Signs and Symptoms
Commotio retinae, formerly known as Berlin’s edema, presents as an area of retinal pallor following direct blunt ocular trauma. Symptoms are associated with the location and extent of the retinal bruising along with the collateral consequences of the blunt trauma.1-18 Any amount of retinal disruption located centrally can cause patients to observe metamorphopsia or reduced visual acuity without decreased red or brightness saturation.
The associated findings from blunt trauma may range from mild diffuse injection, chemosis, subconjunctival hemorrhage, photophobia and pain upon ocular motility to orbital fracture, iridodialysis, lens luxation, traumatic iritis, vitreous hemorrhage and globe rupture.2-13 While specific data for ocular injuries have fluctuated over the last 10 years, one thing has remained constant: injury rates are consistently highest among males of all ages.6-11
The classic work of Sipperly, Quigley and Gass demonstrated that the predominant retinal abnormality in commotio retinae was disruption of the photoreceptor outer segments caused by hydraulic ocular distention induced by blunt force trauma, and not actually retinal edema.15 This mechanism altered the hydrodynamics of the intraretinal and choroidal vascular systems, creating fluid leakage.
The condition is not merely an accumulation extracellular fluid, as originally postulated by Berlin.1-4,14,15 It has been documented in animal models that the predominant pathophysiology is destruction of the vulnerable and delicate photoreceptor outer segments along with the concomitant imbibition of multiple intraretinal cellular elements (RPE, axons of the photoreceptor cells, Müller cells and selected ganglion cells) with intracellular fluid.1-4,14,15 Visual disability depends upon the degree and location of permanently lost photoreceptors. Interestingly, the RPE’s response to traumatic photoreceptor damage seems similar to that observed in experimental retinal detachment and light-induced retinal damage.13,14
Recent in-vivo investigations using spectral-domain optical coherence tomography (SD-OCT) confirm what was postulated by histological studies: commotio retinae is a disruption and fragmentation of the photoreceptor outer segments with resultant fluid incursion and collateral damage to retinal elements.1-4,14-17 The location of the commotio injury is traditionally in the contrecoup position, or directly opposite the site of the impact.1,18
SD-OCT imaging has been used to create a grading scale for macular commotio retinae based upon four distinct photoreceptor morphologic features that have been consistently observed:4
Grade 1: An increase in inner segment-outer segment (IS-OS) junction reflectivity with the disappearance of the thin hyporeflective optical space.
Grade 2: Cone outer segment tip (COST) defects only.
Grade 3: COST and IS-OS junction defects.
Grade 4: COST defects, IS-OS junction and external limiting membrane (ELM) defects.
Eyes with higher grades at baseline had significantly worse visual and anatomic outcomes.4
Cystoid macular edema (CME) is a classical complication of ocular inflammation and is a possible comorbidity of commotio retinae.21 CME can result either from an insult to the inner or outer blood/ocular barrier.12,21
There is no treatment for commotio retinae.12-14 Management consists of attending to accompanying damage (facial or orbital fractures, tissue lacerations, corneal abrasion, traumatic uveitis, subconjunctival hemorrhage) and emotionally supporting the patient when vision is reduced. Acuity monitoring, Amsler grid testing, interferometry and SD-OCT can provide comparative data indicating progress of recovery.1-4,14-17 Patients can be counseled that in the absence of associated damage to the cornea, lens and macula, visual recovery typically returns to pre-injury levels.16-18 In the event it does not, the majority of incompletely resolved cases return to levels better than 20/30.18
Complications such as premature cataractogenesis and the symptoms associated with epiretinal membrane formation, posterior vitreous detachment and macular hole formation should also be mentioned as possible sequelae of the inciting blunt ocular trauma.1,3,5,6,11-13
Facial fractures should be prophylactically medicated with an oral antibiotic. Lacerations and abrasions to the epidermis, conjunctiva and cornea should be protected with topical antibiotic. Concurrent iritis should be treated using a topical cycloplegic and a topical corticosteroid. Hyphema should be managed with bed rest, elevated head position to promote blood settling with the additions of a nasal decongestant, stool softener and ocular hypotensives as necessary. Topical nonsteroidal and steroidal medications along with oral carbonic anhydrase inhibitors and injected steroidal depots have been used to manage recalcitrant cases of CME with variable results.20
• Commotio retinae should be used as an indicator to carefully examine all ocular structures post-trauma.
• A 360° subconjunctival hemorrhage carries the risk of ruptured globe.
• Significant blunt ocular trauma mandates the consideration of imaging to rule out facial and orbital fracture.
• Blunt trauma cases should be monitored for late glaucoma over the patient’s lifetime.
• In cases of peripheral commotio retinae with no visual loss or coexistent ocular damage, the best management is simple observation and patient reassurance.
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