Commotio Retinae

From EyeWiki

Disease Entity

Commotio retinae


Commotio retinae refers to traumatic maculopathy secondary to shock waves caused by blunt trauma either directly or indirectly to the globe. Retinal injury can occur centrally with macular involvement (Berlin's edema) or peripherally without macular involvement and occurs sequentially, progressing from outer to inner layers. The photoreceptor outer segment is always involved; damage to inner retinal layers requires more force.


Commotio retinae is the result of blunt trauma or blast injury to the globe.

Risk Factors

High impact sports activities, motor vehicle accidents causing blunt trauma.

General Pathology

The primary pathology is traumatic disruption of the photoreceptor outer segment.[1] Injury to inner retinal layers and retinal pigment epithelium (RPE) also has been reported.[2]


Commotio retinae is the result of a closed globe blunt trauma or blast injury to the eye.

Blunt trauma causes displacement of the lens-iris diaphragm with expansion of peripheral structures outward. This causes stretching and tearing of ocular tissues secondary to vitreoretinal traction caused by transmission of hydraulic forces. [3][4]

With blast injury, external shockwaves are generated secondary to heat-induced expansion of explosive products. When external shockwaves hit the body, they create internal shock waves throughout the body and within the eye.[3]

Macular commotio retinae is presumed to be a countercoup mechanism of injury secondary to retropulsion and an increase in intraorbital pressure. Because the globe is elastic, it compresses under pressure and can absorb shock waves. The retina, however, is inelastic and bears the full effect of shock waves resulting in injury to the outer segment of photoreceptor and RPE junction. Extramacular commotio retinae, on the other hand, is thought to be a result of direct trauma to sclera overlying the injured retina.[5]

Regeneration of photoreceptor outer segment begins at 1 week and continues for at least 2 months which may explain course of visual acuity recovery.[1]

Primary prevention

Primary prevention includes protective eye wear for patients playing sports. 2-mm polycarbonate lenses in normal streetwear is recommended for athletes in low impact sports. Sports frames with a 3-mm polycarbonate lens is recommended for moderate to high impact sports. Eye protection with sports frame that meets impact-resistance standards should be used by athletes who wear contact lenses and by those who do not need corrective lenses. Face masks attached to a helmet should be used in sports such as hockey, football, baseball, and lacrosse.[6]


Diagnosis is clinical and is made with characteristic findings on dilated funduscopic exam and history of trauma or blast injury. DFE shows gray-white opacification of the neurosensory retina with occasional RPE mottling.


Commotio retinae was first described by Berlin in 1873 and is commonly known as Berlin’s Edema when it involves the posterior pole,[7] though there is no increased thickness of the retina on optical coherence tomography (OCT). Commotio retinae represents about 30% of all eye traumas presenting for hospital treatment.[3]

Physical examination

Dilated funduscopic exam reveals gray-white opacification of the neurosensory retina with occasional RPE mottling[3] secondary to disrupted or fragmented photoreceptor cells or intracellular edema but no extracellular edema. Cherry red macular spot can be seen when commotio involves the fovea.  

Commotio retinae From Tripathy K, Chawla R. Extensive commotio retinae involving peripheral retina. Natl Med J India [serial online] 2017 [cited 2018 Dec 5];30:242. Available from:


Retinal examination shows grayish-white opacification of macula seldom with RPE mottling and cherry red macular spot. Signs on OCT include hyperreflectivity of nerve fiber layer, photoreceptor outer (OS) and inner segments (IS) and disruption of OS-IS junction.


Blurry vision or vision loss occurs within hours after trauma. 

Diagnostic procedures

OCT shows outer photoreceptor segment disruption, RPE – Outer segment junction disruption, and intra-retinal edema in the outer nuclear layer. These changes usually resolve over time. Leakage on FA is seen with RPE changes; “salt and pepper” fundus appearance may indicate more severe injury. DFE is always the first step for diagnosis and to assess for retinal tears. If view is obscured, a gently performed ultrasound should be obtained to assess for retinal tears.

Differential diagnosis

Includes choroidal rupture, Purtscher retinopathy, traumatic macular hole, retinal artery occlusion, chorioretinitis sclopetaria, retinal detachment


Serial retinal examinations are necessary to diagnose development of choroidal neovascularization, macular hole, retinal tear, detachment, zonular dehiscence, angle close glaucoma and lens dislocation. Patient should be followed closely during the first few days and weeks following trauma to monitor and treat for complications.

General treatment

There is no approved or commonly used medical treatment for commotio retinae. However, in cases that do not resolve spontaneously, high dose IV steroids have been anecdotally shown to reduce retinal swelling and improve visual acuity. [8]


Associated injuries: acute commotio commonly associated with macular hole, hyphema, retinal tears, choroidal rupture, dislocated lens, late glaucoma, late cataract, late retinal tears, widespread chorioretinal atrophy.[9] 


While most patients recover completely, some patients will remain visually impaired with reduced vision or paracentral scotoma. These patients may be identifiable by early by ONL hyperreflectivity on OCT, leakage on FA suggesting RPE damage and/or choroidal occlusion. Those who do not recover completely may have RPE atrophy evident on funduscopic exam with time. There are no treatments to improve outcomes in these patients.[3]

Most cases resolve within 4 weeks of injury although some improvement can continue for up to 6 months.[3] However, some patients can have permanent macular damage with absolute or relative scotoma.[10] Patients with commotio retinae involving macula have poorer prognosis because of the increased risk of macular hole or permanent RPE atrophy as a secondary complication.[9] 26% of patients with macular involvement are permanently visually impaired with a VA of <20/30.[3] This is in comparison with 3% of patients sustaining permanent visual consequences after extramacular injury.

Ahn et al created a 4 step grading system for prognosis by evaluating damage in photoreceptor layers including cone outer segment, inner segment and external limiting membrane. The classification is based on OCT findings[2]: Grade 1: increased reflectivity of the inner and outer segment (IS-OS) junction with disappearance of the thin hyporeflective optical space. Grade 2: loss of reflection in cone outer segment tips (COST) Grade 3: loss of reflection in COST and IS-OS junction Grade 4: loss of reflection in the COST, IS-OS junction, and external limiting membrane

This study demonstrated that the extent of photoreceptor injury and the involvement of multiple layers of retina as seen on OCT were predictors of poor visual recovery.[2]

Additional Resources


  1. 1.0 1.1 Hart, J.C. and R. Blight, Commotio retinae. Arch Ophthalmol, 1979. 97(9): p. 1738.
  2. 2.0 2.1 2.2 Ahn, S.J., et al., Optical coherence tomography morphologic grading of macular commotio retinae and its association with anatomic and visual outcomes. Am J Ophthalmol, 2013. 156(5): p. 994-1001.e1.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 BLANCH, R.J., UNDERSTANDING AND PREVENTING VISUAL LOSS IN COMMOTIO RETINAE, in College of Medical and Dental Sciences. 2014, University of Birmingham: Birmingham, UK. p. 581.
  4. Mansour, A.M., W.R. Green, and C. Hogge, Histopathology of commotio retinae. Retina, 1992. 12(1): p. 24-8.
  5. Blanch, R.J., et al., Animal models of retinal injury. Invest Ophthalmol Vis Sci, 2012. 53(6): p. 2913-20.
  6. JB, J., An ongoing tragedy: pediatric sports-related eye injuries. Semin Ophthalmol, 1990. 5: p. 216-223.
  7. 7 R, B., Zur sogenannten commotio retinae. Klin Monatsbl Augenheilkd, 1873. 1: p. 42-78.
  8. Mendes S, Campos A, Beselga D, Campos J, Neves A. Traumatic Maculopathy 6 Months after Injury: A Clinical Case Report. Case Reports in Ophthalmology. 2014;5(1):78-82. doi:10.1159/000360692.
  9. 9.0 9.1 David Browning, M.P. What You Should Know About Blunt Trauma to the Eye: Commotio Retinae, Hyphema, Lens Dislocation, Vitreous Hemorrhage, Retinal Breaks, and Early and Late Glaucoma.  [cited 2016 May 30th, 2016]; Available from:
  10. EM, E., Ocular damage after blunt trauma to the eye. Its relationship to the nature of the injury. Br J Ophthalmol, 1974. 58: p. 126-140.