FM13.11 | Corrosive Poisons (Acids) — Summary & Reflection

KEY TAKEAWAYS

Corrosive acid poisoning (FM13.11) encompasses six agents with distinct mechanisms, clinical presentations, and management requirements:

• Strong mineral acids (H₂SO₄, HNO₃, HCl): local coagulation necrosis with characteristic signs (black charring with H₂SO₄; xanthoproteic yellow staining with HNO₃; white eschar with HCl). No specific antidotes; supportive care and no alkali neutralisation.

• Carbolic acid/phenol: rapidly absorbed systemically → CNS depression, renal failure, carboluria (green-black urine). Treat systemically; supportive care.

• Oxalic acid: systemic hypocalcaemia (oxalate chelates Ca²⁺) → tetany, arrhythmia, renal calcium oxalate crystal deposition. Antidote: IV calcium gluconate.

• Acetylsalicylic acid (aspirin): systemic salicylate toxicity — biphasic acid-base disturbance (early respiratory alkalosis → late metabolic acidosis). Key treatments: urinary alkalinisation (ion trapping) and haemodialysis for severe cases (serum salicylate >350 mg/L).

Forensically: acid attacks are governed by IPC §326A/326B (2013 amendments); injuries almost always constitute grievous hurt (IPC §320). The MLR must document acid type, injury distribution and depth, permanent disfigurement, and prognosis.

REFLECT

Consider the 24-year-old woman from the opening scenario. As her treating physician and the first to document her injuries, how would you ensure your clinical record serves both her immediate treatment needs and the subsequent legal proceedings? Specifically: what information must you capture in the first hour that cannot be reconstructed later? How would you handle the chain of custody for biological samples collected during emergency treatment? And if the police ask you to give a verbal opinion on the type of acid used before laboratory results are available — what can you ethically and scientifically say?