ABSTRACT
Hyperbaric osteonecrosis is a form of non-traumatic bone necrosis associated with prolonged or repeated hyperbaric exposures such as experienced by tunnel and caisson workers and by diving fishermen. Hyperbaric osteonecrosis, also called dysbaric osteonecrosis, can be induced experimentally in sheep long bones by hyperbaric exposures similar to those which cause osteonecrosis in humans. Osteonecrosis was induced in five sheep by 12–13 twenty-four hour hyperbaric exposures to compressed air pressures of 2.5-2.9 atm abs with no-stop decompression. At 26-36 weeks after the first hyperbaric exposure, lesions included extensive fatty marrow necrosis, endosteal thickening in bone shafts and juxta-articular osteonecrosis. Even single 24-h hyperbaric exposures of sheep to compressed air pressures of 2.2-2.4 atm abs with no-stop decompression also induced osteonecrosis. Bone scans with 99mTc-methylene diphosphonate revealed ‘hot spots’ two weeks after hyperbaric exposure in those limbs which were affected by persistent limb bends. Roentgenographic films of these limbs at eight weeks revealed endosteal thickening and medullary opacities at ‘hot spot’ sites, and MRI at eight weeks indicated fatty marrow infarction. Necropsy at nine weeks confirmed extensive fatty marrow and bone necrosis. In our view, the early pathogenesis of hyperbaric osteonecrosis involves a bone compartment syndrome initiated by N2 bubble formation in the fatty marrow of long bones after decompression from prolonged hyperbaric exposure.
