Copper sulphate (nila thotha): six complications and one dangerous reflex

The vomit is blue-green. That single observation is usually enough to make the diagnosis of nila thotha — copper sulphate — ingestion, and it is often the last thing about this poisoning that is straightforward.

What follows is a warning as much as a guide. There is no clinical guideline for copper sulphate poisoning anywhere. The best available source is a published discussion of three cases, which itself states that the efficacy of chelating agents is unproven, that activated charcoal is of unproven benefit, and that the duration of chelation is not established by evidence. Doses appear below because you need to find them quickly at 3 a.m., not because anyone has validated them.

What you are dealing with

Copper sulphate is sold as bright blue crystals for fungicide, algaecide and dyeing use, and is a common agent of deliberate self-harm. Early: metallic taste, burning epigastric pain, profuse vomiting. The lethal dose of ingested copper sulphate is between 10 and 20 g, though that is a rough threshold and depends on the individual. Mortality in severe poisoning is high.

It is also a corrosive. Gastrointestinal manifestations are predominantly due to corrosive injury, and haematemesis and melaena occur with severe overdose. Erosive gastropathy is the rule, not the exception — so the corrosive rules apply here too, chiefly never inducing vomiting.

Six things go wrong, roughly in this order

Note the pairing in rows two and three. This poisoning produces methaemoglobinaemia and intravascular haemolysis simultaneously, and that combination is what makes the standard treatment dangerous.

The methylene blue trap

The textbook answer for methaemoglobinaemia is methylene blue, 1–2 mg/kg intravenously, repeated if cyanosis persists beyond an hour. Here, three separate things can go wrong with that:

1. It is contraindicated in G6PD deficiency — which is common in Pakistan and frequently undiagnosed. You will usually not know the status of the patient in front of you.
2. High doses cause haemolysis themselves — in a patient who is already haemolysing.
3. It needs intact red cells to work, and this poisoning is actively destroying them, so the response is blunted exactly when you need it.

Where methylene blue fails, is contraindicated, or the haemolysis is severe, the described alternatives are exchange transfusion, hyperbaric oxygen, and ascorbic acid — the last being a much weaker reducing agent.

This does not mean never give methylene blue. It means think for ten seconds first, which is more than the reflex allows.

Reducing absorption

Management rests on four principles: reducing absorption, close observation for complications, supportive therapy, and chelation.

Dilution with large quantities of milk and water minimises contact damage to the mucosa. Never induce emesis — repeated exposure of the oesophagus to a corrosive inflicts further damage, and this agrees with the AACT/EAPCCT position paper, which names corrosives explicitly. Activated charcoal is described at 50 g in 200 ml of water, repeated 6-hourly if necessary, but is of unproven benefit; the position paper's view is that charcoal should not be given routinely and is contraindicated without a protected airway.

What to monitor, from the first 24 hours

All complications mentioned above must be monitored for from the first 24 hours onwards (daily full blood counts, serum electrolytes, liver and renal function tests).

Add a daily blood picture and reticulocyte count — that is how you catch the haemolysis. A baseline chest radiograph if the patient has vomited, because aspiration pneumonia or chemical pneumonitis should be anticipated. A coagulation profile if there is spontaneous bleeding, a methaemoglobin level if cyanosed, creatine kinase for rhabdomyolysis, and serum copper if available to guide how long chelation continues.

One diagnostic trap: acute kidney injury alone raises serum amylase, so a high amylase does not by itself confirm pancreatitis.

Organ support is most of the treatment

Correct anaemia from haemolysis or bleeding with red cell concentrate. A proton pump inhibitor for the erosive gastropathy — the published cases used an intravenous omeprazole infusion. Haemodialysis for the kidney injury; in the reported cases it was started on day four to five and continued for up to four weeks, with renal recovery taking nearly five weeks. Exchange transfusion is an option where haemodialysis is not available.

Plasmapheresis rescued a patient with severe poisoning who had not improved on D-penicillamine and supportive care — it removes protein-bound copper, which dialysis does not.

Chelation: commonly given, never proven

Read the caveat before the numbers. The efficacy of these agents is unproven, and the duration of therapy is not established by evidence; the published recommendation is to continue as long as the serum copper remains elevated.

• D-penicillamine (oral) — 1–1.5 g/day in 2–4 divided doses; the reported cases used 500 mg six-hourly without ill effect. The commonly used agent, but nephrotoxic — and acute kidney injury is the commonest complication of the poisoning it is treating. Use carefully where renal replacement therapy is not available.
• Dimercaprol / BAL (intramuscular) — 3–5 mg/kg/dose four-hourly for the first two days, then tailed off over a total of 7–11 days. Used when oral penicillamine is difficult or contraindicated, such as severe corrosive injury to the alimentary tract, which is common here. Some authors question its efficacy against penicillamine.
• Edetate calcium disodium — an alternative, and recommended by some as first-line when penicillamine is unsafe. Also carries a risk of acute tubular necrosis and needs dose reduction in kidney injury.
• DMPS — described as probably the best chelator on experimental grounds. Experimental is the operative word: rarely available, no clinical trial evidence in this poisoning.

Bottom line

Blue-green vomit makes the diagnosis. Treat it as a corrosive as well as a systemic poison, which means no emesis. Expect six complications in sequence and start daily bloods within the first 24 hours. Pause before giving methylene blue — G6PD, haemolysis and the need for intact red cells all work against it. Watch the kidneys hardest, and remember that the chelator most people reach for is nephrotoxic. And be clear with yourself that almost none of this rests on evidence stronger than case reports.

Our copper sulphate tool lays this out in six steps with the evidence tier shown on every recommendation. Also in the suite: Harpic and corrosives, wheat pill and rat poison, and anticoagulant rat poison.

ReviseFCPS1 is built by doctors in Pakistan, for doctors in Pakistan. All our clinical tools are free. If you are preparing for FCPS Part 1, try it free for 7 days — 10,176 doctor-verified MCQs and 8,236 real exam recalls.