Document Type: Case Report

Authors

Department of Forensic Medicine and Toxicology, Lady Hardinge Medical College, New Delhi, India

Abstract

Background: Copper sulfate ingestion is a relatively popular method for committing suicide in Indian subcontinent. It causes a high mortality rate, and so a growing concern has been raised to identify the severe alarming signs suggestive of poor prognosis and to improve treatment approaches.
Case report: A 22-year-old unmarried man working as a painter was found unconscious at his friend residence. The patient developed hypotension, hemorrhagic gastroenteritis with hematemesis and melena, renal and hepatic failure, severe metabolic acidosis and intravascular hemolysis during admission at hospital. His signs were refractory to treatment with fluid replacement therapy, vasoactive drugs, antiemetic drugs, ranitidine, furosemide, methylene blue and 2,3 dimercaptopropane-1-sulphonate. He died six hours post-admission. In post-mortem examinations, there were multiple sub-pleural and sub-epicardial hemorrhages and the gastrointestinal mucosa was congested, hemorrhagic, and greenish blue in color. The liver, on histological examination, showed sub-massive hepatic necrosis. On toxicological analyses, copper sulfate was detected in preserved viscera and results for other heavy metals were negative.
Conclusion: Hypotension, cyanosis, uremia and jaundice can be considered as signs of poor prognosis in copper sulfate poisoning. Copper sulfate ingestion is life-threatening due to its deleterious effects on the upper GI, kidneys, liver and blood. Having no time to waste, aggressive treatments should be immediately instituted and signs of poor prognosis should be kept in mind.

Keywords

How to cite this article: Meena MC, Bansal MK. Acute Copper Sulfate Poisoning: Case Report and Review of Literature. Asia Pac J Med Toxicol 2014;3:130-3.

 

Introduction

Copper sulfate occurs in nature as large blue crystals, soluble in water, containing five molecules of water [CuSO4. 5H2O]. It is commonly known as "blue vitriol" or "blue stone". It is mainly used for agricultural purposes as a pesticide and in leather and paint industry (1-4). It has metallic taste, and for human, it is rated as moderately toxic. The occurrence of copper sulfate poisoning varies in different regions depending on availability of this toxic agent. In case of poisoning, it is commonly consumed with suicidal intentions; however, accidental poisonings have been reported from children as well (1-3).

Copper sulfate is a powerful oxidizing agent, which is corrosive to mucous membranes (3,4). Concentrated solutions are acidic with pH 4. Cellular damage and cell death may result from excessive copper accumulation through which free reduced copper in the cell binds to sulfhydryl groups and inactivates enzymes such as glucose-6-phosphate dehydrogenase and glutathione reductase (4). Copper sulfate ingestion is a relatively popular method for committing suicide in Indian subcontinent and is able to kill as many as one out of four poisoned patients (2,4,5). This high mortality rate has raised a growing concern to identify the severe alarming signs suggestive of poor prognosis and to improve treatment approaches. In this paper a fatal case of copper sulfate ingestion is presented with a brief review of literature on clinical manifestations, determinants of prognosis and essential treatments.

Case report

A 22-year-old unmarried man working as a painter in paint industry was found unconscious at his friend residence on April 2012. On admission to the Lady Hardinge Medical College Hospital, he was presented with hemorrhagic gastroenteritis with nausea, hematemesis, melena and dehydration. He was hypotensive (blood pressure = 80/60 mmHg) and tachycardic (pulse rate = 120 bpm). Complete blood test revealed a normocytic normochromic anemia (hemoglobin = 11.2 mg/dL), an increase in leucocyte count with a marked shift to left, and a decrease in platelet count (82,000/mm3). On blood smear, features of hemolysis including presence of microspherocytes, elliptocytes, nucleated red blood cells and polychromatophils were evident. The patient had also a severe metabolic acidosis (pH = 5.2). In liver function tests, increase in aspartate transaminase (189 IU/L) and total bilirubin (4.8 mg/dL) was found, while alanine transaminase (12 IU/L) and direct bilirubin (0.2 mg/dL) were in normal limits. Albumin, prothrombin time and partial thromboplastin time were normal. Renal function was abnormal with a creatinine of 4.9 mg/dL and blood urea nitrogen of 153 mg/dL in biochemical tests. Urine analysis showed presence of 2+ protein, 2-4 WBCs and 1-2 RBCs/HPF. In the police report, it was stated that a copper sulfate container was found inside the house and that the time of ingestion could not be determined.

The patient received gastric lavage, fluid replacement therapy, vasoactive drugs, antiemetic drugs, ranitidine and furosemide. The gastric lavage returned fluid appeared dark green in color with no peculiar odor. Based on the history of patient as a paint industry worker, findings on police report, color of gastric lavage returned fluid and clinical picture at hospital, the diagnosis of copper sulfate poisoning was suspected for the patient and specific antidotes including methylene blue (1-2 mg/kg/dose in 5% dextrose intravenously) and 2,3 dimercaptopropane-1-sulphonate (DMPS; 250 mg every four hours intravenously) were administered to the patient. He was also given one transfusion of packed red cells (10 mL/kg/dose) during admission. Despite the treatments, patient’s condition deteriorated and he died 6 hours post-admission.

Post-mortem findings

On external examination, cyanosis was present over lips and nail beds (Figure 1).

Figure 1. Post-mortem findings of the patient (external examination): A) cyanosis on lips, B) cyanosis on nail beds

Self-inflicted injury marks were present over flexor aspect of left forearm (Figure 2). A yellowish discoloration was seen all over the body. Internal examination revealed all internal organs were congested. There were multiple sub-pleural and sub-epicardial hemorrhages.

Figure 2. Self-inflicted injury marks over flexor aspect of left forearm of the patient

The gastrointestinal (GI) mucosa was congested, hemorrhagic, and greenish blue in color (Figure 3). The liver, on histological examination, showed sub-massive hepatic necrosis. On toxicological analyses, copper sulfate was detected in preserved viscera and results for other heavy metals were negative.