Six complications, one dangerous reflex, and a set of chelation doses that nobody has proven. What is known, and what only looks known.
Before you reach for methylene blue. This poisoning causes methaemoglobinaemia and intravascular haemolysis at the same time. Methylene blue is contraindicated in G6PD deficiency — common and often undiagnosed in Pakistan — can itself cause haemolysis at high dose, and needs intact red cells to work at all. Step 4 covers it properly.
This is the weakest-evidence tool in the suite, and we would rather tell you than hide it.Guideline / position paperCohort or seriesCase reports / expert opinion
There is no clinical guideline for copper sulphate poisoning anywhere. The primary source below is a discussion of three cases, and it states plainly that chelation efficacy is unproven, charcoal is of unproven benefit, and chelation duration is not established. Doses are reproduced as published so you can find them quickly — not because they are validated.
National Poisons and Drug Information Centre, Jinnah Postgraduate Medical Centre (JPMC), Karachi — 0800-77767 Reported as a round-the-clock toll-free service. Confirm the current number against your own hospital directory before relying on it in an emergency.
Decision-support only. This reproduces published practice so you can apply it quickly. It does not replace clinical judgement or your hospital protocol, and in this arm the published practice is itself uncertain.
✓ Clinically reviewed by Dr Syed Usama Hussain, MBBS, BSc · 05 Aug 2026.
Step 1 · Recognise it
Gamakaranage et al. 2011
Blue-green vomit is the giveaway Case reports / expert opinion
Copper sulphate is sold as bright blue crystals — nila thotha, blue vitriol, blue stone — for fungicide, algaecide and dyeing use, and it is a common agent of deliberate self-harm. The vomit is characteristically blue or green. A metallic taste, burning epigastric pain and profuse vomiting come early.
Dose and mortality. The lethal dose of ingested copper sulphate is between 10–20 g, though this is only a rough threshold for toxicity and depends on individual factors. Mortality in cases of severe poisoning is high.
It is also a corrosive Case reports / expert opinion
Common gastrointestinal manifestations of copper poisoning are predominantly due to corrosive injury. Haematemesis and melaena are observed with severe overdose, probably due to bleeding from mucosal injury. Erosive gastropathy is the rule rather than the exception — so the corrosive principles apply here too, including never inducing vomiting.
The management of copper sulphate poisoning centres on four key principles: reducing absorption, close observation for complications, supportive therapy, and chelation therapy to remove active copper from the body.
Dilution with milk or water Case reports / expert opinion
After ingestion, the contact damage to mucosa can be minimised by drinking large quantities of milk and water. Dilution reduces the direct mucosal injury.
Never induce emesis Guideline / position paper
Emesis must be avoided as repeated exposure of the oesophagus to the corrosive agent may inflict further damage on the mucosa. This agrees with the AACT/EAPCCT position paper, which names corrosives explicitly.
Activated charcoal — unproven Case reports / expert opinion
Some authors recommend activated charcoal (50 g dissolved in 200 ml of water, administered in multiple doses if necessary at 6-hourly intervals) to reduce absorption, but it is of unproven benefit. The AACT/EAPCCT position is that charcoal should not be given routinely and is contraindicated without an intact or protected airway.
Step 3 · The six complications
Gamakaranage et al. 2011
Select one to see when it appears and what to do about it. They tend to arrive in this order.
What to monitor, from the first 24 hours Case reports / expert opinion
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).
Daily full blood count, electrolytes, liver and renal function from the first 24 hours.
Daily blood picture and reticulocyte count — this is how you catch the haemolysis.
Baseline chest radiograph if the patient has vomited: anticipate aspiration pneumonia or chemical pneumonitis.
Coagulation profile if there is spontaneous bleeding.
Methaemoglobin level if the patient is cyanosed.
Creatine kinase for rhabdomyolysis, and serum copper if available to guide chelation duration.
Step 4 · Methaemoglobinaemia and the methylene blue trap
Gamakaranage et al. 2011
Methylene blue — the step to slow down on Case reports / expert opinion
Methaemoglobinaemia is treated with methylene blue (intravenous injection of 1–2 mg/kg/dose and repeated if cyanosis persists beyond one hour).
Three reasons the reflex can fail or harm:
High doses of methylene blue itself can cause haemolysis, and it is contraindicated in G6PD deficiency. G6PD deficiency is common in Pakistan and is frequently undiagnosed.
Methylene blue needs intact red cells to work. This poisoning is actively destroying them, so severe haemolysis blunts the response.
Alternatives to methylene blue in such situations would be hyperbaric oxygen and ascorbic acid — a much weaker reducing agent.
Where methylene blue fails, is contraindicated, or the haemolysis is severe, exchange transfusion has been used.
Gamakaranage et al., J Occup Med Toxicol 2011;6:34; case reports of exchange transfusion
Step 5 · Organ support
Gamakaranage et al. 2011 · case reports
Supportive therapy is most of the treatment Case reports / expert opinion
Anaemia from haemolysis or bleeding must be corrected with transfusion of red cell concentrates.
Haemodialysis for acute kidney injury — started on day 4 to 5 in the reported cases and continued for up to four weeks until renal function recovered.
Exchange transfusion is an option when haemodialysis facilities are not available.
Plasmapheresis has rescued a patient with severe copper sulphate poisoning who did not improve on D-penicillamine and supportive care — it removes protein-bound copper, which dialysis does not.
Proton pump inhibitor for the erosive gastropathy; supportive management for the hepatitis.
Gamakaranage et al. 2011; case report of rescue with plasmapheresis
Step 6 · Chelation
Gamakaranage et al. 2011
Chelation — commonly given, never proven
Read this before the doses. The efficacy of these chelating agents is unproven, and the duration of chelation therapy is not established by evidence. It is recommended to treat with chelators as long as the serum copper level remains elevated. Everything in this section is practice, not proof.
D-penicillamine (oral) Case reports / expert opinion
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. Nephrotoxic — it must be used carefully in places without access to renal replacement therapy, and acute kidney injury is the commonest complication of this poisoning.
Dimercaprol / British anti-Lewisite, BAL (intramuscular) Case reports / expert opinion
3–5 mg/kg/dose four-hourly for the first two days, then tailed off over a total of 7–11 days.
Recommended when oral administration of penicillamine is difficult or contraindicated — for example severe corrosive injury in the alimentary tract, which is common here. Some authors question its efficacy compared with penicillamine.
Edetate calcium disodium Case reports / expert opinion
Dose-reduced in the presence of acute kidney injury.
Another option, and some recommend it as first-line when penicillamine is deemed unsafe. Case reports describe success with edetate calcium disodium followed by oral penicillamine or dimercaprol. It also carries a risk of acute tubular necrosis and must be given carefully.
DMPS (2,3-dimercapto-1-propane sulphonate) Case reports / expert opinion
Not established in this setting.
Described as probably the best chelator on the basis of experimental studies, but experimental is the operative word — it is rarely available and there is no clinical trial evidence in copper sulphate poisoning.
Almost all of these ingestions are deliberate self-harm.
Psychiatric evaluation is mandatory in all patients prior to hospital discharge (Grade 2C). Long-term control of the psychiatric disease is important to avoid recurrence.
A patient who is medically fit for discharge is not therefore fit for discharge. The guideline makes the psychiatric assessment a requirement, not a courtesy — and the ingestion pattern (deliberate versus accidental) is itself among the strongest predictors of how bad the injury will be.
WSES Esophageal Emergencies guidelines, 2019
Common questions
What are the signs of copper sulphate poisoning?
Blue or green vomit is the giveaway, with a metallic taste, burning epigastric pain and profuse vomiting early. Then six complications appear in sequence: erosive gastropathy, intravascular haemolysis, methaemoglobinaemia, hepatitis, acute kidney injury and rhabdomyolysis.
Can I give methylene blue for the methaemoglobinaemia?
Slow down before you do. Methylene blue is contraindicated in G6PD deficiency, which is common and often undiagnosed in Pakistan. High doses can themselves cause haemolysis. And methylene blue needs intact red cells to work, while this poisoning is actively destroying them. Where it fails or is contraindicated, alternatives include exchange transfusion, hyperbaric oxygen and ascorbic acid — the last being a much weaker reducing agent.
Should I induce vomiting or do gastric lavage?
No. Copper sulphate causes corrosive injury and erosive gastropathy is the rule, so emesis must be avoided — repeated exposure of the oesophagus to the corrosive agent inflicts further mucosal damage. Dilution with large quantities of milk and water reduces contact injury.
Does activated charcoal help?
It is of unproven benefit. Some authors recommend 50 g in 200 ml of water, repeated 6-hourly if necessary, but there is no evidence it changes outcome, and the AACT/EAPCCT position is that charcoal should not be given routinely and is contraindicated without a protected airway.
Which chelating agent should I use?
The efficacy of all of them is unproven. D-penicillamine 1–1.5 g/day in 2–4 divided doses is the commonly used agent, but it is nephrotoxic and acute kidney injury is the commonest complication of this poisoning. Dimercaprol (BAL) 3–5 mg/kg/dose four-hourly for two days then tailed off over 7–11 days is used when oral penicillamine is difficult or contraindicated, such as with severe corrosive injury.
How long should chelation continue?
The duration is not established by evidence. The published recommendation is to continue as long as the serum copper level remains elevated.
What is the lethal dose of copper sulphate?
The lethal dose of ingested copper sulphate is between 10 and 20 g, though this is only a rough threshold and depends on individual factors. Mortality in severe poisoning is high.
When does the kidney injury appear and how long does it last?
Acute kidney injury is the commonest complication, reported at 40–60% in some case series. Recovery is slow and incomplete — in the published cases haemodialysis was started on day 4 to 5 and continued for up to four weeks, with one patient taking nearly five weeks to recover.
Clinically reviewed by Dr Syed Usama Hussain, MBBS, BSc
MBBS, BSc — active medical practitioner in Pakistan. Graduated from Federal Medical & Dental College, Islamabad (2021) and completed a one-year clinical internship at the Pakistan Institute of Medical Sciences (PIMS), Islamabad (2022).
Sources
Gamakaranage CSSK, Rodrigo C, Weerasinghe S, Gnanathasan A, Puvanaraj V, Fernando H. Complications and management of acute copper sulphate poisoning; a case discussion. Journal of Occupational Medicine and Toxicology 2011;6:34. — open access, and the source of nearly every statement and dose quoted here.
Case report of severe copper sulphate poisoning rescued with plasmapheresis after failure of D-penicillamine and supportive care.
Reports of exchange transfusion where methylene blue failed, was contraindicated, or haemolysis was severe.
AACT/EAPCCT Position Paper: single-dose activated charcoal; and Position Paper Update 2013: ipecac syrup — for the decontamination statements.
NOTE ON EVIDENCE: no clinical guideline exists for copper sulphate poisoning. The primary source above is a discussion of three cases. Doses are reproduced as published so you can find them quickly, not because they are validated.
Background reading — the six complications in sequence and the three reasons methylene blue can fail or harm: copper sulphate poisoning.