Pediatric Ocular Trauma — Posterior Segment & Orbital

Retinal Findings After Blunt Trauma

Blunt trauma sends a shock wave through the globe that can injure the retina well away from the point of impact. A child with a history of blunt impact to the eye (a ball, a fist, a fall) can develop several distinct posterior-segment findings:

• Commotio retinae (Berlin's edema): transient retinal whitening in the posterior pole, most prominent perifoveally, from shock-wave disruption of the photoreceptor outer segments. The name is misleading: histology shows photoreceptor disruption, not true fluid accumulation. It usually resolves on its own without specific treatment.
• Traumatic retinal dialysis: a disinsertion of the retina at the ora serrata from equatorial scleral compression and vitreous base traction at the moment of impact. The inferotemporal quadrant is affected most often, since it is the retina's firmest point of attachment and therefore where traction concentrates. A dialysis can progress slowly to a retinal detachment, so it needs to be identified and, when indicated, treated with laser demarcation or cryotherapy before that happens.
• Chorioretinitis sclopetaria: a full-thickness chorioretinal rupture with hemorrhage from a high-velocity projectile passing tangentially near the globe without actually penetrating it. The concussive shockwave alone ruptures choroid, retina, and sclera, and the injury heals with dense chorioretinal scarring.
• Purtscher retinopathy: follows severe chest compression or long-bone trauma, classically a severe motor vehicle collision, rather than a direct blow to the eye. It presents with sudden vision loss, multiple cotton-wool spots, hemorrhages, and characteristic Purtscher flecken that spare the fovea. The proposed mechanism is complement-mediated leukoembolization causing precapillary arteriolar occlusion: a systemic process reaching the eye rather than an injury delivered to it directly.

Orbital Floor Fracture & the White-Eyed Trapdoor

The orbital floor overlies the maxillary sinus and is further weakened by the infraorbital groove. It is the thinnest, structurally weakest orbital wall, which makes it the most common site of a blowout fracture from blunt impact.

That pattern flips in young children. Before the frontal sinus pneumatizes, a process not complete until later childhood, the orbital roof has little air space or bone cushioning beneath the brow to absorb blunt impact, so force reaches the thin roof directly instead. One series put a child under seven at roughly two and a half times the odds of an adult for a roof fracture rather than a floor fracture, and roof fractures at this age often carry intracranial injury alongside the orbital one. Once the frontal sinus aerates later in childhood, it functions as a crumple zone, and the floor becomes the more frequent fracture site again.

Forced duction testing distinguishes mechanical restriction from a neurogenic cause of limited eye movement: the examiner grasps the conjunctiva near the limbus and rotates the globe manually. Resistance to passive rotation, a positive test, indicates mechanical restriction such as muscle entrapment. A negative test with limited motility instead points toward a neurogenic cause, such as a cranial nerve palsy.

Intraocular Foreign Body Imaging

When an intraocular foreign body is suspected, particularly after a penetrating injury from a metallic object, imaging choice matters as much as the decision to image at all. MRI is contraindicated if a metallic fragment is a possibility, since the scanner's strong magnetic field can move it and cause further intraocular damage. Thin-cut, non-contrast CT of the orbit is the imaging study of choice instead. The same logic applies in children as in adults: a history that is vague or incomplete, common in pediatric trauma, is not a reason to skip appropriate imaging before choosing between MRI and CT.

Angle Recession Glaucoma

Blunt globe contusion can tear the ciliary body face between its longitudinal and circular muscle fibers, a finding called angle recession and visible on gonioscopy as a widened ciliary body band. Angle recession itself is not glaucoma; it is a structural consequence of the contusion. It does carry a lifelong risk of secondary glaucoma from trabecular meshwork scarring in the injured area, and that risk persists for decades, often well after the child has forgotten the original injury. A history of significant blunt eye trauma in childhood therefore warrants periodic intraocular pressure monitoring well into adulthood, not only during the acute post-injury period.

Traumatic Optic Neuropathy

Traumatic optic neuropathy classically presents with vision loss and a relative afferent pupillary defect despite an initially normal-appearing fundus. The injury is to the nerve itself, typically from a shear or contusive force at the optic canal, not to any visibly damaged retinal structure. That combination, a normal fundus paired with an abnormal pupil, is what should raise suspicion for optic nerve injury rather than commotio retinae, traumatic hyphema, or angle recession glaucoma: none of those produce this exact pairing of findings.

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