低磷血症
呼吸性碱中毒
医学
过度换气
低碳酸血症
头部受伤
磷酸盐
病理生理学
内科学
内分泌学
胃肠病学
外科
呼吸系统
生物化学
代谢性酸中毒
高碳酸血症
化学
作者
Philippe Gadisseux,Domenic A. Sica,John D. Ward,Donald P. Becker
出处
期刊:Neurosurgery
[Oxford University Press]
日期:1985-07-01
卷期号:17 (1): 35-40
被引量:16
标识
DOI:10.1227/00006123-198507000-00006
摘要
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.
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