Red mercurochrome‐associated acute kidney injury successfully treated by chelation therapy

An 85-year-old, otherwise healthy female was referred to our hospital because of un-intentional ingestion of 40 mL Red Mercurochrome (2% merbromin) half a day ago. The symptoms of mercury toxicity were mild and consisted of non-specific gastrointestinal upset and red coloured stool. On arrival, she was clearly conscious (E4M6V5), without neurological deficit, but hypertensive (207/104 mmHg). Blood tests revealed leukocytosis with left-shift (white blood cells 14 000/μL (normal 3500–11 000), neutrophils 85.2%), acute renal failure (urea nitrogen 20 mg/dL (normal 6–21), creatinine 1.19 mg/dL (normal < 1.03)), but normal liver function and electrolytes. Toxicology investigations showed elevated serum and urine level of mercury, at 78.7 μg/L (normal < 60) and 380 μg/L (normal < 10), respectively. Detoxification protocol was immediately performed with gastric lavage, followed by intravenous infusion of 250 mg 2,3-dimercapto-1-propansulfonacid (DMPS, Dimaval, Heyl, Taiwan) every 4 h. The patient recovered uneventfully and was discharged 2 days later. There was no chronic sequel. A follow-up laboratory examination after 2 months found normal renal function (serum creatinine level 0.96 mg/dL) and absence of mercury burden (serum and urine mercury 4.8 μg/L and 8.2 μg/L, respectively). Merbromin is a topical antiseptic used for minor wounds. Merbromin is an organomercuric disodium salt compound and a fluorescein. The US Food and Drug Administration banned the medical use of merbromin in 1998 due to its mercury content. Nevertheless, merbromin remains widely available in many Asian countries. Very few data are available in the literature regarding the renal outcome of merbromin poisoning. In 1997, Luk et al. reported a 24-year-old schizophrenic case of elevated blood mercury (880 nmol/L (normal < 50 nmol/L)) following ingestion of Mercurochrome. The presentations were nausea and vomiting, but without renal or hepatic function impairment. Chelating therapy with dimercaprol was immediately started and the gastrointestinal symptoms subsided by day 4. Ayala Curiel et al. described a 10-day-old newborn infant who was given Mercurochrome orally for 7 days due to misunderstanding of the medical instructions. The initial symptoms included loss of appetite and low weight increase but without renal deterioration. Elevated blood mercury concentrations were found. Chelating therapy with dimercaprol was also initiated and the overall outcome was good. Notably, Stark et al. reported a case of accidental intrathecal mercury (5 mL Mercurochrome) application, which was complicated with acute meningitis and encephalitis. There was no renal damage. The patient was also successfully treated with lumbar drainage and chelation therapy (DMPS and 2,3dimercaptosuccinatacid (DMSA)). Eighteen months after intoxication, polyneuropathy and slight neuropsychological deficiencies were detectable. Therefore, this is the first known case in the literature of oral merbromin-associated acute kidney injury that was successfully treated by DMPS chelation therapy. What we have learned from this case is, although a number of chelating agents (dimercaprol, edetate calcium disodium, D-penicillamine, DMPS and DMSA) are currently in clinical use for treating mercury intoxication, no standard guidelines are available at present that specify the conditions under which chelation is indicated or contraindicated, thereby contributing to a growing confusion over the appropriate use of these chelating agents.