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UC Davis UC Davis Previously Published Works UC Davis UC Davis Previously Published Works Title Hemodialysis Complications of Hydroxocobalamin: A Case Report Permalink https://escholarship.org/uc/item/26s763wr Journal Journal of Medical Toxicology, 6(2) ISSN 1937-6995 Authors Sutter, Mark Tereshchenko, Nadia Rafii, Rokhsara et al. Publication Date 2010-06-01 DOI 10.1007/s13181-010-0067-9 Peer reviewed eScholarship.org Powered by the California Digital Library University of California J. Med. Toxicol. (2010) 6:165–167 DOI 10.1007/s13181-010-0067-9 TOXICOLOGY OBSERVATION Hemodialysis Complications of Hydroxocobalamin: A Case Report Mark Sutter & Nadia Tereshchenko & Rokhsara Rafii & G. Patrick Daubert Published online: 30 March 2010 # The Author(s) 2010. This article is published with open access at Springerlink.com Abstract Hydroxocobalamin is a new antidote approved aware of its effects on hemodialysis machines which could by the FDA for the treatment of cyanide poisoning. Our delay the initiation of this important treatment modality in the report describes a patient with cyanide poisoning who severely acidemic patient. survived after treatment with hydroxocobalamin and com- plications we encountered with hemodialysis. A 34-year- Keywords Hydroxocobalamin . Hemodialysis . Cyanide old female presented to the emergency department after a syncopal event and seizures. Her systolic blood pressure was 75 mmHg, her QRS complex progressively widened, Introduction and pulses were lost. She was intubated and resuscitated with fluids, sodium bicarbonate for her QRS widening and The lethal effects of cyanide poisoning have been well vasopressors. Venous blood gas demonstrated a pH of 6.36 described [1]. Cyanide is a potent cellular toxin that with an O2 saturation of 99%. Due to the acidemia with a interferes with aerobic metabolism by blocking cytochrome normal pulse oximetry, simultaneous venous and arterial a-a3 of the electron transport system. This blockade blood gases were obtained. Venous gas demonstrated a pH eventually leads to a significant increase in anaerobic of 6.80 with a PO2 of 222 mmHg, an O2 saturation of 99%. metabolism and a profound lactic acidosis. Death from The arterial blood gas showed a pH of 6.82, a PO2 518 mmHg, cyanide toxicity is the result of multi-system organ failure an O2 saturation of 100%. Cyanide was suspected and that stems from the body’s inability to utilize oxygen [2]. hydroxocobalamin and sodium thiosulfate were given. Within On December 15, 2006, a new antidote for the treatment of 40 min of hydroxocobalamin administration, vasopressors cyanide poisoning, hydroxocobalamin, (Cyanokit™,Dey were discontinued. Initially, nephrology attempted dialysis for Laboratories, Napa, CA, USA) was approved by the FDA metabolic acidosis; however, the dialysis machine repeatedly [3]. In contrast to previously utilized antidotes, hydroxoco- shut down due to a “blood leak”. This was an unforeseen balamin binds cyanide without decreasing the oxygen effect attributed to hydroxocobalamin. Cyanide level, drawn carrying capacity of hemoglobin. Hydroxocobalamin binds 20 min after the antidote was completed, was elevated at to cyanide to form cyanocobalamin which can then be 22 mcg/dL. Her urinary thiocyanate level could not be excreted in the urine. Additionally, sodium thiosulfate can analyzed due to an “interfering substance”. Hydroxocobala- also be administered to provide another mechanism to min is an effective antidote. However, clinicians must be enhance cyanide excretion [4]. The side effects of hydroxocobalamin are minimal making : : M. Sutter (*) N. Tereshchenko G. P. Daubert it advantageous to previous antidotes. Hydroxocobalamin is Department of Emergency Medicine, University of California, known to cause an orange/red discoloration of the blood, Davis Medical Center, urine, and secretions. This discoloration of the bodily fluids PSSB 2100, 2315 Stockton Blvd, Sacramento, CA 95817, USA has been shown to interfere with several chemistry method- e-mail: [email protected] ologies. This interference has been established to cause statically significant alterations in aspartate aminotransferase, R. Rafii bilirubin, creatinine, magnesium, and iron [5–7]. Other Department of Internal Medicine, Division of Pulmonary and Critical Care, University of California, Davis, colorimetric tests have also been influenced by both Sacramento, CA 95817, USA hydroxocobalamin and the resulting cyanocobalamin. This 166 J. Med. Toxicol. (2010) 6:165–167 can lead to interferences and calculation errors by co-oximeter blood gas showed a pH of 6.82, a PO2 518 mmHg, an O2 measurements of carboxyhemoglobin, methemoglobin, oxy- saturation of 100%, a PCO2 of 55 mmHg, and bicarbonate hemoglobin, and hemoglobin [8, 9]. An additional side effect of 9 mEq/L. Additionally, a carboxyhemoglobin level was of hydroxocobalamin is hypertension; however, this is often 0.4% and methemoglobin was 0.6%. Cyanide toxicity was a desired effect in the critically ill patient [5]. suspected given the profound metabolic acidosis and A classical presentation of cyanide often includes the limited systemic oxygen extraction. The oxygen extraction sudden onset of syncope, seizures, and eventual cardiovascu- from arterial to venous side was markedly decreased as the lar collapse [1]. We present a case consistent with cyanide calculated oxygen extraction was only 6%. The patient poisoning who survived neurologically intact, after treatment received 5 g of hydroxocobalamin over 15 min followed by with hydroxocobalamin and sodium thiosulfate. We also 12.5 g of sodium thiosulfate infused over 30 min. describe some challenges encountered after hydroxocobalamin Within 15 min of the start of the hydroxocobalamin administration. infusion, blood pressure had increased, and norepinephrine was weaned. Forty minutes after the start of the hydrox- ocobalamin infusion, norepinephrine was discontinued and Case Report the patient’s systolic blood pressure was 115 mmHg. Twenty minutes later, a repeat arterial blood gas demon- A 34-year-old female with bipolar disorder presented after strated a pH of 7.32, a PO2 of 445 mmHg, an O2 saturation her roommate witnessed a syncopal event followed by of 100%, a PCO2 of 41 mmHg, and a bicarbonate of tonic-clonic seizure activity. She arrived in the emergency 23 mEq/L. Initial laboratories subsequently returned with a department 11 min after her roommate called 911. Her potassium of 4.1 mEq/L and a dramatically elevated lactic initial systolic blood pressure was 75 mmHg, and the acid level of 32.4 mEq/L (normal 0.2–2.2 mEq/L). cardiac monitor showed a narrow complex rhythm that During the initial resuscitation, the nephrology service began to widen just before carotid pulses were lost. The attempted to dialyze the patient for overwhelming metabolic patient was intubated, intravenous fluids started and two acidosis. However, the hemodialysis machine (Fresenius ampoules of sodium bicarbonate were rapidly administered 2008 K) repeatedly alarmed and shut down due to a “blood due to the QRS widening on the monitor. Cardiopulmonary leak”. It took several hours to turn off the internal alarms to resuscitation was begun and pulses returned following the allow for hemodialysis to begin. Fortunately, by this time the administration of epinephrine and atropine. A critical lab acidosis had corrected and hemodialysis was no longer value demonstrated a venous blood pH of 6.36. Two needed. Ethylene glycol and methanol levels returned as additional ampoules of sodium bicarbonate were pushed, undetectable. The patient was extubated the next day and was and repeat venous blood gas exhibited a pH of 6.41. neurologically intact. On hospital day4, whole blood cyanide Norepinephrine was initiated and simultaneous placement levels, which were drawn 20 min after the antidote was of both an internal jugular venous line and a radial arterial completely infused in the emergency department, returned line occurred with both returning bright red blood. Because elevated at 22 μg/dL (normal 0–20 μg/dL, ARUP Laborato- of the findings of bright red venous blood in this severely ries, Salt Lake City, UT, USA). Repeat cyanide levels from acidemic patient with a pulse oximetry of 99–100%, we hospital day3 were undetectable. Unfortunately, blood sam- obtained simultaneous arterial and venous blood gases. The ples obtained prior to antidote administration were utilized for internal jugular venous gas demonstrated a pH of 6.80 with immediate testing and a sample was not available for send-out aPO2 of 222 mmHg, an O2 saturation of 99%, a PCO2 of analysis. Urinary thiocyanate levels were unable to be 57 mmHg and bicarcarbonate of 9 mEq/L. The radial artery analyzed due to an “interfering substance”. Fig. 1 Hemodialysis blood leak Light Light alarm source source Dialysate Interfering column Substance Photodetector Photodetector Left: Normal light transparency. Right: Interfering substance decreases transparency and shuts off dialysis machine J. Med. Toxicol. (2010) 6:165–167 167 The patient denied a suicidal ingestion of cyanide or hemodialysis might be delayed or prevented altogether. This potential exposure to any other cellular toxins, such as delay in dialysis initiation would be unacceptable in most hydrogen sulfide, that would explain her clinical condition cases of overwhelming metabolic acidosis. and rapid response to the therapy provided. However, there Another problem we encountered was the inability to assay were several concerning factors in the patients social for urinary thiocyanate which is often
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