Burn-induced bone loss: importance, mechanisms, and management

The purpose of this article is to familiarize the reader with the issue of bone loss that accompanies severe burn injury. Why is this important? How does it happen? How can we treat it?

The published findings on this subject are reviewed and integrated into a conceptual framework.

Bone loss occurs quickly following a severe burn, is sustained, and increases the risk of postburn fracture. The likely mechanisms responsible are the increase in endogenous glucocorticoid production resulting from the stress response and resorptive cytokines resulting from the systemic inflammatory response and likely aggravated by progressive vitamin D deficiency. Calcium metabolism is also disrupted as the patients develop hypocalcemic hypoparathyroidism likely due to an upregulation of the parathyroid calcium-sensing receptor, possibly due to inflammatory cytokine stimulation. Treatment is achieved by use of anabolic agents and vitamin D supplementation. Studies of acute administration of the antiresorptive agent pamidronate are also promising.

Postburn bone loss should be looked for in patients with a burn injury of 40% or greater total body surface area. The cause is inherent to the adaptive mechanisms following burn injury. Methods are available to treat this condition.