Mystical Fire Ingestion: An Illustrative Case of Accidental Copper Intoxication

Abstract

SESSION TITLE: Poisoning and Drug Overdose 2 SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Copper is a micronutrient that plays an important role in cellular respiration acting as a cofactor for cytochrome c oxidase and Zinc-copper superoxide dismutase. Toxicity can impair production of adenosine triphosphate (ATP) resulting in lactic acidemia, hematologic derangements and cardiac arrest. We present a case of an accidental ingestion of copper salts in the form of Mystical Fire. CASE PRESENTATION: A 65 year old man presented with acute onset of nausea and vomiting 18 hours after an accidental ingestion of mystical fire, by having confused it with candy. His vomitus was initially bilious and then became coffee ground. He had known type II diabetes, hypertension and coronary artery disease. He was a non-smoker and non- alcoholic. On presentation, he was initally normotensive. His abdominal exam was significant for epigastric tenderness. His laboratory evaluation was notable for leukocytosis of 15,000, haemoglobin of 16.5 gm/dl and a methemoglobin level of 7.5%. He also had elevations in serum creatinine of 2.7, total creatinine kinase of 3469, lactic acid of 5.5 and a serum copper level of 738 mcg/dl (Figure 1). His lactate dehydrogenase (LDH) peaked at 2968 IU/L reflective of haemolytic anemia. He was supported with dimercaprol, penicilliamine, ascorbic acid and renal replacement therapy (RRT). Plasmapheresis was also attempted. The patient had an esophagogastroduodenoscopy (EGD) revealing a normal esophagus, but a friable gastric mucosa. A diagnostic laparoscopy revealed discoloured gastric mucosa but no necrosis or perforation. Despite clearance of his serum copper level via chelation therapy and RRT, he died from refractory shock and cardiac arrest. DISCUSSION: This case illustrates the entire spectrum of cellular and metabolic derangements associated with acute copper poisoning, secondary to the irreversible enzymatic inhibition of Cytochrome c oxidase and Superoxide Dismutase (1). These enzymes are vital in cellular respiration and free radical scavenging (figure 2). Acute copper poisoning is rare (2), and the degree of intoxication seen in this case is limited to case reports. In a review of case reports, 37.5% of patient with toxic copper ingestion died with a few hours (3). Management includes minimising absorption using chelating agents such as dimercaprol and penicillamine, RRT and providing supportive care. Early endoscopy for muscosal damage has been described. CONCLUSIONS: Acute copper toxicity can present with multi-system failure. Recognition and early intervention is key to prevent and treat the complications. Reference #1: Beer, S., Bradberry, S., and Vale, J. (1998). Copper sulfate (UK PID) (United Kingdom: National Poisons Information Service Centre Reference #2: Bremner, I. (1998). Manifestations of copper excess. Am. J. Clin. Nutr. 67, 1069S - 1073S Reference #3: Nastoulis N et al. Greenish- blue, gastric content: Literature review and case report of acute copper sulphate poisoning. Forensic Sci Rev. 2017 Jan; 29(1):77-91 DISCLOSURE: The following authors have nothing to disclose: Shah Ravi, Sunkaru Touray, Sumera Ahmad No Product/Research Disclosure Information