October 2014

Case of the Month

Author: Adrian Fung


Figure 1. Colour fundus photograph of the right eye reveals a whitish discolouration of the retina temporal to the fovea.

Figure 1. Colour fundus photograph of the right eye reveals a whitish discolouration of the retina temporal to the fovea.


A 28-year-old Asian male was referred by his optometrist after being hit in his right eye by a basketball.


Case History

A 28-year-old Asian male was referred by his optometrist after being hit in his right eye by a basketball the day before. He reported slight blurring of his vision and was moderately myopic but otherwise had no significant past ocular or medical history.

On examination his visual acuities were right (OD) 6/9 and left (OS) 6/4.8 (no improvement with pinhole). Intraocular pressures were 14mmHg OD and 12mmHg OS. Anterior segment examination showed some mild corneal oedema, 3+ microhyphema and 1mm anisocoria with the right pupil being larger than the left. This anisocoria was greatest in lighted conditions and was less pronounced in the dark. There was no relative afferent pupillary defect. Posterior segment examination demonstrated whitening of the retina temporal to the fovea (Figure 1). This had a well demarcated border and extended superotemporally (Figure 2). A scleral depressed peripheral retinal examination failed to detected any retinal breaks or dialysis. Optical coherence tomography through the fovea was normal.


Figure 2
Figure 2. The retinal whitening extends along the superotemporal vascular arcade.




What is your diagnosis?


Differential Diagnosis

The differential diagnosis of retinal whitening includes:

  • Infective retinitis (CMV; HSV/VZV in acute retinal necrosis)
  • Cotton-wool spots
  • Retinal arteriolar occlusions
  • Commotio retinae



Given the history of blunt ocular trauma, a diagnosis of commotion retinae with microhyphaema and traumatic mydriasis was made.


Clinical Course

The patient was prescribed dexamethasone (Maxidex™) eyedrops 6X/day and told to minimise activity with elevated bedrest for his hyphaema. He was warned of the symptoms of retinal detachment and asked to present urgently if these occurred. At the one week review the hyphaema, traumatic anisocoria and commotio retinae were resolving. By 1 month his vision had improved to 6/6 in the right eye and all signs had resolved. Gonioscopy showed a normal drainage angle without evidence of angle recession. Follow-up care was arranged with his optometrist.



Blunt ocular trauma is a common cause of visual impairment in the younger population. Frequent causes include assault, ball sports (soccer, golf, squash, basketball) and work place related injuries.1 The mean age of injury is around 30 years, with a higher incidence in males.1 Almost any structure in the eye can be damaged, including the:


  1. Orbit
  • Wall fracture: Enophthalmos, hypoglobus, restricted extraocular movements


  1. Eyelid
  • Laceration


  1. Globe rupture


  1. Anterior segment
  • Hyphaema
  • Irido(cyclo)dialysis
  • Cataract
  • Phacodonesis


  1. Intraocular pressure
  • Elevated: Red cell/ghost cell/phacoanaphylactic/angle recession glaucoma
  • Reduced: Globe rupture, cyclodialysis


  1. Posterior segment
  • Vitreous haemorrhage
  • Commotio retinae
  • Retinal haemorrhages
  • Retinodialysis
  • Retinal tear
  • Rhegmatogenous retinal detachment
  • Choroidal rupture with or without secondary choroidal neovascularisation
  • Macular hole
  • Traumatic optic neuropathy
  • Optic nerve avulsion


Commotio retinae refers to transient, self-limited deep retinal whitening that follows up to 10% of cases of blunt ocular trauma.2 This whitening can take several hours to manifest ophthalmoscopically3 and is most commonly found inferotemporally (37%), temporal (17%) or superotemporally (17%)4. Originally described in 1873, it was initially thought to be due to extracellular oedema.5 However, experimental animal studies have shown it to actually represent disruption of the photoreceptor outer segments and retinal pigment epithelium (RPE) with variable degrees of necrosis and apoptosis.3,4,6-8 This has been confirmed by a single case of a human eye with commotion retinae that was enucleated and examined less than 24 hours following blunt trauma. In addition, high-resolution optical coherence tomography (OCT) studies concur with these findings.9-11 The retinal changes are thought to be secondary to the concussive forces being transmitted to the posterior segment.


Although the clinical features of commotio retinae usually resolves spontaneously, permanent visual defects can ensue. This is most commonly seen following macular involvement where the median presenting visual acuity is 6/12 and improves to ≥6/9 on final follow up in 74% of patients.4 Grading by OCT of macular commotio has been proposed, with loss of reflection in the cone outer segment tips (COST), inner segment-outer segment junction (ellipsoid layer) and external limiting layer being associated with a poorer final visual acuity.1 Surprisingly, even extramacular commotio can be associated with visual deficits, perhaps due to occult macular injury.4 No known specific treatment exists for commotion retinae.



Take home points


  • Commotio retina refers to transient opacification of the retina secondary to blunt ocular trauma.
  • Histological and optical coherence tomography studies have shown that the whitening represents disruption of the photoreceptor outer segments and retinal pigment epithelium.
  • Although the clinical findings usually resolve, permanent visual effects may ensue, particularly if the macula is involved and there is severe disruption of the outer retina on optical coherence tomography.



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