Severe hypophosphatemia after head injury.
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.
D000293:Adolescent; D000328:Adult; D001924:Brain Concussion / Q000097:blood; D001929:Brain Edema / Q000097:blood; D001930:Brain Injuries / Q000097:blood*; D002543:Cerebral Hemorrhage / Q000097:blood; D005260:Female; D006407:Hematoma, Epidural, Cranial / Q000097:blood; D006408:Hematoma, Subdural / Q000097:blood; D006801:Humans; D008297:Male; D008875:Middle Aged; D010710:Phosphates / Q000097:blood*
D010710:Phosphates