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.