Fatality from potassium gold cyanide poisoning

Abstract

While potassium cyanide poisoning has been well described, the toxicity of potassium gold cyanide is less well understood. This case describes an 84-year-old man who presented after an intentional ingestion of 0.5–1 teaspoons of potassium gold cyanide. Despite antidotal therapy, the patient rapidly developed severe lactic acidosis, multiorgan dysfunction and ultimately expired. While the patient’s clinical findings were consistent with acute cyanide poisoning, a serum cyanide level was below the toxic threshold. Previous reports have suggested that gold toxicity may also contribute to the effects of potassium gold cyanide, and may have played a role in the patient’s rapid decline. In addition to treatment of cyanide toxicity, management of acute gold toxicity should also be considered in potassium gold cyanide ingestion.

Background

Potassium gold cyanide (KAuCN₂) is a compound used in industrial electroplating and found as a by-product of gold mining.¹ Ingestion of this substance is rarely reported in the literature and previous reports are limited to occupational exposures.^2–5 Cyanide and gold can both have toxic effects in acute ingestion. Cyanide is a well-known mitochondrial toxin that inhibits oxidative phosphorylation and results in multiorgan system failure. Initial symptoms of cyanide poisoning are non-specific and include headache, anxiety, confusion and abdominal pain.⁶ Patients with cyanide ingestion often present with hypertension, tachycardia, tachypnoea and lactic acidosis, but rapidly progress to respiratory and circulatory collapse. Acute gold toxicity is less understood, as most adverse effects of gold result from chronic gold therapy for rheumatological conditions. Gold poisoning commonly presents with dermatitis, stomatitis, proteinuria and enterocolitis, but can have severe haematological effects, including aplastic anaemia, neutropaenia and thrombocytopaenia.⁷ In this report, we describe a fatal case of intentional KAuCN₂ ingestion, despite antidotal therapy.

Case presentation

An 84-year-old man presented to the emergency department after ingesting 0.5–1 teaspoons of KAuCN₂, containing approximately 0.4–0.8 g cyanide and 1.5–3 g gold, in an intentional suicide attempt (figure 1). He had previously used the compound in his occupation of metal plating jewellery. He informed his wife, who called the regional poison control centre and emergency medical services. Prehospital providers found the patient with severe vomiting, diarrhoea and respiratory distress. Prehospital providers intubated the patient and administered 5 g of hydroxocobalamin approximately 3 hours after initial ingestion. On arrival to the hospital, the patient had labile blood pressures, and initial laboratories were notable for a creatinine of 1.66 mg/dL and a lactate of 2.9 mmol/L. His ECG demonstrated sinus tachycardia. No other coingestants were identified. He was initially hypertensive, but developed severe hypotension, requiring vasopressor support. After admission to the intensive care unit, the patient received an additional 10 g of hydroxocobalamin and 12.5 g of sodium thiosulfate. A serum cyanide level, obtained after administration of 10 g of hydroxocobalamin, 6 hours after initial ingestion, was 0.25 mg/L.

Figure 1.

Bottle of potassium gold cyanide powder, ingested by the patient.

Outcome and follow-up

Despite antidotal therapy for cyanide toxicity, the patient rapidly developed worsening lactic acidosis, multiorgan dysfunction and respiratory failure. The patient subsequently had cardiovascular collapse and expired approximately 12 hours after initial ingestion.

Discussion

While potassium cyanide ingestion has been well described in the literature, the toxicity of KAuCN₂ is less well understood. Cyanide is a well-established mitochondrial toxin that inhibits oxidative phosphorylation and results in multiorgan system failure from histotoxic hypoxia. The patient’s clinical presentation and amount of ingested cyanide were consistent with acute cyanide poisoning (toxic dose 100–200 mg (1.5 mg/kg), ingested dose 400–800 mg (4–8 mg/kg)).⁸ However, the obtained cyanide level (0.25 mg/L) was below the toxic level of 0.5 mg/L; interpretation of this level is challenging as it was obtained after antidotal therapy and may not reflect cyanide bound in cyanocobalamin.^{9 10} Two previous case reports describing KAuCN₂ ingestion had similarly low serum cyanide levels, implicating gold as a possible cause of acute toxicity.^{4 5}

Despite frequent exposure to gold products in both domestic and industrial settings, exposure to gold through ingestion remains rare in literature. In part, this may be a consequence of limited systemic gold absorption from the gastrointestinal tract as metallic gold does not ionise. However, systemic gold absorption from soluble gold compounds, such as cyanide, bromide, iodide and thiosulfate, is thought to be higher.¹¹ It has been suggested that KAuCN₂ may dissociate after ingestion to form aurocyanide (Au(CN)₂-), a known metabolite of gold compounds used for immunotherapy. Although considered stable ex vivo, aurocyanide may interact with intracellular thiols to liberate hydrogen cyanide and produce other soluble gold compounds through redox cycles.¹² These gold compounds may exert toxic effects.

The diagnosis and management of acute gold toxicity is not well described. Chelation therapy has been suggested, but cobalt ethylenediaminetetraacetic acid was unsuccessful in one fatal case of metallic cyanide and gold ingestion.⁴ Historically, 2,3-dimercaptopropanol has been described as treatment for toxicity related to gold salt applications for rheumatoid arthritis. In addition to treatment of cyanide toxicity, management of acute gold toxicity should be considered in acute KAuCN₂ ingestion.

Learning points.

• Potassium gold cyanide (KAuCN₂) is a readily available occupational compound used in metal plating and gold mining.

• KAuCN₂ is an uncommon exposure that can result in multiorgan dysfunction and death.

• The toxic effects of KAuCN₂ may result from both cyanide and gold toxicity.

• Management of both gold and cyanide toxicity should be considered in cases of acute KAuCN₂ ingestion.