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The differential diagnosis of retinal whitening includes:

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

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
2. Eyelid
   
   • Laceration
3. Globe rupture
   
4. Anterior segment
   
   • Hyphaema
     
   • Irido(cyclo)dialysis
     
   • Cataract
     
   • Phacodonesis
5. Intraocular pressure
   
   • Elevated: Red cell/ghost cell/phacoanaphylactic/angle recession glaucoma
     
   • Reduced: Globe rupture, cyclodialysis
6. 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 ophthalmoscopically(3) 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.