Dalhousie University, Halifax, NS, Canada.
Ann Pharmacother. 2012 Mar;46(3):e6. doi: 10.1345/aph.1Q560. Epub 2012 Feb 28.
To report a case of methylene blue extravasation and subsequent tissue necrosis in a patient with refractory septic shock.
A 47-year-old female presented with febrile neutropenia secondary to chemotherapy. The patient quickly decompensated to refractory septic shock in the critical care unit despite implementation of early goal-directed therapy as well as intravenous norepinephrine and vasopressin to stabilize her hemodynamic status. She received a 16-hour infusion of 1% methylene blue 0.25 mg•kg(-1)•h(-1), titrated up to 0.5 mg•kg(-1)•h(-1), via a peripheral intravenous catheter. Ten hours after the start of the methylene blue infusion, she experienced a local extravasation injury, which led to distal digital necrosis. While her hemodynamic status improved dramatically, allowing discharge from the intensive care unit and eventually to home, the extravasation site became necrotic and required debridement and skin graft.
Methylene blue is a vasoactive chemical that has been shown to provide hemodynamic stability in the treatment of refractory septic shock. Methylene blue administration is not considered standard of practice in the treatment of refractory septic shock and many aspects of its dosing, route, duration, and adverse effects are poorly described. As such, there is little guidance for its administration. We postulate that, in our patient, in the presence of systemic vasopressin and norepinephrine, methylene blue caused extensive vasoconstriction at the site of extravasation, resulting in tissue ischemia and necrosis. Tissue necrosis secondary to peripheral intravenous extravasation has not been previously described and is not listed as an adverse outcome on the drug monograph. The Naranjo probability scale indicates that the tissue necrosis was probably caused by the methylene blue extravasation.
To mitigate future risk to limb and skin, we recommend that methylene blue infusions be delivered via central venous catheter. Extra care should be given to patients with risk factors for extravasation, such as sedation, presence of systemic disease, proximal intravenous puncture sites, and improperly placed catheters.
报告 1 例难治性感染性休克患者甲烯蓝外渗及随后组织坏死。
一名 47 岁女性因化疗引起发热性中性粒细胞减少症。尽管早期目标导向治疗以及静脉给予去甲肾上腺素和加压素以稳定其血流动力学状态,但患者在重症监护病房中迅速失代偿为难治性感染性休克。她接受了 16 小时的 1%甲烯蓝 0.25mg·kg(-1)·h(-1)输注,通过外周静脉导管滴定至 0.5mg·kg(-1)·h(-1)。甲烯蓝输注开始后 10 小时,她出现局部外渗损伤,导致远端指端坏死。尽管她的血流动力学状态显著改善,允许从重症监护病房出院并最终回家,但外渗部位出现坏死,需要清创和植皮。
甲烯蓝是一种血管活性化学物质,已被证明可在治疗难治性感染性休克中提供血流动力学稳定性。甲烯蓝的给药不被认为是难治性感染性休克治疗的标准实践,其剂量、途径、持续时间和不良反应的许多方面描述得很差。因此,对其给药的指导很少。我们推测,在我们的患者中,在全身血管加压素和去甲肾上腺素存在的情况下,甲烯蓝在外渗部位引起广泛的血管收缩,导致组织缺血和坏死。外周静脉外渗引起的组织坏死以前没有描述过,也没有被列在药物专论的不良后果中。Naranjo 概率量表表明,组织坏死可能是由甲烯蓝外渗引起的。
为了降低肢体和皮肤的未来风险,我们建议通过中心静脉导管给予甲烯蓝输注。对于有外渗风险的患者,如镇静、存在全身疾病、近端静脉穿刺部位和放置不当的导管,应给予特别关注。