Question:
A person comes to emergency after consumption of substance, the form & dose of which is not known to relatives. The patient shows tachypnea, hypotension. On metabolic assessment high anion gap acidosis is noted with hypocalcemia. Diagnosis
A person comes to emergency after consumption of substance, the form & dose of which is not known to relatives. The patient shows tachypnea, hypotension. On metabolic assessment high anion gap acidosis is noted with hypocalcemia. Diagnosis
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High anion gap acidosis is non-specific – but acidosis PLUS hypocalcaemia (calcium being chelated by oxalate) points to one alcohol.
Updated On: Jun 22, 2026
- Methyl alcohol
- Ethylene glycol
- Dhatura
- Ethyl alcohol
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The Correct Option is B
Solution and Explanation
Step 1: List the discriminating findings. The patient has (i) an unknown ingested substance, (ii) tachypnoea and hypotension, (iii) a HIGH ANION GAP metabolic acidosis and - the key clue - (iv) hypocalcaemia.
Step 2: Use hypocalcaemia to localise the toxin. Among the options, the toxin that classically combines high-anion-gap acidosis WITH hypocalcaemia is ethylene glycol. Ethylene glycol is metabolised to glycolic acid (causing the high anion gap acidosis) and then to oxalic acid, which binds serum calcium to form insoluble calcium oxalate. This chelation drops the serum calcium (hypocalcaemia) and the calcium-oxalate crystals deposit in renal tubules, causing acute kidney injury. Tachypnoea is the respiratory compensation for acidosis; hypotension reflects the toxic/metabolic decompensation.
Step 3: Eliminate the distractors.
• Methyl alcohol (A): Also causes a high anion gap acidosis, but its hallmark is VISUAL loss from formic acid, and it does NOT characteristically cause hypocalcaemia.
• Dhatura (C): An anticholinergic plant poison - dry mouth, dilated pupils, hot dry flushed skin, delirium, tachycardia; it does not produce high-anion-gap acidosis with hypocalcaemia.
• Ethyl alcohol (D): Ordinary alcohol; can cause a mild ketoacidosis but not the calcium-oxalate hypocalcaemia picture, and it is the antidote (competitor for alcohol dehydrogenase) rather than the cause here.
Step 4: Conclude. High anion gap metabolic acidosis PLUS hypocalcaemia (from calcium-oxalate formation) points specifically to ethylene glycol.
Final answer: B - Ethylene glycol.
Step 2: Use hypocalcaemia to localise the toxin. Among the options, the toxin that classically combines high-anion-gap acidosis WITH hypocalcaemia is ethylene glycol. Ethylene glycol is metabolised to glycolic acid (causing the high anion gap acidosis) and then to oxalic acid, which binds serum calcium to form insoluble calcium oxalate. This chelation drops the serum calcium (hypocalcaemia) and the calcium-oxalate crystals deposit in renal tubules, causing acute kidney injury. Tachypnoea is the respiratory compensation for acidosis; hypotension reflects the toxic/metabolic decompensation.
Step 3: Eliminate the distractors.
• Methyl alcohol (A): Also causes a high anion gap acidosis, but its hallmark is VISUAL loss from formic acid, and it does NOT characteristically cause hypocalcaemia.
• Dhatura (C): An anticholinergic plant poison - dry mouth, dilated pupils, hot dry flushed skin, delirium, tachycardia; it does not produce high-anion-gap acidosis with hypocalcaemia.
• Ethyl alcohol (D): Ordinary alcohol; can cause a mild ketoacidosis but not the calcium-oxalate hypocalcaemia picture, and it is the antidote (competitor for alcohol dehydrogenase) rather than the cause here.
Step 4: Conclude. High anion gap metabolic acidosis PLUS hypocalcaemia (from calcium-oxalate formation) points specifically to ethylene glycol.
Final answer: B - Ethylene glycol.
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