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.