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Slide 1 |
Jane Loman, MD
The term traumatic glaucoma incorporates a variety of posttraumatic mechanisms that lead to a rise in IOP. Traumatic glaucoma often occurs from a blunt injury that causes anterior segment deformation during impact, but it can also occur with penetrating injuries. A prospective examination of 100 traumatic glaucoma cases revealed 75% were caused by blunt trauma and 25% by penetrating injuries.1 High IOP can occur acutely or long after the initial traumatic event and is most commonly related to hyphema, posttraumatic inflammation and/or angle recession.
The incidence of traumatic hyphema is 17/100,000 and 30% to 94% of these patients exhibit angle recession.1,2 The typical patient is a man younger than 30 years of age. In the United States, sporting injuries account for 60% of traumatic hyphemas.3 Globally, numerous reports mention rates of ocular trauma caused by assault, specific sports, and elastic cords. Twenty to 30% of reported patients had traumatic glaucoma or IOP > 21 mm Hg. A 10-year prospective study in 31 patients with traumatic hyphema and angle recession revealed a 9% incidence of traumatic glaucoma, with 6% of the cases being late onset.2 Late-onset glaucoma from blunt trauma ranges from 1.3% to 20% in other studies.
The pathogenesis of traumatic glaucoma occurs when at initial impact of an object to the eye, the cornea and anterior sclera are rapidly displaced posteriorly with a compensatory expansion at the equator of the eye. The expansion causes tears in various parts of the anterior segment that are affected by hemorrhage, inflammation, and scarring and have been referred to as the seven anterior rings of tissue3,4:
Although aqueous production may be temporarily reduced by an inflamed posttraumatic ciliary body, outflow channels are also affected, which may lead to a rise in IOP. Outflow can be damaged by the actual tear or blocked by hemorrhage, platelets, inflammatory cells, ghost cells (degenerated red blood cells from a prior traumatic vitreous hemorrhage), fibrous ingrowth or scar tissue.
In addition, subluxation of the lens in blunt and penetrating trauma can lead to glaucoma in a variety of mechanisms. Traumatic rupture of the lens capsule can release lens proteins and cause phacoanaphylactic uveitis, leading to uveitic glaucoma. This inflammation can also cause peripheral anterior synechiae (PAS), closing the angle. Relative pupillary block can occur with posterior synechiae, an anterior sublaxated lens, or traumatic lens swelling.5
The pathogenesis of late-onset glaucoma is not completely understood. Late-onset glaucoma is usually related to damage of a significant amount of trabecular meshwork or PAS formation. Through time, these patients are already experiencing a normal age-related decrease in outflow facility. Thus, with already damaged meshwork or a partially closed angle, there is inadequate healthy meshwork to compensate for this change. Interestingly, there is an increase risk of developing primary open-angle glaucoma in the other eye (50%), suggesting that they may already have impaired outflow facility.6 Less commonly, penetrating images with metal foreign objects can cause siderosis or chalcosis leading to open-angle glaucoma.
In patients with angle recession glaucoma, some surgeons may assume that there is damaged trabecular meshwork adjacent to the recessed angle or that damage to the ciliary muscle disrupts the tension exerted on the trabecular meshwork reducing its function.4 Some studies also report a hyaline membrane forming over the angle reflecting a posterior extension of Descemet's membrane.
In cases of an acute rise in IOP, symptoms of headache, nausea, blurry vision, or photophobia may be present. Late-onset glaucoma from gradual IOP rise is usually asymptomatic. Therefore, a detailed history of the event should be taken.
Acutely, a ruptured globe or penetrating injury should be ruled out. Some critical signs that aid in diagnosis are 360° of chemosis, shallow anterior chamber (AC), scleral show on indirect examination, and limitiation of eye movement. Pressure on the globe should be avoided until surgical intervention is taken. Once a ruptured globe has been ruled out or repaired, accurate IOP readings may be taken. Then, critical signs suggesting equatorial expansion of the globe should be evaluated by slit lamp examination.
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In patients with acute hyphema, pressure on the globe should be avoided to prevent rebleeding. Therefore, gonioscopy should be postponed until 1 month after the initial trauma. Gentle gonioscopy with a Zeiss lens should be performed only if there is intractable IOP rise of unknown cause (Slide 3). Gonioscopic findings and evaluation include:
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The amount in degrees of angle recession, PAS, and fibrous ingrowth should be recorded because they may be markers for adjacent damaged trabecular meshwork. Numerous studies have shown that those with more than 180° of angle recession are at risk for developing late-onset glaucoma. Patients with 360° of angle recession will not necessarily have a rise in IOP because there may be some viable trabecular meshwork adjacent to the atrophic circular fibers causing the recessed angle.
The diagnosis of traumatic glaucoma is mainly clinical and includes a detailed history of the mechanism of injury, slit lamp examination, IOP measurements, gonioscopy, optic nerve head, and nerve fiber analysis. Most importantly, patients with a history of blunt trauma (especially in those with documented angle recession or hyphema) should have yearly examinations for life to look for late-onset glaucoma. These patients are similar to glaucoma suspects. Thus, if they have other risk factors such as high IOP and suspicious cup-to-disc ratios, baseline disc photos, an automated Humphrey visual field, and optical coherence tomography (OCT) of their nerve fiber layer should also be considered. OCT can be used as a baseline measure of the nerve fiber layer and may be helpful in demonstrating nerve fiber loss before visual field loss.
Black patients have an 8% risk for sickle cell and are a subset of patients that may need a sickle cell preparation and hemoglobin electrophoresis in the presence of hyphema.7 These patients will produce sickled cells that may not easily pass through the trabecular meshwork and lead to rapid increases in IOP. Laboratory tests in patients with a history of a bleeding disorder should also be considered: platelet counts, liver function tests protime, and patial thromboplastin time.8
Treatment of traumatic glaucoma involves lowering IOP or precluding its rise to prevent optic nerve damage. Treatment also depends on the cause of the unstable IOP and the amount of time after the traumatic event.
Acutely, the increase in IOP is usually caused by blockage of the angle with hyphema, debris, and inflammatory cells. Because these patients are usually young, they can tolerate acute increases in IOP without nerve damage. Therefore, most ophthalmologists advocate treatment with aqueous suppressants such as beta blockers, alpha-2 agonists, and carbonic anhydrase inhibitors (CAIs) when IOP>30mm Hg. CAIs should not be used in patients with sickle-cell. Parasympathomimetics are associated with increased inflammation and should be avoided. Topical steroids should also be used for up to 6 weeks to decrease inflammation and cellular infiltration of the damaged angle.
Another concern in the acute phase of traumatic hyphema is the risk of rebleeding (usually in the first 2 to 5 days), which increases the risk of IOP rise and the development of total hyphema. First-line tactics include no use of anticoagulation or nonsteroidal anti-inflammatory drugs such as aspirin, no exertional activities, head elevation of 30°, and the use of an eye shield at all times. Hospital admission in hyperactive children, those with a large hyphema or high IOP, and those with sickle cell or a bleeding disorder should be considered, though this is controversial given the variable cost and effectiveness. In patients with a bleeding disorder such as hemophilia, clotting factors should be administered as soon as possible.
Controversy exists regarding the use of antifibrinolytic agents to prevent rebleeding. Tranexamic acid and 
-aminocaproic acid have been shown in numerous studies to significantly reduce the incidence of rebleeding by stabilizing the fibrin clot.7 However, more recent studies do not show an improvement in visual outcome and thus these drugs have fallen out of favor. Furthermore, these patients have to be monitored closely for the many side effects of these drugs such as dizziness, hypotension, and vomiting. It is also contraindicated in patients with renal or hepatic insufficiency or hemophilia. A topical preparation of -aminocaproic acid with promising results is not yet available commercially. Of note, topical and oral steroids, drugs commonly used in eye trauma, may also help to prevent rebleeding by inhibiting fibrinolysis and stabilizing the blood-ocular barrier.7 If rebleeding occurs, an IOP check will help evaluate further treatment options, which may include the use of an antifibrinolytic drug.
In the subacute period, a persistent IOP rise of >50mm Hg for 5 days, an IOP>35mm Hg for greater than 7 days, or a persistent hyphema for >10 days on maximal medical therapy may constitute an anterior chamber washout. This is meant to decrease the rate of optic nerve damage, PAS formation, and corneal blood staining, respectively. In those with sickle cell, an AC washout should be considered if IOP is >30mm Hg for more than 24 hours.7
An AC washout includes creating two paracentesis incisions with saline irrigation through one incision and a depression of the posterior lip of the second paracentesis. This technique allows for easy transition to bimanual irrigation/aspiration or cutting to further control bleeding. Furthermore, the paracentesis can be performed at the slit lamp to lower IOP postoperatively.
Numerous studies report different treatment options for late-onset glaucoma. Many patients may need life-long treatment with topical medications. In those refractory to medical therapy, argon laser trabeculoplasty and trabeculectomy without antimetabolite have yielded disappointing results.10 Failure may be due to increased fibroblast proliferation in younger patients or a change in their aqueous humor after trauma. The use of mitomycin and 5-fluorouracil has decreased the rate of trabeculectomy failure. Also, glaucoma drainage implants (except Molteno implants) in eyes with past failed filtering procedures have been shown to control IOP.4,11
