Choroidal Rupture

A break in the choroid, Bruch membrane and retinal pigment epithelium after blunt injury, caused by globe compression and expansion. The retina typically remains intact, and the sclera (elastic) does not tear.

• Types:
  • Direct rupture: located anteriorly near the ora serrata, parallel to it, at the site of impact; often missed.
  • Indirect rupture: posterior pole, crescent shaped, concentric to the optic disc, usually on the temporal side, due to contre coup; more frequently affects the macula.
• Present in about 5 to 10 percent of blunt eye injuries (and in up to 25 percent of severe injuries).
• Bilateral in about 10 percent. Often accompanies subretinal and vitreous haemorrhage that obscures the rupture in the first days.
• Complications: choroidal neovascularisation (5 to 30 percent, months to years later), submacular haemorrhage, macular scar, fibrous proliferation, retinal detachment.

• Variable visual loss (moderate to severe if the macula is involved); vision may be normal in peripheral ruptures.
• Initial haemorrhage hides the lesion; after clearing (2 to 6 weeks), a yellow white crescentic or curvilinear subretinal streak with pigmented margins, often multiple, and sometimes with underlying bare sclera.
• Central scotoma and metamorphopsia (macular rupture or choroidal neovascularisation).
• Late: pigment migration, retinal pigment epithelium atrophy, and fibrovascular scar.

• Dilated fundus examination with scleral depression once the media clear.
• Optical coherence tomography: break in the retinal pigment epithelium and Bruch membrane complex, subretinal fluid or choroidal neovascular membrane.
• Fluorescein angiography (hyperfluorescence from window defect and late staining; leakage in active neovascularisation) and indocyanine green angiography (best for rupture outline); optical coherence tomography angiography to detect neovascularisation.
• Amsler grid, visual acuity and field tests; B-scan ultrasound to exclude retinal detachment if vitreous haemorrhage prevents a view.
• Surveillance for neovascularisation: Amsler grid weekly at home, clinic review at 1 to 2 weeks, 4 to 6 weeks, 3 months, 6 months, 12 months, then yearly for at least 2 years.

• Observation of uncomplicated ruptures; vision recovers as haemorrhage resolves, if the fovea is spared. No treatment prevents the rupture.
• Choroidal neovascularisation (suspected from new metamorphopsia, haemorrhage or fluid on optical coherence tomography): intravitreal anti-vascular endothelial growth factor therapy: ranibizumab 0.5 mg, bevacizumab 1.25 mg, or aflibercept 2 mg monthly for 3 doses, then as needed according to optical coherence tomography activity (young patients usually need only a few injections and often have a good outcome).
• Alternative or adjunct: photodynamic therapy with verteporfin (6 mg/m2 IV over 10 minutes, laser at 15 minutes), thermal laser for extrafoveal membranes, and surgical excision in refractory cases.
• Submacular haemorrhage threatening the fovea: intravitreal tissue plasminogen activator (25 to 50 micrograms in 0.1 mL) with expansile gas (sulphur hexafluoride 20 percent or perfluoropropane 14 percent) and prone or face down positioning, or subretinal tPA with vitrectomy.
• Vitreous haemorrhage: observation, head elevation; vitrectomy if no clearing in 4 to 6 weeks.
• Counselling on visual prognosis, protective eyewear, regular self-testing and prompt reporting of symptoms.