous system lesions (stroke, hemorrhage, tumor) were excluded based on neuroimaging. A non-contrast head CT revealed no abnormalities, and the patient exhibited no focal neurological deficits, altered mental status, or fever—making acute intracranial pathology unlikely.  

This case reinforces key principles of toxicologic resuscitation: early suspicion, aggressive correction of acidosis, and rapid toxin elimination. Even in the absence of standard antidotes, timely bicarbonate therapy and hemodialysis proved effective in preventing blindness and ensuring survival. Emergency physicians, especially in resource-limited settings, must remain vigilant for the triad of “eyes, acid, alcohol”—a clinical pattern that demands immediate action to avert devastating outcomes.¹¹ 

Learning Points 

• Methanol toxicity should be suspected in any patient presenting with bilateral vision loss, high-anion-gap metabolic acidosis, and a history of unregulated alcohol ingestion. 

• In the absence of fomepizole or ethanol, early bicarbonate therapy and hemodialysis can still lead to survival and partial visual recovery. 

• Optic disc edema is an early, objective finding and may guide diagnosis before imaging. 

• Severe metabolic acidosis (pH < 7.0) and methanol >100 mg/dL strongly predict poor outcomes—intervention must be immediate. 

• Emergency physicians in resource-limited settings must recognize this triad: “eyes, acid, alcohol.” 

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