Edward Hines, Jr. Veterans Affairs Hospital, Hines, IL 60141, USA.
Heart Lung. 2013 Jul-Aug;42(4):287-9. doi: 10.1016/j.hrtlng.2013.03.004. Epub 2013 May 11.
A 56-year-old woman with a history of paraplegia and chronic pain due to neuromyelitis optica (Devic's syndrome) was admitted to a spinal cord injury unit for management of a sacral decubitus ulcer. During the hospitalization, she required emergency transfer to the intensive care unit (ICU) because of progressive deterioration of respiratory muscle function, severe respiratory acidosis, obtundation and hypotension. Upon transfer to the ICU, arterial blood gas revealed severe acute-on-chronic respiratory acidosis (pH 7.00, PCO2 120 mm Hg, PO2 211 mm Hg). The patient was immediately intubated and mechanically ventilated. Intravenous fluid boluses of normal saline (10.5 L in about 24 h) and vasopressors were started with rapid correction of hypotension. In addition, she was given hydrocortisone. Within 40 min of initiation of mechanical ventilation, there was improvement in acute respiratory acidosis. Sixteen hours later, however, the patient developed life-threatening hypokalemia (K(+) of 2.1 mEq/L) and hypomagnesemia (Mg of 1.4 mg/dL). Despite aggressive potassium supplementation, hypokalemia continued to worsen over the next several hours (K(+) of 1.7 mEq/L). Urine studies revealed renal potassium wasting. We reason that the recalcitrant life-threatening hypokalemia was caused by several mechanisms including total body potassium depletion (chronic respiratory acidosis), a shift of potassium from the extracellular to intracellular space (rapid correction of respiratory acidosis with mechanical ventilation), increased sodium delivery to the distal nephron (normal saline resuscitation), hyperaldosteronism (secondary to hypotension plus administration of hydrocortisone) and hypomagnesemia. We conclude that rapid correction of respiratory acidosis, especially in the setting of hypotension, can lead to life-threatening hypokalemia. Serum potassium levels must be monitored closely in these patients, as failure to do so can lead to potentially lethal consequences.
一位 56 岁的女性，因视神经脊髓炎（Devic 综合征）导致截瘫和慢性疼痛而入院，以治疗骶骨褥疮。住院期间，由于呼吸肌功能进行性恶化、严重呼吸性酸中毒、意识障碍和低血压，她需要紧急转入重症监护病房（ICU）。转入 ICU 后，动脉血气显示严重的急性加重慢性呼吸性酸中毒（pH 值 7.00，PCO2 120mmHg，PO2 211mmHg）。患者立即进行气管插管和机械通气。静脉输注生理盐水（约 24 小时内输注 10.5L）和血管加压药，迅速纠正低血压。此外，还给予患者氢化可的松。在开始机械通气后的 40 分钟内，急性呼吸性酸中毒得到改善。然而，16 小时后，患者出现危及生命的低钾血症（K+为 2.1mEq/L）和低镁血症（Mg 为 1.4mg/dL）。尽管进行了积极的补钾治疗，但在接下来的几个小时内，低钾血症仍持续恶化（K+为 1.7mEq/L）。尿液研究显示肾脏钾丢失。我们推断，顽固的危及生命的低钾血症是由多种机制引起的，包括全身钾耗竭（慢性呼吸性酸中毒）、钾从细胞外转移到细胞内空间（机械通气快速纠正呼吸性酸中毒）、向远曲小管输送增加的钠（生理盐水复苏）、醛固酮增多症（继发于低血压加用氢化可的松）和低镁血症。我们得出结论，呼吸性酸中毒的快速纠正，尤其是在低血压的情况下，可导致危及生命的低钾血症。在这些患者中，必须密切监测血清钾水平，否则可能导致潜在的致命后果。
