A 32 year old lethargic male was brought to emergency depament with history of consumption of some drug .On investigation, he had low calcium, serum Creatinine -3.8 mg/dL, raised BUN . On ABG, metabolic acidosis was noted. On urine examination, calcium oxalate crystals were observed. He was treated with 4-methyl pyrazole. What could be the probable drug ingestion leading to following condition ?
First, I need to recall the drugs that lead to metabolic acidosis and calcium oxalate crystals. Ethylene glycol comes to mind because it's a common cause of toxic alcohol ingestion. When metabolized, ethylene glycol is converted to glycolic acid and oxalic acid, which can form calcium oxalate crystals in the urine. This leads to renal failure, which explains the high creatinine and BUN. The low calcium is due to calcium binding with oxalate, forming the crystals.
The treatment mentioned is 4-methyl pyrazole, which is the antidote for ethylene glycol poisoning. It works by inhibiting alcohol dehydrogenase, preventing the conversion of ethylene glycol into its toxic metabolites. So the correct answer here is likely ethylene glycol.
Looking at the options, the possible other drugs could be methanol, isopropanol, or maybe something else. Methanol also causes metabolic acidosis but its metabolites are formic acid, leading to optic nerve damage. The crystals in methanol might be different. Isopropanol is metabolized to acetone, causing a different pattern. Also, isopropanol poisoning doesn't typically produce calcium oxalate crystals. So methanol and isopropanol can be ruled out based on the crystals present.
The other option might be something like aspirin, but aspirin overdose causes a mixed acid-base disorder and doesn't lead to calcium oxalate crystals. So the presence of those crystals is a key clue pointing towards ethylene glycol.
So the correct answer should be ethylene glycol. The other options are incorrect because they don't produce calcium oxalate crystals. The treatment with 4-methyl pyrazole also aligns with ethylene glycol poisoning, confirming that.
**Core Concept**
This question tests knowledge of toxic alcohol poisoning, specifically ethylene glycol toxicity, which causes metabolic acidosis, acute kidney injury, and calcium oxalate crystals in urine. The antidote 4-methyl pyrazole (fomepizole) inhibits alcohol dehydrogenase, preventing toxic metabolite formation.
**Why the Correct Answer is Right**
Ethylene glycol is metabolized by alcohol dehydrogenase to glycolic acid and oxalic acid. Oxalic acid binds calcium to form **calcium oxalate crystals** (observed in urine) and causes hypocalcemia. Metabolic acidosis arises from glycolic acid accumulation. Acute kidney injury (elevated creatinine/BUN) results from crystal-induced tubular obstruction and direct nephrotoxicity. Fomepizole blocks this cascade by competitively inhibiting alcohol dehydrogenase.
**Why Each Wrong Option is Incorrect**
**Option A:** Methanol poisoning causes formic acid accumulation (not oxalate crystals) and optic neuropathy.
**Option B:** Isopropanol is metabolized to acetone (not oxalate crystals) and causes a high an