Background: Sodium nitroprusside (SNP) is a vasodilator used primarily to treat hypertensive emergencies and improve cardiac output in heart failure. Toxicity results from conversion of SNP to cyanide (CN) and can occur when SNP is infused at doses ðn 2 mcg/kg/min for prolonged periods. The diagnosis of superimposed cyanide toxicity in critically ill patients is challenging: the patient may deteriorate without the usual laboratory markers of acute cyanide overdose. Concomitant administration of sodium thiosulfate (STS) prevents accumulation of CN and is considered standard of care for patients receiving prolonged SNP infusion. Currently there is only one FDA-approved distributor of STS and the drug has been on national shortage since 2011. Case Report: A 23-year-old woman with recent diagnosis of severe dilated cardiomyopathy was admitted to the intensive care unit and started on an infusion of SNP, with documented maximum rate of 3.0 mcg/kg/min. Despite initial improvement she deteriorated on hospital day 4. Respiratory failure prompted intubation, which was complicated by a PEA arrest. Return of spontaneous circulation was achieved after 15 minutes of ACLS. After confirming that she had not received STS during her hospital course, healthcare providers (HCPs) suspected CN toxicity secondary to prolonged SNP infusion. She was empirically treated with 300 mg sodium nitrite (SN) and 12.5 g of STS (NithiodoteR), then re-dosed (per package guidelines) with 150 mg SN and 6.25 g STS. CN levels were sent pre and post-treatment, returning at 6.289 mg/L and 0.128 mg/L respectively. Never recovering from her PEA arrest, she required increasing vasopressor support for cardiogenic shock and hemodialysis for acute kidney failure. Unfortunately, ARDS progressed. Her family ultimately withdrew care, and she expired on hospital day 5. Prior to the national shortage, STS was routinely administered with all NPS infusions at this institution per standardized order set. Case Discussion: CN toxicity from SNP infusion is well-documented in the literature, but it appears that significant morbidity related to SNP infusion is rare due to the routine administration of STS. The ongoing shortage of STS may result in further cases of SNP toxicity. HCPs are unlikely to be familiar with SNPfs mechanism of toxicity and likely rely on standardized order sets that may be altered without sufficient warning by hospital pharmacies during drug shortages. Conclusions: HCPs should be cognizant of drug shortages and their negative effects on previously standardized treatment modalities. Additionally, in the setting of prolonged SNP infusion, HCPfs must maintain vigilance for CN toxicity.
