Open Angle and Traumatic Glaucoma
Soshian Sarrafpour
Magdalena Robak
THE CLINICAL CHALLENGE
Although often thought of as a disease of increased intraocular pressure (IOP), the term glaucoma refers to a group of diseases characterized by degeneration of retinal ganglion cells and is thus best understood as an optic neuropathy that is often, but not always, associated with elevated IOP. Glaucomatous damage occurs at the level of the ganglion cells, and thus thinning of the retinal nerve fiber layer (axons of the ganglion cells) and ganglion cell layer is seen in glaucoma. A variety of etiologies can present as open angle glaucomas, including traumatic glaucomas. Evaluation for other concerning ophthalmic conditions such as tumor or retinal detachment is essential in anticipation of treatment.
Glaucoma can lead to irreversible vision loss. The vision loss is classically peripheral vision (Figure 46.1); however, patients often describe blurry vision and require increased lighting to see well owing to a loss of contrast sensitivity.1 More importantly, vision loss from glaucoma is oftentimes devastating to patients and can be associated with loss of independence, depression, falls, and motor vehicle collisions.2,3 As such, whereas acute angle closure glaucoma is more readily recognized by emergency providers, the vision loss of open angle glaucomas may indirectly lead to a broader array of chief complaints, particularly in an aging population. Given the rapid irreversible vision loss that can happen, swift diagnosis and treatment are often essential to optimizing outcomes.
The most important and only known modifiable risk factor is elevated IOP. Other historical risk factors include increasing age, family history, race, and thinner central corneal thickness.4 Other risk factors may include myopia, diabetes, systemic hypoperfusion, and trauma.5
Elevated IOP in open angle glaucomas presents a serious and urgent threat of damage to the optic nerve and thus the peripheral (and eventually central) vision of a patient. If left uncontrolled, persistently elevated IOPs can lead to irreversible blindness (“time is vision”). Patients usually present in the emergency setting because of pain and nausea associated with markedly high IOP, which may reduce penetrance and efficacy of traditional topical medications. Trauma-associated glaucoma can be challenging to evaluate owing to associated eyelid swelling, hyphema, vitreous hemorrhage, or corneal edema that limit ocular exam and visualization of the optic nerve. IOP measurement and other parts of the exam may also have to be deferred in the setting of trauma until a ruptured globe is ruled out. Additionally, patients presenting with trauma may have other life-threatening injuries that require immediate attention, leading to prolonged untreated elevations of IOPs and potential vision loss.
 Figure 46.1: Optic Nerve and visual field findings of mild, moderate, and advanced glaucoma. |
Open angle Glaucoma
Glaucoma is a leading cause of irreversible blindness in both the United States and abroad.6 Globally, the prevalence of glaucoma in patients 40 to 80 years old is 3.54% as of 2014 and is predicted to impact almost twice as many people (111.8 million) by 2040.7 In the United States, racial differences have been observed, although it is unclear due to methodological flaws whether this is due to genealogical differences or social injustices tracing back to slavery and continued structural racism. The most notable of these studies, “Racial Variations in the Prevalence of Primary Open-angle Glaucoma,” identified at least a fourfold increase in age-adjusted prevalence of primary open angle glaucoma (POAG) in Black compared with white patients in East Baltimore. In the study, “race” was defined by self-reported census terms without respect to ancestry and all designations other than “Black” or “white” were included in the white cohort.8
Pathophysiology
The etiology of open angle glaucoma varies, and multiple mechanisms and etiologies are described. In general, outflow is typically obstructed past the visible trabecular meshwork (hence “open angle”) or episcleral vascular pressures can be elevated (as in carotid-cavernous fistula, Sturge-Weber syndrome, etc.). Please refer to the differential diagnosis section for some potential etiologies of open angle glaucomas. POAG is a diagnosis of exclusion when no other cause is found.
Traumatic Glaucoma
Traumatic glaucoma is multifactorial and can occur following penetrating, blunt, chemical, and surgical trauma. Glaucoma occurs most commonly after blunt trauma, with an incidence of about 3.39% at 6 months after the inciting incident.9 Risk factors include poor presenting visual acuity, older age, injury involving the lens, angle recession, presence of hyphema, and elevated IOP at presentation.9 As a consequence of this, after emergency evaluation and treatment for acute conditions, referral to ophthalmology for follow-up and surveillance is appropriate.
Pathophysiology
Blunt trauma causes a sudden compression of the eye posteriorly, forcing the globe to expand at the equator and stretching tissues within the eye. This causes trauma to the pupil sphincter, the iris base, the ciliary body, the trabecular meshwork, the zonules holding the lens, and the peripheral retina.10 Damage to the angle and trabecular meshwork can lead to lifelong glaucoma. Additionally, elevations in ocular pressure can occur from hyphema, vitreous hemorrhage, pigmentary debris, or inflammation after trauma.
Inflammation and dispersion of pigment and debris in the eye obstruct the trabecular meshwork and leads to IOP spikes. This is usually self-limited and clears spontaneously, although IOP control with medication may be required while waiting for resolution.
Traumatic hyphema can exacerbate posttraumatic IOP elevations by clogging the trabecular meshwork with red blood cells. Elevation of IOP can occur and should be managed appropriately, although these elevations tend to be self-limited. These patients should be followed closely for rebleeding, usually within the first 5 days of trauma.
Alkaline agents penetrate through tissue and cause glaucoma (uncommon in acid injuries). The IOP initially goes up to 40 to 50 mm Hg within 10 minutes, then returns to normal before gradually rising to high levels again over the next 1 to 2 hours. The initial IOP spike may be from distortion of the trabecular meshwork from contraction of the outer collagen layers of the eye, whereas the second elevation of IOP is thought to be from prostaglandin release. Long-term damage from inflammation can induce peripheral synechiae of the angle, which can lead to angle closure glaucoma.
Late manifestations of glaucoma from trauma can occur from a variety of etiologies as well. These include ciliary body muscle tears (angle recession), lens-induced glaucomas, ghost cell glaucoma (long-standing heme in the vitreous or anterior chamber can lead to khaki colored “ghost cells” which can obstruct outflow), choroidal hemorrhages, and retinal detachment. Lens-induced glaucomas are worth additional mention. Traumatic lens dislocation can lead to pupillary block or lens swelling that mechanically closes the angle (phacomorphic glaucoma). Additionally, if mature cataracts develop (phacolytic glaucoma) or if the lens capsule is violated (phacoantigenic or lens particle glaucoma), lens debris and inflammatory material can obstruct the outflow pathways.
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