ABSTRACT
Limitation of Ocular Motility The patient with an orbital floor blowout fracture may have vertical diplopia due to a variety of different mechanisms. Horizontal diplopia in the presence of a medial orbital wall
blowout fracture is less commonly seen. The mechanisms which may be responsible for limitation of ocular motility are:
1. Entrapment of connective tissue septa or of an extraocular muscle within the fracture
2. Hematoma and/or edema in the orbital fat adjacent to the fracture
3. Hematoma or contusion of an extraocular muscle(s) 4. Palsy of an extraocular muscle(s) due to neuronal
damage 5. Volkmann’s ischemic contracture of an entrapped
extraocular muscle
Enophthalmos/Proptosis/Hypoglobus Enophthalmos is produced by an enlarged orbital volume and varies from insignificant to cosmetically disfiguring depending
on the degree of orbital bony expansion. Fat atrophy usually contributes little if anything to the enophthalmos. Enophthalmos may be masked by orbital hematoma, edema, or air, which may even cause proptosis in the first few days following trauma. Proptosis, however, may be associated with a “blow-in” fracture where the fragmented bones of the orbital floor are displaced into the orbit. This is more often seen in the context of fractures involving the roof of the orbit. Enophthalmos is always significant in the presence of combined fractures of the orbital floor and medial orbital wall. Hypoglobus is seen in the presence of extensive orbital floor blowout fractures. In some patients, the maxillary antrum extends laterally for some distance beyond the infraorbital neurovascular bundle, with the ensuing orbital floor defect occupying almost the whole of the orbital floor. Very rarely, the globe may come to lie within the maxillary antrum or even within the ethmoid sinus (Figs. 25.3 and 25.4).
