Abstract and Introduction
Introduction: Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life-threatening features and acute renal failure. Previous reports on the use of extracorporeal procedures such as haemodialysis and haemoperfusion have shown no significant removal of mercury. We report here the successful use of the chelating agent 2,3-dimercaptopropane-1-sulphonate (DMPS), together with continuous veno-venous haemodiafiltration (CVVHDF), in a patient with severe inorganic mercury poisoning.
Case Report: A 40-year-old man presented with haematemesis after ingestion of 1 g mercuric sulphate and rapidly deteriorated in the emergency department, requiring intubation and ventilation. His initial blood mercury was 15 580 µg/l. At 4.5 hours after ingestion he was started on DMPS. He rapidly developed acute renal failure and so he was started on CVVHDF for renal support and in an attempt to improve mercury clearance; CVVHDF was continued for 14 days.
Methods: Regular ultradialysate and pre- and post-filtrate blood samples were taken and in addition all ultradialysate generated was collected to determine its mercury content.
Results: The total amount of mercury in the ultrafiltrate was 127 mg (12.7% of the ingested dose). The sieving coefficient ranged from 0.13 at 30-hours to 0.02 at 210-hours after ingestion. He developed no neurological features and was discharged from hospital on day 50. Five months after discharge from hospital he remained asymptomatic, with normal creatinine clearance.
Discussion: We describe a patient with severe inorganic mercury poisoning in whom full recovery occurred with the early use of the chelating agent DMPS and CVVHDF. There was removal of a significant amount of mercury by CVVHDF.
Conclusion: We feel that CVVHDF should be considered in patients with inorganic mercury poisoning, particularly those who develop acute renal failure, together with meticulous supportive care and adequate doses of chelation therapy with DMPS.
Ingestion of inorganic mercury compounds can result in severe toxicity, and blood mercury concentrations in excess of 220 µg/l are associated with severe clinical effects. Fatalities have been reported after ingestion of 0.5 g by an adult, with a mean lethal adult dose of 1-4 g. Inorganic mercury causes toxicity by two mechanisms. First, mercuric ions precipitate proteins that cause direct necrosis on contact with tissues; this occurs in the mouth, stomach, large bowel and kidney. Mercuric ions accumulate in the kidneys (accounting for 85-90% of the body burden), causing acute renal failure due to necrosis of the proximal tubular epithelium, usually within 24 hours. Second, inorganic mercury complexes with a number of ligands, particularly sulphydryl groups, causing inhibition of enzymes and protein transport mechanisms. This causes a metabolic acidosis and, in the early phases of toxicity, it can cause death due to metabolic acidosis, vasodilatation and shock.
Previously, dimercaprol (British anti-Lewsite [BAL]) was the chelating agent of choice for inorganic mercury poisoning. It is lipophilic and is given by intramuscular injection formulated in peanut oil. It mobilizes tissue mercury by forming soluble complexes, which are excreted in the urine. In the anuric patient these complexes accumulate, resulting in increased toxicity of both BAL and mercury. The chelating agent of choice for inorganic mercury poisoning is now 2,3-dimercaptopropane-1-sulphonate (DMPS), which is much better tolerated and results in greater mercury excretion.
We describe here a case of severe poisoning due to mercuric sulphate, which was treated successfully with a combination of DMPS and high-flux continuous veno-venous haemodiafiltration (CVVHDF) with no neurological or renal sequelae. Data are also presented describing the toxicokinetics of the mercuric salt and its clearance by CVVHDF.
Crit Care. 2003;7(3) © 2003 BioMed Central, Ltd.
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Cite this: Case Report: Severe Mercuric Sulphate Poisoning Treated With 2, 3-Dimercaptopropane-1-Sulphonate and Haemodiafiltration - Medscape - Feb 17, 2003.