Commotio Retinae

From EyeWiki


Disease Entity

Commotio retinae

Disease

Commotio retinae refers to traumatic retinopathy secondary to direct or indirect trauma to the globe. Retinopathy may be present at areas of scleral impact (coup) and or distant sites (contrecoup) including the macula. Commotio retinae in the posterior pole is also referred to as Berlin's edema.[1]

Etiology

Closed globe trauma or blast injury. Commotio retinae is present in about 30% of all eye traumas presenting for hospital treatment.[2]

Risk Factors

High impact sports activities (most commonly ball sports), violence, motor vehicle accidents and other activities associated with blunt trauma to the face and orbits.

General Pathology

Retinal whitening as seen in commotio retinae always involves loss or disruption of the photoreceptor outer segments,[3] but may include damage to additional retinal layers with sufficient force.[4]

Pathophysiology

Blunt trauma causes displacement of the lens-iris diaphragm with expansion of peripheral structures outward. Indirect injuries such as blast trauma or orbital trauma transmit shockwaves to the globe causing similar deformation related force injuries.[2] This causes stretching and tearing of ocular tissues secondary to vitreoretinal deformation caused by transmission of hydraulic forces. [2][5] The retina is inelastic and absorbs the full effect of shock waves resulting in injury to various layers mainly the outer segment of photoreceptor and RPE junction.[6] It has been postulated that the injury is most severe at the photoreceptor processes as they are not suspended by the Muller cells, in contrast to the remainder of the neurosensory retina.[5]

There is no significant blood retina barrier breakdown associated with commotio retinae.[3] The retinal blood flow does not appear to be altered,[7] though the choroidal circulation may be impaired.[8]

Mansour et al. showed disruption of photoreceptor outer segments, deposition of debris in the subretinal space and RPE cell injury in a cadaveric human eye processed within 24 hours of trauma.[5] The characteristic glistening appearance described below is likely related to increased scattering of light by the abnormal photoreceptor processes and subretinal debris, which is well characterized by OCT.[4][7]

Restoration of photoreceptor outer segments begins at 1 week and continues for at least 2 months which may explain course of visual acuity recovery.[3] The clinical appearance of commotio retinae resolves within 1 week, with restoration of normal fundus appearance or pigmentary changes depending on the severity of the injury.[4]

Primary prevention

Primary prevention includes protective eye wear for athletes. 2-mm polycarbonate lenses in normal streetwear is recommended for low impact sports. Impact resistant sports frames with a 3-mm polycarbonate lens are recommended for moderate to high impact sports. Face masks attached to a helmet should be used in the highest risk sports including ice and field hockey, football, baseball, and lacrosse.[9]

Diagnosis

Diagnosis is clinical and is made based on characteristic appearance listed below Physical Examination.

History

Patients or bystanders will often offer a mechanism of trauma. It is important to screen for child abuse and domestic abuse as indicated.

Physical examination

A complete ophthalmoscopic exam to rule out open globe injury and orbital fracture including dilated fundus examination is indicated after significant trauma.  

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: http://www.nmji.in/text.asp?2017/30/4/242/218686
  

Signs

Dilated funduscopic exam reveals glistening gray-white opacification of the neurosensory retina with or without intraretinal hemorrhages and RPE mottling.[2] A pseudo cherry red spot may be seen when commotio involves the fovea. The fundus reflex may be notably white as opposed to red.

Optical coherence tomography (OCT) signs include disruption of ellipsoid zone (EZ), interdigitation zone (IZ) and occasionally inner retinal layers.[4]

Symptoms

Blurry vision or vision loss occurs immediately following trauma. 

Diagnostic procedures

  1. Dilated fundus examination
  2. OCT
  3. Fundus photography
  4. Ultrasonography in cases with unclear media due to vitreous hemorrhage or anterior segment injury.

Differential diagnosis

  1. Retinal ischemia
  2. Choroidal rupture
  3. Purtscher retinopathy
  4. Traumatic macular hole
  5. Chorioretinitis sclopetaria
  6. Retinal detachment

Management

Patients suffering substantial ocular trauma with commotio retinae should be followed with serial eye exams to evaluate for any additional treatable conditions.

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. [10]

Complications

Acute commotio retinae is commonly associated with traumatic macular hole, retinal tears, choroidal rupture, lens subluxation, hyphema, orbital fractures, late glaucoma, late cataract, late retinal tears, widespread chorioretinal atrophy.[4][11] 

Prognosis

While most patients recover completely, some patients will remain visually impaired with reduced vision or paracentral scotoma.

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[4]: Grade 1: increased reflectivity of the EZ with loss of ordinary definition of the photoreceptor lines. Grade 2: loss of reflection in cone outer segment tips (IZ) Grade 3: loss of reflection in IZ and EZ Grade 4: loss of reflection in the IZ, EZ and ELM. In this study increasing grades of pathology were predictors of poor visual recovery.[4]

Most cases resolve within 4 weeks of injury although some improvement can continue for up to 6 months.[2] However, some patients can have permanent macular damage with absolute or relative scotoma.[12] Patients with commotio retinae involving macula have poorer prognosis because of damage to the fovea along with increased risk of macular hole or permanent RPE atrophy as a secondary complication.[11] 26% of patients with macular involvement are permanently visually impaired with a VA of <20/30.[2] This is in comparison with 3% of patients sustaining permanent visual consequences after extramacular injury. There are no treatments to improve outcomes in these patients.[2]

Additional Resources

  • The University of Alabama at Birmingham. US Eye Injury Registry. https://useir.org/ Accessed 14 August 2019.

References

  1. Berlin R. Sogenannten commotio retinae. So-called commotio retinae. Klin Monatsbl Augenheilkd 1873;1:42–78.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 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.
  3. 3.0 3.1 3.2 Hart, J.C. and R. Blight, Commotio retinae. Arch Ophthalmol, 1979. 97(9): p. 1738.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 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.
  5. 5.0 5.1 5.2 Mansour, A.M., W.R. Green, and C. Hogge, Histopathology of commotio retinae. Retina, 1992. 12(1): p. 24-8.
  6. Blanch, R.J., et al., Animal models of retinal injury. Invest Ophthalmol Vis Sci, 2012. 53(6): p. 2913-20.
  7. 7.0 7.1 Mansour AM and Shields CL. Microvascular Capillary Plexus Findings of Commotio Retinae on Optical Coherence Tomography Angiography. Case Rep Ophthalmol 2018; 9:473-478.
  8. Hashimoto R, Hirota A and Maeno T. Choroidal blood flow impairment demonstrated using laser speckle flowgraphy in a case of commotio retinae. Am J Ophthalmol Case Rep 2016; 4:30-34.
  9. JB, J., An ongoing tragedy: pediatric sports-related eye injuries. Semin Ophthalmol, 1990. 5: p. 216-223.
  10. 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.
  11. 11.0 11.1 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: http://www.retinareference.com/diseases/9c563c5794aacd24/documents/9c563c5794/document.pdf.
  12. 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.