Choroidal ruptures are breaks in the choroid, the Bruch membrane, and the retinal pigment epithelium (RPE), and are the result of blunt ocular trauma.
Traumatic choroidal rupture in children can occur in all ages following blunt injury.
Choroidal rupture may occur at the time of delivery, particularly when forceps are used.
• Blunt ocular trauma is the most common type of eye injury. Approximately 5–10% of these patients develop a choroidal rupture.
• Most eyes have a single rupture, but up to 25% of eyes have multiple ruptures.
• About 80% of ruptures occur temporal to the disc, and 66% involve the macula.
Rare (approximately 1/10,000), except in patients with a history of ocular trauma.
• Ocular trauma
• More common in eyes with angioid streaks following minor ocular trauma
Currently, no genes have been mapped indicating a predilection for eyes sustaining choroidal ruptures.
• Protective eyewear (e.g., polycarbonate lenses) during any contact sports and activities exposing eyes to possible trauma
• When Bruch’s membrane is abnormal, minor trauma can result in extensive choroidal rupture.
• High-risk patients should be advised of the hazards associated with blunt ocular trauma related to contact sports and other activities.
• After blunt trauma, the eye undergoes mechanical compression and then sudden expansion. Because of its tensile strength, the sclera can resist this insult; the retina is also protected because of its elasticity. The Bruch membrane does not have enough elasticity or tensile strength; therefore, it breaks.
• Concurrently, the small capillaries in the choriocapillaris are damaged, leading to subretinal or sub-RPE hemorrhage. The larger choroidal vessels are usually spared. Hemorrhage along with retinal edema may obscure the choroidal rupture during the acute phases. As the blood clears, a white, curvilinear, crescent-shaped streak concentric to the optic nerve is seen.
• Classified as:
– Direct, occurring at the site of impact, most commonly anterior and parallel to the limbus; or
– Indirect, occurring away from the site of impact, usually in the posterior pole concentric to the optic disc or through the fovea
Choroidal rupture occurs most commonly as a result of trauma, usually in young males.
COMMONLY ASSOCIATED CONDITIONS
Choroidal neovascularization (CNV) may occur. (1)[B]
• Choroidal ruptures typically present after an episode of blunt trauma to the globe
• Also commonly associated with patients having a history of previous angioid streaks
• Patients complain of new onset decreased vision and/or a paracentral or central scotoma
• A thorough search for other signs of trauma to the, head, orbit, ocular adnexa, and eye (2)
• Ophthalmologic findings may include:
– Subretinal hemorrhage, which may obscure rupture of Bruch’s membrane
– White subretinal streak(s) concentric to the optic nerve in areas of previous subretinal hemorrhage.
– The nerve fiber layer usually intact
– Chorioretinal membranes
– Macular hole, retinal tears, retinal dialysis, and retinal detachment may occur
DIAGNOSTIC TESTS & INTERPRETATION
None generally necessary as it is a clinical diagnosis.
• Fluorescein angiography (FA) often is helpful in confirming the presence, location, and extent of choroidal ruptures.
– FA demonstrates a hypofluorescent curvilinear streak early followed by hyperfluorescence in the late phase.
• Indocyanine green angiography (IGGA) is useful in localizing ruptures obscured by hemorrhage.
• CT scan of the head to assess possibility of intraocular foreign body, ruptured globe or other head injury not previously detected
• B scan of globe and orbit
Follow-up & special considerations
Serial examinations may be necessary to establish a diagnosis of choroidal rupture
• Chorioretinal scars – may be related to old infectious process such as toxoplasmosis or histoplasmosis
• Angioid Streaks – red or brown irregular lesions that radiate from the optic nerve
• Exudative Age-Related Macular Degeneration (ARMD)
• Valsalva retinopathy
• There is no treatment for choroidal ruptures, but a careful examination is important to exclude other ocular injuries associated with blunt ocular trauma, such as commotio retinae, retinal dialysis, hyphema, angle recession, and traumatic iritis.
• Inflammation of the anterior segment can be treated with topical steroids and cycloplegics.
• CNV is a common sequelae of choroidal ruptures. CNV may be treated as needed, with anti-VEGF therapy showing the most promise. (3)
Issues for Referral
Vitreoretinal specialists should be consulted in instances of suspected choroidal rupture.
• If CNV is extrafoveal, it may be treated with laser photocoagulation. Recurrences are rare.
• Prior to anti-VEGF therapy, pars plana vitrectomy with membrane extraction was considered for subfoveal or juxtafoveal CNV.
Patients will need close monitoring until the disease is brought under control. Patients may need follow-up with other specialists.
Patients should be followed closely.
Teach patients to monitor each eye using an Amsler grid and a near card.
• A prognostic indicator of the patient’s eventual vision is the location of the rupture in relation to the fovea. In patients with:
– Subfoveal rupture, the vision tends to remain poor
– Extrafoveal rupture, the vision may remain excellent until and unless CNV develops
– Contusion maculopathy, the visual potential is limited
• Most do not reach a final visual acuity of 20/40 or better
• If rupture does not involve the fovea, good vision is expected.
• CNV is the most common late complication of choroidal ruptures.
• Retinal detachment is occasionally found in anterior choroidal ruptures.
• A variety of visual field defects have been observed.
1. Ament CS, Zacks DN, Lane AM, et al. Predictors of visual outcome and choroidal neovascular membrane formation after traumatic choroidal rupture. Arch Ophthalmol 2006;124(7):957–66. (B)
2. Dubinski W, Sharma S. Choroidal rupture. Can Fam Phys 2006;52:1071–1079. (C)
3. Liang F, Puche N, Soubrane G, et al. Intravitreal ranibizumab for choroidal neovascularization related to traumatic Bruch’s membrane rupture. Graefes Arch Clin Exp Ophthalmol 2009;247(9):1285–8. (C)