Acute mercury chloride inioxication. effects of hemodialysis and plasma exchange on mercury kinetic

Abstract

A 27 year-old man developed after ingestion of mercury chloride, 6 g, a hypovolemic shock, an acute renal failure and a necrosis of the stomach which required a total gastrectomy. The anuria did not improve and required 42 hemodialyses. Subsequent evolution showed numerous complications and the patient died on the 91st day. On admission mercury plasma concentration was 5 mg/L and decreased slowly with an apparent half-life of 226 hours. Hemodialyses were ineffective for mercury elimination: mercury clearances varied between -10 and + 1.5 ml/min. Seventeen mg of mercury were removed by six plasma exchanges: the mercury clearance was mean 17.3 ml/min. Among the extracorporeal elimination methods, plasma exchange appears to be the most efficient for inorganic mercury and it could be usefull in association with chelation therapy at the early phase of the intoxication.

Being alive after a severe inorganic mercury intoxication

“…It has been stated that hemodialysis, peritoneal dialysis, hemoperfusion, plasma exchange, and exchange transfusion produced no convincing clinical benefit in mercury intoxication [8,12,17]. In our patient, peritoneal dialysis was continued till the end of the 3rd week of hospitalization which was compatible with the 2nd week of chelation theraphy with DMSA.…”

Full Recovery from a Potentially Lethal Dose of Mercuric Chloride

“…The lowered potassium concentration in this patient is not typical; some case reports have recorded hyperkalemia, sometimes attributed to rhabdomyolysis. [4,5]. However, hypokalemia in this patient is not surprising given the possibility of marked potassium losses as a result of significant vomiting and diarrhea.…”

“…Previous case reports have also reported gastrointestinal symptoms including nausea, vomiting, diarrhea, abdominal pain, hematemesis, and melena [5][6][7]. Due to the corrosive properties of this salt, additional gastrointestinal complications may include mucosal inflammation, ulceration, and necrosis of the gastrointestinal tract [4,5,8]. Subsequent to the initial gastrointestinal injury, patients may suffer oliguria and renal failure, due to a combination of impaired perfusion and direct renal toxicity [6], the latter typically involving proximal tubular injury [9].…”

“…Gastrointestinal blood losses may be sufficient to produce anemia, requiring transfusion of blood or blood products [5]. In patients with severe gastric necrosis, surgical intervention may be required [4]. Caustic injury to the oropharyngeal mucosa may produce oropharyngeal and laryngeal edema; developing obstruction requires airway protection and ventilatory support, and tracheostomy may be required [5].…”

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

“…Mercuric chloride is also nephrotoxic, and acute oliguric renal failure from acute tubular necrosis may develop within several days. Renal failure is usually reversible, although haemodialysis may be required for 1-2 weeks (Arena, 1971;Sauder et al, 1988).…”