Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Graduate Institute of Medical Science, National Defense Medical Center, Taipei, Taiwan.
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Department of Medicine, Armed Forces Taoyuan General Hospital, Taoyuan, Taiwan.
Am J Med. 2015 Mar;128(3):289-96.e1. doi: 10.1016/j.amjmed.2014.09.027. Epub 2014 Oct 15.
Hypokalemic nonperiodic paralysis represents a group of heterogeneous disorders with a large potassium (K(+)) deficit. Rapid diagnosis of curable causes with appropriate treatment is challenging to avoid the sequelae of hypokalemia. We prospectively analyzed the etiologies and therapeutic characteristics of hypokalemic nonperiodic paralysis.
Over an 8-year period, patients with hypokalemic nonperiodic paralysis were enrolled by excluding those with hypokalemic periodic paralysis due to acute shift of K(+) into cells. Blood and spot urine samples were collected for the measurements of electrolytes, pH, and biochemistries. Intravenous potassium chloride (KCl) at a rate of 10-20 mmol/h was administered until muscle strength recovered.
We had identified 58 patients with hypokalemic nonperiodic paralysis from 208 consecutive patients with hypokalemic paralysis, and their average K(+) concentration was 1.8 ± 0.2 mmol/L. Among patients with low urinary K(+) excretion (n = 17), chronic alcoholism, remote diuretic use, and anorexia/bulimia nervosa were the most common causes. Among patients with high urinary K(+) excretion (n = 41) and metabolic acidosis, renal tubular acidosis and chronic toluene abuse were the main causes, while primary aldosteronism, Gitelman syndrome, and diuretics were the leading diagnoses with metabolic alkalosis. The average KCl dose needed to restore muscle strength was 3.8 ± 0.8 mmol/kg. Initial lower plasma K(+), volume depletion, and high urinary K(+) excretion were associated with higher recovery KCl dosage. During therapy, patients with paradoxical hypokalemia (n = 32) who required more KCl supplementation than patients without (4.1 ± 0.7 vs 3.4 ± 0.7 mmol/kg, P < 0.001) often exhibited significantly higher plasma renin activity and received a higher volume of normal saline before its appearance.
Understanding the common etiologies of hypokalemic nonperiodic paralysis may aid in early diagnosis. Patients with initial lower plasma K(+), renal K(+) wasting, and hypovolemia required higher recovery K(+) dosage. Paradoxical hypokalemia is prone to develop in hypovolemic patients even during K(+) supplementation with volume repletion.
低钾非周期性瘫痪是一组钾(K(+))大量缺乏的异质性疾病。快速诊断可治愈病因并进行适当治疗具有挑战性,因为这可能会导致低钾血症的后遗症。我们前瞻性分析了低钾非周期性瘫痪的病因和治疗特征。
在 8 年期间,通过排除由于细胞内 K(+)急性转移引起的低钾周期性瘫痪患者,我们纳入了低钾非周期性瘫痪患者。采集血和即时尿样,用于测量电解质、pH 值和生化指标。静脉滴注氯化钾(KCl)的速度为 10-20mmol/h,直至肌力恢复。
我们从 208 例低钾性瘫痪患者中发现了 58 例低钾非周期性瘫痪患者,他们的平均 K(+)浓度为 1.8±0.2mmol/L。在尿 K(+)排泄量低的患者中(n=17),慢性酒精中毒、长期使用利尿剂和神经性厌食/贪食症是最常见的病因。在尿 K(+)排泄量高且代谢性酸中毒的患者中(n=41),肾小管酸中毒和慢性甲苯滥用是主要病因,而原发性醛固酮增多症、Gitelman 综合征和利尿剂是代谢性碱中毒的主要诊断。恢复肌力所需的平均 KCl 剂量为 3.8±0.8mmol/kg。初始较低的血浆 K(+)、容量耗竭和高尿 K(+)排泄与更高的恢复 KCl 剂量有关。在治疗期间,需要更多 KCl 补充的低钾血症患者(n=32)出现了矛盾性低钾血症,比不需要补充 KCl 的患者(4.1±0.7 比 3.4±0.7mmol/kg,P<0.001)需要补充更多的 KCl,且在出现矛盾性低钾血症之前通常接受了更高剂量的生理盐水。
了解低钾非周期性瘫痪的常见病因可能有助于早期诊断。初始较低的血浆 K(+)、肾 K(+)丢失和低血容量的患者需要更高的恢复 K(+)剂量。在补充 KCl 并补充容量时,低血容量患者容易出现矛盾性低钾血症。