should be avoided.

Many treatments have been proposed to prevent rebleeding in traumatic hyphema, although none is universally accepted. They include an antifibrinolytic agent (aminocaproic acid or tranexamic acid) administered orally, topical aminocaproic acid, and oral prednisolone.

Surgical evacuation of hyphema is usually performed in adults when early corneal blood staining is detected or when significant IOP elevation has persisted for 5–7 days. The difficulty of detecting early blood staining in a child and the risk that corneal staining may cause severe deprivation amblyopia, coupled with the problems of accurately measuring IOP, justify earlier surgical intervention whenever a total hyphema persists for 4–5 days. Even earlier surgery may be necessary if elevated pressures occur in a patient with sickle cell trait or disease. Various operative techniques have been employed; none has been shown to offer particular advantages in children.

Late glaucoma is a potential complication of traumatic hyphema in children, as in adults, and may present with no symptoms. Gonioscopy can be performed after the eye has healed and the child can cooperate. Annual follow-up should be continued in children who are found to have angle recession.

Orbital Fractures

Orbital floor fractures

Blunt facial trauma is the usual cause of orbital floor fractures. When the rim remains intact, this is termed blowout fracture. Orbital floor fracture is thought to be caused by an acute increase in intraorbital pressure from direct impact that closes the orbital entrance, or by compression of the rim, which results in buckling of the floor. Orbital floor fracture can be part of more extensive fractures of the orbit and midface. In some cases, the mechanism causing floor fractures extends to include the medial wall as well.

Injury to the inferior rectus muscle or to its nerve, with resulting weakness, may be caused by hemorrhage or ischemia, in addition to restriction. It can occur either at the time of injury or during repair of the fracture.

Clinical features Injury to the inferior rectus muscle can present as either limited elevation or depression. Hypoesthesia in the cutaneous distribution of the infraorbital nerve can also occur.

In a patient with limited elevation, a positive forced-duction test indicates the presence of restriction. Bradycardia, heart block, nausea, or syncope can occur as a vagal response to entrapment. When the entrapment involves the more anterior portion of the orbital floor or when there is associated injury to the inferior rectus muscle or its nerve, there can also be limited depression. Reduced saccadic velocity and force generation on attempted downgaze suggest weak muscle action. Orbital computed tomography and high-resolution, multipositional magnetic resonance imaging are useful for revealing the presence and extent of the injury.

A special presentation, the white-eyed blowout fracture, is characterized by marked restriction (in both directions) of vertical ocular motility despite minimal signs of soft-tissue injury. This restriction is due to entrapment of the inferior rectus muscle either beneath a trapdoor fracture or, in the case of children, in a linear opening caused by flexion deformity of the floor. Early surgery, rather than observation, is required in order to minimize permanent muscle and nerve damage.

Criden MR, Ellis FJ. Linear nondisplaced orbital fractures with muscle entrapment. J AAPOS. 2007;11(2):142–147.

Management There are several approaches to the management of orbital floor fractures. Some clinicians advocate surgical exploration in all cases, irrespective of the results of forced-duction testing. The justification for this approach is that, especially with large bony defects, progressive