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Commotio Retinae

ROUTINE — Trauma

Symptoms

  • Decreased central or peripheral vision, depending on the site of impact.
  • Can be asymptomatic if localized outside the macula.
  • Positive history of recent blunt ocular trauma.

Clinical Findings

Ophthalmoscopic appearance

  • Confluent, well-demarcated area of gray-white retinal opacification at or directly opposite the site of impact.
  • Retinal blood vessels course normally and undisturbed over the area of whitening (distinguishes it from ischemic CRAO).

Berlin'S EDEMA

  • The specific eponym used when commotio retinae involves the macula/posterior pole.
  • May present with a "cherry-red spot" mimicking a central retinal artery occlusion (CRAO).

Pathophysiologic signature

  • Despite the term "edema," this is NOT true extracellular fluid accumulation.
  • The retinal whitening is caused by fragmentation and disruption of the photoreceptor outer segments and intracellular RPE swelling.

Associated traumatic findings

  • Commotio rarely occurs in isolation following significant trauma.
  • Must look for: Choroidal rupture, traumatic macular hole, hyphema, and peripheral retinal tears/dialyses at the vitreous base.

Etiology

Mechanism of injury

  • Blunt concussive force to the globe generates a shockwave transmitted to the posterior segment.
  • The shockwave physically disrupts the fragile photoreceptor outer segments and RPE cell layer.

Healing and recovery

  • The disrupted outer segments typically regenerate, allowing the retinal whitening to fade and vision to improve over days to weeks.
  • Severe forces can cause permanent photoreceptor loss or delayed RPE atrophy.

Red Flags

  • Central vision loss that fails to improve: Indicates permanent photoreceptor damage or a developing traumatic macular hole.
  • Concurrent choroidal rupture: High risk for secondary choroidal neovascularization (CNV) months to years later.
  • Peripheral commotio without a full peripheral exam: A missed retinal tear or dialysis leading to retinal detachment.

Investigations

Clinical exam

  • Complete comprehensive ophthalmic evaluation including dilated fundoscopy.
  • 360° scleral depressed examination of the peripheral retina to rule out tears/dialysis.
  • CAUTION: Defer scleral depression if there is a ruptured globe, active hyphema, microhyphema, or severe iritis.

Macular OCT

  • Key diagnostic tool: Confirms the absence of true retinal edema.
  • Demonstrates focal disruption or fragmentation of the ellipsoid zone (IS/OS junction), confirming outer segment damage.

Treatment

Primary management

  • Supportive observation is the only indicated management.
  • Because there is no true extracellular edema, therapies such as topical NSAIDs, corticosteroids, or dehydrating agents offer ZERO benefit.

Management of complications

  • Retinal tears or dialyses: Require immediate prophylactic laser retinopexy or cryotherapy to prevent detachment.
  • Traumatic macular hole: May require pars plana vitrectomy if it fails to close spontaneously.

Clinical Pearl

Commotio retinae is photoreceptor outer-segment disruption, not true edema. Steroids and NSAIDs are useless. While the commotio itself usually resolves, the mandatory task is to search for the hidden complications: peripheral retinal tears and choroidal ruptures.

Differential Diagnosis

  • Central retinal artery occlusion (CRAO)
  • White without pressure (benign peripheral variant)
  • Chorioretinitis sclopetaria (full-thickness rupture)
  • Retinal detachment

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