Mechanisms of extraocular muscle injury in orbital fractures

The gross and microscopic events that occur after orbital blowout fractures were evaluated to assess the mechanisms of diplopia and muscle injury. Int ramuscular and intraorbital pressures were evaluated in experimental animal s, in cadavers, and at the time of orbital fracture explorations for repair of orbital fractures in humans. Histologic and circulatory changes, muscle pressure recordings, and operative observations were evaluated. Creation o f a compartment syndrome was evaluated to include a histologic evaluation o f the orbital fibrous sheath network for the extraocular muscles and the in tramuscular vasculature. These experiments and observations do not support the role of a compartment syndrome in ocular motility disturbances because (1) intramuscular pressur es were subcritical in both humans and animals; (2) no limiting fascial com partment could be demonstrated; and (3) microangiograms and histologic eval uations did not confirm areas of compartmental ischemic necrosis. Muscle co ntusion, scarring within and around the orbital fibrous sheath network, ner ve contusion, and incarceration within fractures remain die probable causes of diplopia, with the most likely explanations being muscle contusion and fibrosis or incarceration involving the muscular fascial network.