Trauma and Surgery
Nonpenetrating, or blunt, trauma to the eye may cause a variety of anterior segment conditions that can then lead to secondary glaucoma, including
These findings, particularly when in combination, often lead to elevated IOP initially after trauma. This elevation tends to be brief but may be protracted and result in glaucoma.
Siderosis or chalcosis from a retained intraocular metallic foreign body in penetrating or perforating injuries may lead to IOP elevation and glaucoma. Chemical injuries, particularly those involving alkali, may cause acute IOP elevation as a result of inflammation, shrinkage of scleral collagen, release of chemical mediators such as prostaglandins, direct damage to the anterior chamber angle, or compromised anterior uveal circulation. Recurrent inflammation or damage to the trabecular meshwork may progress to glaucoma over months or years after a chemical injury.
The risk of elevated IOP after a traumatic hyphema is increased with recurrent hemorrhage, or rebleeding. The average reported frequency of rebleeding after an initial hyphema is 5%–10%, but it varies significantly with different study populations. Rebleeding usually occurs within 3–7 days of the initial hyphema and may be related to normal clot retraction and lysis. In general, the larger the hyphema, the higher the incidence of increased IOP, although small hemorrhages may also be associated with marked elevation of IOP, particularly when the angle is already compromised. Increased IOP occurs as a result of obstruction of the trabecular meshwork with red blood cells (RBCs), inflammatory cells, debris, and fibrin, as well as from direct injury to the trabecular meshwork from the blunt trauma. Gentle gonioscopic examination in individuals with blunt trauma may reveal a subtle hyphema. In addition to glaucomatous damage, prolonged IOP elevation in an eye with a hyphema increases the risk of corneal blood staining (Fig 15-8).
Individuals with sickle cell hemoglobinopathies have an increased risk of elevated IOP following hyphema and are more susceptible to the development of optic neuropathy. Normal RBCs pass through the trabecular meshwork without difficulty. However, in the sickle cell hemoglobinopathies (including sickle cell trait), the low pH of the aqueous humor causes the RBCs to sickle and become rigid. These more rigid cells become trapped in the trabecular meshwork, and even low numbers of sickle-shaped RBCs may cause marked elevations in IOP. In addition, the optic nerves of patients with sickle cell disease are much more sensitive to elevated IOP and are prone to development of anterior ischemic optic neuropathy and central retinal artery occlusion, as a result of compromised microvascular perfusion.
Figure 8-15 Corneal blood staining following trauma. Note the area of layered heme in the inferior angle.
In general, conservative management is appropriate for the patient with an uncomplicated hyphema and includes use of an eye shield, limited physical activity, and head elevation. Topical and oral corticosteroids may reduce associated inflammation, although their effect on rebleeding is debatable. If significant ciliary spasm or photophobia occurs, cycloplegic agents may be helpful, but they have no proven benefit for prevention of rebleeding. Oral administration of aminocaproic acid has been shown to reduce rebleeding in some studies. However, this has not been confirmed in all studies, and systemic adverse effects, such as hypotension, syncope, abdominal pain, and nausea, can be significant. Also, discontinuation of aminocaproic acid may be associated with clot lysis and additional IOP elevation.
Treatment of elevated IOP in patients with hyphema includes ocular hypotensive agents, particularly aqueous suppressants, and hyperosmotic agents. It has been suggested that patients with sickle cell hemoglobinopathies avoid carbonic anhydrase inhibitors, because these agents may increase the sickling tendency in the anterior chamber by further lowering the pH; however, this relationship has not been firmly established. The use of systemic carbonic anhydrase inhibitors and hyperosmotic agents may induce a sickle crisis in susceptible individuals who are significantly dehydrated. Adrenergic agonists with significant α1-agonist effects (apraclonidine, dipivefrin, epinephrine) should also be avoided in patients with sickle cell disease, because of the potential for anterior segment vasoconstriction with their use. Parasympathomimetic agents may not be appropriate in patients with traumatic hyphema as they may increase inflammation and result in more centrally located posterior synechiae.
For patients with sickle cell disease, the threshold for surgical intervention may be lower, given these patients’ increased risk of optic neuropathy from elevated IOP. In young children, vision obstruction by the hyphema or corneal blood staining may justify early surgical intervention to reduce the risk of amblyopia. If surgery for elevated IOP becomes necessary, an anterior chamber irrigation is commonly performed first. If a total hyphema is present, pupillary block may occur, and an iridectomy is helpful at the time of the washout. If the IOP remains uncontrolled, filtering surgery may be required. Some surgeons prefer to perform glaucoma filtering surgery with the anterior chamber washout to obtain immediate control of IOP, relieve any pupillary block, and reduce the risk of elevated IOP in the future from damage to the trabecular meshwork.
Campagna JA. Traumatic hyphema: current strategies. Focal Points: Clinical Modules for Ophthalmologists. American Academy of Ophthalmology; 2007, module 10.
Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database Syst Rev. 2013;12:CD005431. Epub 2013 Dec 3.
Hemolytic and ghost cell glaucoma
Hemolytic glaucoma, ghost cell glaucoma, or both may develop after a vitreous hemorrhage. In hemolytic glaucoma, hemoglobin-laden macrophages block the trabecular meshwork. Red-tinged cells can be seen floating in the anterior chamber, and the trabecular meshwork may appear reddish brown. In ghost cell glaucoma, degenerated RBCs (ghost cells) obstruct the trabecular meshwork.
Ghost cells are small, khaki-colored RBCs that have lost their intracellular hemoglobin (Fig 16-8). Because they are less pliable than normal RBCs, they obstruct the trabecular meshwork and cause elevated IOP. RBCs degenerate within 1 to 3 months after a vitreous hemorrhage. They gain access to the anterior chamber through a disrupted hyaloid face, which can occur spontaneously or as a result of trauma or previous surgery (eg, pars plana vitrectomy, cataract extraction, capsulotomy).
Patients with ghost cell glaucoma typically present with elevated IOP and a history of or current vitreous hemorrhage from trauma, surgery, or preexisting retinal disease. The IOP may be markedly elevated, with accompanying corneal edema. The anterior chamber may contain degenerated RBCs. The cellular reaction is often out of proportion to the aqueous flare, and the conjunctiva tends not to be inflamed unless the IOP is markedly elevated. On gonioscopy, the angle appears normal except for possible layering of ghost cells in the inferior angle. A long-standing vitreous hemorrhage may be present, with characteristic khaki coloration and clumps of extracellular pigmentation from degenerated hemoglobin.
Figure 8-16 Ghost cell glaucoma: the classic appearance of ghost cells in the anterior chamber. These small, khaki-colored cells can become layered, as occurs in a hyphema or hypopyon.
(Courtesy of Ron Gross, MD.)
In these conditions, IOP typically normalizes once the hemorrhage has cleared. Medical therapy with aqueous suppressants is the preferred initial approach. If medical therapy fails to control the IOP, some patients may require anterior chamber irrigation, pars plana vitrectomy, and/or incisional glaucoma surgery. When a collection of RBCs or ghost cells is present in the vitreous, a pars plana vitrectomy is likely necessary for IOP control.
Traumatic, or angle-recession, glaucoma
Angle recession is a common finding after blunt trauma and involves a tear between the longitudinal and circular muscle fibers of the ciliary body. Although angle recession is not necessarily associated with immediate IOP elevation and glaucoma, it is a sign of probable damage to the trabecular meshwork. Traumatic glaucoma is chronic and usually unilateral and may occur immediately after the ocular trauma or months to years later. It resembles POAG in presentation and clinical course but can be distinguished by its classic gonioscopic findings (Figs 8-17, 8-18):
widening of the ciliary body band
absent or torn iris processes
white, glistening scleral spur
irregular and dark pigmentation in the angle
PAS at the border of the recession
Figure 8-17 Goniophotograph of angle recession. Angle recession occurs when the ciliary body is torn, usually between the longitudinal and circular fibers of the ciliary body, resulting in a deepened angle recess (arrows). The dark circular deposits located on the peripheral iris represent old heme.
(Reproduced from Alward WLM, Longmuir RA. Color Atlas of Gonioscopy. 2nd ed. American Academy of Ophthalmology; 2008:89. Fig 9-50.)
Figure 8-18 Typical gonioscopic appearance of angle recession. Torn iris processes (arrows), a whitened and increasingly visible scleral spur, and a localized depression in the trabecular meshwork are shown.
(Courtesy of Steven T. Simmons, MD.)
Traumatic glaucoma should be considered in a patient with unilateral IOP elevation. The patient’s history may reveal the contributing incident, although it may have occurred in the distant past and hence forgotten. Examination may reveal findings consistent with previous trauma, such as corneal scars, iris injury, abnormalities in the angle, focal anterior subcapsular cataracts, and phacodonesis. Comparing gonioscopic findings in the affected eye to those in the fellow eye may help the clinician identify areas of recession.
More extensive angle recession is associated with a greater reduction in outflow facility and an increased risk of glaucoma. However, even with substantial angle recession, this risk is not high. Although the risk of developing glaucoma decreases appreciably after several years, it is still present even 25 years or more after injury. In a significant proportion (up to 50%) of fellow eyes, elevated IOP may occur, suggesting that some eyes with trauma that go on to develop glaucoma may have been predisposed to POAG. Alternatively, it is possible the fellow eyes were more likely to have sustained trauma as well. Because it is not possible to predict which eyes will develop glaucoma, regular monitoring of all eyes with angle recession and their fellow eyes is recommended.
The treatment of traumatic glaucoma is often initiated with aqueous suppressants, prostaglandin analogues, and α2-adrenergic agonists. Miotics may be useful, but paradoxical responses of increased IOP may occur. Laser trabeculoplasty has reduced efficacy in these patients. Incisional glaucoma surgery may be required to control the IOP in patients not responding to medical therapy.
Surgically induced IOP elevation
Conventional surgical procedures such as cataract extraction are occasionally associated with transient IOP elevation. Similarly, laser surgery—including trabeculoplasty, iridotomy, and posterior capsulotomy—may be complicated by posttreatment IOP elevation. Although the IOP may rise as high as 50 mm Hg or more, these elevations are usually transient, lasting from a few hours to a few days. Other procedures, including vitrectomy and penetrating keratoplasty (PKP), may be followed by a sustained increase in IOP. The exact mechanism of the IOP elevation is not always known. However, the presence of inflammatory cells, RBCs, debris, pigment release, mechanical deformation of the trabecular meshwork, oxidative damage, and angle closure may be involved.
Agents used as adjuncts to intraocular surgery or postoperative treatment (eg, corticosteroids) may also cause secondary IOP elevation. For example, the injection of viscoelastic substances into the anterior chamber may result in a transient and possibly severe postoperative increase in IOP. Cohesive viscoelastic agents, especially in higher-molecular-weight forms, may be more likely to cause an increase in IOP than dispersive viscoelastics.
Postoperative IOP elevation, even over a short period, can cause considerable damage to the optic nerve in susceptible individuals. Eyes with preexisting glaucoma are particularly at risk of further damage; thus, it is extremely important to monitor IOP soon after conventional or laser surgery and to consider treatment with IOP-lowering medications at the time of surgery. If a substantial rise in IOP occurs, IOP-lowering therapy may be required, including the use of topical β-blockers, α2-adrenergic agonists, or carbonic anhydrase inhibitors. If postoperative inflammation is present, prostaglandin analogues may be deferred until the inflammation has resolved. Paracentesis with release of aqueous fluid (and possibly viscoelastic) can be used to rapidly lower the IOP if it is substantially high. Persistent IOP elevation may require filtering surgery.
The implantation of an intraocular lens (IOL) can lead to a variety of secondary glaucomas, including
uveitis-glaucoma-hyphema (UGH) syndrome
secondary pigmentary glaucoma
pseudophakic pupillary block (see Chapter 10)
UGH syndrome is a secondary inflammatory glaucoma classically caused by chafing of the iris or ciliary body by a malpositioned or rotated anterior chamber IOL. It is characterized by 1 or more of the following:
cystoid macular edema
This condition can also occur after implantation of a posterior chamber IOL in the ciliary sulcus or one that is suture-fixated to the iris or sclera. Implantation of single-piece acrylic IOLs in the sulcus is a particular risk factor for this condition and should be avoided. Gonioscopy and ultrasound biomicroscopy may be helpful in revealing the IOL’s exact position in relation to the iris and ciliary body. Persistent or recurrent cases often require IOL repositioning or IOL exchange, which can be technically challenging because of possible synechiae and/or an open posterior capsule. This syndrome may be mimicked in patients with neovascularization of the internal lip of a corneoscleral wound, which may result in recurrent spontaneous hyphemas and elevated IOP. Laser ablation of the vessels may successfully resolve these cases.
Secondary glaucoma is a common complication after PKP and occurs with greater frequency in aphakic and pseudophakic patients and after a second graft. Wound-induced distortion of the trabecular meshwork and progressive angle closure are the most common causes of glaucoma after PKP. Attempts to minimize these changes with different-sized donor grafts, peripheral iridectomies, and surgical repair of the iris sphincter have been only partially successful. Alternative procedures, such as lamellar stromal or endothelial grafts, may have a lower risk of elevated IOP. Long-term use of topical corticosteroids after PKP is another potential cause of elevated IOP and secondary glaucoma in these patients. Surgical interventions to treat glaucoma after PKP are associated with an increased risk of graft rejection and failure. See BCSC Section 8, External Disease and Cornea, for further discussion of PKP.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.