Commotio Retinae or Berlin’s Oedema is grey-white discolouration of the retina due to disruption of outer segment photoreceptor layer following blunt trauma. This is caused due to contrecoup injury. Shock waves caused due to impact traverses the fluid- filled eye and then strike retina.
Commotio retinae or Berlin’s oedema was first described by a German physician, Rudolph Berlin in the year 1873, as a transient grey-white opacification of the macular/ peripheral retina following blunt trauma to eye.
Commotio retinae may involve any part of retina and may be accompanied by choroidal rupture or retinal haemorrhage. Macular oedema reduces central vision, but vision usually improves as the oedema resolves. After an acute attack of oedema, there may be scarring of retina with pigment dispersal. Vision may be acutely reduced or normal depending upon whether the macula is involved or not. It may permanently reduce vision if the fovea centralis is involved.
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Symptoms of Commotio retinae may be
Commotio retinae is caused due to pressure waves emanating from blunt trauma to the eye resulting in retinal injury. There may also be associated choroidal rupture or retinal haemorrhage. Following acute episode of oedema, retina may develop scarring and pigment dispersal. Macular commotio retinae reduces central vision. The vision usually improves on resolution of oedema, unless there is development of macular hole or disruption of retinal pigment epithelium of the fovea.
Studies suggest that commotio retinae is probably caused due to disruption of the photoreceptor outer segments, and is not a true extracellular oedema.
This is more common in young males.
Diagnosis depends upon the history of injury to the eye and clinical features.
There are two variations of commotio retinae depending upon the severity of injury to the eye.
Clinical features on examination may include:
Commotio retinae is a self-limiting opacification of retina following direct ocular trauma, and is characterised by transient whitening at the level of deep sensory retina. Retinal whitening may take hours to develop before it may be seen with the help of ophthalmoscope. The lesion may affect both central or peripheral retina.
Histopathologically, animal models have suggested that there is disruption of photoreceptor outer segments with associated damage to retinal pigment epithelium.
Histologic studies do not separate cases into retinal concussion or contusion.
Differential diagnosis includes
There is no approved medical therapy for commotio retinae. The patient should be observed closely during first few days to weeks following trauma, to monitor development of any complication and its treatment thereof.
The cases which do not resolve spontaneously may be tried with intravenous steroids. This may reduce retinal swelling and thus may help in improvement of vision.
Most patients recover spontaneously, but some with more severe trauma may remain visually impaired with reduced vision or paracentral scotoma.
Most of the cases resolve within four weeks of injury, although some improvement may continue for up to even six weeks. Some patients have permanent macular damage with absolute or relative scotoma. Patients with involvement of macular area have poor prognosis.
There may be complications due to associated injuries such as macular hole, retinal tears, choroidal rupture, hyphaema, lens dislocation, late development of cataract, glaucoma or retinal tears, or chorioretinal atrophy.