Baylor University Medical Center Proceedings April 2017 - 167

Hemodialysis failure secondary to hydroxocobalamin
exposure
Kenneth Lim, MD, PhD, Eliot Heher, MD, David Steele, MD, Andrew Z. Fenves, MD, John Kevin Tucker, MD, Ravi Thadhani,
MD, MPH, Kenneth Christopher, MD, and Nina Tolkoff-Rubin, MD

Hydroxocobalamin is a recently approved antidote for the treatment of
cyanide poisoning. The case presented involves a young patient administered empiric hydroxocobalamin due to suspected cyanide overdose.
Due to the development of acute kidney injury and severe metabolic
derangement, emergent hemodialysis was initiated. Unfortunately,
hemodialysis was confounded by a recurrent "blood leak" alarm. This
unforeseen effect was secondary to interference from hydroxocobalamin.
Hydroxocobalamin causes orange/red discoloration of bodily fluids and
permeates the dialysate. This leads to defraction of light in the effluent
path of the blood leak detector from discolored dialysate, which can
result in activation of the blood leak alarm and an inability to continue
hemodialysis treatment. This case highlights several new and emerging
critical concerns with this medication, including the potential consequence of delayed initiation of emergent renal replacement therapy
with empiric administration, the need for increased awareness among
clinicians of various disciplines, and the need for multidisciplinary
communication.

ydroxocobalamin was approved by the Food and Drug
Administration in December 2006 for the treatment of
cyanide poisoning. For decades, cyanide poisoning has
been treated using the cyanide antidote kit (1, 2). This
kit contains amyl nitrite, sodium nitrite, and sodium thiosulfate, which can cause hypotension and reduced oxygen-carrying
capacity of hemoglobin (3-5). In contrast, hydroxocobalamin
does not cause these complications. This property makes it advantageous for patients with already decreased oxygenation,
those who have been exposed to carbon monoxide, and pregnant
patients. Hydroxocobalamin can therefore be safely used in
cases where combined carbon monoxide and cyanide toxicity is
suspected. The side-eﬀect proﬁle of hydroxocobalamin is considered minimal compared to its predecessor cyanide antidote
kit (6). It can, however, cause orange/red discoloration of skin,
blood, urine, and secretions, and this can lead to statistically signiﬁcant alterations in certain colorimetric tests and co-oximetry
measurements (7-9). A newly recognized problem associated
with the increasing usage of hydroxocobalamin is the interference of hemodialysis. This is particularly concerning due to the
potential ramiﬁcations of limiting the provision of life-saving
treatment in critically ill intoxicated patients. Here we describe a

Proc (Bayl Univ Med Cent) 2017;30(2):167-168

case of a young patient administered empiric hydroxocobalamin
with failure of emergent hemodialysis secondary to interference
from hydroxocobalamin.
CASE REPORT
A 24-year-old man with asthma was found unresponsive
and profoundly hypotensive by emergency medical services. No
eyewitnesses were available. On arrival to the emergency room,
he was found in extremis with signiﬁcant agonal breathing, a
Glasgow coma scale score of 3, temperature of 35.3°C, blood
pressure of 60/45 mm Hg, heart rate of 74 beats/min, respiratory rate of 24 breaths/min, and cool extremities. His serum
creatinine was 1.3 mg/dL; sodium, 145 mmol/L; potassium,
4.6 mmol/L; bicarbonate, 10 mmol/L; anion gap, 39; phosphate, 4.9 mmol/L; lactate, 21.3 mmol/L; and white blood cell
count, 27.3 K/uL. A bedside arterial blood gas was signiﬁcant
for a pH of 6.99, a partial pressure of carbon dioxide of 47, and
a partial pressure of oxygen of 76. A blood and urine toxicology
screen were negative.
Sonography was negative for blunt abdominal trauma.
Echocardiogram showed a severely diminished ejection fraction.
Radiographs showed mildly increased interstitial markings
bilaterally. Despite emergent intubation and intravenous ﬂuid
resuscitation, he required rapid escalation to multiple vasopressors. He was administered hydroxocobalamin empirically in the
emergency room due to concern for cyanide intoxication. Due
to profound acid-base disturbance and concern for intentional
overdose, emergent dialysis was initiated using the Fresenius
2008K machine. This was confounded by a recurrent "blood
leak alarm" that repeatedly shut down the machine despite a
change to a new dialyzer. Emergent salvage extracorporeal membrane oxygenation was commenced, but the patient died. It
was later revealed that instead of cyanide, the patient was most
likely intoxicated with sodium azide.
From the Division of Nephrology, Massachusetts General Hospital, Harvard
Medical School, Boston, Massachusetts (Lim, Heher, Steele, Fenves, Tucker,
Thadhani, Tolkoff-Rubin); and the Renal Division, Brigham and Women's Hospital,
Harvard Medical School, Boston, Massachusetts (Lim, Tucker, Christopher).
Corresponding author: Kenneth Lim, MD, PhD, Division of Nephrology,
Massachusetts General Hospital, Harvard Medical School, 165 Cambridge Street,
Suite 302, Boston, MA 02114 (e-mail: kjlim@mgh.harvard.edu).
167

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