The management of acute bone loss in severe catabolism due to burn injury

Reduced bone formation has been documented in both children and adults following burn injury of ≤ 40% total body surface area. In children, reduced bone formation and hypercalciuria may be the underlying causes of acute and sustained reduction in bone mineral density. The possible consequences of this reduction are an increase in extrapolated annual fracture incidence and reduced peak bone mass. Excessive endogenous glucocorticoid production, immobilization, bone marrow suppression, and magnesium depletion are all postulated as underlying causes. The most promising potential management agent is recombinant human growth hormone, which can stimulate bone formation via production of insulin-like growth factor I(IGF-I) and its associated binding protein, IGFBP-3, which correlates with bone mineral density in adults. Long-term treatment may be necessary to see a positive effect on bone formation and bone density. Correcting any detected magnesium depletion, and exercise as tolerated, are two other management strategies that might improve bone formation in this population.