Sanson Gianfranco, Russo Savino, Iudicello Alessandra, Schiraldi Fernando
School of Nursing, University of Trieste, Trieste, Italy.
High Dependency Unit, Azienda Ospedaliero-Universitaria, Trieste, Italy.
J Emerg Med. 2015 May;48(5):555-61.e3. doi: 10.1016/j.jemermed.2014.12.048. Epub 2015 Mar 9.
In severe hyperkalemia, neurologic symptoms are described more rarely than cardiac manifestations. We report a clinical case; present a systematic review of available literature on secondary hyperkalemic paralysis (SHP); and also discuss pathogenesis, clinical effects, and therapeutic options.
A 75-year-old woman presented to the emergency department complaining of tetraparesis. Her serum potassium level was 11.4 mEq/L. Electrocardiogram (ECG) showed a pacemaker (PMK)-induced rhythm, with loss of atrial capture and wide QRS complexes. After emergency treatment to restore cell membrane potential threshold and lower serum potassium, neurologic and ECG signs completely disappeared. An acute myocardial infarction subsequently occurred, possibly linked to tachycardia induced by salbutamol therapy. We reviewed 99 articles (119 patients). Mean serum potassium was 8.8 mEq/L. In most cases, ECG showed the presence of tall T waves; loss of PMK atrial capture was documented in 5 patients. In 94 patients, flaccid paralysis was described and in 25, severe muscular weakness; in 65 patients, these findings were associated with other symptoms. Concurrent renal failure was often documented. The most frequent treatments were dialysis and infusion of insulin and glucose. Eighty-seven percent of patients had complete resolution of symptoms. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Severe hyperkalemia is always a life-threatening medical emergency, as it can precipitate fatal dysrhythmias and paralysis. SHP should be considered in the differential diagnosis of neurologic signs and symptoms of uncertain etiology, especially in a subject with kidney failure or who is taking medications that may worsen renal function. The presence of a PMK does not necessarily impede hyperkalemic cardiac toxicity.
在严重高钾血症中，神经症状的描述比心脏表现更为罕见。我们报告一例临床病例；对继发性高钾性麻痹（SHP）的现有文献进行系统综述；并讨论其发病机制、临床影响和治疗选择。
一名75岁女性因四肢无力就诊于急诊科。她的血清钾水平为11.4 mEq/L。心电图（ECG）显示起搏器（PMK）诱发的心律，心房捕捉丧失，QRS波群增宽。在进行紧急治疗以恢复细胞膜电位阈值并降低血清钾后，神经和心电图体征完全消失。随后发生急性心肌梗死，可能与沙丁胺醇治疗诱发的心动过速有关。我们回顾了99篇文章（119例患者）。平均血清钾为8.8 mEq/L。在大多数情况下，心电图显示高耸T波；5例记录有PMK心房捕捉丧失。94例患者描述有弛缓性麻痹，25例有严重肌无力；65例患者中，这些表现与其他症状相关。常记录有并发肾衰竭。最常用的治疗方法是透析以及输注胰岛素和葡萄糖。87%的患者症状完全缓解。
为什么急诊医生应该了解这个情况？：严重高钾血症始终是危及生命的医疗急症，因为它可引发致命性心律失常和麻痹。在病因不明的神经体征和症状的鉴别诊断中，应考虑SHP，尤其是在肾衰竭患者或正在服用可能使肾功能恶化药物的患者中。PMK的存在不一定能阻止高钾血症的心脏毒性。
