CALM EYE WITH SLOWLY DECLINE OF VISUAL LOSS

Dwi Permana Putra – 1011131066Tanjungpura University

Hypertensive Retinopathy

Hypertensive Retinopathy

• Retinal vascular damage caused by hypertension

Clinical Manifestation

• Most patients are asymptomatic• Some presents headaches and blurred vision• On ophthalmoscopy:

– Generalized arteriolar narrowing– Changes of the arterovenous crossings– Flame Haemorrhage– Microaneurysms– Exudates– Arteriolar macroaneurysms– Cotton-wool spots– Optic disc swelling– FIPT (Focal Intraretinal Periarterioal Transudates)

Grading of Hypertensive RetinopathyKeith and Wegner Classification (1939)

• Grade I (Figure.A)• Slight narrowing • It consists of mild

generalized arteriolar attenuation, particularly of small branches broadening of the arteriolar light reflex and vein concealment

• asymptomatic hypertension

• Grade II (Figure B)• It comprises marked

generalized narrowing and focal attenuation of arterioles associated with deflection of veins at arteriovenous crossings (Salus’ sign)

• BP is higher and sustained

• Grade III (Figure C)• This consists of Grade II changes

plus copper-wiring of arterioles• banking of veins distal to

arteriovenous crossings (Bonnet sign)

• tapering of veins on either side of the crossings (Gunn sign) and right-angle deflection of veins (Salu’ s sign)

• Flame-shaped haemorrhages, cotton-wool spots and hard exudates are also present

• Grade IV (Figure.D)• This consists of all

changes of Grade III plus silver-wiring of arterioles and papilloedema

• Headache, asthenia, loss of weight, dyspnea, visual disturbaces, impairment of cardiac, cerebral and renal function

Diagnosis

• history of the patients• ophthalmoscopy (direct

or indirect)• May reveal decrease of

patient vision, occipital headache and high Blood pressure

• Physical Examination• detect elevation of

blood pressure

• Ophthalmoscopy– Generalized arteriolar

narrowing– Changes of the arterovenous

crossings– Flame Haemorrhage– Microaneurysms– Exudates– Arteriolar macroaneurysms– Cotton-wool spots– Optic disc swelling– FIPT (Focal Intraretinal

Periarterioal Transudates)

Diffrential Diagnosis

• Diabetic Retinopaty• The presence of

microaneurysms:– Dilation of the veins,

which will be visible on funduscopic examination in the form of a small red dot near blood vessels

• Found in patients with Diabetes Mellitus.

Management

• A major purposes of treatment – prevent, limit, or reverse such target organ damaged by

lowering the patient’s high blood pressure• Lifestyle changes promote healthy lifestyle

exercise, consume healthy foods• Advice patient to reduce the blood pressure– Taking the medication– Referral to medical team (Surgical management is

indicated to address certain secondary causes of systemic hypertension)

Complication

• hypertensive retinopathy complications– venous occlusion branch / central retinal artery– macular edema– proliferative vitreoretinopati

• All of these changes ultimately lead to decreased visual acuity and blindness

Retinitis Pigmentosa

Retinitis Pigmentosa

• Retinitis pigmentosa (RP) is a group of inherited disorders characterized by progressive peripheral vision loss and night vision difficulties (nyctalopia) that can lead to central vision loss

Pathophysiology

• RP is typically thought of as a rod-cone dystrophy in which the genetic defects cause cell death (apoptosis)– predominantly in the rod photoreceptors– the genetic defects– cone photoreceptors

• RP has significant phenotypic variation patients with the same genetic mutation can present with very different retinal findings

• Photoreceptors is shortening of the rod outer segments loss of the rod photoreceptor occur in mid periphery of the retina These regions of the retina reflect the cell apoptosis by having decreased nuclei in the outer nuclear layer

• the degeneration tends to be worse in the inferior retina suggesting a role for light exposure

• The final common pathway in RP is typically death of the rod photoreceptors that leads to vision loss most densely found in the midperipheral retina, cell loss in this area tends to lead to peripheral vision loss and night vision loss

Etiology

• Photoreceptor cell death (most of the photoreceptor cells are rods)

• Molecular defect more than one hundred different genes

• Autosomal recessive• Autosomal dominant X-linked recessive

Incidence

• Occurs 5 persons per 1000 of the world population

• Appears in the childhood progresses slowly blindness in advance middle age

• Male are more commonly affected than females in ratio of 3:2

Clinical Features

• 1. Visual Symptoms• Night blindness It is the characteristic feature

and may present several years before the visible changes in the retina appear due to degeneration of the rods

• Dark adaptation Light threshold of the peripheral retina is increased the process of dark adaptation itself is not affected until very late

• Tubular vision occurs in advanced cases

2. Fundus Changes (fig.1)• Retinal pigmentary changes

these are typically perivascular and resemble bone corpuscles in shape

• Retinal arterioles are narrowed and may become thread-like in late stages

• Optic disc becomes pale and waxy in later stages and ultimately consecutive optic atrophy occurs (Fig.2).

• Other associated changes which may be seen are colloid bodies, choroidal sclerosis, cystoid macular oedema, atrophic or cellophane maculopathy.

3. Visual Field Changes• Annular or ring-shaped

scotoma is a typical feature which corresponds to the degenerated equatorial zone of retina

• As the disease progresses, scotoma increases anteriorly and posteriorly and ultimately only central vision is left (tubular vision)

• Eventually even this is also lost and the patient becomes blind.

Treatment• No effective treatment for the disease• Measures to stop progression, which have been tried from time to time,

without any breakthrough include: vasodilators, placental extracts, transplantation of rectus muscles into suprachoroidal space, light exclusion therapy, ultrasonic therapy and acupuncture therapy. Recently vitamin A and E have been recommended to check its progression.

• Low vision aids (LVA) in the form of ‘magnifying glasses’ and ‘night vision device’ may be of some help.

• Rehabilitation of the patient should be carried out as per his socio-economic background

• Prophylaxis Genetic counselling for no consanguinous marriages may help to reduce the incidence of disease. Further, affected individuals should be advised not to produce children

•

Age-Related Macular Degeneration

• senile macular degeneration• is a bilateral disease of persons of 59 years of

age or older• It is a leading cause of blindness in

population above the age of 65 years• It is of two types non-exudative and

exudative

Risk Factors

• Heredity• Nutrition• Smoking• Hypertension• Exposure to sun light

Clinical types

• 1. Non-exudative or atrophic ARMD• dry or geographic ARMD 90 percent cases• causes mild to moderate, gradual loss of

vision• Patients may complain of distorted vision,

difficulty in reading due to central shadowing

• Ophthalmoscopically (Fig. 11.26A)• it is characterised by • occurrence of drusens (colloid

bodies)• pale areas of retinal pigment

epithelium atrophy• irregular or clustered pigmentation• Drusens appear as small discrete,

yellowish-white, slightly elevated spots

• later stages enlargement of the atrophic areas within which the larger choroidal vessels may become visible

2. Exudative ARMD• Wet or neovascular ARMD

10% rapidly progressive marked loss of vision

• Stages:– Stage of drusen formation, – Stage of retinal pigment

epithelium (RPE) detachment– Stage of CNV (Fig. 11.26B)– Stage of haemorrhagic

detachment of RPE– Stage of haemorrhagic

detachment of neurosensory retina

– Stage of disciform (scarring) macular degeneration

Diagnosis

• Examination of the macula slitlamp biomicroscopy with a +90D/+78D non-contact lens

• Fundus fluorescein angiography indocyanine green angiography help in detecting CNV in relation to foveal avascular zone

Treatment

• There is no effective treatment for non-exudative ARMD

• some treatment options are available for exudative ARMD

• Certain specific:– antioxidants, vitamins and minerals (vitamin C

and E, beta carotene, zinc and copper) prevent or delay the progression of ARMD

Treatment for exudative ARMD• Argon green-laser photocoagulation is the treatment of choice for extrafoveal of

CNVM• Photodynamic therapy (PDT) is the treatment of choice for subfoveal and

juxtafoveal classic CNVM. In PDT, vertiporfin, a photosensitizer or light activated dye is injected intravenously. The area of CNVM is then exposed to light from a diode laser source at a wavelength (689 nm) that corresponds to absorption peak of the dye. The light-activated dye then causes disruption of cellular structures and occlusion of CNVM with minimum damage to adjacent RPE, photoreceptors and capillaries.

• Transpupillary thermotherapy (TTT) with a diode laser (810 nm) may be considered for subfoveal occult CNVM PDT is definitely better than TTT but is very costly.

• Surgical treatment in the form of submacular surgery to remove CNVM and macular translocation surgery are being evaluated

• Pharmacologic modulation with antiangiogenic agent like interferon alfa-29, and inhibitor of vascular endothelial growth factor (VEGF)

Eye Intoxification

Introduction

• The toxic retinopathies form a diverse group of conditions that result from retinal damage caused by systemically administered drugs

• relatively rare particularly when features of bilateral pigmentary disturbance or retinal crystal deposition are present

CHLOROQUINE AND HYDROXYCHLOROQUINE

• Chloroquine was popularized first for the prophylaxis and treatment of malaria

• as an effective treatment for various connective tissue diseases (rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) )

• Chloroquine and hydroxychloroquine can produce identical retinopathy– related to their affinity for pigmented structures, especially

in the eye– difficulty with reading or with other fine visual tasks caused

by central or paracentral scotomas

• The earliest fundus are irregularity in the macular pigmentation and blunting of the foveal reflex

• the central irregular pigmentation may become surrounded by a concentric zone of hypopigmentation, usually horizontally oval and more prominent inferior to the fovea (Figure 1)

• This paracentral depigmentation results in the classical bull’s-eye maculopathy

• continued exposure to the drug generalized pigmentary changes

• End-stage appearance may be indistinguishable from that of a cone-rod dystrophy, with peripheral pigment irregularity and bone spicule formation, vascular attenuation, and optic disc pallor

Thioridazine• antipsychotic drug • After 2 weeks blurring, nyctalopia,

and a brownish visual discoloration• vision was normal to profoundly

reduced• fundus could appear normal change

a couple of weeks• Pigment granularity developed

posterior to the equator• geographic areas of depigmentation

and loss of choriocapillaris developed ( Fig.2)

• If the drug was withdrawn early after the onset of symptoms, the patients usually reported improvement in vision

Niacin• nicotinic acid, vitamin B6 to lower serum

cholesterol• patients who take 1.5 g or more daily

develop maculopathy Rarely• central visual changes in weeks or

months after the initial administration of the drug

• Reduction in visual acuity is usually mild to moderate

• The patients develop a bilateral maculopathy that has the clinical appearance of cystoid macular edema, but there is no dye leakage or accumulation with fluorescein angiography

• Optical coherence tomography (OCT) reveals the presence of cystoid spaces in the inner nuclear and outer plexiform layers ( Fig.3)

Tamoxifen• Tamoxifen is a nonsteroidal estrogen

antagonist breast cancer• Retinopathy was first described

among women treated with more than 180 mg/day for longer than a year

• These patients usually had a symptomatic decrease in vision

• The characteristic fundus findings were small, white, refractile deposits in the inner retina

• Associated pigmentary irregularity ( Fig.4)

• Fluorescein angiography demonstrated macular edema in most cases

Deferoxamine• Deferoxamine mesylate is a chelating agent

used to remove toxic levels of heavy metals from the body

• reduce iron levels in patients with transfusion-dependent anemia and to treat aluminum toxicity Chronic Renal

• The onset of visual symptoms occur after long exposure

• Patients usually complain of blurred vision, nyctalopia, color vision abnormalities, or visual field restriction

• the fundus may appear normal or subtle pigment

• Color vision is frequently abnormal, typically with a tritan dyschromatopsia

• The maculopathy may progress develop into coarse macular pigmentary changes ( Fig.5) occasionally, peripheral pigmentary clumping

Didanosine• Didanosine is an antiretroviral drug

human immunodeficiency virus infection• Of 43 children receiving didanosine

followed prospectively, 3 (7%) developed an asymptomatic peripheral retinal degeneration first noted after 9–19 months of therapy

• The findings consisted of small, sharply demarcated areas of retinal and retinal pigment epithelial atrophy around the midperiphery ( Fig. 6)

• Visual acuity remained normal in all patients• One patient who was able to undergo

reliable testing demonstrated mild restriction of the peripheral visual field

• Clinical findings included normal visual acuity, field defects, and abnormal electro-oculogram (EOG)

Thank You