Monitoring intraocular pressure is critical in the early stages of chemical injury, especially with alkali burns. Acute secondary glaucoma may occur as a result of inflammation, shrinkage of scleral collagen, release of chemical mediators such as prostaglandins, direct injury to the angle, or compromise of the anterior uveal circulation. Oral carbonic anhydrase inhibitors may be used to lower intraocular pressure until the corneal epithelium adequately heals to allow for the introduction of topical intraocular pressure lowering agents. Chronic secondary open angle glaucoma may also occur months to years following chemical injury due to trabecular damage. (A more detailed discussion of chemical injury can be found in chapter Corneal Trauma on section Chemical Injury.)

Traumatic hyphema, following blunt or penetrating ocular trauma or intraocular surgery may cause acute rises in intraocular pressure. Typically, increased intraocular pressure leading to glaucomatous nerve damage occurs following a recurrent hemorrhage or in patients with sickle cell hemoglobinopathies. Elevated intraocular pressure may occur acutely following obstruction of the trabecular meshwork, pupillary block by a “buttonhole clot” involving both the anterior and posterior chambers, trauma to the trabecular meshwork, angle recession, or chronically by the formation of peripheral anterior synechiae.

The three most common anterior chamber angle injuries found in a sample of posttraumatic glaucoma patients were angle recession, iridodialysis, and cyclodialysis [1]. Iridodialysis refers to a separation of the iris root from the ciliary body. Secondary glaucoma may develop acutely if associated with significant hyphema or chronically by the formation of peripheral anterior synechiae if untreated. Cyclodialysis refers to a separation of the ciliary body from its attachment at the scleral spur, resulting in a cleft. Cyclodialysis typically causes hypotony that may result in visual damage; however, delayed closure of a cleft may result in an acute rise in intraocular pressure with a formed anterior chamber and open angle.

Recession of the anterior angle may occur following blunt ocular trauma by tears in the ciliary body, usually between the longitudinal and circular fibers. Angle recession is often associated with injury to the trabecular meshwork as well. Glaucoma associated with angle recession, referred to as angle recession glaucoma or traumatic glaucoma, presents as chronic secondary open angle glaucoma with an insidious rise in intraocular pressure leading to glaucomatous nerve damage and visual field loss months to years following the trauma.

A population-based study conducted on inhabitants in Mamre, South Africa revealed a prevalence of angle recession at 14.6% of 987 inhabitants screened with gonioscopy, over half of which having bilateral angle recession. The prevalence of glaucoma in those with angle recession was 5.5 to 8.0% in eyes identified as having 360° angle recession [2]. Possible risk factors for the development of glaucoma with angle recession include increased pigmentation of the angle, elevated baseline intraocular pressure, hyphema, lens displacement, and angle recession of more than 180° [3].

All individuals sustaining blunt ocular trauma should undergo gonioscopic evaluation of the angle for recession, typically 6–8 weeks following the trauma. Gonioscopic findings may include a broad angle recess, absent or torn iris processes, a white glistening scleral spur, depression in the overlying trabecular meshwork, and peripheral anterior synechiae in the border of the recession (Fig. 5.1). Patients identified with recessed angles should be monitored routinely with intraocular pressure checks and adjunctive glaucoma testing.

Treatment of angle recession glaucoma is often initiated with topical medications such as aqueous suppressants, prostaglandin analogs, and alpha-2 adrenergic agonists. Laser trabeculoplasty has little utility [4]. Surgical intervention may be undertaken to lower the intraocular pressure. Angle recession glaucoma had been associated with a high rate of bleb failure in trabeculectomy; however, trabeculectomy with adjunctive mitomycin C has been shown to be effective [5, 6]. Glaucoma drainage devices are also gaining popularity for the treatment of this condition.

Ghost cell glaucoma and hemolytic glaucoma are related forms of secondary open angle glaucoma that develop following a traumatic vitreous hemorrhage with a disrupted anterior hyaloid face that provides a communication between the posterior and anterior chambers. In ghost cell glaucoma, de-hemoglobinized red blood cells or “ghost cells” migrate to the anterior chamber to block trabecular outflow channels leading to elevated intraocular pressure; while in hemolytic glaucoma, hemoglobin-laden macrophages are the source of the obstruction. Theoretically, patients with a disruption of the anterior hyaloid face from previous ocular trauma or surgery are at risk for the development of hemolytic or ghost cell glaucoma following vitreous hemorrhage of any cause.

On examination, khaki-color cells are visualized in the anterior chamber out of proportion to aqueous flare and can be seen layering over the inferior trabecular meshwork on gonioscopy in ghost cell glaucoma. In hemolytic glaucoma, red-tinged cells are seen in the anterior chamber and a reddish-brown pigment is seen covering the trabecular meshwork on gonioscopy. Given the time course for the natural degradation of red blood cells, elevation in intraocular pressure tends to occur a few weeks to three months following the vitreous hemorrhage [7].

The incidence of hemolytic and ghost cell glaucoma following traumatic vitreous hemorrhage is not known. Regardless, intraocular pressure should be monitored closely in the posttraumatic vitreous hemorrhage patient for the development of secondary open angle glaucoma. Following clearance of the hemorrhage, which removes the source hemoglobin and red blood cells, the secondary open angle glaucoma typically resolves. Intraocular pressure may be managed with traditional topical aqueous suppressants although some patients may require anterior chamber washout or glaucoma filtration surgery. Pars plana vitrectomy may be indicated to clear the vitreous hemorrhage for visual improvement and for control of intraocular pressure.

Retained intraocular foreign body from previous penetrating ocular trauma composed of iron causes siderosis. If untreated, iron deposited in neuroepithelial tissue oxidizes to form powerful free radicals that promote chronic intraocular inflammation, where secondary chronic open angle glaucoma may develop. Also known as siderotic glaucoma, the retained iron-containing foreign bodies may also be associated with heterochromia, mydriasis, and rustlike discoloration of the anterior capsular and posterior corneal surfaces.

Secondary glaucoma may follow anterior segment surgery or various ophthalmic laser procedures. Peripheral iridotomy with neodymium:yttrium–aluminum–garnet (Nd:YAG) laser may cause an immediate spike in intraocular pressure that is usually transient but may occasionally be clinically significant. The photodisruptive properties of Nd:YAG laser on pigment-containing iris epithelial tissue can cause bleeding and secondary pigment dispersion that can obstruct aqueous outflow at the trabecular meshwork. A series of 734 Chinese patients reported intraocular pressure rises of >8 mmHg in 9.8 and 0.8% of treated patients at one hour and two weeks post-procedure, respectively [8]. The series also revealed an association between the incidence of intraocular pressure spikes with higher amounts of laser energy used for the procedure. Similarly, patients undergoing posterior capsulotomy with Nd:YAG laser can have long-term elevations in intraocular pressure when higher amounts of energy are used, as reported in one series comparing groups receiving <80 and >80 mJ treatments [9].

Patients undergoing Nd:YAG laser iridotomy typically are pretreated with intraocular pressure lowering agents such as brimonidine 0.15% and pilocarpine 2%. Previous series have shown higher incidences of intraocular pressure spikes, including clinically significant rises, in patients not receiving intraocular pressure lowering pretreatment [10]. Following the procedures with Nd:YAG laser, patients are typically given a short course of topical nonsteroidal or corticosteroids to reduce inflammation and associated intraocular pressure rises.

Intraocular pressure rise is relatively common following cataract surgery that may occur by a variety of mechanisms with either an open or closed anterior chamber angle (Table 5.2). Frequently, intraocular pressure can acutely rise in the immediate postoperative period due to retention of high viscosity dispersive viscoelastic material (sodium hyaluronate, sodium chondroitin sulfate-sodium hyaluronate), commonly utilized in the modern era of phacoemulsification for intraoperative endothelial cell protection [11]. In this scenario, the peak of intraocular pressure rise occurs about 4–6 hours following surgery usually due to an obstruction in aqueous outflow through the trabecular meshwork. Patients may present with acute pain and corneal haze with an open anterior chamber angle due to significantly elevated pressure. In addition to medical management, the surgeon may also provide gentle pressure on the posterior lip of the surgical paracentesis wound to release a small amount of aqueous humor to provide immediate pressure lowering. Over the course of a few days, intraocular pressure tends to normalize as the retained material resorbs.

Secondary glaucoma is also a common complication following penetrating keratoplasty. The glaucoma typically progresses in a chronic insidious nature due to wound distortion of the trabecular meshwork and progressive angle closure. Aphakic and pseudophakic patients and those with a second graft are more frequently affected. Various treatment options may be utilized. Glaucoma drainage implants and trabeculectomy combined with antimetabolite (mitomycin C) have shown similar efficacy [12].

Inflammation, hyphema, and increased intraocular pressure can occur as a result of contact between the iris or ciliary body and a malpositioned intraocular lens implant. This entity, known as uveitis-glaucoma-hyphema syndrome, was first recognized in 1978 with the creation of poorly developed anterior chamber lens implants that resulted in iris chafing. This syndrome can lead to chronic inflammation, cystoid macular edema, hemorrhage, and glaucomatous optic neuropathy. Although the number of cases has been reduced with the advent of posterior chamber intraocular lenses, it can still occur because of posterior iris chafing. Treatment usually involves intraocular lens removal, repositioning, or exchange. Medical management involves the use of intraocular pressure lowering drops for glaucoma and topical steroids for uveitis [13].