What is the treatment for a patient with suspected copper sulphate poisoning?

Treatment of Copper Sulphate Poisoning

Immediate supportive care with early gastric decontamination, aggressive fluid resuscitation, and chelation therapy with D-penicillamine are essential for survival in acute copper sulphate poisoning, with plasmapheresis reserved for severe cases unresponsive to initial chelation. 1, 2, 3

Immediate Emergency Management

Initial Stabilization

• Secure airway, breathing, and circulation first - copper sulphate poisoning causes severe hemorrhagic gastroenteritis, hypotension, and potential coma requiring immediate hemodynamic support 1, 2
• Administer 100% oxygen and establish IV access for aggressive fluid replacement to manage dehydration and hypotension 2
• Monitor for signs of shock and administer vasoactive drugs (vasopressors) if hypotension persists despite fluid resuscitation 2

Early Decontamination

• Perform gastric lavage as early as possible if the patient presents within 1-2 hours of ingestion to remove residual copper sulphate 2
• Do not induce vomiting, as the patient likely already has severe hemorrhagic gastroenteritis with hematemesis 1, 2

Specific Antidotal Therapy

Chelation with D-Penicillamine

• Start D-penicillamine immediately at 250-500 mg/day initially, then increase by 250 mg increments every 4-7 days to a maximum of 1000-1500 mg daily in divided doses 1, 4
• Administer on an empty stomach (at least 1 hour before meals or 2 hours after) and at least 1 hour apart from any other medications 4
• Add pyridoxine (vitamin B6) supplementation daily, as penicillamine increases pyridoxine requirements 4
• Monitor 24-hour urinary copper excretion - aim for initial cupriuresis >2 mg in the first week, then maintain urinary copper at 200-500 µg/day during ongoing treatment 5, 4

Alternative Chelation Options

• If D-penicillamine is not tolerated or unavailable, consider 2,3-dimercaptopropane-1-sulphonate (DMPS) as an alternative chelating agent 2
• Zinc administration (competes with copper for absorption) may be used as adjunctive therapy in chronic toxicity but is not first-line for acute poisoning 1

Management of Specific Complications

Methemoglobinemia

• Administer methylene blue immediately if methemoglobinemia is present (typically manifests as cyanosis with saturation gap on pulse oximetry) 2, 6
• Standard dose: 1-2 mg/kg IV over 5 minutes 2

Intravascular Hemolysis

• Monitor hemoglobin, haptoglobin, LDH, and indirect bilirubin closely 2, 3
• Provide blood transfusions as needed for severe anemia 2
• Consider plasmapheresis (therapeutic plasma exchange) for severe hemolysis unresponsive to chelation - copper is protein-bound and not dialyzable, but plasmapheresis can remove it effectively 3
• Perform 4 cycles of plasma exchange if clinical deterioration continues despite D-penicillamine 3

Acute Kidney Injury and Rhabdomyolysis

• Administer furosemide for diuresis and to prevent acute tubular necrosis 2
• Initiate hemodialysis for severe renal failure (though it does not remove copper directly, it manages uremia and fluid overload) 2, 3
• Monitor creatine kinase levels for rhabdomyolysis 7

Hepatic Failure

• Monitor liver function tests (AST, ALT, bilirubin, INR, albumin) serially 1, 2
• Provide supportive care with N-acetylcysteine if indicated for hepatotoxicity 2
• Consider liver transplantation consultation if fulminant hepatic failure develops 5

Gastrointestinal Hemorrhage

• Administer ranitidine or proton pump inhibitors for gastric protection 2
• Give antiemetic drugs to control severe vomiting 2
• Monitor for melena and hematemesis; transfuse blood products as needed 1, 2

Adrenal Insufficiency

• Administer IV hydrocortisone if adrenal insufficiency develops (hypotension refractory to fluids and vasopressors, hyponatremia, hyperkalemia) 2

Diagnostic Monitoring

Essential Laboratory Tests

• Measure serum copper and ceruloplasmin levels (though serum copper may be normal initially despite severe toxicity) 1, 2
• Complete blood count with attention to hemolysis markers 1
• Comprehensive metabolic panel including liver function tests, renal function, and electrolytes 1, 2
• Arterial blood gas to assess for metabolic acidosis 2
• Methemoglobin level if cyanosis or saturation gap present 6
• 24-hour urinary copper excretion to guide chelation therapy 5, 4

Clinical Monitoring

• Look for Kayser-Fleischer rings on slit-lamp examination (pathognomonic brown ring-shaped markings in the cornea) 1, 4
• Monitor for neurological deterioration, behavioral changes, and coma 1, 2
• Watch for signs of multi-organ failure progression 2, 3

Critical Pitfalls to Avoid

• Do not delay chelation therapy while waiting for serum copper levels - clinical presentation and history of exposure are sufficient to initiate treatment 1, 2
• Do not rely on serum copper levels alone - they may be normal on admission despite severe toxicity 2
• Do not use hemodialysis as primary copper removal strategy - copper is protein-bound and not dialyzable; use plasmapheresis instead for refractory cases 3
• Do not underestimate the lethal dose - as little as 10 grams can be fatal 7
• Do not stop D-penicillamine if neurological symptoms worsen initially - this can occur during early treatment but does not indicate treatment failure 4

Prognosis and Follow-up

• Even with aggressive treatment, patients may develop chronic kidney disease requiring long-term dialysis 3, 6
• Persistent mild hepatic impairment may remain after recovery 2
• Long-term monitoring of renal and liver function is essential in survivors 1
• Psychiatric evaluation and follow-up are necessary for intentional ingestions 2