Pathologically Apparent Sequelae of Ocular Trauma
Ocular trauma can lead to a variety of pathologically apparent sequelae involving different parts of the eye, depending on the nature of the trauma. Rupture of Descemet membrane may occur after minor trauma (eg, in keratoconus; Fig 4-4) or major trauma (eg, forceps delivery; Fig 4-5).
The anterior chamber angle structures, especially the trabecular beams, are vulnerable when the anterior segment is distorted during trauma. Traumatic recession of the anterior chamber angle occurs when there is a tear in the anterior ciliary body between the longitudinal fibers and the circular fibers of the ciliary muscle with posterior displacement of the iris root (Fig 4-6). Concurrent damage to the trabecular meshwork with subsequent fibrosis may lead to glaucoma.
Iridodialysis is a tear in the iris at the thinnest portion of the diaphragm, the iris root, where it inserts into the supportive tissue of the ciliary body (Fig 4-7). Only a small amount of supporting tissue surrounds the iris sphincter. If the sphincter muscle is torn, contraction of the remaining muscle will create a notch at the pupillary border.
Cyclodialysis results from disinsertion of the longitudinal ciliary muscle fibers from the scleral spur (Fig 4-8). This condition can lead to hypotony because the aqueous humor of the anterior chamber now has free access to the suprachoroidal space, resulting in increased outflow; in addition, because the blood supply to the ciliary body is reduced, the production of aqueous humor is decreased.
The uveal tract is attached to the sclera at 3 points: the scleral spur, the internal ostia of the vortex veins, and in the peripapillary region. This anatomical arrangement is the basis of the evisceration technique and explains the vulnerability of the eye to expulsive choroidal hemorrhage. The borders of a dome-shaped suprachoroidal hemorrhage are delimited by the position of the vortex veins and the scleral spur (Fig 4-9).
A Vossius ring appears when iris pigment epithelial cells are compressed against the anterior surface of the lens, depositing a ring of melanin pigment concentric with the pupil.
If the lens capsule is disrupted, a cataract may form immediately. The capsule is thinnest at the posterior pole, the point farthest from the lens epithelial cells. The epithelium of the lens may be stimulated by trauma to form an anterior fibrous plaque just inside the capsule. The lens zonular fibers are points of relative weakness; if they rupture, lens displacement occurs, either partial (subluxation) or complete (luxation). Focal areas of zonular rupture may allow formed vitreous to enter the anterior chamber.
Commotio retinae (Berlin edema) often complicates blunt trauma to the eye. Although it is most prominent in the macula, commotio retinae can affect any portion of the retina. The retinal opacification seen clinically results from disruption in the architecture of the photoreceptor outer segments and the RPE, which can be seen with optical coherence tomography (OCT) or on histologic examination.
Retinal dialysis is most likely to develop in the inferotemporal or superonasal quadrant. The retina is anchored anteriorly to the nonpigmented epithelium of the ciliary pars plana. This union is reinforced by the attachment of the vitreous base, which straddles the ora serrata. Deformation of the eye can result in a circumferential retinal tear at the point of attachment of the ora serrata or immediately posterior to the point of attachment of the vitreous base (Fig 4-10). The interface between necrotic and normal neurosensory retina is also vulnerable to retinal tears.
After a penetrating injury, intraocular fibrous or fibrovascular proliferation may occur. This proliferation may lead to vitreous, subretinal, and/or choroidal hemorrhage; tractional retinal detachment; proliferative vitreoretinopathy (PVR), including anterior PVR (Fig 4-11); hypotony; and phthisis bulbi (discussed in Chapter 1). Formation of proliferative intraocular membranes may affect the timing of vitreoretinal surgery. Sequelae of intraocular hemorrhage include hemosiderosis bulbi secondary to iron deposition from breakdown of red blood cells, and cholesterolosis, also from red blood cell breakdown.
Rupture of Bruch membrane or a choroidal rupture may occur after direct or indirect injury to the globe. Choroidal neovascularization, granulation tissue proliferation, and scar formation may occur in areas where the choroid has ruptured or where there are disruptions in the Bruch membrane. A subset of direct choroidal ruptures, usually those occurring after a projectile injury, may result in focal posttraumatic choroidal granulomatous inflammation (Fig 4-12). This inflammation may be related to foreign material introduced into the choroid. A chorioretinal rupture and necrosis is known as chorioretinitis sclopetaria.
Excerpted from BCSC 2020-2021 series: Section 4 - Ophthalmic Pathology and Intraocular Tumors. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.