44

Glaucoma Due to Trauma

Carla I. Bourne, MD and Bradford J. Shingleton, MD

Glaucoma due to trauma is a multifactorial disease. Intraocular pressure (IOP) may increase after blunt trauma, lacerating trauma, chemical exposure, electromagnetic radiation, or surgery. Elevated IOP may develop immediately after the injury or years later. The angle may be open or closed. The injured eye may demonstrate obvious signs of damage, or clinical signs of trauma may be largely unapparent. Eyes that are predisposed to glaucoma after ocular injury may actually have a low IOP initially rather than a high IOP. Low IOP may result from aqueous hyposecretion due to ciliary contusion and inflammation, increased uveoscleral/vortex outflow due to a cyclodialysis cleft, tears through trabecular meshwork (TM) into Schlemm’s canal, or loss of integrity of the globe due to scleral or corneal perforation. Low IOP can often convert to high IOP as a result of treatment, normal healing processes, and the long-lasting effect of the injury itself on TM outflow. Elevated IOP has multiple causes, but they all tend to reflect a reduced facility of outflow of aqueous humor through the TM drainage channels (Table 44-1).¹

Glaucoma-causing injuries to the anterior segment most commonly follow blunt injury, and the US Eye Injury Registry² reports that, at 6 months following the injury, the incidence of glaucoma was 3.39%. Factors highly predictive of developing glaucoma have been identified as poor initial visual acuity, advancing age, lens injury, angle recession, higher initial IOP, and hyphema.^2–4

The impact from the blunt injury results in a sudden compressive deformation of the eye. The cornea and anterior sclera are displaced posteriorly, and there is a compensatory expansion of the globe in the equatorial direction.⁵ Campbell⁶ has graphically described 7 rings, or circles, of tissue anterior to the equator of the globe that suddenly expand with blunt impact. Because the internal fluids of the eye cannot compress, the forces are transmitted to the 7 rings of tissue. This often results in splitting or tearing of tissues that may manifest as radial sphincter tears, iridodialysis, angle recession, cyclodialysis, TM tears, zonule separation, or peripheral retinal dialysis. Damage in many of these areas may result in either early onset or delayed onset glaucoma.

EARLY-ONSET GLAUCOMA AFTER EYE INJURY

Contusion With Intraocular Inflammation

Blunt trauma commonly results in inflammation of the anterior segment visualized as flare and cells at the slit lamp. Red blood cells and gross angle disruption are often not identified, but IOP may still be elevated. The elevation of IOP in this setting is presumably due to reduced aqueous outflow as a result of inflammatory cells and debris obstructing TM outflow channels. Edema and direct damage to TM beams may not be identified on gonioscopy but may still contribute to a temporary rise in IOP. This situation tends to be self-limited and clears spontaneously or with the use of topical steroids.

Trabecular Meshwork Damage

Herschler⁷ has shown that gonioscopy early after blunt injury may demonstrate trauma-related changes in the trabecular zone. A full-thickness tear in TM may occur, and a trabecular flap may be created at the point of rupture. This tends to arise just below the insertion of the trabecular sheets at Schwalbe’s line. Inflammation is invariably associated with this type of injury. IOP may or may not be elevated depending on the amount of aqueous production. Indeed, IOP may actually be subnormal in the early peritraumatic period due to direct access of aqueous to Schlemm’s canal, bypassing the TM. A small clot may be noted in the area of the TM tear due to bleeding from Schlemm’s canal. Healed TM tears are difficult to see, as gonioscopy is more commonly performed at a time remote from the injury. If IOP elevation develops at a later time, it is probably associated with more extensive angle recession.

Significant bleeding in the anterior chamber associated with blunt ocular trauma increases the chance for elevation of IOP.8 The high-impact compression and expansion secondary to blunt injury leads to rupture of iris stromal or ciliary body blood vessels. The IOP may be elevated due to all the factors noted under “Contusion With Intraocular Inflammation” and “Trabecular Meshwork Damage” as well as red blood cell obstruction of the outflow pathway.

Moderate IOP elevation up to 10 mm Hg above baseline may occur in as many as 30% of patients with traumatic hyphema.⁹ Because the vast majority of these patients have healthy optic nerves, they can tolerate an elevation of IOP for a moderate period of time. The elevation tends to be self-limited and clears as the blood cells are normally processed through the aqueous drainage channels. A given patient’s susceptibility to IOP elevation in the setting of trauma is highly variable. Read and Goldberg^9,10 found that IOP levels to 35 mm Hg or more that persist beyond 5 to 7 days may be associated with an increased risk of glaucomatous optic atrophy, particularly in the presence of sickle cell disease, but not restricted to that group. Higher pressures for a shorter period may be even more poorly tolerated.

One of the groups at highest risk for optic nerve damage in the setting of traumatic hyphema are those patients with sickle cell hemoglobinopathy.¹⁰ These patients are susceptible to even marginal IOP elevation and are also predisposed to profound IOP spikes. The sensitivity of the optic nerve to marginal IOP elevation is presumably related to restricted blood flow to the optic nerve in the setting of the sickle cell disease. A high increase of IOP that may occur in these patients seems to be related to the restricted egress of rigid, sickled red blood cells through the TM outflow pathway. A vicious circle develops in that the sickle cells cannot clear from the anterior chamber, and there is a stagnation of cells. A relatively acidotic pH develops in the anterior chamber, leading to further sickling. The accumulating sickled red cells have no greater chance of clearing through the trabecular outflow pathway, and the cycle feeds on itself. Treatment has been proposed to increase the oxygen content of aqueous with the goal of reducing sickling and theoretically lowering IOP. Early positive results have been demonstrated in an animal study using intracameral hyperbaric oxygen¹¹ and another study using humidified oxygen delivered transcorneally in human eyes.¹² Our traditional means for treating glaucoma in this setting may actually contribute to an exacerbation of the sickling process. These are theoretical concerns without confirmation clinically, but these factors must be considered by any physician treating patients with sickle disease or sickle trait. Use of a carbonic anhydrase inhibitor (CAI) and the associated metabolic acidosis that results may increase sickling. Methazolamide theoretically causes less systemic acidosis than acetazolamide. If a systemic CAI is required in this situation, methazolamide may be the preferred choice. Epinephrine derivatives may exacerbate sickling due to their vasoconstrictive effect and subsequent hypoxia that develops in the anterior chamber. Miotics and prostaglandin agonists may increase inflammation. Topical aqueous suppressants are the treatment of choice, and the role of topical apraclonidine remains to be determined.

In patients with normal hemoglobin, the greatest concern for serious elevation of IOP is in those hyphema patients who suffer rebleeding. The incidence of rebleeding is highly variable depending on type of injury and patient population. It may be associated with clot lysis and clot retraction from damaged blood vessels. If rebleeding occurs, it tends to occur in the first 2 to 5 days after the injury. Although the majority of patients who lose vision in the setting of traumatic hyphema do so secondary to macular problems rather than secondary to glaucoma, every effort should be made to minimize the risk for sudden elevation of IOP. Treatment is directed toward minimizing the rate of rebleeding.

Several studies13–18 prove the efficacy of oral aminocaproic acid and tranexamic acid in reducing the rate of rebleeding; however, there is variability in the reports dealing with its side effects (eg, nausea, vomiting, postural hypotension) and extension of duration of the clot. Some patients have a dramatic elevation of IOP on cessation of aminocaproic acid,¹⁹ and for this reason, we rarely use this drug. In low-risk groups, the side effects of oral antifibrinolytic therapy may actually outweigh the risks of no treatment at all. The use of topical aminocaproic acid²⁰ is also being studied. One randomized study²¹ showed a decreased risk of rebleeding by approximately 67% in patients receiving topical aminocaproic acid. However, the continued need for a large-scale trial has left many questions unanswered, including its efficacy in sickle cell patients. Groups that appear to be at higher risk from rebleeding are Black Americans, patients who present more than 24 hours after injury,²² and patients taking anticoagulants. Antifibrinolytics are not the only oral medicines used to decrease rate of rebleeding. A study in 1992 by Farber and colleagues²³ claimed efficacy for systemic prednisone at a dosage of 40 mg per day to reduce rebleeding. This dosage was equivalent in effect to the reduction in rebleeding obtained at the same institution several years earlier with aminocaproic acid. However, as with aminocaproic acid and tranexamic acid, there are no large trials demonstrating a definitive improvement in outcomes.^24,25 Current recommendations include discontinuation of salicylates and anticoagulant therapy to decrease the risk of rebleed.²⁵ Intracameral tissue plasminogen activator has been suggested to speed clot resorption. However, use is limited to eyes with no active bleeding site, and results are mixed in reducing rebleeding.^26–28

Medical treatment for glaucoma in the setting of traumatic hyphema involves aqueous suppressants as the first line of defense (Table 44-2). Cycloplegic agents and topical steroids are often used to reduce the associated iritis and minimize outflow pathway edema. Activity limitation, shield protection, and elevation of the bed have traditionally been used during the first 5 to 7 days following injury.

Surgical treatment is indicated for those patients who do not respond satisfactorily to medical therapy. Traditional indications for surgery have included an IOP higher than 40 mm Hg for more than 48 hours, corneal blood staining in the setting of a large hyphema, or a stagnant, nonresorbing blood clot involving a significant amount of the angle circumference. The threshold for surgery is less in sickle cell patients with intervention recommended for IOP higher than 30 mm Hg at any time or more than 24 mm Hg for more than 24 hours (see Table 44-2). A host of surgical procedures has been described, including anterior chamber washout,²⁹ clot expression,³⁰ delivery of the clot with a cryoprobe,³¹ automated hyphemectomy,³² ultrasonic fragmentation or aspiration,³³ and peripheral iridectomy and/or trabeculectomy.^34,35 Washing out of the circulating red cells from the anterior chamber may be all that is required. If that does not lower IOP to an acceptable level, the washout can be repeated or additional techniques employed as noted in Table 44-2. Paracentesis and anterior chamber washout seems to be the simplest procedure,²⁹ and this may be coupled with a coaxial manual irrigation system. The entire clot does not need to be removed as only the circulating red blood cells obstruct the outflow pathways. Subsequent release of aqueous and blood can be achieved via the paracentesis at the slit lamp postoperatively, as needed.

Alkaline agents have the capability of penetrating ocular tissues and may lead to glaucoma. This is uncommon with acid burns. A number of researchers have studied the nature of the IOP rise following alkali exposure.36 A dicrotic pressure rise has been noted with an immediate IOP rise up to the level of 40 to 50 mm Hg within the first 10 minutes of the injury. The pressure tends to return to normal after a short time and then gradually rises to high levels at the end of the first hour or two. It is believed that shrinkage of the outer collagen coats of the eye resulting in distortion of the TM³⁷ may cause the initial IOP spike. Prostaglandin release has been implicated as the major factor in the second hypertensive phase. Weeks to months later, the IOP may be elevated due to angle closure as a result of peripheral anterior synechiae (PAS) formation. In addition, if aqueous pH remains elevated higher than 11.5 for prolonged periods, ciliary body damage can lead to hypotony and phthisis bulbi, and decreased secretion of ascorbate can limit keratocyte collagen repair.³⁷ Studies^38,39 on rabbits have shown that rinsing with borate-buffered eyewash is significantly better at neutralizing pH compared to isotonic saline.

Because of the impressive corneal changes that may arise from a chemical injury, IOP elevation may be overlooked. It is critical to monitor IOP because Kuckelkorn et al have shown early development of glaucoma in 15.6% of chemically injured eyes and late-onset secondary glaucoma in 22.2% of such eyes.40 Treatment of the IOP elevation, if necessary, is focused on aqueous suppressant therapy, both topically and systemically. Miotics are generally avoided because of the intense inflammation that is associated with chemical burns. Topical steroids, if not contraindicated from a corneal basis, may reduce inflammation, and cycloplegic agents may maximize comfort and help to stabilize the blood-aqueous barrier. Brodovsky et al⁴¹ and Ralph⁴² demonstrated that in cases of severe burns, oral vitamin C and tetracycline, in addition to topical citrate, ascorbate, and tetracycline drops, decrease collagenolytic activity. However, no large, long-term randomized studies on humans have been documented. Anterior chamber paracentesis had been favored by some in the past but is less commonly used at this time. Trabeculectomy is largely unsuccessful due to extensive conjunctival scarring. Glaucoma drainage devices and cyclophotocoagulation procedures may have better IOP outcomes. Cyclophotocoagulation has been shown to have a reasonably low complication rate and may be a better option when the anterior chamber view and ocular surface are compromised.⁴³

LATE-ONSET GLAUCOMA AFTER EYE INJURY

Angle Recession

A tear in the ciliary body results in angle recession. The typical tear occurs between the circular and longitudinal muscles in the ciliary body. There is a resulting posterior displacement of the iris root, which results in the clinical appearance of a broadening of the ciliary body band. Collins⁴⁴ was the first to give a pathologic description of angle recession in 1892. Wolff and Zimmerman⁴⁵ presented a classic correlation between traumatic glaucoma and angle recession in 1962.

Angle recession is remarkably common after blunt injury. The incidence of angle recession in the setting of traumatic hyphema has been reported from 50% to 100%.^22,46,47 The incidence of glaucoma with angle recession appears to be directly related to the extent of angle involvement. The risk of glaucoma appears to be greatest if 240 degrees or more of the angle are involved. The elevation in IOP after blunt trauma with angle recession may occur months or years after the initial injury. Blanton observed a bimodal pattern with glaucoma occurring within the first year or after 10 years of injury.⁴⁷

The diagnosis of angle recession is made by careful gonioscopic examination (Figure 44-1). The ciliary body band tends to be broader in certain zones, and there may be baring of ciliary processes. The scleral spur may appear abnormally white. Differences between the eyes may be remarkably subtle. The most useful technique for documenting angle recession is to compare quadrants between the injured eye and the noninvolved eye of a given patient. Traditionally, bilateral, simultaneous Koeppe gonioscopy (Ocular Instruments)⁴⁸ with 2 lenses has been an excellent way to detect these differences. Anterior segment optical coherence tomography and ultrasound biomicroscopy are newer techniques that permit objective and quantitative documentation of the angle configuration.^49,50

The treatment of angle-recession glaucoma follows the pattern used for primary open-angle glaucoma. Inadequate control with topical and oral therapy may lead one to consider laser trabeculoplasty (LTP). LTP is rarely effective and may also be associated with a higher incidence of acute IOP elevation. Filtration surgery is often required. Trabeculectomy success is strongly dependent on the use of adjunctive antimetabolites, as most patients are young and predisposed to fibrosis.^51,52

The mechanism for glaucoma in angle recession depends on the timing of the IOP elevation after injury. Early IOP increase is due to trabecular inflammation and the presence of circulating blood and inflammatory products. This often resolves within weeks to months, and the patient may enter a honeymoon period with normalization of IOP. The ophthalmologist must be aware that this period of normal IOP can be short lived; eyes with significant angle recession deserve close follow-up at least every 6 months initially.

Late angle-recession glaucoma may be secondary to the formation of a glass-like membrane over the TM, thought to be an extension of Descemet’s membrane. This explains the poor response to conventional medical and laser treatment in angle-recession glaucoma. Indeed, in such eyes treated with LTP, the surgeon may see a spreading, whitening of cracked glass–like appearance at the site of laser impact. In contrast, if instead of LTP the surgeon performs neodymium:yttrium-aluminum-garnet laser goniopuncture (YLT), a transient reduction in IOP is seen, supporting the suggestion that obstruction to outflow in angle-recession glaucoma is due to the presence of a glass-like membrane covering the TM. Unfortunately, such IOP reductions tend to be short-lived, as Melamed and colleagues53–55 have shown in monkeys that the openings made by goniopuncture tend to be covered by Descemet’s membrane over time. When goniopuncture was repeated in humans, more than 50% required further surgery within 1 year of YLT.⁵⁶

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