Glaucoma Following Trauma
Scott J. Fudemberg
Jonathan S. Myers
L. Jay Katz
George L. Spaeth
Following trauma, intraocular pressure (IOP) may become elevated for many reasons (Table 54C.1). A common mechanism for elevated IOP is obstruction of, or damage to, the trabecular meshwork, leading to reduced aqueous outflow. Glaucoma may follow blunt or penetrating trauma to the eye and orbit, chemical exposures, and trauma to nonocular structures. Glaucoma may develop immediately or soon after the trauma or may only manifest itself years or decades later.
Table 54C.1. Mechanisms of Glaucoma Following Trauma | ||
|---|---|---|
|
Early Posttraumatic Glaucoma
Immediately following blunt and penetrating trauma, IOP may be elevated or reduced. According to the United States Eye Injury Registry, in the first 6 months following an ocular contusion injury, the risk of developing glaucoma is 3.4%.1 Risk factors for developing glaucoma during the early postcontusion period include increasing age, baseline visual acuity worse than 20/200, angle recession, hyphema, and lens injury.1 Corneal and vitreal injuries have also been found to be significant predictors of development of early glaucoma.2 Reduced IOP may result from aqueous hyposecretion secondary to the effects of inflammation and prostaglandins on the ciliary body, increased outflow through a cyclodialysis cleft, retinal detachment, or a penetrating injury to the globe. Careful clinical examination is crucial following any significant trauma to exclude retinal detachment or an occult rupture to the globe. The presence of elevated IOP does not exclude the possibility of a penetrating injury. Penetrating trauma may lead to a suprachoroidal hemorrhage or aqueous misdirection, with a flat anterior chamber and high IOP. Moreover, various tissues may block the site of penetrating trauma yielding IOP in the normal range. Glaucoma develops in more than 2.67% of penetrating ocular injuries with independent risk factors for subsequent glaucoma including increasing age, baseline visual acuity worse than 20/200, and anterior chamber inflammation independently associated.3 The ultimate need for surgical management of traumatic glaucoma is independently associated with hyphema, corneal injury, optic atrophy, visual acuity worse than 20/200, and penetrating ocular injury.4
Blunt trauma to the globe typically compresses the cornea, shortening the globe along its anterior-posterior axis. The fluid and other intraocular contents are relatively noncompressable, and the globe deforms with elongation in the equatorial plane. This stretching may lead to rupture of one or more of the seven relatively nondistensible rings within the eye: the pupillary sphincter (radial tears), the iris insertion (iridodialysis), the ciliary body (angle recession) and its attachment to the sclera (cyclodialysis), the trabecular meshwork (trabeculodialysis), the zonular fibers, and the ora serrata (retinal dialysis). Damage to these structures leads to many of the various forms of glaucoma following trauma.
Hyphema
Blood in the anterior chamber is one of the most common findings after ocular contusion.5 Immediately following blunt and penetrating trauma, damage to the iris and ciliary body compromises the blood aqueous barrier, with the release of protein into the anterior chamber, or actual bleeding. Protein and blood cells may obstruct the trabecular meshwork, thus increasing IOP.6,7,8
Inflammation following trauma is typically treated with topical steroids. Cycloplegics are helpful to reduce discomfort, to stabilize the blood-aqueous barrier, and to enhance uveoscleral outflow. This aids IOP control and helps prevent posterior synechiae formation and resultant pupillary block. Cycloplegics may also help prevent rebleeds following hyphemas by immobilizing the iris and ciliary body.
Hyphema is a frequent complication of ocular trauma (Fig. 54C.1). Bleeding results from tears between the circular and longitudinal muscles of the ciliary body, disrupting the major arterial circle of the iris. These tears produce angle recession. Hyphemas may lead to elevated IOP; the larger the hyphema, the greater is the likelihood of pressure elevation. The mechanism of glaucoma is obstruction of the trabecular meshwork by trabecular beam swelling, fibrin, and red blood cells. Because of their pliability, red blood cells, in small amounts, pass through normal trabecular meshwork with relative ease.6 However, in larger quantities, especially when accompanied by fibrin and trabecular swelling, red blood cells may obstruct the meshwork.6,7 Microhyphemas, in which the suspended red blood cells do not form an observable layer, still may lead to elevated IOP. Glaucoma occurs in over 25% of hyphemas filling 50% of the anterior chamber, over 50% of near total hyphemas, and in almost all “black ball” or “eight ball” hyphemas.
In a black ball hyphema, the blood is so concentrated and the anterior chamber so stagnant and hypoxic that the blood within the anterior chamber appears black (Fig. 54C.2). Such a black ball hyphema may consist of a dumbbell-shaped clot filling the anterior chamber, pupil, and posterior chamber. These hyphemas are more difficult to manage and lead to glaucoma through pupillary block as well as trabecular obstruction.9
Optimal treatment for hyphema has not been clearly established. Most clinicians recommend treatment with topical steroids and cycloplegics. Patients are often instructed to keep their heads elevated to promote settling of the red blood cells in the inferior anterior chamber angle, thus improving vision and allowing more of the trabecular meshwork to clear. Bed rest and the avoidance of nonsteroidal anti-inflammatories or other agents with blood thinning properties are recommended to reduce the incidence of rebleeds, which commonly occur in the first 4 days.
Rebleeds often are more severe than the initial bleeding episode and may lead to more serious complications and vision loss. Oral aminocaproic acid and steroids have been shown to reduce the rate of rebleeds. Oral aminocaproic acid, however, may cause nausea, vomiting, and systemic hypotension; thus, its use typically requires inpatient hospitalization. Topical aminocaproic acid may also reduce rebleeding.10 Most hyphemas can be managed on an outpatient basis unless the patient is at high risk of rebleeding and complications.11,12 Such patients include those receiving anticoagulant therapy, children, African Americans, patients who have tested positive for sickle cell (including trait), patients with greater than one-third hyphemas, and patients at high risk for noncompliance with therapy or follow-up.
Aqueous suppressants are helpful to control elevated IOP. Miotics are avoided because they may increase inflammation or rebleeding. Latanoprost should also be avoided, given concerns regarding increased inflammation and current lack of evidence that it is effective in this setting. Most patients without pre-existing nerve damage or sickle cell disease or trait may be observed, despite moderately elevated IOPs (up to 35 to 40 mm Hg) for 2 to 4 weeks, with only conservative medical therapy.
Patients with severely or persistently elevated pressures may be treated with paracentesis, anterior chamber washout, clot extraction (either manual or facilitated by a mechanical vitrector), or guarded filtration procedures. Some clinicians routinely perform a guarded filtration procedure at the time of anterior chamber washout to help ensure short-term IOP control. The expectation with this combined procedure is that the filtration surgery will most likely fail in the intermediate future, by which time the trabecular meshwork should have recovered adequate function. Trabeculectomy with iridectomy has been recommended as the initial treatment for total hyphemas, because most require surgery eventually.13 During anterior chamber washout, it is not necessary to remove all of the clot, because it is the circulating red blood cells that obstruct the meshwork, and clot removal may lead to rebleeding and damage to intraocular structures. When necessary, an automated vitrectomy-cutting handpiece with irrigating sleeve can be helpful to debulk clots without disturbing the structures to which the clots are attached. Ideally, if the clinical situation allows, surgical procedures should be done on or after the fourth day following the trauma, because the highest incidence of rebleeding is between the second and fourth days. Additionally, by this time, clots may have retracted from adjacent structures, facilitating their removal with reduced surgical manipulation and trauma.
All African-American patients or patients with a family history of sickle cell trait or disease who present with a hyphema or microhyphema must be screened for sickle cell trait. The sickle cell gene is present in approximately 9% of African Americans. In the setting of a hyphema, patients with sickle cell trait alone or sickle cell disease may have clinically significant sickling of red blood cells in the relatively hypoxic and low pH conditions of the anterior chamber. Sickled red blood cells are less pliable and easily obstruct the trabecular meshwork, leading to high IOPs even with remarkably little blood in the anterior chamber.14 In addition, patients with sickle cell trait or disease are at risk of ischemic complications to the optic nerve or retina at relatively low IOPs.15,16 For this reason, it has been suggested that sickle patients with hyphemas or microhyphemas be monitored more closely and that their IOP be managed aggressively to be maintained below 30 mm Hg at all times and not be allowed to remain higher than 24 mm Hg for more than 24 hours. Additionally, in a report of 99 eyes of 97 children hospitalized with hyphema after blunt trauma, sickle cell trait was a significant risk factor for rebleed.5
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
