Commotio Retinae

From EyeWiki



Disease Entity

Commotio retinae

Disease

Commotio retinae is a disease pathology that involves degeneration of the layers of the retina secondary to shock waves caused by blunt trauma or blast injury. Damage can occur centrally with macular involvement or peripherally without macular involvement and occurs sequentially, progressing from outer to inner layers. The photoreceptor outer segment is always involved; damage to more interior layers requires more force.  

Etiology

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

Risk Factors

High impact sports activities

General Pathology

The primary pathology is traumatic disruption of the photoreceptor outer segment and reversible loss of cone pigment in the retinal pigment epithelial [1]. Damage to blood vessels in the nerve fiber layer also occurs with greater force of shock wave[2].

Pathophysiology

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 and hydraulic forces transmitted[3, 4]. 

With blast injury, external shockwaves are generated secondary to heat-induced expansion of explosive products. External shockwaves hit the body and create internal shock waves throughout the body and within the eye. These cause shearing and tearing at tissue surface interfaces [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 passed on by the elastic globe. 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 meeting 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

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 neuroretina with occasional RPE mottling.

History

Commotio retinae was first described by Berlin in 1873 and is commonly known as Berlin’s Edema when it involves the posterior pole[7]. 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 neuroretina with occasional RPE mottling[3] secondary to disrupted or fragmented photoreceptor cells or intracellular edema. Cherry red macular spot can be seen when commotio involves the fovea.  

Signs

Signs on DFE include gray-white opacification of neuroretina, RPE mottling and cherry red macular spot.

Signs on OCT include hyperreflectivity of nerve fiber layer, photoreceptor OS, photoreceptor IS and disruption of OS-IS junction. 

Symptoms

Pain, blurry vision or vision loss occurs within hours after trauma. 

Diagnostic procedures

OCT shows level of disruption of commotio retinae and hyperreflectivity. In all cases photoreceptor OS is involved, with rare IS involvement. These changes are likely to resolve over time. There is also sometimes hyperreflectivity of the ONL which is likely predictive of future degeneration.

Leakage on FA and “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

Choroidal rupture, Purtscher retinopathy, traumatic retinal hole, chorioretinitis sclopetaria, retinal detachment

Differential diagnosis broadens when history cannot be elicited and etiologies characterized by retinal whitening must be ruled out. Differential can include cotton wool spot, BRAO and viral retinitis. 

Management

Serial subsequent examinations are necessary to detect possible late developing problems including choroidal neovascularization, 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 BCVA(11).

Complications

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]. 

Prognosis

While most patients recover completely, some patients will remain visually impaired with reduced vision or paracentral scotoma. These patients may be identifiable by early ONL hyperreflectivity on OCT, choroidal leakage on FA and/or choroidal occlusion. Those who do not recover completely may have RPE atrophy evident on funduscopic exam. 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[8].

Patients with commotio retinae involving macula have poorer prognosis because of the increased risk of macular hole 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. This study demonstrated that the number of photoreceptors lost and the number of layers damaged on OCT were predictors of poor visual recovery[2]. 

Additional Resources

References

1.           Hart, J.C. and R. Blight, Commotio retinae. Arch Ophthalmol, 1979. 97(9): p. 1738.

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.           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.           R, B., Zur sogenannten commotio retinae. Klin Monatsbl Augenheilkd, 1873. 1: p. 42-78.

8.           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.

9.           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.

10.        www.useir.org

11.       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.