The Many Faces of Traumatic Glaucoma

Ocular trauma is a common reason for emergency appointments in optometric practice, with an estimated 7.5% of Americans experiencing an eye injury at some point in their lives.¹ Patients presenting in the aftermath of trauma require thorough evaluation and prompt management.

A significant concern in the immediate and chronic phases of management is the potential development of trauma-induced glaucoma. Glaucoma occurring secondary to trauma is multifactorial in nature, and can be obvious at presentation, or masquerade in the acute phase.^2,3

Elevated intraocular pressure (IOP) following an injury is most often due to impaired outflow of aqueous humor through the trabecular meshwork. However, not all cases will initially manifest with elevated IOP.

In some instances, decreased IOP may be present at the time of evaluation secondary to dysfunction of the ciliary body, inflammation, or an open-globe injury.² IOP may subsequently rise after the acute phase has resolved if underlying damage has impaired outflow pathways.

Pathophysiologies of trauma-induced glaucoma

Traumatic glaucoma is classified based on the mechanism of trauma, timing of IOP elevation, and the underlying pathophysiological changes it causes.

Closed-globe trauma

Early onset

Several conditions can cause closed-globe trauma with an early onset of days to weeks, including:

Trabecular meshwork damage: Following blunt force trauma, tears in the trabecular meshwork, inflammation, and clots from Schlemm’s canal may impede outflow and impact IOP.²
Hyphema: Aggregation of blood within the anterior chamber can arise secondary to the shearing impact of the compression-decompression forces to the globe that occur during blunt trauma (Figure 1).³ The red blood cells present may obstruct and impede outflow, resulting in elevation of IOP.²
Traumatic iritis: An innate immune response may be provoked secondary to trauma, where permeability of the blood vessels and inflammatory mediators increase.³ The trabecular meshwork can then be obstructed by inflammatory debris resulting in elevated IOP (Figure 2).
Choroidal hemorrhage: An anterior shift to the retina and choroid can cause stress on the posterior ciliary arteries resulting in a suprachoroidal hemorrhage (Figure 3).³ The anterior shift can push the lens-iris diaphragm forward, resulting in a blockage of the trabecular meshwork, elevating IOP secondary to angle closure.²

Figure 1: Slit lamp image of traumatic hyphema.

^{Figure 1: Courtesy of Devyn Moran Glover, OD.}

Figure 2: Slit lamp image of traumatic iritis.

^{Figure 2: Courtesy of Devyn Moran Glover, OD.}

Figure 3: Fundus photograph of choroidal hemorrhage.

^{Figure 3: Courtesy of Devyn Moran Glover, OD.}

Late onset

Causes of closed-globe trauma with late onset of months to years can range from angle recession to lens dislocation, as follows:

Angle recession: Gonioscopic views will reveal a broadening of the ciliary body band (Figure 4) that occurs secondary to a tear typically between the circular and longitudinal muscles of the ciliary body and the retrodisplacement of the iris root.²
- Angle recession is closely linked to traumatic hyphema and higher rates of glaucoma are apparent in cases where broader damage to the angle are noted.²
Ghost cell glaucoma: When a traumatic vitreous hemorrhage occurs, or a hyphema is long-standing; this secondary open-angle glaucoma can develop. The outflow of the trabecular meshwork can be impeded by “ghost cells”—dehemoglobinized red blood cells—and potentially increase IOP.²
Lens subluxation or dislocation: Displacement of the lens can occur with trauma. The mechanism in which IOP raises is dependent on the location of the dislocated lens. Pupillary block, chronic or acute angle closure, and blocking of the trabecular meshwork by vitreous strands can elevate IOP.³
Steroid-induced glaucoma: A temporary elevation in IOP can occur with topical steroid use. The mechanism of which this often short-lived elevation occurs is thought to be from elevated resistance in outflow through the trabecular meshwork.³
- Timing and magnitude of elevation is often related to potency, frequency, duration, administration route, and patient individual risk factors.³

Figure 4: Gonioscopic view of angle recession.

^{Figure 4: Courtesy of Devyn Moran Glover, OD.}

Open-globe trauma

The initial goal following open-globe trauma is to allow for healing by closing all wounds. IOP can become elevated due to a variety of mechanisms including angle closure, inflammation, hemorrhage, lens displacement, and epithelial or fibrous downgrowth.³ The incidence of developing glaucoma secondary to open-globe trauma is approximately 2.7%.⁵

Deeper dive into downgrowth

The following mechanisms are specific to eye injuries in which the corneoscleral envelope is breached through penetration or rupture:

Epithelial downgrowth: The introduction of epithelial cells from the external portion of the eye can lead to the growth of membranes, pearls, or cysts on a variety of structures in the anterior segment.² If structures like the trabecular meshwork are impacted and impeded, IOP can rise.
Fibrous downgrowth: Like epithelial downgrowth, a fibrovascular tissue can proliferate on a variety of anterior segment structures leading to impairment of outflow through the trabecular meshwork.³

Clinical evaluation of suspected traumatic glaucoma

A detailed case history is the first and most crucial step when evaluating patients post ocular trauma. It is crucial to determine what type of injury occurred and the nature of the object that the eye encountered. Additionally, timing of the injury must be known to guide clinical decisions and management in the acute phase.

When assessing patients with a traumatic injury, it is important to note whether the patient is taking blood thinners and whether there is a personal or family history of sickle cell disease, as these factors potentially influence the course of treatment.

All symptoms should be documented, including the level of pain, changes in visual acuity, presence of diplopia, and new onset photopsia or other visual disturbances.

Initial exam

Initial examination should assess the pupils, extraocular muscles, visual fields, visual acuity, and IOP. Rebound tonometry may be useful in the immediate aftermath of an injury, especially if concern for an open-globe injury. However, long-term management may be best monitored with Goldmann applanation tonometry (GAT).

Slit lamp exam

A thorough slit lamp evaluation of the anterior segment is then warranted. Sodium fluorescein should be instilled to assess for positive Seidel sign, and to rule out open-globe trauma. If safe and possible, prior to dilation, gonioscopy should be performed to evaluate structures of the angle for trauma related damage.

A dilated fundus exam should then be done to rule out any retinal, vitreous, or choroidal abnormalities. A thorough assessment of the optic nerve should be done noting signs of edema, pallor, or other signs of damage.

If the posterior segment cannot be visualized, a B-scan ultrasound should be considered to identify pathology. In cases involving orbital trauma, additional diagnostic imaging, such as CT scan, MRI, or X-Ray may be indicated.

Address IOP elevations

Immediate concerns should be addressed, including elevated IOP. The treatment plan should be guided by the ocular structures involved and the suspected mechanism causing the acute rise in IOP. It is important to note that IOP may be low in the initial evaluation phase of traumatic glaucoma.

When appropriate, baseline glaucoma testing—such as pachymetry, visual field testing, optical coherence tomography (OCT), and corneal hysteresis—should be performed to assess the severity of disease and establish a long-term follow-up plan for effective ongoing management.

Treatment and management of traumatic glaucoma

Treatment for traumatic glaucoma is dependent on the state of the globe and time of onset.

Closed-globe trauma with early onset

In the acute phase of ocular trauma, if IOP is elevated, aqueous suppressants (e.g., timolol, dorzolamide, brinzolamide, or brimonidine) are recommended to reduce aqueous production, thus lowering pressure. The choice of which agents and dosing schedule to utilize is dependent on how severely elevated the IOP is.

When inflammation is present following an injury, topical corticosteroids are often indicated. Potency, dosage, and frequency depends on the magnitude of inflammation present. Furthermore, patients need to be monitored closely, as steroid use can potentially induce a secondary elevation in IOP.

For blood-related pathologies (e.g., hyphema, vitreous hemorrhage), a combination of aqueous suppressants, topical corticosteroids, and cycloplegics are recommended to manage symptoms and promote healing. Patients should be encouraged to elevate their head while sleeping to facilitate blood clearance.

Special consideration is needed for patients with sickle cell disease, as carbonic anhydrase inhibitors (CAIs) need to be avoided due to increased sickling of red blood cells; consider avoiding drugs that have antiplatelet activity.

Surgical management

If limited or no improvement is made with topical management, surgical intervention such as an anterior chamber washout can remove clotted or persistent hyphemas.

Approximately 5% of cases involving hyphemas secondary to trauma require surgical intervention.³ The decision to intervene surgically depends on the patient’s risk of permanent vision loss as well as the severity and duration of elevated IOP.³

^{Courtesy of Steven R. Sarkisian, Jr, MD.}

Table 1: Guidelines for surgical intervention based on duration of severely elevated IOP in healthy eyes.³

IOP Elevation	Duration
> 50mmHg	5 days
> 45mmHg	7 days
> 35mmHg	14 days

^{Table 1: Courtesy of Razeghinejad et al.}In cases of choroidal hemorrhage, it is recommended to manage pain and mitigate elevated IOP. Cycloplegics and corticosteroids can be used to stabilize vascular integrity.² Miotics are contraindicated as they may adversely impact the depth of the anterior chamber.²

Closed-globe trauma with late onset

Treatment guidelines for cases of closed-globe trauma with late onset are as follows:

Angle recession glaucoma: Patients who develop angle recession secondary to trauma are managed similarly to those with primary open-angle glaucoma (POAG).
- Topical hypotensive medications may be able to effectively manage IOP; however, surgical procedures such as laser trabeculoplasty, minimally invasive glaucoma surgery (MIGS), or filtration procedures are sometimes warranted.
Ghost cell glaucoma: Typically, conservative topical therapy with aqueous suppressants is utilized as first line therapy. Cycloplegics and corticosteroids may be needed to clear the anterior chamber of lingering ghost cells. Surgical intervention is required if IOP is not responding to medical treatment.
- In most cases, a pars plana vitrectomy will eliminate residual ghost cells. However, surgical intervention such as filtration surgery or cyclophotocoagulation may additionally be needed to manage the glaucomatous component of these cases.²
Lens dislocation or subluxation: IOP elevation secondary to lens dislocation should be managed depending on the position of the lens. Surgical evaluation is almost always indicated. It is crucial to remove the dislocated lens and replace or exchange the intraocular lens.

Open-globe trauma

Post open-globe trauma, epithelial and fibrous downgrowth may manifest and are managed similarly. In non-progressive cases, observation may be appropriate.

However, the associated glaucoma can be aggressive and challenging to control.³ Management often requires surgical removal of the downgrowth, glaucoma drainage implants, and/or cyclophotocoagulation to effectively manage IOP.³

Differential diagnoses for traumatic glaucoma

According to data from the US Eye Injury Registry, approximately 3.4% of individuals develop glaucoma within 6 months of sustaining blunt ocular trauma.⁴ Several risk factors may increase the likelihood of development of traumatic glaucoma, including poor initial visual acuity, advanced age, angle recession, lens trauma, hyphema, and elevated IOP at presentation.²

In the acute phase following ocular trauma, a careful assessment can identify the specific mechanism responsible for the pressure increase. The leading differential diagnoses include corticosteroid-induced IOP elevation and previously undiagnosed POAG. Elevation in IOP secondary to corticosteroid use can occur within one to two weeks of use.²

Other conditions, such as hyphema, intraocular inflammation, angle abnormalities, and lens-related pathology, can lead to transient elevation in IOP or progress to chronic traumatic glaucoma.

Potential complications of traumatic glaucoma

Glaucoma secondary to trauma can lead to serious complications, including optic nerve damage, progressive visual field loss, and ultimately irreversible vision impairment. Prompt identification of the underlying mechanism of elevated IOP is crucial to provide the most appropriate treatment approach.

In some cases, topical medications—such as aqueous suppressants, miotics, mydriatics, and corticosteroids—may be able to effectively manage IOP elevation and limit damage. However, if medical management is inadequate, surgical intervention ranging from MIGS to more invasive procedures, such as filtration surgery, may be necessary to prevent further glaucomatous progression.

Additionally, the contralateral, uninjured eye should be treated as a glaucoma suspect. Patients with a history of traumatic glaucoma are at an elevated risk for the development of POAG in the contralateral eye.⁶

Tips for educating patients on trauma-induced glaucoma

Patients should receive individualized education regarding their immediate concerns following ocular injury. Furthermore, it is equally important to educate patients on long-term risks, including the potential for glaucomatous progression. Emphasizing the elevated risk of glaucoma development is especially important in patients with known risk factors.

Patients should understand that glaucoma can lead to irreversible and progressive vision loss, and the absence of elevated IOP or optic nerve damage in the acute phase does not eliminate future risk. Long-term follow-up and treatment compliance are crucial to preserve vision and prevent disease progression.

At a minimum yearly glaucoma testing (e.g., OCT, visual fields, gonioscopy) is recommended; however, patients at higher risk may need more frequent monitoring.

Conclusion

Traumatic glaucoma can pose an immediate threat to vision loss or remain a silent, progressing condition that is diagnosed years or even decades after the initial injury. One of the most important tasks of the provider in the aftermath of injury is to obtain a thorough case history to guide clinical evaluation and management.

Equally important is patient education. As providers, we must clearly communicate both short- and long-term risks associated with traumatic glaucoma. Empowering patients with this knowledge fosters a deeper understanding of the importance of ongoing care.

Additionally, education reiterates their responsibility to attend follow-up visits, which are essential for detecting late-onset complications that may otherwise go undetected.