The gross and microscopic events that occur after orbital blowout fractures were evaluated to assess the mechanisms of diplopia and muscle injury. Intramuscular and intraorbital pressures were evaluated in experimental animals, 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 of a compartment syndrome was evaluated to include a histologic evaluation of the orbital fibrous sheath network for the extraocular muscles and the intramuscular vasculature. These experiments and observations do not support the role of a compartment syndrome in ocular motility disturbances because (1) intramuscular pressures were subcritical in both humans and animals; (2) no limiting fascial compartment could be demonstrated; and (3) microangiograms and histologic evaluations did not confirm areas of compartmental ischemic necrosis. Muscle contusion, scarring within and around the orbital fibrous sheath network, nerve contusion, and incarceration within fractures remain the probable causes of diplopia, with the most likely explanations being muscle contusion and fibrosis or incarceration involving the muscular fascial network.
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