Dr Mohaimen Al-Zubaidy MBBS BSC (Hons)

F2 Doctor
Newcastle University Healthcare Trust

Introduction

Rhegmatogenous retinal detachment (RRD) is one of the major causes of blindness worldwide. It is caused by single or multiple breaks in the retina and is defined by the separation of the neurosensory retina from the retinal pigment epithelium (1). Treatment for these cases is time sensitive with many studies advising for treatment within 24 hours to improve visual outcomes, thus early recognition and management of these cases is important particularly in cases involving the macula (2).

This article will discuss the clinical features associated with rhegmatogenous retinal detachment, its underlying pathogenesis as well as the steps taken in managing patients with this condition.

Epidemiology

RDD is predominantly a disease of the population older than 50 years, with a male predominance. The annual RRD incidence is highly dependent on demographic characteristics but is generally estimated at about 1 in 10,000 per of RD occurring in approximately 1 in 10 000 of the population per annum (3, 4).

Risk factors

Blunt eye trauma is a common cause for development of secondary RRD however more than 50% of RRDs are primary and occur spontaneously with no history of surgical or non-surgical trauma (5). Other risk factors include retinal tear formation at the time of PVD (6). Myopic patents are also at greater risk of developing RRD. Patients with pre-existing retinal thinning such as lattice degeneration, atrophic retinal holes and retinal dialyses are also at higher risk (7,8). RRD risk also varies by gender and ethnicity with men, and Caucasian and Asian populations at relatively higher risk (9,10).

Pathogenesis

Rhegmatogenous retinal detachment development is closely related to changes in the ageing more liquified vitreous. There is a higher likelihood of developing posterior vitreous detachment secondary to regions of persistent vitreoretinal traction predisposing to retinal tear formation. A complex interaction of factors such as weakening of vitreoretinal adhesion and molecular changes at the vitreoretinal interface are important in predisposing to focal areas that are more at risk of progressing into retinal tears.  These tears predispose to liquified vitreous being able to seep into the break and displace the neurosensory retinal pigment epithelium adhesion, resulting in detachment and visual loss (11).

Clinical Presentation

Patients with RRD commonly present with photopsias, flashing lights secondary to the mechanical stimulation of vitreoretinal traction, more noticeable in the dark. Visual field defects are also a common complaint, often described as a black curtain effect by patients (1).

The level of visual field defect depends on the location of the detachment with more severe visual loss in foveal involving cases with loss of central vision. Patients with RRD also mention being able to see floaters, caused by opacities in the vitreous that cast dark shadows in the field of vision (2).

Investigations

In conjunction with clinical symptoms, retinal examination with binocular indirect ophthalmoscope or slit lamp is the mainstay of definitively diagnosing cases of RRD which would reveal bullous separation of the retinal layers. Occasionally the media may not be clear, impairing retinal examination and thus ultrasound in the forms of an B scan is a useful adjunct to aid diagnosis. Optical Coherence Tomography may also be used in diagnosis to reveal sub-foveal fluid in affected eyes (12).

Treatment

All patients diagnosed with RRD require admission to hospital for surgical intervention within 72 hours in foveal sparing cases and 24 hours in foveal involving cases (2).

Irrespective of the surgical method chosen, the aims are to pinpoint and close all the breaks with minimum iatrogenic damage to reduce the chance of further vitreoretinal traction. This occlusion results in recontact and healing of the break with the underlying retinal pigment epithelium. This is accomplished in two ways; either by pushing the detached retinal epithelium towards the eye wall with an intraocular gas tamponade (pars plana vitrectomy) or bringing the eye wall closer to the detached retina (scleral buckle). In some cases, a combination of these techniques is used.

Sealing of the breaks is further solidified and accomplished by creating a strong chorioretinal adhesion around the breaks; this may be completed with partial thickness scleral diathermy, trans-scleral cryotherapy, or laser photocoagulation (1,5,12).

Surgical intervention does not come without risk and in a small number of cases complications my arise including subretinal haemorrhage, iatrogenic breaks and hypertony (13). However untreated cases will often result in complete visual loss thus early intervention is encouraged. (14)

Conclusion

Though potentially sight-threatening, in the majority of cases which receive early treatment RDD carries an excellent prognosis. Its thus important for us as clinicians to be able to recognise the clinical features associated with RRD and execute early surgical intervention for optimal visual outcomes.

References

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13. Lv Z, Li Y, Wu Y, Qu Y. Surgical complications of primary rhegmatogenous retinal detachment: a meta-analysis. PLoS One. 2015;10(3):e0116493. Published 2015 Mar 3. doi:10.1371/journal.pone.0116493
14. Ivanisević M. The natural history of untreated rhegmatogenous retinal detachment. Ophthalmologica. 1997;211(2):90-92. doi:10.1159/000310766