Oud Lavi
Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, Texas Tech University School of Medicine, Odessa, TX 79762, USA.
Med Sci Monit. 2009 Mar;15(3):CS49-53.
Respiratory failure in severely hypophosphatemic patients has been attributed to respiratory muscle weakness, leading to ventilatory failure. While frequently documenting hypercarbic respiratory failure, previous reports of hypophosphatemia-related respiratory failure in patients otherwise free of pulmonary or airway disease often did not provide sufficient information on gas exchange and pulmonary function, precluding inference on alternative or additional sources of respiratory dysfunction in this population.
We report a case of acute hypoxic respiratory failure in a 26 year-old bulimic woman with severe hypophosphatemia. The patient presented with acute onset of dyspnea, paresthesias, limb shaking, and severe hyperventilation. SpO2 was 74%, requiring administration of 100% O2, with normal chest radiograph. Serum phosphate was <0.3 mmol/liter (1.0 mg/dL). Further evaluation did not support pulmonary, vascular, neurogenic or external exposure-related causes of hypoxic respiratory failure, which rapidly resolved with parenteral correction of hypophosphatemia.
To date, hypoxic respiratory failure has not been reported in association with hypophosphatemia. Increased awareness and further investigations can help elucidate the mechanisms of hypophosphatemia-associated hypoxemia.
严重低磷血症患者的呼吸衰竭被认为是由于呼吸肌无力导致通气衰竭。虽然既往报告经常记录高碳酸血症性呼吸衰竭，但之前关于无肺部或气道疾病患者的低磷血症相关呼吸衰竭的报道往往没有提供足够的气体交换和肺功能信息，无法推断该人群呼吸功能障碍的其他或额外来源。
我们报告一例26岁贪食症女性发生急性低磷血症并伴有急性低氧性呼吸衰竭。患者表现为急性起病的呼吸困难、感觉异常、肢体震颤和严重的通气过度。血氧饱和度（SpO2）为74%，需给予100%氧气，胸部X线片正常。血清磷酸盐<0.3 mmol/升（1.0 mg/dL）。进一步评估不支持低氧性呼吸衰竭的肺部、血管、神经源性或外部暴露相关病因，经胃肠外纠正低磷血症后，呼吸衰竭迅速缓解。
迄今为止，尚未有低磷血症相关低氧性呼吸衰竭的报道。提高认识并进一步开展研究有助于阐明低磷血症相关低氧血症的机制。
