Gadisseux P, Sica D A, Ward J D, Becker D P
Neurosurgery. 1985 Jul;17(1):35-40. doi: 10.1227/00006123-198507000-00006.
Hypophosphatemia occurs in a variety of clinical conditions. It develops in parallel with phosphate depletion from body losses or more commonly as a sequel to the redistribution of phosphate from the extracellular to the intracellular compartment. Hypophosphatemia is a multisystem disturbance capable of involving the neurological, immunological, and muscular systems, among others. In this report, we describe five patients with severe head injury who developed marked hypophosphatemia (less than 1 mg/dl) within 24 hours of hospitalization. This fall in serum phosphate coincided with the induction of respiratory alkalosis consequent to mechanical ventilation. In four of the five patients, as acid-base parameters returned to normal, serum phosphate values rose, in all instances reaching values greater than 2.5 mg/dl. Urinary phosphorus excretion, ordinarily negligible after hypophosphatemia induced by hypocapnia, was still present in Cases 1 and 4 (greater than 600 mg/24 hours). This is unexplained by any of the known hormonal or fluid alterations that accompany head injury. These five patients developed severe, yet transient, hypophosphatemia that resolved upon correction of hyperventilation-induced acid-base abnormalities. We discuss the pathophysiology of this entity and the implications for the head trauma patient.
低磷血症发生于多种临床情况。它与因身体失磷导致的磷耗竭同时出现,或更常见的是作为磷从细胞外转移至细胞内区室后的后遗症而发生。低磷血症是一种多系统紊乱,可累及神经、免疫和肌肉等系统。在本报告中,我们描述了5例重度颅脑损伤患者,他们在住院24小时内出现了明显的低磷血症(低于1mg/dl)。血清磷的这种下降与机械通气导致的呼吸性碱中毒的发生同时出现。在这5例患者中的4例,随着酸碱参数恢复正常,血清磷值上升,所有情况下均达到大于2.5mg/dl的值。低碳酸血症诱导的低磷血症后通常可忽略不计的尿磷排泄,在病例1和病例4中仍然存在(大于600mg/24小时)。这无法用颅脑损伤伴随的任何已知激素或液体改变来解释。这5例患者出现了严重但短暂的低磷血症,在纠正过度通气引起的酸碱异常后得以缓解。我们讨论了这种情况的病理生理学以及对颅脑创伤患者的影响。