A Game of Paintball Leads to a Potentially Devastating Eye Injury

Jessica Lee, MD; Ronald C. Gentile, MD


January 24, 2017

Case Diagnosis

The circumstance of the patient's injury and the findings seen on fundus exam in the right eye support a diagnosis of a choroidal rupture with Berlin edema. Choroidal ruptures, which result from blunt trauma and are typically seen in closed-globe injuries, are defined as a break in Bruch membrane involving both the underlying choroid and overlying retinal pigment epithelium layer. In the acute phase, they are associated with subretinal hemorrhages,[1] as was seen in this case. The patient also had commotio retinae, also known as Berlin edema, which is characterized by transient deep whitening of the retina believed to be related to extracellular edema and disruption of the photoreceptor outer segments.

Lacquer cracks can be seen in eyes that are highly myopic and are often observed bilaterally with other signs of myopia like a tilted disc and/or posterior staphylomas. Clinically, lacquer cracks appear as fine, yellow, single or multiple irregular lines in the posterior pole, which was not seen in this case. Although a retinal detachment appears lighter than an attached retina, the appearance of the peripheral whitening in this case was much more dramatic and typical of Berlin edema. In addition, the absence of outer hydration lines or subretinal fluid goes against a rhegmatogenous retinal detachment.

Angioid streaks are often in the differential of choroidal ruptures, as they also result from breaks in Bruch membrane. Angioid streaks are located deep to the retinal vessels and originate from the peripapillary area as dark red-to-brown bands. As opposed to this case's choroidal ruptures concentric to the optic disc, angioid streaks radiate out from the optic disc. Angioid streaks are usually bilateral and can be associated with medical conditions such as pseudoxanthoma elasticum, Ehlers-Danlos syndrome, Paget disease, and sickle cell disease. The retina of eyes with angioid streaks has a peau d'orange appearance, which is easily differentiated from the retinal whitening seen in our patient.

Acute retinal necrosis is caused by a reactivation of latent viral infection, most commonly from varicella zoster virus, followed by herpes simplex virus 1 and 2, and rarely cytomegalovirus. It manifests as acute unilateral panuveitis or retinal arteritis and can progress to diffuse necrotizing retinitis and retinal detachment.[2] Patients typically present with eye redness, periorbital pain, photophobia, and vision loss. In this patient, the areas of peripheral whitening were deep and not associated with periarteritis and prominent inflammation, going against the diagnosis of acute retinal necrosis. In addition, cystoid macular edema is not associated with subretinal hemorrhage, as was seen in this patient.

Clinical Course

The patient was initially treated with a topical antibiotic, corticosteroid, cycloplegic, and alpha adrenergic agonist. Once the corneal abrasion healed, the patient underwent an intravitreal injection of sulfur hexafluoride (SF6) gas and tissue plasminogen activator (tpA) to displace the subretinal hemorrhage from under the fovea.

Four weeks after the intravitreal injection, vision in the right eye improved to 20/40 with resolution of the submacular hemorrhage and better visibility of the choroidal rupture located temporal and inferior to the fovea (Figure 3).

Figure 3. Optical coherence tomography and corresponding infrared fundus image (top, horizontal; bottom, vertical) of the right eye 1 month after the injury.

Six months after the injury, visual acuity improved to 20/20 with persistence of a small scotoma. Despite the choroidal rupture being complicated by a choroidal neovascular membrane (Figure 4), treatment with intravitreal anti-vascular endothelial growth factor (VEGF) injections allowed the patient to maintain 20/20 vision.

Figure 4. Fluorescein angiography (late phase) of the right eye 1 year after the injury.


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