ACQUIRED MACULOPATHIES SOLAR RETINOPATHY Solar retinopathy also known as photo retinitis, or eclipse retinopathy , refers to retinal injury induced by direct or indirect sun viewing. Solar retinopathy is associated with religious sun gazing, solar eclipse observing, telescopic solar viewing, sun bathing and sun watching in psychiatric disorders . Causes of photic retinopathy, other than solar retinopathy : • Welding arc exposure, • Lightening retinopathy, • Retinal phototoxicity from ophthalmic instruments like operating microscope.
CLINICAL FEATURES
CENTRAL SEROUS CHORIORETINOPATHY Central serous chorioretinopathy (CSCR) is characterised by spontaneous serous detachment of neurosensory retina in the macular region, with or without retinal pigment epithelium detachment. Risk factors include: • Age and sex - The disease affects typically young adult (20–50 years), males more than females, • Personality- Type A personality individuals are more prone, • Steroid intake is an important risk factor, • Emotional stress, Hypertension, • Pregnancy (usually 3rd trimester), and • Cushing’s disease.
SYMPTOMS Sudden painless loss of vision (6/9–6/24) associated with Relative positive scotoma , micropsia and metamorphopsia. SIGNS Fundus examination shows • Mild elevation of macular area, demarcated by a circular ring reflex. • Small yellow grey elevations may be seen due to RPE detachment. • Foveal reflex is absent or distorted • Subretinal deposists may be seen. • Multifocal pigmentary changes suggest chronicity. CLINICAL FEATURES
CSR is usually self-limiting but often recurrent. Three patterns are known Acute classic CSCR is characterized by short clinical course with spontaneous resolution within 3–6 months with near normal visual recovery. Recurrences are known in 30–50% of all the cases. Chronic CSCR , also termed as diffuse retinal pigment epitheliopathy (DRPE), is seen in few cases. It is characterized by a chronic course lasting more than 12 months, typically affecting individuals above 50 years of age. Such cases may have permanent visual impairment due to progressive RPE atrophy and photoreceptor degeneration. Bullous CSCR is rare presentation characterized by larger and more numerous areas of serous retinal and RPE detachments often confused with bullous retinal detachment. CLINICAL COURSE
INVESTIGATIONS
1. Conservative measures. Reassurance is the only treatment required in majority of the cases, since CSR undergoes spontaneous resolution in 80 to 90% cases. Visual acuity returns to normal or near normal within 3 to 6 months. • Discontinuation of steroids, if possible, should be done at the earliest. • Life style changes to reduces stress in life, should be adopted. 2. Laser photocoagulation is indicated in following cases : • Long-standing cases (more than 6 months). • Patients having recurrent CSR with visual loss. • Patients having permanent loss of vision in the other eye due to this condition. Contraindications include the cases having leak near or within the FAZ. 3. Photodynamic therapy (PDT) may be beneficial for those with severe disease not amenable to conventional laser treatment, e.g., with sub-foveal leaks and chronic cases. 4. Anti-VEGF can be considered if CNV develop TREATMENT
CYSTOID MACULA EDEMA It refers to collection of fluid in the outer plexiform (Henle’s layer) and inner nuclear layer of the retina, centred around the foveola. Etiology It is associated with a number of disorders. A few common causes are as follows: 1. Complication of ocular treatment such as : Ocular surgery, e.g., cataract extraction, penetrating keratoplasty, glaucoma filteration surgery and retinal detachment surgery. Ocular laser therapy, e.g , panretinal photocoagulation (PRP), and Nd:YAG laser capsulotomy. Topical ocular therapy with eye drops like epinephrine, dipivefrine and prostaglandin analogues, especially in patients who have undergone cataract surgery.
CYSTOID MACULA EDEMA 2. Retinal vascular disorders e.g., diabetic retinopathy and central retinal vein occlusion (CRVO), branch retinal vein occlusion (BRVO), retinal telangiectasia (e.g., Coats’ disease), peri phlebitis retinae (Eales disease), and hypertensive retinopathy. 3. Intraocular inflammations , e.g., pars planitis , posterior uveitis and anterior uveitis. 4. Retinal dystrophies, e.g., retinitis pigmentosa. 5. Vitreomacular traction as seen in macular epiretinal membrane (ERM) and vitreo macular traction (VMT) syndrome. 6. Systemic diseases such as leukaemia, chronic renal failure and multiple myeloma. 7. Miscellaneous causes include intraocular tumours, choroidal neovascularization (CNV) and collagen vascular diseases.
PATHOGENESIS
CLINICAL FEATURES COMPLICATIONS Long-standing CME may end in lamellar macular hole.
TREATMENT
MACULAR HOLE CAUSES Senile or idiopathic (83%), more common in females aged 60–80 years than males (F:M, 3:1). Traumatic macular hole account for (5%) cases. Other causes of macular hole include: cystoid macular oedema, vitreomacular traction, postsurgical, myopia, post-laser treatment, epiretinal membrane traction and post-inflammatory. PATHOGENESIS: Senile macular holes are caused by tractional forces associated with early PVD.
SYMPTOMS Decreased vision, typically around 6/60 level for a full thickness hole and better for a partial hole. Metamorphopsia or distortion of vision may be there. Central scotoma may be reported by some patients. SIGNS Based on the fundus appearance the macular hole can be classified into four stages CLINICAL FEATURES
CLINICAL FEATURES
Fundus fluorescein angiography reveals early foveal hyper fluorescence without leak in the late phase in patients with stage 2 to 4 macular holes. Optical coherence tomography (OCT) is useful for: Differentiating true holes from the lamellar holes and cysts, Staging of the macular hole, Determining the degree of traction from the epiretinal membrane, and Planning the surgery INVESTIGATIONS