Gelbenegger Georg, Buchtele Nina, Schoergenhofer Christian, Roeggla Martin, Schwameis Michael
Department of Emergency Medicine, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.
Department of Internal Medicine I, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria.
Drug Saf Case Rep. 2017 Nov 3;4(1):17. doi: 10.1007/s40800-017-0058-8.
A 66-year-old Caucasian male became unconscious 2 weeks after initiation of add-on therapy with empagliflozin for poorly controlled type 2 diabetes mellitus. The inpatient had recently suffered focal pontine stroke, rendering him bedridden and requiring increased nursing care, including assistance with drinking. The patient had received empagliflozin 10 mg once daily for glycaemic control. Investigations revealed hypernatraemia (164 mmol/l), a urine glucose level of 3935 mg/dl, and a creatinine level of 2.1 mg/dl. The patient was diagnosed with severe hypernatraemic dehydration due to iatrogenic glucosuria and prerenal kidney failure. Empagliflozin was discontinued and the patient received hypotonic fluids (including 5% dextrose and free water). Over the following 4 days, glucosuria subsided, blood sodium levels and kidney function normalized and the patient regained full consciousness. He was discharged for rehabilitation 40 days after admission. A Naranjo assessment score of 6 was obtained, indicating a probable relationship between the patient's hypernatraemic dehydration and administration of empagliflozin. In this care-dependent inpatient, who lost the ability to replace water loss autonomously because of a stroke, continuous administration of empagliflozin caused persistent glucosuria and contributed to progressive volume depletion. Excessive dehydration resulted from ignorance of both the populations that are susceptible to dehydration under sodium-glucose cotransporter 2 (SGLT2) inhibitor therapy and the drug's mechanism of action. In patients who depend on support from others in daily tasks, including fluid intake, patients with an impaired sense of thirst and those who have lost the ability to communicate thirst, SGLT2 inhibitor therapy should not be initiated or might be (temporarily) discontinued.
一名66岁的白种男性在开始使用恩格列净作为附加治疗药物来控制2型糖尿病（控制不佳）2周后失去意识。该住院患者近期发生了局灶性脑桥中风，导致卧床不起，需要更多护理，包括饮水协助。患者每日服用一次10mg恩格列净以控制血糖。检查发现高钠血症（164mmol/L）、尿葡萄糖水平为3935mg/dl以及肌酐水平为2.1mg/dl。患者被诊断为因医源性糖尿和肾前性肾衰竭导致的严重高钠性脱水。停用恩格列净，患者接受低渗液体（包括5%葡萄糖和自由水）治疗。在接下来的4天里，糖尿消退，血钠水平和肾功能恢复正常，患者完全恢复意识。入院40天后出院进行康复治疗。Naranjo评估得分为6分，表明患者的高钠性脱水与恩格列净的使用之间可能存在关联。在这名依赖他人护理的住院患者中，由于中风而失去自主补充水分流失的能力，持续使用恩格列净导致持续性糖尿，并导致渐进性容量耗竭。由于忽视了钠-葡萄糖协同转运蛋白2（SGLT2）抑制剂治疗下易发生脱水的人群以及该药物的作用机制，导致了过度脱水。对于在日常任务（包括液体摄入）中依赖他人支持的患者、口渴感觉受损的患者以及失去表达口渴能力的患者，不应开始使用SGLT2抑制剂治疗，或者可能需要（暂时）停用。
