Ophthalmic Care of the Combat Casualty Chapter 11 Glaucoma

Glaucoma Associated With Ocular Trauma Chapter 11 GLAUCOMA ASSOCIATED WITH OCULAR TRAUMA NEIL T. CHOPLIN, MD* INTRODUCTION GLAUCOMA OCCURRING EARLY FOLLOWING OCULAR TRAUMA Inflammation Alterations in Lens Position Hyphema Phacoanaphylactic Glaucoma Increased Episcleral Venous Pressure Glaucoma Following Chemical Injuries Glaucoma Due to Trauma to Nonocular Structures GLAUCOMA OCCURRING LATE FOLLOWING OCULAR TRAUMA Steroid-Induced Glaucoma Secondary Angle Closure Ghost Cell (Hemolytic) Glaucoma Posttraumatic Angle Deformity (Angle Recession) Chemical Injuries Glaucoma Following Penetrating and Perforating Injuries Siderosis Bulbi TREATMENT SUMMARY *Captain, US Navy (Ret); Eye Care of San Diego, 3939 Third Avenue, San Diego, California 92103; Adjunct Clinical Professor of Surgery, Uniformed Services University of Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799; formerly, Chairman, Depart- ment of Ophthalmology, Naval Medical Center, San Diego, California 185 Ophthalmic Care of the Combat Casualty INTRODUCTION The definition of glaucoma has undergone con- the eye following trauma can result in significant siderable change in the last 20 years. As commonly elevations of IOP, it is presumed that optic nerve used today, glaucoma refers to a diverse group of damage will occur if the pressure remains high eye disorders characterized by progressive loss of enough long enough, even if the optic nerve is nor- axons from the optic nerve, resulting in loss of vi- mal at the time of presentation. sual function as manifested in the visual field.1 The Although glaucomatous optic neuropathy may structural changes in the optic nerve head are rec- take some time to develop, elevated IOP after ocu- ognizable, and the patterns of visual field damage lar trauma can occur immediately after the injury are characteristic but not specific. Glaucoma may or at any time in the future, even years later. Con- thus be considered to be an optic neuropathy. For ditions associated with elevated IOP at the time of purposes of this discussion, the term glaucoma is injury include the following: used to describe conditions resulting in high intraocular pressure (IOP); eventual optic neuropa- •alterations in outflow from inflammation thy is presumed to be the long-term result if the and inflammatory byproducts, elevated IOP is not adequately lowered. • hyphema with or without pupillary block, In the population without glaucoma, approxi- •subluxation of the lens, and mately 95% of people have IOPs between 11 and 21 •increased episcleral venous pressure. mm Hg. An IOP above 24 mm Hg is considered elevated. Although the exact etiology of glaucomatous Elevated IOP may also be a consequence of optic neuropathy is not known, many risk factors changes in ocular tissues due to chemical injuries have been identified, with elevated IOP considered or from damage to nonocular structures. Weeks, to be one of the most important. The risk of glau- months, or years following injury, IOP may become coma increases with the level of IOP, and the risk elevated due to chronic use of corticosteroids for of disease progression decreases as the pressure is control of inflammation, secondary angle closure, lowered. Nevertheless, not all patients with el- ghost cells, scar tissue formation, effects of retained evated IOP develop glaucoma, and not all pati- foreign bodies, or damage to the drainage structures ents with glaucoma have elevated IOP. In the con- (angle recession). For purposes of this discussion, text of ocular trauma, patients with glaucoma may early refers to the period from the time of injury present with optic neuropathy but almost assuredly through the first 2 weeks following injury, whereas will present with elevated IOP. Because changes in late refers to any time after the first 2 weeks. GLAUCOMA OCCURRING EARLY FOLLOWING OCULAR TRAUMA Inflammation struction. Blunt trauma can also cause direct damage to trabecular endothelial cells or to meshwork Inflammation of varying degrees invariably fol- extracellular components, resulting in elevated lows any injury to the eye. Although iritis and iri- IOP.3 docyclitis usually cause lower IOP because of de- creased aqueous formation, elevated IOP may Alterations in Lens Position occur through a variety of mechanisms.2 Leakage of proteins into the anterior chamber from the in- Blunt trauma may cause zonular disruption, re- creased vascular permeability that accompanies sulting in dislocation of the lens. Partial subluxation inflammation may result in elevated IOP through may allow prolapse of vitreous into the anterior the osmotic influx of water. Inflammatory cells and chamber. This process may, in itself, result in el- other particulate debris (eg, blood, fibrin, iris pig- evated IOP, probably by an osmotic mechanism. ment, lens material, vitreous) can mechanically Anterior movement of vitreous may also cause a block the outflow pathways. Figure 11-1 shows a pupillary block with secondary angle closure. Par- typical inflammatory reaction in the anterior cham- tial subluxation of the lens is illustrated in Figure ber with fibrin formation, which may lead to pu- 11-2. Complete dislocation of the lens into the ante- pillary block and secondary angle closure, or an rior chamber may result in pupillary block and open-angle glaucoma due to outflow pathway ob- angle closure as shown in Figure 11-3. 186 Glaucoma Associated With Ocular Trauma Fig. 11-3. This photograph shows subluxation of the lens into the anterior chamber, causing pupillary block and secondary angle closure glaucoma. Reproduced with permission from Liebmann JM, Ritch R, Greenfield DS. Fig. 11-1. Intraocular inflammation. Severe intraocular The angle-closure glaucomas. In: Choplin NT, Lundy DC, inflammation, as can occur following trauma, may re- eds. Atlas of Glaucoma. London, England: Martin Dunitz, sult in the formation of a fibrinous exudate, seen here. Ltd; 1998: Figure 10.6. Fibrin, inflammatory debris, and cells may obstruct the outflow pathways and cause elevated intraocular pressure. Reproduced with permission from Meyer J, Katz L. Hyphema Secondary open-angle glaucomas. In: Choplin NT, Lundy DC, eds. Atlas of Glaucoma. London, England: Martin Bleeding into the anterior chamber, or hyphema Dunitz, Ltd; 1998: Figure 9.14(a). (Figure 11-4), is discussed in detail in Chapter 8, Blunt Trauma and Nonpenetrating Injuries of the Anterior Segment. Blood in the anterior chamber may cause elevated IOP by mechanically blocking outflow channels. A total, or “eight-ball,” hyphema Fig. 11-2. Blunt trauma may rupture zonules and cause total or partial dislocation of the crystalline lens. This lens is partially dislocated inferiorly and temporally. Vit- Fig. 11-4. Hyphema. Blood in the anterior chamber from reous may come around the edge of the lens and cause a trauma may elevate intraocular pressure by blocking pupillary block or direct elevation of intraocular pres- outflow pathways or by causing pupillary block and sec- sure. Reproduced with permission from Meyer J, Katz L. ondary angle closure. Reproduced with permission from Secondary open-angle glaucomas. In: Choplin NT, Lundy American Academy of Ophthalmology. Ophthalmology DC, eds. Atlas of Glaucoma. London, England: Martin Study Guide. San Francisco, Calif: American Academy of Dunitz, Ltd; 1998: Figure 9.13. Ophthalmology; 1987: Figure 42. 187 Ophthalmic Care of the Combat Casualty a b Fig. 11-5. Ultrasound biomicroscope image of an eye following blunt trauma. (a) This image shows a subluxed lens (L) and broken zonules (arrows), disinserted from the ciliary body (C). The angle is closed (indicated with an aster- isk) due to pupillary block caused by the clotted blood and (b) anteriorly displaced vitreous (arrows). The iris (I) is pushed up against the cornea. Reproduced with permission from Berinstein DM, Gentile RC, Sidoti PA, et al. Ultra- sound biomicroscopy in anterior ocular trauma. Ophthalmic Surg Lasers. 1997;28:201–207. or an organized clot of sufficient size can cause the inflammatory response accompanying the in- pupillary block. Figure 11-54 is an ultrasound biomi- jury. Alkali can also cause direct damage to the out- croscope image from an eye with a subluxed lens flow pathways, leading to elevated IOP.5 However, with clotted blood and anterior movement of vitre- elevation of IOP may occur almost immediately fol- ous, resulting in pupillary block. The iris is apposed lowing the injury, due to scleral shrinkage and pros- to the trabecular meshwork, resulting in secondary angle closure. Phacoanaphylactic Glaucoma Lens protein is normally sequestered within the capsular bag from the time of embryonic develop- ment. If the lens is ruptured by trauma (usually penetrating trauma), the immune system reacts to the released lens protein with a granulomatous inflammatory response, often associated with elevated IOP. This phenomenon is illustrated in Fig- ure 11-6. Increased Episcleral Venous Pressure Orbital hemorrhage from trauma may result in proptosis and marked congestion within the orbit, Fig. 11-6. Phacoanaphylactic uveitis and glaucoma. The compressing the orbital veins and preventing drain- lens in this eye has been ruptured; cortical material has age from the outflow channels. The resulting in- been released into the anterior chamber, resulting in a crease in episcleral venous pressure may cause a massive inflammatory response. The inflammation, along significant rise in IOP. with the osmotic effect of the lens protein’s pulling water into the anterior chamber, may

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