Corrosive Poisons
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Direct answer
Acids kill tissue by coagulative necrosis, forming a dry eschar that limits depth, while alkalis liquefy tissue and burrow deeper — which is why caustic strictures of the oesophagus follow alkali ingestion more often than acid. Management in the first hours is airway first (hoarseness and stridor mean supraglottic oedema), then early dilution with water or milk if there is no perforation, and two absolute prohibitions: no induced emesis and no attempted neutralisation, since the exothermic reaction burns again. Each acid stains its own eschar — sulphuric brown-black, nitric yellow, hydrochloric grey-white — and the exam remembers carbolic acid by its white eschar and the urine that darkens on standing.
What you must remember
- Eschar colours: sulphuric acid a characteristic brown-black, nitric acid yellow from the xanthoproteic reaction, hydrochloric grey-white, carbolic (phenol) white later turning bronze — with darkening "carbolic urine" on standing and systemic toxicity.
- Alkalis — sodium and potassium hydroxide, ammonia — produce liquefactive necrosis with soapiness of the mouth mucosa; classically acids burn the stomach worse (the alkaline saliva buffers the oesophagus) and alkalis burn the oesophagus worse.
- Oxalic acid poisoning is different in kind: absorbed oxalate chelates calcium, producing hypocalcaemia with tetany, convulsions, envelope-shaped calcium oxalate crystals in the urine and acute tubular injury.
- Airway outranks everything: drooling, hoarseness and stridor predict airway compromise; early intubation is safer than watching.
- Early dilution with water or milk helps only within the first thirty to sixty minutes and only when perforation is not suspected; the absolute prohibitions stand regardless — no emetics, no lavage for strong corrosives (perforation), no neutralisation (exothermic re-burn), no oils.
- Endoscopy within the first day, once stable, grades the injury and predicts the stricture; steroids remain controversial; antibiotics accompany full-thickness injury.
- Strictures declare themselves at two to four weeks, more often after alkali ingestion, and require dilatation — with a recognised late risk of squamous carcinoma at the stricture decades later.
- Vitriolage — acid throwing, usually sulphuric or nitric on the face — demands immediate copious water irrigation for a prolonged period, eye irrigation first if the eye is involved, and it is a medico-legal case of assault with specific statutory compensation provisions.
Airway, dilute, scope — one swallow of lye
A toddler drinks from a bottle under the sink; a woman swallows toilet-cleaner acid in despair. Both are handled in the same order. First the airway: a hoarse voice or stridor means supraglottic burn, and the anaesthetist is called before the oedema closes the door. Second, dilution: if seen early and perforation is not suspected, water or milk dilutes the residual corrosive; once perforation is likely, nothing by mouth.
Third, the scope: endoscopy in the first twelve to twenty-four hours, once stabilised, grades the burn — hyperaemia, ulceration, or full-thickness — and forecasts the stricture; nothing accelerates healing pharmacologically. Fourth, the watch for the two disasters: perforation with mediastinitis or peritonitis in the first days, and the fibrosing stricture at weeks two to four, when the dilatation programme begins. In the vitriolage casualty meanwhile, the irrigation never stops early — copious water for half an hour, the eye flooded if involved — because the acid keeps burning while it is wet.
Where students slip
The neutralisation instinct is the most punished error in this chapter: the acid-base reaction releases heat and burns the mucosa a second time, which is why dilution is the answer, not titration. Second, examinees forget the acid-alkali geography — acids burn the stomach (the alkaline saliva and oesophageal squamous mucosa resist acid) while alkalis spare the stomach more and destroy the oesophagus — and this inversion is what the single-best-answer question tests. Third, the colour table is half-remembered: nitric yellow and sulphuric brown-black are quoted safely, but carbolic's white-then-bronze eschar with darkening urine and oxalic's hypocalcaemic tetany with envelope crystals are the distinguishing marks examiners reserve for the viva. Finally, emesis and lavage are wrongly advised "if early" — with corrosives, never.
Frequently asked questions
Why do acids and alkalis injure differently?
Acid coagulates proteins into a dry eschar that walls off deeper penetration; alkali liquefies proteins and saponifies fats, so it digs through tissue planes — the reason alkali strictures are more common.
Which acid produces a yellow eschar and why?
Nitric acid, from the xanthoproteic reaction with tissue proteins; sulphuric gives brown-black and hydrochloric grey-white, forming the classic colour trio.
Why is neutralisation of a corrosive forbidden?
The neutralising reaction is strongly exothermic, causing a second thermal burn on already necrotic mucosa; dilution with water or milk achieves safety without the heat.
When and how is endoscopy performed after corrosive ingestion?
Within the first twelve to twenty-four hours in a stable patient, to grade the burn and predict stricture; beyond about forty-eight hours the perforation risk of the instrument rises.
What distinguishes oxalic acid poisoning?
Systemic absorption of oxalate chelates calcium: hypocalcaemia with tetany and seizures, acute kidney injury, and envelope- or crystal-shaped calcium oxalate crystals in urine microscopy.