producing fibrous plaques intermixed with basement membrane.

Retina

The retina is made of terminally differentiated cells that typically do not regenerate when injured. Glial cells (Müller cells and fibrous astrocytes) proliferate in response to retinal trauma. Surgical techniques to close openings in the peripheral retina are successful when the neurosensory retina and retinal pigment epithelium (RPE) are destroyed (eg, cryotherapy, photocoagulation) and the surrounding tissues form an adhesive, atrophic scar.

Retinal scars are produced by glia rather than fibroblasts. After inflammatory cells have cleared away the debris, the tissues most damaged by the therapeutic modality remain as a thin, atrophic area in the center of the scar. Increasing numbers of residual viable cells encircle the zone of greatest destruction. Adhesion between the residual neurosensory retina and Bruch membrane develops according to the size of the original wound and the type of injury. The internal limiting membrane and the Bruch membrane provide the architectural planes for glial scarring. Adhesions from the internal limiting membrane to the Bruch membrane may incorporate a rare residual glial cell, and variable numbers of retinal cells and RPE may be present between the membranes. If the wound has damaged the Bruch membrane, choroidal fibroblasts and vessels may participate in the formation of the final scar. The end result is a metaplastic collagenous plaque in the sub–neurosensory retina and sub-RPE areas. The RPE usually proliferates rather exuberantly in such scars, giving rise to the dense black clumps seen clinically in scars of the fundus.

Vitreous

The vitreous has few cells and no blood vessels. Nonetheless, in conditions that cause vitreal inflammation, mediators stimulate the formation of membranes composed of new vessels and the proliferation of glial and fibrous tissue. With contraction of these membranes, the retina becomes distorted and detached.

Eyelid, Orbit, and Lacrimal Tissues

The rich blood supply of the skin of the eyelids supports rapid healing. On about the third day after injury to the skin, myofibroblasts derived from vascular pericytes migrate around the wound and actively contract, resulting in a volumetric decrease in the size of the wound. The eyelid and orbit are compartmentalized by intertwining fascial membranes enclosing muscular, tendinous, fatty, lacrimal, and ocular tissues that are distorted by scarring. Exuberant contracting distorts muscle action, producing dysfunctional scars. The striated muscles of the orbicularis oculi and extraocular muscles are made of terminally differentiated cells that do not regenerate, but the viable cells may hypertrophy.

Histologic Sequelae of Ocular Trauma

Rupture of the Descemet membrane may occur after minor trauma (eg, in keratoconus; Fig 2-3) or major trauma (eg, after forceps injury; Fig 2-4).

The anterior chamber angle structures, especially the trabecular beams, are vulnerable to distortion of the anterior globe. Cyclodialysis results from disinsertion of the longitudinal muscle of

the ciliary body from the scleral spur (Fig 2-5). This condition can lead to hypotony because the aqueous of the anterior chamber now has free access to the suprachoroidal space; and because the blood supply to the ciliary body is diminished, the production of aqueous is decreased.

Traumatic recession of the anterior chamber angle is due to a tear in the ciliary body between the longitudinal and circular muscles with posterior displacement of the iris root (Fig 2-6). Concurrent damage to the trabecular meshwork may lead to glaucoma.

The uveal tract is attached to the sclera at 3 points: the scleral spur, the internal ostia of the vortex veins, and the peripapillary tissue. This anatomical arrangement is the basis of the evisceration technique and explains the vulnerability of the eye to expulsive choroidal hemorrhage. The borders of the dome-shaped choroidal hemorrhage are defined by the position of the vortex veins and the scleral spur (Fig 2-7).

Figure 2-3 A break in the Descemet membrane in keratoconus shows anterior curling of Descemet membrane toward the

corneal stroma (arrow). (Courtesy of Hans E. Grossniklaus, MD.)

Figure 2-4 A break in the Descemet membrane as a result of forceps injury shows anterior curling of the original membrane (arrow) and production of a secondary thickened membrane.

Figure 2-5 Cyclodialysis (arrow) shows disinsertion of ciliary body muscle (asterisk) from the scleral spur (arrowhead).

(Courtesy of Hans E. Grossniklaus, MD.)

Figure 2-6 Angle recession shows a rupture in the ciliary body in the plane between the external longitudinal muscle fibers and the internal circular and oblique fibers (arrow); the iris root is displaced posteriorly (arrowhead). Note the scleral spur

(asterisk).

An iridodialysis is a rupture of the iris at the thinnest portion of the diaphragm, the iris base, where it inserts into the supportive tissue of the ciliary body (Fig 2-8). Only a small amount of supporting tissue surrounds the iris sphincter. If the sphincter muscle is ruptured, contraction of the remaining muscle will create a notch at the pupillary border. The iris diaphragm may be lost completely through a relatively small limbal rupture associated with 360° iridodialysis.

Figure 2-7 A, This eye developed an expulsive hemorrhage after a corneal perforation. B, The intraocular choroidal hemorrhage is dome shaped (arrowheads), delineated anteriorly by the insertion of the choroid at the scleral spur (arrow).

(Courtesy of Hans E. Grossniklaus, MD.)

Figure 2-8 A, Clinical photograph showing iridodialysis with a tear in the base of the iris. B, Gross photograph showing

posterior view of iridodialysis (arrows). (Part A courtesy of Hans E. Grossniklaus, MD.)

A Vossius ring appears when compression and rupture of iris pigment epithelial cells against the anterior surface of the lens occur, depositing a ring of melanin pigment concentric to the pupil.

A cataract may form immediately if the lens capsule is ruptured. The lens capsule is thinnest at the posterior pole, a point farthest away from the lens epithelial cells. The epithelium of the lens may be stimulated by trauma to form an anterior lenticular fibrous plaque. The lens zonular fibers are points of relative weakness; if they are ruptured, displacement of the lens can be 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. Most prominent in the macula, commotio retinae can affect any portion of the retina. Originally, the retinal opacification seen clinically was thought to result from retinal edema (extracellular accumulation of fluid), but experimental evidence shows that a disruption in the architecture of the photoreceptor elements causes the loss of retinal transparency.

Retinal dialysis is most likely to develop in the inferotemporal or superonasal quadrant. The retina is anchored anteriorly to the nonpigmented epithelium of the 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 or immediately posterior to the point of attachment of the vitreous base. Vitreoretinal traction may cause tears in a retina weakened by necrosis.

Intraocular fibrocellular proliferation may occur after a penetrating injury. Such proliferation may lead to vitreous/subretinal/choroidal hemorrhage; traction retinal detachment; proliferative vitreoretinopathy (PVR), including anterior PVR (Fig 2-9); hypotony; and ultimately phthisis bulbi. Formation of proliferative intraocular membranes may affect the timing of vitreoretinal surgery. The timing of the drainage of a ciliochoroidal hemorrhage is based on lysis of the blood clot (10–14 days). Hemosiderin forms at approximately 72 hours after hemorrhage. Sequelae of intraocular hemorrhage include siderosis bulbi, cholesterosis, and hemoglobin spherulosis.

Figure 2-9 Anterior proliferative vitreoretinopathy (PVR). A, Traction of the vitreous base on the peripheral retina (arrow) and ciliary body epithelium (asterisks). B, Incorporation of peripheral retinal (arrow) and ciliary body tissue (arrowheads) into the vitreous base. C, Condensed vitreous base (asterisk), adherent retina (arrow), and RPE hyperplasia (arrowhead). (Courtesy of

Hans E. Grossniklaus, MD.)

Figure 2-10 Focal posttraumatic choroidal granulomatous inflammation. A, Enucleated eye with a projectile causing a perforating limbal injury that extends to the posterior choroid. B, Microscopic examination shows a focus of choroidal

granulomatous inflammation (between arrowheads). (Courtesy of Hans E. Grossniklaus, MD.)

Rupture of the Bruch membrane or choroidal rupture may occur after direct or indirect injury to the globe. Choroidal neovascularization, granulation tissue proliferation, and scar formation may occur in an area of choroidal rupture. A subset of direct choroidal ruptures, those usually occurring after a projectile injury, may result in focal posttraumatic choroidal granulomatous inflammation (Fig 2-10). This may be related to foreign material introduced into the choroid. A chorioretinal rupture and necrosis is known as sclopetaria.

Phthisis bulbi is defined as atrophy, shrinkage, and disorganization of the eye and intraocular contents. Not all eyes rendered sightless by trauma become phthisical. If the nutritional status of the eye and near-normal intraocular pressure (IOP) are maintained during the repair process, the globe will remain clinically stable. However, blind eyes are at high risk of repeated trauma with cumulative destructive effects. Slow, progressive functional decompensation may also prevail. Many blind eyes pass through several stages of atrophy and disorganization into the end stage of phthisis bulbi:

Atrophia bulbi without shrinkage. Initially, the size and shape of the eye are maintained. The atrophic eye often has elevated IOP. The following structures are most sensitive to loss of nutrition: the lens, which becomes cataractous; the retina, which atrophies and becomes separated from the RPE by serous fluid accumulation; and the aqueous outflow tract, where anterior and posterior synechiae develop.

Atrophia bulbi with shrinkage. The eye becomes soft because of ciliary body dysfunction and progressive diminution of IOP. The globe becomes smaller and assumes a squared-off configuration as a result of the influence of the 4 rectus muscles. The anterior chamber collapses. Associated corneal endothelial cell damage results initially in corneal edema followed by opacification from degenerative pannus, stromal scarring, and vascularization. Most of the remaining internal structures of the eye will be atrophic but recognizable histologically.

Phthisis bulbi (Fig 2-11). The size of the globe shrinks from a normal average diameter of 24– 26 mm to an average diameter of 16–19 mm. Most of the ocular contents become disorganized.

In areas of preserved uvea, the RPE proliferates and drusen may be seen. Extensive calcification of the Bowman layer, lens, retina, and drusen usually occurs. Osseous metaplasia of the RPE with bone formation may be a prominent feature. The sclera becomes massively thickened, particularly posteriorly.

Figure 2-11 Phthisis bulbi. A, Gross photograph showing globe with irregular contour, cataractous lens with calcification (asterisk), cyclitic membrane with adherent retina (arrowheads), organized ciliochoroidal effusion (open arrows), and bone formation (between green arrows). B, Photomicrograph demonstrating histopathologic correlation with gross photograph in A.