Pin the diagnosis on the calcium clue.
Two of the findings - high anion gap metabolic acidosis with tachypnoea - are shared by several alcohols, so they cannot settle the answer alone. The deciding feature is the hypocalcaemia.
Why ethylene glycol causes hypocalcaemia: Ethylene glycol is oxidised through glycolaldehyde to glycolic acid (the main driver of the anion gap) and finally to oxalic acid. Oxalate avidly binds free serum calcium, precipitating as calcium oxalate. This does two things: it lowers serum calcium (hypocalcaemia) and it deposits crystals in the kidney, producing acute renal failure with characteristic oxalate crystalluria. Tachypnoea is Kussmaul-type compensation for the acidosis and hypotension reflects the severe metabolic insult.
Ruling out the other toxins:
- Methanol also gives a high anion gap acidosis, but its signature is decreased/loss of vision from formate toxicity, and it is NOT associated with hypocalcaemia, so the calcium clue excludes it.
- Dhatura is an anticholinergic (mydriasis, dry hot skin, delirium, urinary retention) with no oxalate-driven acidosis or hypocalcaemia.
- Ethyl alcohol does not chelate calcium; clinically it is used to block alcohol dehydrogenase as treatment, not as the offending poison here.
The combination of high anion gap acidosis $+$ hypocalcaemia (from calcium-oxalate formation) is essentially unique to ethylene glycol among these choices.
Answer: B (Ethylene glycol).