Papadakis M A, Wexman M P, Fraser C, Sedlacek S M
Am J Kidney Dis. 1985 Jan;5(1):64-6. doi: 10.1016/s0272-6386(85)80139-6.
We describe the occurrence of hyperkalemia in a stable hemodialysis patient who developed digoxin toxicity. The patient had been receiving digoxin for 2 years. His maintenance digoxin dose was increased from 0.125 to 0.25 mg three times a week, which resulted in a toxic serum level of 4.9 ng/mL (therapeutic range is 0.8 to 2.0 ng/mL). As a consequence of the digoxin toxicity, he became hyperkalemic (7.8 mEq/L), and this value returned to normal only after the digoxin level was lowered by a combination of oral charcoal and dialysis. This study shows how readily hyperkalemia can occur in an anephric patient manifesting digoxin toxicity. Thus, potentially lethal hyperkalemia can occur in hemodialysis patients who ingest therapeutic quantities of digoxin. Digoxin toxicity should be added to the differential diagnosis of hyperkalemia in patients with renal failure. This can occur despite the absence of a history of massive ingestion of a cardiac glycoside.
我们描述了一名稳定的血液透析患者发生高钾血症并出现地高辛中毒的情况。该患者接受地高辛治疗已达2年。他维持服用的地高辛剂量从每周三次每次0.125毫克增加至0.25毫克,导致血清地高辛水平达到中毒值4.9纳克/毫升(治疗范围为0.8至2.0纳克/毫升)。由于地高辛中毒,他出现了高钾血症(7.8毫当量/升),且仅在通过口服活性炭和透析联合治疗使地高辛水平降低后,该值才恢复正常。本研究表明,在表现出地高辛中毒的无肾患者中,高钾血症很容易发生。因此,摄入治疗剂量地高辛的血液透析患者可能会发生潜在致命的高钾血症。在肾衰竭患者中,地高辛中毒应被列入高钾血症的鉴别诊断范围。即使没有大量摄入强心苷的病史,这种情况也可能发生。