Severe hypophosphatemia after head injury.

Abstract

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.

• Authors: P Gadisseux, D A Sica, J D Ward, D P Becker
• Journal: Neurosurgery (Neurosurgery) Vol. 17 Issue 1 Pg. 35-40 (Jul 1985) ISSN: 0148-396X [Print] United States
• PMID: 4022285 (Publication Type: Journal Article)

Chemical References

• Phosphates

Topics

• Adolescent
• Adult
• Brain Concussion (blood)
• Brain Edema (blood)
• Brain Injuries (blood)
• Cerebral Hemorrhage (blood)
• Female
• Hematoma, Epidural, Cranial (blood)
• Hematoma, Subdural (blood)
• Humans
• Male
• Middle Aged
• Phosphates (blood)