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Accidental Inorganic Mercury Chloride Poisoning in a 2Year Old Child

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Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life threatening features and acute renal failure. A 2-year old well thriving child presented with alleged history of accidental ingestion of inorganic mercury
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  CLINICAL BRIEFS Accidental Inorganic Mercury Chloride Poisoningin a 2-Year Old Child Sanjay Verma  &  Ramesh Kumar  &  Alka Khadwal  & Sunit Singhi Received: 29 March 2010 /Accepted: 23 April 2010 /Published online: 19 August 2010 # Dr. K C Chaudhuri Foundation 2010 Abstract  Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life threateningfeatures and acute renal failure. A 2-year old well thrivingchild presented with alleged history of accidental ingestionof inorganic mercury chloride. He presented with evidenceof corrosive trauma to the gastrointestinal tract mucosa, but with normal renal function at admission, which wasmanaged with BAL and other supportive treatment. But he developed non-oliguric renal failure after admission,which also improved gradually. On follow-up, two monthslater, the patient  ’ s renal function was normal; indicating that renal failure caused by acute inorganic mercury poisoning produced no permanent renal damage. We have hereby presented a case of mercury intoxication in a 2-year oldchild, with an excellent clinical improvement and normal-ization of laboratory results. Keywords  Mercury chloride poisoning.Dimercaprol.Renal failure Introduction Mercury exists in three forms: elemental (metallic) mercury,organic mercury and inorganic mercury. Elemental mercuryis shiny, silver, odourless liquid used in thermometers.Organic mercury is formed when combined with carbon.Methyl mercury is a common form of organic mercury.Inorganic mercury is formed when combined with non-carbon substances. These mercury salts are usually white powder or crystals. This form of mercury has been used inmedicines and also for folk remedies in Asian countries.Inorganic mercury poisoning usually occurs as a result of occupational exposure. However, accidental or suicidalingestion has also produced poisoning at non-occupationalsettings [1  –  3]. When ingested accidently it mainly causesdamage to GI tract and kidneys. Accidental ingestion of inorganic mercury chloride in small children leading toacute renal failure has been rarely reported.We describe here a case of accidental poisoning due tomercuric chloride ingestion in a 2-year old child, leading torenal failure which was successfully treated with dimercap-rol along with supportive management. Case Report A 2-year-old well thriving child from a village of Haryanawas admitted to our emergency department with history of alleged ingestion of unknown quantity of mercury chloride powder at home. His grandfather used to work in a societyagainst superstition and he used to show some magicaltricks by using this powder. Child developed vomiting andswelling of lips and cheeks immediately after this. He wastaken to a local hospital where gastric lavage was donewithin 30 min of ingestion and transferred to our center.On reaching our hospital, he was afebrile, fully conscious but irritable. His heart rate was 190 beats per minute,respiratory rate 32 breaths per minute and blood pressure was96/68 mm of Hg. There was no cyanosis or pallor. He was S. Verma :  R. Kumar  : A. Khadwal : S. SinghiAdvanced Pediatric Center,Post Graduate Institute of Medical Education and Research,Chandigarh 160012, IndiaS. Verma ( * )House no. 3001/1, sector - 38-D,Chandigarh 160012, Indiae-mail: sanjay06verma@yahoo.comIndian J Pediatr (2010) 77:1153  –  1155DOI 10.1007/s12098-010-0143-9  having swelling of lips, cheeks and submandibular region but there was no airway compromise. Upper GI endoscopyrevealed oropharyngeal hyperemia and superficial ulcerationin stomach but there was no laryngeal edema on ENTevaluation. Urine output was adequate and rest of systemicexamination was normal. Blood was drawn for sampling andactivated charcoal was started. Initial investigations showedHb of 11.6 gm%, TLC 9,500/mm 3 , platelets 5,10,000/mm 3 .Metabolic profile showed S.bilirubin of 0.8 mg/dl, SGOT86U/l, SGPT 38U/l, ALP 207U/l, total protein 7.2 gm%,albumin 3.7 gm/dl, globulin 3.5 gm/dl, B Urea 24 mg/dl,creatinine 0.8 mg/dl. His ECG was normal & radiologyincluding X-ray chest and soft tissue neck was normal. Theinitial blood mercury level by ICPMS was 35 microgm/dl(  N  =<1microgm/dl) and urinary mercury levels were 24microgm/dl (  N  =<10microgm/dl). He was treated with injec-tion BAL (dimercaprol in oil 100 mg/ml) 4 mg/kg/dose every4 hourly initially on first day then 2 mg/kg/dose 6 hourlydeep intramuscularly thereafter. Child was shifted to PICU for vital monitoring and supportive management.Three days later, child developed non oliguric renal failurewith progressive increase in serum creatinine and blood urea(Table 1). Because of worsening renal function tests, BALwas discontinued on 7th day of admission and intravenousfluids were continued because of poor oral intake. Urine pHwas kept alkaline with parentral NaHCo 3  as child haddeveloped painful ulcers in the vestibule of mouth secondaryto chemical burns. Renal function gradually improved over next 2 weeks and patient was discharged. At a follow-upexamination, about two months later, the patient  ’ s renalfunction was normal; indicating that renal failure caused byacute inorganic mercury poisoning produced no permanent renal damage. During the hospital stay and follow-up, parentswere also counseled about hazards of storing chemicals at home and prevention of accidental poisonings and injuries. Discussion This patient exhibited the typical signs and symptoms of acute inorganic mercury chloride toxicity. He presentedwith evidence of corrosive trauma to the gastrointestinaltract mucosa, but with normal renal function at admission,unlike the children reported earlier  [4, 5]. Absorption, distribution, excretion and toxicity depend upon thecompound to which the patient is exposed [6]. Inorganic mercury causes toxicity by two mechanisms. First, mercuricions precipitate proteins that cause direct necrosis, oncontact with tissues; this occurs in the mouth, stomach,large bowel and kidney. Mercuric ions accumulate in thekidneys (accounting for 85  –  90% of body burden), causingacute renal failure due to necrosis of the proximal tubular epithelium, usually within 24 h. Second, inorganic mercurycomplexes with a number of ligands, particularly sul- phydryl groups, causing inhibition of enzymes and proteintransport mechanisms. This causes metabolic acidosis and,in the early phases of toxicity, it can cause death due tometabolic acidosis, vasodilatiation and shock  [7]. Rate of excretion of inorganic mercury is complex, whichoccurs in three phases: 35% of single dose is excreted withinfew days, a second phase with half life of 30 days account for 50%,andrestisexcretedinslowthirdphasewithahalf-life of 100 days [8]. Renal failure due to acute tubular necrosis usually becomes evident within few hours, but in our case it occurred after 3 days. In severe cases, death may occur dueto cardiovascular collapse. Because of its solubility, mercuricchloride is the most toxic of the inorganic salts with a meanlethal dose in the adult 0.2  –  1.0 g.Acute mercury poisoning is best managed by discontin-uing the exposure, providing supportive therapy andenhancing the removal of the metal from the body.Elimination of mercury from the body is achieved bychelation therapy and self-excretion. Hemodialysis, hemo- perfusion and peritoneal dialysis have been reported to havelittle efficacy or to be completely ineffective in removingmercury [1, 3, 9].The appropriate treatment for acute inorganic mercury poisoning is chelation therapy usingdimercaprol (BAL), if renal failure develops, dialysis may be needed [9, 10]. Though hemodialysis, hemoperfusion and peritoneal dialysis have been reported to have littleefficacy or to be completely ineffective in removingmercury [1, 3, 11]. Dimercaprol mobilizes tissue mercury  by forming soluble complexes, which are excreted in urine.Early recognition of this potentially lethal poisoning andappropriate treatment saved this boy ’ s life. Monitoring biochemical parameters along with blood and urinarymercury levels can help in guiding the appropriatemanagement. We have hereby presented a case of mercuryintoxication in a 2-year old child, with an excellent clinicalimprovement and normalization of laboratory results. Day of admission 1st 2nd 3rd 5th 6th 8th 10th 12th 60thBlood Urea (mg %) 40 45 143 184 189 167 154 144 25S. Creatinine (mg%) 0.4 0.7 2.8 4.1 4.7 4.2 3.4 2.1 0.6S. Sodium (meq/l) 149 147 135 147 145 134 139 136 137S. Potassium (meq/l) 4.5 3.6 4.7 5.6 5.2 4.2 5.3 4.5 4.3 Table 1  Renal function testsduring treatment and follow-up1154 Indian J Pediatr (2010) 77:1153  –  1155  Contributions  SV, RK & AK were involved in the diagnosis &treatment of the patient. SV & RK reviewed the literature and draftedthe manuscript. SV, AK, SS supervised the patient  ’ s management.SV, RK & AK & SS approved the final draft. Role of Funding Source  None. Conflict of Interest  None. References 1. Worth DP, Davison AM, Lewins AM, Ledgerwood MJ. Haemo-dialysis and charcoal haemoperfusion in acute inorganic mercury poisoning. Postgrad Med J. 1984;60:636  –  8.2. SamuelsER,HeichHM,McLaineMN,FarantJP.Acaseofaccidentalinorganic mercury poisoning. J Anal Toxicol. 1982;6:120  –  2.3. Sauder PH, Livardjani F, Jaeger J, Kopfershmitt J, Heimburger R,Waller CH, et al. Acute mercury chloride intoxication, effects of hemodialysis and plasma exchange on mercury kinetic. ClinToxicol. 1988;26:189  –  97.4. Stack T, Bissenden JG, Hoffman G, Yeoman WB. Mercuricchloride poisoning in a 23-month old child. Br Med J.1983;287:1513.5. Yossef YM, Berkovitch M, Goldman M. Mercury intoxication ina 2-year old girl: a diagnostic challenge for the physician. Pediatr  Nephrol. 2007;22:903  –  6.6. Clarkson TW. The pharmacology of mercury compounds. AnnuRev Pharmacol. 1972;12:373.7. Winship KA. Toxicity of mercury and its inorganic salts. AdvDrug React Ac Pois Rev. 1985;3:129  –  60.8. Rothstein A, Hayes AD. The metabolism of mercury in the rat studied by isotope techniques. J Pharmacol Exp Ther.1960;130:166.9. Counter SA, Buchanan LH. Mercury exposure and childdevelopment outcomes. Pediatrics. 2004;198:209  –  30.10. Carl RB. Treatment of mercury intoxication. Curr Opin Pediatr.1999;11:265  –  8.11. Yoshida M, Satoh H, Igarashi M, Akashi K, Yamamura Y,Yoshida K. Acute mercury poisoning by intentional ingestion of mercuric chloride. Tohoku J Exp Med. 1997;182:347  –  52.Indian J Pediatr (2010) 77:1153  –  1155 1155
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