Fatal Mercuric Chloride Ingestion

Winek, Charles L.; Fochtman, Frederick W.; Bricker, J. Douglas; Wecht, Cyril H.

doi:10.3109/15563658108990034

Cited by 18 publications

(5 citation statements)

References 10 publications

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“…The initial blood mercury concentration is the highest recorded level in the literature that has been associated with a favourable outcome. (There is one report of a patient with a blood mercury of 22 000 μg/l who died soon after presentation to hospital [ 5 ].)…”

Section: Discussionmentioning

confidence: 99%

Case report: Severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration

et al. 2003

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Correspondence: Paul Dargan, paul.dargan@gstt.sthames.nhs.uk R1 BAL = British anti-Lewsite (dimercaprol); CVVHDF = continuous veno-venous haemodiafiltration; DMPS = 2,3-dimercaptopropane-1-sulphonate; ICU = intensive care unit. AbstractIntroduction Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, lifethreatening 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.

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Section: Discussionmentioning

confidence: 99%

Case report: Severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration

et al. 2003

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“…This concentration is supposed to be associated with fatal outcome due to multiple organ failure. 2 Because of anuric renal failure, haemodialysis was necessary. Kidney function returned to normal within 10 days.…”

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confidence: 99%

Mercury Kinetics in a Case of Severe Mercuric Chloride Poisoning Treated with Dimercapto-1-propane Sulphonate (DMPS)

Toet

Dijk²,

Savelkoul

et al. 1994

Hum Exp Toxicol

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1 A case of severe mercuric chloride poisoning with clinical signs of mucosal damage of the gastrointestinal tract and anuric renal failure, is presented. The initial whole blood mercury concentration was 14,300 ?g 1-1. This concentration is supposed to be associated with fatal outcome due to multiple organ failure. 2 Because of anuric renal failure, haemodialysis was necessary. Kidney function returned to normal within 10 days. Haemodialysis proved to be ineffective with regard to total mercury elimination. 3 Treatment with DMPS was started because of very severe poisoning, anuric renal failure and optimistic reports on the 'new' chelating agent 2,3-dimercapto-1-propanesulphonic acid (DMPS) in mercury poisoning. DMPS was administered by parenteral route initially and was continued thereafter by oral route, until whole blood and urine mercury concentrations had decreased below a level considered as toxic. Except for a temporary pruritic erythema of the skin, no side effects of DMPS treatment were observed. 4 The clinical course was mild, despite continuing high whole blood mercury concentrations, Recovery was uneventful and complete. DMPS treatment, administered by intravenous and oral route, was shown to be an effective alternative for BAL in life-threatening mercuric chloride intoxication. 5 The pharmacokinetic data presented in this case report suggest that non-renal mercury clearance may considerably exceed renal mercury clearance.

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“…Blood concentrations in groups S2 and S3 were extremely toxic ( Fig. 2A) and concentrations of >20 µg dl −1 are fatal (Winek et al, 1981). The total amounts of mercury unabsorbed or taken up in the intestinal tissue, expressed as the intestinal mercury, was higher in rats given HgCl 2 in water than given HgCl 2 in milk (Fig.…”

Section: Long-term Experimentsmentioning

confidence: 97%

Effect of milk on intestinal fluid accumulation and renal injury following mercuric chloride ingestion in rats

Kamijo

Hayashi

Yoshimura

et al. 2004

J of Applied Toxicology

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To investigate the effect of milk on intestinal fluid accumulation and renal injury following mercuric chloride (HgCl(2)) ingestion, 10 ml kg(-1) of saline or 10 mg kg(-1) of HgCl(2) dissolved in 10 ml kg(-1) of water or raw milk was administered enterally to rats and the mercury content in biological samples was determined by cold vapour atomic absorption spectrometry. Three hours after administration, the intestinal water content in rats that received HgCl(2) in water (group S2) was significantly higher than in rats that received saline (group S1) (P < 0.01) or HgCl(2) in milk (group S3) (P < 0.01). The amount of mercury detected per gram dry weight of small intestine was higher in group S2 than in group S3 (P < 0.05). Seventy-two hours after administration, both the serum urea nitrogen and creatinine concentrations in rats that received HgCl(2 )in milk (group L3) were significantly higher than in rats that received saline (group L1) (P < 0.05) or HgCl(2) in water (group L2) (P < 0.05). Mercury levels in many of the biological samples in group L3 were higher than in group L2 (P < 0.05). Milk may reduce the intestinal cytotoxicity of mercury but it promotes its absorption, which may lessen intestinal fluid accumulation but worsen renal injury.

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Fatal Mercuric Chloride Ingestion

Cited by 18 publications

References 10 publications

Case report: Severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration

Case report: Severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration

Mercury Kinetics in a Case of Severe Mercuric Chloride Poisoning Treated with Dimercapto-1-propane Sulphonate (DMPS)

Effect of milk on intestinal fluid accumulation and renal injury following mercuric chloride ingestion in rats

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