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INTRODUCTION: Methylene blue (MB) has recently gained traction as an adjunctive therapy in the management of vasoplegia. Due to risk of inducing oxidative hemolysis its use should be avoided in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency Although rare, drug induced oxidative hemolysis can still occur in patients without G6PD deficiency. In this report, we describe a case of severe oxidative hemolysis in a G6PD sufficient adult following administration of a large dose of MB.

CASE REPORT: A 78-year-old male with a history of coronary artery disease was admitted for coronary artery bypass graft surgery. Patient underwent surgery without any major complications. Post operatively however he developed severe shock refractory to multiple vasopressors and inotropes. A presumptive diagnosis of vasoplegia was made for which the patient was given multiple boluses of MB. Hemodynamics improved thus the patient was started on a MB infusion. Approximately 24 hours later the patient was noted to have an acute drop in his hemoglobin from 9.9 to 8.0 g/dl. He was transfused multiple units of blood with only transient improvements in his hemoglobin. Physical exam and imaging revealed no evidence of bleeding. Additional workup was notable for an LDH of 7222 U/L and an elevated bilirubin raising concern for hemolytic anemia.

Review of his peripheral smear was notable for the presence of numerous bite cells. A diagnosis of oxidative hemolytic anemia secondary to MB administration was made. MB infusion was discontinued and within 48 hours the patient’s LDH normalized and hemoglobin had stabilized. A quantitative G6PD test ordered during the acute hemolytic period and was reported as normal. Due to the possibility of a falsely normal result in the setting of active hemolysis, G6PD testing was repeated two months following discharge and was also normal.

CONCLUSIONS: Methylene blue can be a lifesaving medication in the setting of severe vasoplegia. However, clinicians should be aware of the possibility of inducing severe oxidative hemolytic anemia even in G6PD sufficient patients when giving this agent in large doses. Management of oxidative hemolysis secondary to MB is supportive care with prompt discontinuation resulting in resolution of hemolysis.

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Correspondence: Chris Nevala-Plagemann (chris.nevala-plagemann@hci.utah.edu)

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Correspondence: Chris Nevala-Plagemann (chris.nevala-plagemann@hci.utah.edu)

Author and Disclosure Information

Correspondence: Chris Nevala-Plagemann (chris.nevala-plagemann@hci.utah.edu)

INTRODUCTION: Methylene blue (MB) has recently gained traction as an adjunctive therapy in the management of vasoplegia. Due to risk of inducing oxidative hemolysis its use should be avoided in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency Although rare, drug induced oxidative hemolysis can still occur in patients without G6PD deficiency. In this report, we describe a case of severe oxidative hemolysis in a G6PD sufficient adult following administration of a large dose of MB.

CASE REPORT: A 78-year-old male with a history of coronary artery disease was admitted for coronary artery bypass graft surgery. Patient underwent surgery without any major complications. Post operatively however he developed severe shock refractory to multiple vasopressors and inotropes. A presumptive diagnosis of vasoplegia was made for which the patient was given multiple boluses of MB. Hemodynamics improved thus the patient was started on a MB infusion. Approximately 24 hours later the patient was noted to have an acute drop in his hemoglobin from 9.9 to 8.0 g/dl. He was transfused multiple units of blood with only transient improvements in his hemoglobin. Physical exam and imaging revealed no evidence of bleeding. Additional workup was notable for an LDH of 7222 U/L and an elevated bilirubin raising concern for hemolytic anemia.

Review of his peripheral smear was notable for the presence of numerous bite cells. A diagnosis of oxidative hemolytic anemia secondary to MB administration was made. MB infusion was discontinued and within 48 hours the patient’s LDH normalized and hemoglobin had stabilized. A quantitative G6PD test ordered during the acute hemolytic period and was reported as normal. Due to the possibility of a falsely normal result in the setting of active hemolysis, G6PD testing was repeated two months following discharge and was also normal.

CONCLUSIONS: Methylene blue can be a lifesaving medication in the setting of severe vasoplegia. However, clinicians should be aware of the possibility of inducing severe oxidative hemolytic anemia even in G6PD sufficient patients when giving this agent in large doses. Management of oxidative hemolysis secondary to MB is supportive care with prompt discontinuation resulting in resolution of hemolysis.

INTRODUCTION: Methylene blue (MB) has recently gained traction as an adjunctive therapy in the management of vasoplegia. Due to risk of inducing oxidative hemolysis its use should be avoided in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency Although rare, drug induced oxidative hemolysis can still occur in patients without G6PD deficiency. In this report, we describe a case of severe oxidative hemolysis in a G6PD sufficient adult following administration of a large dose of MB.

CASE REPORT: A 78-year-old male with a history of coronary artery disease was admitted for coronary artery bypass graft surgery. Patient underwent surgery without any major complications. Post operatively however he developed severe shock refractory to multiple vasopressors and inotropes. A presumptive diagnosis of vasoplegia was made for which the patient was given multiple boluses of MB. Hemodynamics improved thus the patient was started on a MB infusion. Approximately 24 hours later the patient was noted to have an acute drop in his hemoglobin from 9.9 to 8.0 g/dl. He was transfused multiple units of blood with only transient improvements in his hemoglobin. Physical exam and imaging revealed no evidence of bleeding. Additional workup was notable for an LDH of 7222 U/L and an elevated bilirubin raising concern for hemolytic anemia.

Review of his peripheral smear was notable for the presence of numerous bite cells. A diagnosis of oxidative hemolytic anemia secondary to MB administration was made. MB infusion was discontinued and within 48 hours the patient’s LDH normalized and hemoglobin had stabilized. A quantitative G6PD test ordered during the acute hemolytic period and was reported as normal. Due to the possibility of a falsely normal result in the setting of active hemolysis, G6PD testing was repeated two months following discharge and was also normal.

CONCLUSIONS: Methylene blue can be a lifesaving medication in the setting of severe vasoplegia. However, clinicians should be aware of the possibility of inducing severe oxidative hemolytic anemia even in G6PD sufficient patients when giving this agent in large doses. Management of oxidative hemolysis secondary to MB is supportive care with prompt discontinuation resulting in resolution of hemolysis.

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