Department of Medicine I, University of Luebeck, 23538 Luebeck, Germany.
Am J Emerg Med. 2012 Jan;30(1):250.e1-4. doi: 10.1016/j.ajem.2010.09.027. Epub 2010 Oct 27.
Severe hyperkalemia (>7 mmol/L) is a medical emergency because of possible fatal arrhythmias. We here report the case of a 58-year-old woman surviving extreme hyperkalemia (>10 mmol/L). The patient with a history of congestive heart failure, a DDD pacemaker and mild chronic renal insufficiency was admitted with progressive weakness and sudden onset of hypotension and bradycardia in the absence of any pacemaker action. Laboratory tests revealed an extreme serum potassium level of 10.1 mmol/L, with a slightly elevated serum creatinine of 149 μmol/L. Treatment with norepinephrine, sodium bicarbonate, and insulin improved both the hemodynamic situation and the serum potassium with subsequent regaining pacemaker actions even before additional hemodialysis normalized the potassium level. A thorough investigation demonstrated that several mechanisms contributed to the extreme potassium level: urinalysis and a low transtubular potassium gradient in the presence of metabolic acidosis with normal anion gap pointed to preexisting interstitial nephritis, with renal tubular acidosis type IV as the predisposing factor, whereas several drugs and acute impairment of renal function contributed to the dangerous situation. Despite the odds for fatal outcome, the patient recovered completely, and long-term management was initiated to prevent recurrent hyperkalemia.
严重高钾血症(>7mmol/L)可引发致命性心律失常,属于医学急症。我们报告 1 例血钾极度升高(>10mmol/L)患者的救治经过。患者为 58 岁女性,既往充血性心力衰竭、DDD 起搏器植入和轻度慢性肾功能不全,因进行性肌无力和低血压、心动过缓就诊,且无起搏器活动。实验室检查示血钾极度升高至 10.1mmol/L,血肌酐轻度升高至 149μmol/L。给予去甲肾上腺素、碳酸氢钠和胰岛素治疗后,患者的血流动力学和血钾水平均得到改善,随后起搏器功能恢复正常,而进一步行血液透析后血钾水平恢复正常。深入检查发现多种机制导致血钾极度升高:存在代谢性酸中毒时尿分析和肾小管钾梯度正常提示存在先前存在的间质性肾炎,以肾小管酸中毒 4 型为潜在致病因素,而多种药物和急性肾功能损害也促成了这种危急情况。尽管有致命结局的风险,但患者完全恢复,启动了长期管理以预防复发性高钾血症。