Trauma And Glaucoma

12.3.1 Hyphema. Elevated IOP associated with hyphema usually responds favorably to aqueous suppressants. CAIs may also be added to the treatment regimen. However, caution is warranted with systemic acetazolamide in patients with sickle cell hemoglobinopathy (or sickle trait), because the drug increases the concentration of ascorbic acid in the aqueous, which leads to more sickling in the anterior chamber.53 Systemic acetazolamide also causes systemic acidosis, which may exacerbate eryth-rocyte sickling. Methazolamide may be safer because it causes less systemic acidosis than does acetazolamide.

Surgical intervention is warranted when IOP cannot be controlled medically and threatens to cause glaucomatous damage or if corneal blood staining develops. Unfortunately, the optic disk usually cannot be visually assessed, and many patients will manifest afferent pupillary defects caused by the presence of the blood itself, rather than by the optic nerve injury. Consequently, intervention may need to be undertaken based on somewhat arbitrary criteria. Although a healthy optic nerve may be able to tolerate IOP of 40 to 50 mm Hg for 1 week or longer, a glaucomatous disk may suffer further damage with substantially lower IOP within a shorter time period. Evaluation of the fellow eye for evidence of preexisting glaucomatous optic neuropathy may thus be helpful with regard to guiding therapy.

12.3.2 Angle-Recession Glaucoma. Angle-recession glaucoma usually develops years or even decades after blunt trauma with hyphema. In one series, the mean duration between injury and diagnosis of elevated IOP was 16 years.54 In another, the time between injury and the diagnosis of glaucoma averaged 7.6 ± 9.5 years.55 Late glaucoma is more common if the recession involves 180° or more of the angle. Patients with angle recession who develop glaucoma probably have a predisposition to it. The fellow eyes of patients with unilateral angle-recession glaucoma are more likely to have abnormalities of aqueous dynamics or open-angle glaucoma.

Medical therapy for angle-recession glaucoma is identical to that for idiopathic open-angle glaucoma. Pilocarpine may have little effect or a paradoxical effect on IOP. The response to medical treatment is worse, as is the response to argon laser trabeculoplasty.

12.3.3 Inflammation. Ocular inflammation is a common complication of blunt injury. In one series of 496 consecutive uveitis patients, the inflammation in 24 (4.8%) of the patients was attributed to nonpenetrating trauma.56 Trauma-induced inflammation may compromise outflow and elevate IOP by several mechanisms, including the following:

1. Obstruction of outflow pathways with inflammatory cells, debris, protein, or other serum components that are liberated because of vascular incompetence

2. Inflammation-induced swelling of the trabecular meshwork that impairs outflow

3. Inflammatory damage to trabecular endothelial cells

4. Sclerosis of the trabecular meshwork as a result of chronic inflammation

5. Obstruction of the trabecular meshwork by a hyaline membrane

Treatment with topical corticosteroids and glaucoma medications frequently affords resolution of the intraocular inflammation and IOP reduction.

Inflammation is a common complication of penetrating injury and may be associated with posterior synechiae formation, pupillary block, iris bombe, and angle-closure glaucoma. Glaucoma may result from trabecular obstruction, with inflammatory cells and debris. If there is chronic inflammation in the fellow eye, sympathetic ophthalmia should be suspected.

12.3.4 Foreign Bodies. Whenever possible, foreign bodies should be removed to prevent the complications described above. Once glaucoma is present, a foreign body may be so encapsulated that standard extraction techniques may be problematic. Furthermore, the visual prognosis may already be limited by extensive retinal damage. Corticosteroids to avoid cyclitic membranes and scarring of the meshwork are also of primary importance during the early postinjury period. Antibiotics are required for endophthalmitis prophylaxis. Elevated IOP may be treated with aqueous suppressants. When medical therapy is insufficient, filtering surgery may be appropriate.

12.3.5 Chemical Burns. Management of elevated IOP in the early phase of a chemical burn is limited to aqueous suppressants. However, because re-epithelialization of the ocular surface may be impaired by topical medications, systemic medications may be preferred. Miotics are relatively contraindicated, because they may aggravate anterior segment inflammation, as well as contribute to the formation of posterior synechiae that may eventuate in pupillary block. Corticosteroids may be helpful with respect to minimizing anterior segment inflammation, but concern regarding the increased risk of corneal stromal melting may favor systemic administration.

0 0

Post a comment