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Clindamycin-Associated Hyperphosphatemia in a Child with Renal Dysfunction

机译:克林霉素相关性高磷酸盐血症在肾功能不全的儿童中

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Objective: To report a case of hyperphosphatemia associated with administration of intravenous clindamydn phosphate in a child with renal dysfunction.Case Summary: We describe thg,case of a 12-year-old boy who developed hyperphosphatemia while receiving intravenous clindamycin phosphate. The child had a history of asthma but was otherwise healthy. He was transferred to our facility for management of methicillin-resistant Staphylococcus aureus bacteremia, periorbital cellulitis, osteomyelitis, and necrotizing pneumonia. He received intravenous vancomycin and clindamycin 930 mg administered every 8 hours. Concurrently, he developed acute kidney injury. His baseline phosphorus concentration was within the normal range but increased as high as 11.7 mg/dL while he received clindamycin. Despite receiving oral phosphate binder therapy and a low phosphorus diet, he had little reduction in serum phosphorus values. Intravenous clindamycin was suspected as a potential cause for hyperphosphatemia, and a recommendation was made to switch from intravenous to oral clindamycin solution since it contains a different salt formulation. Given the severity of the child's disseminated infection and questions of whether he could absorb the enteral formulation, the decision was made to continue intravenous clindamycin and he was ultimately transferred to a rehabilitation facility for further care on intravenous clindamycin.Discussion: Excess orator intravenous intake of phosphorus can result in hyperphosphatemia, as the body's plasma phosphate concentration exceeds the kidney's diminished filtration capacity. In this patient, use of the Naranjo probability scale indicated a possible adverse event associated with clindamycin. Phosphate intake from intravenous clindamycin and decreased glomerular filtration rate may have contributed to the child's hyperphosphatemia.Conclusions: While intravenous clindamycin was not the sole cause for this patient's hyperphosphatemia, health care professionals should be aware of the potential for increased phosphate load when administering this drug to a patient with renal dysfunction.
机译:目的:报道一例肾功能不全患儿静脉注射克林霉素高磷酸盐血症的病例。病例摘要:我们描述了一名12岁男孩在接受静脉注射克林霉素磷酸盐治疗时发生高磷酸盐血症的病例。这个孩子有哮喘病史,但身体健康。他被转移到我们的设施,以管理耐甲氧西林的金黄色葡萄球菌菌血症,眶周蜂窝组织炎,骨髓炎和坏死性肺炎。他每8小时接受静脉内万古霉素和克林霉素930 mg的给药。同时,他发展为急性肾损伤。他的基线磷浓度在正常范围内,但在接受克林霉素治疗时增加到了11.7 mg / dL。尽管接受口服磷酸盐结合剂疗法和低磷饮食,他的血清磷值几乎没有降低。怀疑克林霉素可能是引起高磷酸盐血症的潜在原因,并且由于其含有不同的盐配方,因此建议从静脉克林霉素溶液改为口服克林霉素溶液。考虑到儿童的传播感染严重程度以及是否可以吸收肠内制剂的问题,决定继续静脉注射克林霉素,最终他被转到康复机构接受克林霉素静脉注射的进一步护理。磷会导致高磷血症,因为人体血浆中的磷酸盐浓度超过了肾脏过滤能力的下降。在该患者中,使用Naranjo概率量表表明可能与克林霉素有关的不良事件。结论:虽然静脉注射克林霉素不是该患者高磷酸盐血症的唯一原因,但医疗保健专业人员应注意服用这种药物时可能会增加磷酸盐负荷肾功能不全的患者。

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