Mar 28, 2023

Man presents with decreased vision after ocular trauma

A 33-year-old man presented to the Tufts Medical Center emergency department after being assaulted 2 days prior.

The patient was initially seen in the ED at an outside hospital, where he had been evaluated for right eye pain, redness, tearing and blurred vision before eloping. He had been unable to obtain the eye drops prescribed at that time and presented to our institution due to worsening symptoms.

His medical history included schizophrenia and alcohol use disorder with frequent ED visits to local hospitals for associated sequelae. He had no surgical history. He endorsed smoking a quarter pack of cigarettes and drinking approximately 1 L of vodka daily. He had no allergies and was taking an oral antipsychotic. He denied any history of ocular problems.

Visual acuity without correction was 20/60 in the right eye and 20/20 in the left eye. The right pupil was round and nonreactive; the left pupil was round and minimally reactive. There was no relative afferent pupillary defect in either eye. Tonometry demonstrated IOP of 23 mm Hg and 17 mm Hg in the right and left eyes, respectively. Color vision was full bilaterally. He had a prominent right exotropia but with full motility and visual fields to confrontation.

Anterior segment examination of the right eye demonstrated periorbital and eyelid edema, subconjunctival hemorrhage and chemosis, clear cornea without any abrasion or laceration, and a deep anterior chamber with a small fibrinous strand at the inferotemporal pupillary margin. Anterior chamber cells were difficult to appreciate at bedside. On dilated fundus exam, he had areas of commotio retinae in the inferior and inferonasal retinal periphery but no other abnormalities. Examination of the left eye was unremarkable. A CT scan of the orbits showed right periorbital soft tissue swelling, chronic mildly displaced fractures of the nasal bones and no other acute findings.

The patient was seen in the office 2 days later for a comprehensive evaluation. At this visit, visual acuity was measured at 20/100 in the right eye and 20/50 in the left eye. On slit lamp examination, 3 to 4+ fine anterior chamber cells and 2+ flare were noted in the right eye. He was started on prednisolone acetate six times daily and continued cyclopentolate twice daily.

After missing his 1-week follow-up appointment, the patient returned 2 weeks later. He was using his eye drops as directed and reported that his eye pain and light sensitivity had improved, but he continued to have intermittent blurry vision in the right eye. Visual acuity had decreased to 20/400 (20/200 with pinhole) in the right eye and was stable at 20/25- in the left eye. He had a pharmacologically dilated right pupil and full color vision in both eyes. Right eye IOP by applanation was elevated to 41 mm Hg and improved to 25 mm Hg after topical therapy in the office; he was subsequently started on dorzolamide-timolol and brimonidine. On exam, the subconjunctival hemorrhage had resolved, and only rare cells and trace flare were noted. He had signs of an early cataract in the right eye and large cup-to-disc ratios bilaterally, with no evidence of cupping. Retinal examination showed a macular hole in the right eye and was otherwise unremarkable. OCT imaging of the retina was performed.

See answer below.

In the acute setting of ocular trauma, urgent and emergent diagnoses should first be ruled out. Ruptured globe or penetrating ocular injury (with or without intraocular foreign body), retrobulbar hemorrhage leading to orbital compartment syndrome, and orbital fracture with extraocular muscle entrapment are ophthalmic emergencies requiring acute surgical intervention. These conditions are typically obvious based on clinical examination, radiographic imaging and additional supporting history, although some penetrating injuries may be more subtle. Careful evaluation of this patient ruled out these diagnoses.

His worsening vision after trauma, elevated IOP and anterior chamber cells suggest multiple diagnoses contributing to his presentation. For patients with this type of profound deterioration in their vision, OCT can not only be a helpful addition to the clinical examination but also an essential tool in obtaining a diagnosis. In this case, OCT of the retina demonstrated the presence of a full-thickness macular hole of the right eye, providing a likely explanation for his visual acuity (Figure 1).

The presence of anterior chamber cells in the setting of trauma necessitates distinction between red vs. white blood cells. Red blood cells that can only be distinguished microscopically represent microhyphema (in contrast to hyphema, a more apparent accumulation of red blood cells often layering inferiorly). This results from shearing forces to vascular structures in the eye. White blood cells, on the other hand, indicate inflammation in the form of traumatic iritis, a process induced by the necrotic products formed from dead and injured cells. The use of a red-free filter on slit lamp examination can help distinguish between the two, as red blood cells will disappear with the use of this filter and white blood cells will remain visible. In this case, mostly white blood cells were present.

The patient's elevated IOP is likely multifactorial. Given the degree of elevation and amount of inflammation present, obstruction by white blood cells along with potential direct damage to and/or inflammation of the trabecular meshwork could all be contributing factors. The elevation of his IOP after several weeks of treatment with topical prednisolone suggests further impact by steroid-induced ocular hypertension (steroid response).

Given the patient's full extraocular motility and no evidence of a cranial nerve palsy, his persistent right exotropia was thought to be related to the decompensation of an underlying exophoria.

The patient was monitored for his full-thickness traumatic macular hole, which did not spontaneously resolve (Figure 2). He was subsequently evaluated by the retina service, and the decision was made to pursue surgical repair. A 25-gauge pars plana vitrectomy with membrane peel, air-fluid exchange and 15% C3F8 gas was performed 11 weeks after the initial trauma without complication. On postoperative day 1, visual acuity was hand motion and IOP was 19 mm Hg. His early postoperative course was complicated by several missed office appointments and visits to the ED instead for blurred vision and eye pain, but with stable vision and exam noted each time. His right exotropia persisted, suggesting a more chronic history of retinal damage and poor vision in an unreliable patient. Two weeks postoperatively, his vision had improved to counting fingers. Given his normal IOP, the glaucoma drops were stopped.

This patient presented with trauma to the eye, which can lead to damage of any ocular structure. After ruling out emergent diagnoses, evaluation for other pathologies such as eyelid lacerations, corneal abrasions, lacerations or foreign bodies, ocular hypertension or glaucoma, traumatic iritis, hyphema, lens subluxation or dislocation, choroidal hemorrhage, and retinal tear or detachment should take place, as they often require urgent treatment. Traumatic optic neuropathy, commotio retinae, choroidal rupture, retinal or vitreous hemorrhage, zonular damage and iridodialysis/cyclodialysis are important to diagnose and monitor, but early treatment is not typically indicated for these conditions. Cataract formation may be acute or chronic, depending on the extent of the injury and the presence or absence of anterior capsule rupture.

Chronic sequelae and complications of ocular trauma depend on the acute pathology. In particular, secondary glaucoma is common but may be underdiagnosed due to delayed onset. A large cohort study found that 3.39% of patients developed post-traumatic secondary glaucoma within 6 months after blunt ocular injury. Many different mechanisms may be responsible for glaucoma, including direct damage to the eye and/or angle structures (either through blunt or penetrating injury), hyphema, hemolytic glaucoma after hyphema or vitreous hemorrhage, ghost cell glaucoma, inflammation and lens-related problems (such as phacomorphic, lens particle, phacolytic and phacoantigenic glaucomas), among others. Angle-recession glaucoma is especially common after trauma and is strongly associated with hyphema. It is caused by a tear between the longitudinal and circular layers of the ciliary body, evidenced as a widened ciliary body band on gonioscopy. Greater than 180° of angle recession is more likely to result in the development of glaucoma, with more than 270° associated with earlier development of glaucoma. For this reason, monitoring patients and performing careful gonioscopy after their initial injury are essential.

Traumatic macular holes are full-thickness defects of the neurosensory retina, occurring at the fovea after various types of ocular injuries. They occur at an incidence of 1.4% in closed-globe injuries and most commonly occur in young men. Although the pathogenesis is not completely understood, a proposed mechanism suggests that blunt trauma in the anterior-posterior direction of the globe causes a temporary expansion of the globe along the equatorial axis. The tangential forces exerted on the macula then produce a separation of the retinal layers, resulting in a macular hole. Visual acuity may range from 20/30 to 20/400, and in mild cases, patients may complain of metamorphopsia. Huang and colleagues found no correlation between the size of traumatic macular holes and visual acuity (in contrast to idiopathic macular holes, in which a larger diameter corresponds with worse vision).

Management of traumatic macular holes typically begins with observation, as they frequently close spontaneously. Some studies have found a spontaneous closure rate ranging from 28.6% to 44% within the first 2 months. Characteristics suggesting a higher likelihood of spontaneous closure are a smaller size, absence of intraretinal fluid and shorter duration from onset; after more than a year, they are unlikely to close spontaneously. Surgical repair is another option, and although there is no consensus on the optimal timing for operative intervention, the best outcomes are seen when surgery occurs earlier rather than later. Many surgeons elect to operate within the first 1 to 3 months after onset. The surgical technique typically consists of a pars plana vitrectomy with induction of posterior vitreous detachment, epiretinal membrane peel, fluid-gas exchange and head-down positioning for patients postoperatively. Past studies have investigated the application of adjuvants (TGF-beta 2, platelet concentrate, serum) into the hole before infusion of the gas tamponade, which has been thought to facilitate formation of a chorioretinal adhesion and subsequent hole closure. Although silicone oil is an option for tamponade, either SF6 or C3F8 gas is much more commonly used and has a higher success rate for closure. Visual acuity improves when either spontaneous or surgical hole closure occurs. Importantly, anatomic improvement does not necessarily correspond with functional improvement, as damage to the photoreceptor layer and retinal pigment epithelium from the initial trauma can be visually significant.

This patient also had traumatic iritis, which commonly occurs after blunt ocular injury. It manifests as an anterior chamber reaction of variable severity, and primary symptoms include eye pain, photophobia and mildly decreased vision. Occasionally, the impact of trauma may cause a ring of iris pigment, or Vossius ring, to be imprinted on the anterior lens capsule from forces pushing the iris posteriorly. More chronic inflammation can cause synechiae. Traumatic iritis is treated with topical steroids and cycloplegics as first-line therapy. Cycloplegia helps prevent the formation of posterior synechiae and reduces the patient's pain and discomfort from ciliary body spasm. As with other forms of uveitis, steroid treatment should be tapered, but patients often do not require an extended taper as the inflammation responds well to steroids.

Acute trauma can cause either increased or decreased IOP. Increased IOP results from damage to the trabecular meshwork, trabeculitis or obstruction of the trabecular meshwork by either red or white blood cells. Decreased IOP can occur from ciliary body damage and decreased production of aqueous humor. This patient had no hyphema or lens capsule violation, which can also contribute to glaucoma by obstructing flow through the trabecular meshwork by blood cells or lens proteins. Ocular hypertension and glaucoma in the setting of blunt trauma should be managed based on the underlying etiology, but regardless of the mechanism, topical IOP-lowering drops are indicated as first-line therapy. Aqueous suppressants are most effective, and cholinergic agents should be avoided as they impair uveoscleral outflow and may increase IOP in the setting of angle recession and restricted aqueous flow through the trabecular meshwork. Oral agents (eg, acetazolamide, methazolamide) can be added when topical therapy is insufficient. Incisional glaucoma surgery (trabeculectomy, tube shunt) and/or cyclodestructive procedures can play a role for cases refractory to medical treatment. Laser trabeculoplasty has not been found to be significantly effective. Patients should also be monitored with gonioscopy for the development of angle recession, which can cause glaucoma weeks to years after trauma.

Six weeks after macular hole repair, the patient's visual acuity was 20/400 in the right eye, and OCT demonstrated closure of his macular hole (Figure 3). However, IOP was 46 mm Hg, which improved with topical therapy and oral acetazolamide in the office. He was restarted on topical glaucoma drops (dorzolamide-timolol and brimonidine) in addition to oral acetazolamide. He was then referred to the glaucoma service for further management. Examination demonstrated 180° of angle recession in the right eye with a highly pigmented trabecular meshwork. He had a small iris sphincter tear noted in addition to early cortical cataract and anterior and posterior subcapsular opacities. Visual acuity was 20/70, and IOP was 21 mm Hg in the right eye. Visual field testing and OCT of the optic nerves were unreliable. The patient was diagnosed with ocular hypertension in the setting of angle recession, pigmented angle and steroid response, for which he was continued on glaucoma drops, and latanoprost was added. He has since been lost to ophthalmology follow-up but continues to periodically present to the ED for alcohol intoxication.

In patients who may be unreliable with medication adherence or follow-up appointments, interventions that minimize the need for patient-initiated effort should be prioritized. When possible, a multidisciplinary approach to care should be implemented by coordinating care with social workers and case managers, or family members in cases in which patients are willing. Patients who are experiencing homelessness may have assigned case workers through local programs and shelters. These individuals should be involved when patients have vision-threatening conditions and/or require close monitoring, as they may be in closer contact with patients and can help ensure they return for care.

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