In his blog, Doug Rett, OD, FAAO, digs deeper into questions every eye doctor has had at one point in his or her career. He sees patients and works with students and residents at the optometry clinic for the VA Boston Healthcare System and will use his blog to bring the teaching points he sees in clinic to a larger audience. Contact him at doctorrett@gmail.com.

Disclosure: Rett has no relevant financial disclosures.

BLOG: Why are choroidal ruptures always crescent-shaped?

Depending where you see patients, you might see a fair amount of ocular trauma.

As I work in a veteran’s hospital, I see a fair amount of ocular trauma that happened years or decades ago, and some of those old injuries bear the scars of choroidal rupture.

Choroidal ruptures are most often sequelae of trauma and are best described as crescent-shaped lesions in the posterior pole, concentric to the disc. But why this shape? Why are they parallel to the optic disc and not perpendicular? Or a random direction? And why are 82% of choroidal ruptures temporal to the disc (Patel et al.)? This month we’ll tackle the curiously-repetitive shape of choroidal ruptures.

Choroidal ruptures in the posterior pole are caused by contre-coup injuries or – less elegantly – caused by the compressive force of the globe’s contents as a wave of energy travels anterior to posterior. Contre-coup is undoubtedly a top-five best ocular descriptive term, so let’s unpack it here.

Unsurprisingly, it’s French in origin: “contre” meaning “against,” and “coup” meaning “blow” or “shot” (as in “coup de grâce” – a death blow). So choroidal ruptures in the posterior pole are technically described as indirect choroidal ruptures (ICRs), as they are contre-coup injuries. A patient can also have a direct choroidal rupture from the coup injury: the lesion in DCRs is located anteriorly at the site of impact and is parallel to the ora. But the majority of choroidal ruptures are ICRs in the posterior pole.

The characteristic shape of ICRs comes not from a vascular origin but from how the globe moves within the orbit. When an eye takes a blunt trauma – say, a punch – anteroposterior compressive forces propagate down, leading to the posterior displacement of the globe and extraocular muscles. But the crucial point to know is that the optic nerve remains relatively less disturbed in its anatomical position, held in place by the retrobulbar tissue. Essentially, during a punch, the optic nerve pushes back. However, as the nerve is inserted not in the most posterior pole of the globe but 15 degrees nasal to that pole, it pushes back obliquely. This creates a shear force, radiating concentrically from the nerve, and explains why ICRs are crescent-shaped and often temporal to disc – because that’s typically the direction the force vector is traveling relative to the nerve, and that temporal area receives the maximum stress.

But not all ICRs are temporal to the disc, and not all of them are directly through the fovea, the most posterior pole of the globe. The slight difference in the location of the ICRs is likely due to two factors: traumas/punches come in from slightly different angles, propagating compressive forces in different directions relative to the optic nerve location and the soon-to-be-victim often initiates a protective Bell’s phenomenon before impact, protecting the cornea but also changing the direction of the force vector.

So, the temporal ocular wall relative to the optic nerve receives the maximum pressure when a blow is received. But, as we know, the globe has many layers to it, so why does the retina and scleral not show any damage? The retina is elastic enough to rebound, and the sclera has enough tensile strength to resist injury, but Bruch’s membrane is breached because it’s inelastic and fragile and can’t withstand such a force.

Early after the injury, there is often a hemorrhage above and/or below the retinal pigment epithelium (RPE), followed by fibrovascular activity leading to a well-defined scar in the choroid, Bruch’s membrane and RPE. In fact, choroidal ruptures are actually tears of the choroid, Bruch’s membrane and RPE; the retina and sclera remain mostly undisturbed.

Choroidal ruptures greatly increase the risk of choroidal neovascularization membrane (CNVM) formation over the patient’s lifetime, and, perhaps not surprisingly, longer ruptures have a higher risk of CNVM. Ruptures between 1.10 mm and 2.35 mm have an 11% chance of CNVM; ruptures greater than 2.35 mm have a 50% chance (Eliott et al.).

So, the next time you see a crescent-shaped arc in the posterior pole, think about those contre-coup forces that created that shear stress on the globe. And follow that patient closer as you monitor for CNVM. Bonne chance.

References:

Eliott D, Papakostas TD. Traumatic chorioretinopathies. In Ryan’s Retina. 6th ed. Elsevier:2017.

Nair U. Clinical Ophthalmology. 2013;doi:10.2147/OPTH.S46223.

Patel MM, et al. Int Ophthalmol Clin. 2013;doi:10.1097/IIO.0b013e31829ced74.

Pujari A, et al. Medical Hypotheses. 2019;doi:10.1016/j.mehy.2019.02.010.