Choroidal rupture is a condition in which the choriocapillaris, Bruch’s membrane, and retinal pigment epithelium (RPE) are torn due to non-penetrating (closed) blunt trauma to the eye. The sclera withstands the tensile strength, but the less elastic Bruch’s membrane breaks, causing the rupture.
In a retrospective study of 101 patients, the average age was 36 years, and 76% were male. Closed eye injuries are three times more common than open injuries.
The main mechanisms of injury are as follows:
The distribution of rupture sites is reported as: fovea 30%, extrafoveal macula 45%, extramacular 25%.
It is usually caused by blunt ocular trauma. However, in systemic diseases that increase the fragility of Bruch’s membrane (such as pseudoxanthoma elasticum, Ehlers-Danlos syndrome, angioid streaks, etc.), rupture can occur even with minor trauma.
For several days to weeks after injury, the rupture line is often hidden by hemorrhage, making it difficult to confirm on fundus examination. Clear findings are obtained only after the hemorrhage is absorbed.
Yes. Immediately after injury, choroidal hemorrhage and subretinal hemorrhage often cover the rupture line, making it difficult to confirm on fundus examination. After several days to weeks, as the hemorrhage is absorbed, it can be seen as a white to yellowish-white streak.
Immediately after injury, the rupture line is hidden by hemorrhage. After hemorrhage absorption, the following characteristic findings appear.
The following associated findings may be observed.
OCT reveals a break in the inner choroidal layers including Bruch’s membrane and loss of RPE continuity. The neurosensory retina overlying the rupture site is often preserved.
The cause of choroidal rupture is almost always non-penetrating blunt ocular trauma. The following systemic diseases increase the fragility of Bruch’s membrane, making rupture more likely even with minor trauma.
Caution is needed for Bruch’s membrane fragility in the following diseases:
| Disease name | Characteristic fundus findings |
|---|---|
| Pseudoxanthoma elasticum | Angioid streaks / subretinal yellow spots |
| Ehlers-Danlos syndrome | Connective tissue fragility, angioid streaks |
| Angioid streaks of the retina | Radial dark red streaks from the optic disc |
Wearing polycarbonate protective glasses (sports eye guards) is effective. Polycarbonate has higher impact resistance than regular plastic lenses and prevents direct eye trauma.
Diagnosis is based on a combination of history of ocular trauma and characteristic fundus findings. Immediately after injury, examination may be difficult due to bleeding, so re-examination after the bleeding is absorbed is important.
The characteristics of each examination are shown below.
| Examination method | Main findings | Purpose |
|---|---|---|
| FA (fluorescein angiography) | Early hypofluorescence → late staining | CNV detection |
| OCT | Loss of RPE continuity | Rupture confirmation and size assessment |
| Fundus autofluorescence (FAF) | Hypofluorescence (RPE defect) + marginal hyperfluorescence | Size assessment |
Differentiation from the following diseases is important.
There is no drug therapy or surgical procedure to heal choroidal rupture itself. The basic approach is observation, waiting for spontaneous absorption of choroidal hemorrhage (weeks to months).
Choroidal neovascularization (CNV) occurs in about 5-10% of choroidal rupture cases after blunt trauma. Older age, rupture involving the fovea, and long rupture length (especially ≥4000 μm) are reported as independent risk factors. The average time from injury to CNV diagnosis is about 5.7 months, and most cases develop within 1 year. Traumatic CNV typically occurs as type 2 and may be accompanied by serous or hemorrhagic pigment epithelial detachment. When CNV is confirmed, the following treatments are performed.
Anti-VEGF Injection
First-line treatment: Intravitreal injection of anti-VEGF agents is the first-line treatment for traumatic CNV.
Fewer injections: It tends to be controlled with fewer injections (average 4.2) than age-related macular degeneration.
Agents: Ranibizumab, aflibercept, bevacizumab, etc. are used.
Other Treatments
Laser photocoagulation: Indicated for choroidal neovascularization in the macula located more than 200 μm from the fovea. It is difficult to perform when close to the fovea.
Photodynamic therapy (PDT): Reported as an adjunct to anti-VEGF therapy.
Observation only: If the CNV is small and distant from the fovea, observation may be an option.
Intravitreal injection of anti-VEGF drugs is the first choice, and traumatic CNV tends to be controlled with fewer injections (average 4.2 injections) compared to age-related macular degeneration. However, if the fovea is already damaged, complete recovery of vision may be difficult.
When the eye is compressed from the front, the tissue around the firmly fixed optic disc is pushed backward, creating circular stress centered on the disc. The choroid has relatively poor extensibility, and this mechanical action often causes circumferential rupture in the posterior pole, especially around the optic disc. The reactions of each tissue are as follows:
Direct Rupture
Location: The fundus around the site of direct impact (mainly temporal side).
Morphology: Linear fissure parallel to the ora serrata.
Frequency: Less common than indirect rupture.
Indirect Rupture
Location: Occurs at the posterior pole due to countercoup effect, opposite the impact site.
Morphology: Arcuate to crescent-shaped striae concentric with the optic disc.
Frequency: More commonly observed.
Histopathologically, disruption of the choriocapillaris, RPE, and Bruch’s membrane is observed. The overlying neurosensory retina is often preserved.
Secondary changes include the following:
