RETINA

RETINADr. Mandiri Nindiasari, SpM, MScKetebalan retina

Anatomi retina

Pemeriksaan Funduskopi dg:Oftalmoskop direkOftalmoskop indirekLensa kontak goldmannUSGFoto fundusFluoresence angiography

Fundus normal

Wall reflex di makula remaja

RETINOPATI DIABETIKDiabetic retinopathy is an ocular microangiopathy

Epidemiology: the main causes of acquired blindness in the industrialized countries. 90% diabetic patients have retinopathy > 20 yrsPathogenesis and individual stages of diabetic retinopathyDiabetes mellitus can lead to changes in almost every ocular tissue. These include symptoms of keratoconjunctivitis sicca, xanthelasma, mycotic orbital infections, transitory refractory changes, cataract, glaucoma, neuropathy of the optic nerve, oculomotor palsy. 90% of all visual impairments in diabetic patients are caused by diabetic retinopathy.

Symptomsasymptomatic for a long time. Only in the late stages with macular involvement or vitreous hemorrhage will the patient notice visual impairment or suddenly go blind.

Diagnostic considerations stereoscopic examination of the fundus with the pupil dilated (gold standard)Fluorescein angiography : if laser treatment is indicated. slit-lamp examination : rubeosis iridis +/-TreatmentClinically significant macular edema focal laserProliferative diabetic retinopathy scatter photocoagulation (3-5 sessions)

Prophylaxis regular ophthalmologic screening examinations type II diabetics : upon diagnosis of the disorder once a year / more oftentype I diabetics: within 5 years of the diagnosisPregnant patients: once every trimester.Clinical course and prognosisOptimum control of blood glucose can prevent or delay retinopathy. However, diabetic retinopathy can occur despite optimum therapy. The risk of blindness due to diabetic retinopathy can be reduced by optimum control of blood glucose, regular ophthalmologic examination, and timely therapy, but it cannot be completely eliminated.Retinopati diabetik (NPDR sedang)

PDR

PDS high risk

PDR, pre & post laser

Retinal vein occlusionVein occlusion occurs as a result of circulatory dysfunction in the central vein or one of its branches.

Epidemiologythe second most frequent vascular retinal disorder after diabetic retinopathy. The most frequent underlying systemic disorders are arterial hypertension and diabetes mellitusThe most frequent underlying ocular disorder is glaucoma.EtiologyOcclusion due to local thrombosis at sites where sclerotic arteries compress the veins. In CRVO: the thrombus lies at the level of the lamina cribrosaIn BRVO: at an arteriovenous crossing.

Symptomsa loss of visual acuity if the macula or optic disk are involved.Diagnostic considerations and findingsCRVO: hemorrhages in all four quadrants of the retinaBRVO: hemorrhages in the area of vascular supply; this bleeding may occur in only one quadrant Cotton-wool spots and retinal or optic-disk edemaChronic occlusions: lipid deposits. One differentiates between non-ischemic and ischemic occlusion depending on the extent of capillary occlusion.Ischemic occlusion is diagnosed with the aid of fluorescein angiography.Differential diagnosisdiabetic retinopathyAn internist should be consulted

TreatmentIn acute : hematocrit to 3538% by hemodilution. Laser treatment: in ischemic occlusionFocal laser treatment: in BRVO with macular edema when VA < 20/40 within 3ProphylaxisEarly diagnosis and prompt treatment of underlying systemic and ocular disorders is important.

Clinical course and prognosisVA in 1/3 patients remains unchanged in 1/3worsens in 1/3 despite therapy. Complications: preretinal neovascularization, retinal detachment, and rubeosis iridis with angle closure glaucomaCRVO

BRVO

Retinal Arterial OcclusionRetinal infarction due to occlusion of an artery in the lamina cribrosa or a branch retinal artery occlusion.

EpidemiologyRetinal artery occlusions occur significantly less often than vein occlusions.EtiologyEmboli inflammatory processes such as temporal arteritis (Hortons arteritis).

SymptomsCRAO: sudden, painless unilateral blindness.BRAO: a loss of visual acuity or visual field defects.

Diagnostic considerationsOphthalmoscopyacute stage of CRAO: grayish whitefovea centralis: cherry red spot The column of blood will be seen to be interrupted. optic nerve atrophy : in chronic stage of CRAOBRAO: a retinal edema in the affected area of vascular supply Perimetry (visual field testing)a total visual field defect in CRAOa partial defect in BRAO

TreatmentEmergency treatment is often unsuccessful even when initiated immediately: Ocular massagemedications that reduce intraocular pressure Paracentesis to drain the embolus in a peripheral retinal vessel. Calcium antagonists or hemodilution to improve vascular supply.

ProphylaxisExcluding or initiating prompt therapy of predisposing underlying systemic disorders is crucial.Clinical course and prognosisThe prognosis is poor because irreparable damage to the inner layers of the retina occurs within one hour. Blindness usually cannot be prevented in CRAO. The prognosis is better where only a branch of the artery is occluded unless a macular branch is affected.CRAO

BRAO

Hypertensive RetinopathyArterial changes in hypertension are primarily caused by vasospasm

PathogenesisHigh blood pressure breakdown of the blood-retina barrier or obliteration of capillaries intraretinal bleeding, cotton-wool spots, retinal edema, or optic disk swelling SymptomsPatients with high blood pressureHeadache or eye pain. Impaired vision or loss of VA in stage III or IV

Diagnostic considerationsdiagnosed by ophthalmoscopy, preferably with the pupil dilatedDifferential diagnosisother vascular retinal disorders such as diabetic retinopathy.

TreatmentTreating the underlying disorder is crucial Blood pressure < 140/90mm Hg. Stages of hypertensive vascular changes (as described by Keith,Wagener, and Barker)

The WHO distinguishes between HT retinopathy (stages I and II) and malignant HT retinopathy (stages III and IV)ProphylaxisRegular blood pressure monitoring Ophthalmoscopic examination of the fundus

Clinical course and complicationsvascular changes (retinal artery and vein occlusion) and macroaneurysms vitreous hemorrhage. Papilledema t atrophy of the optic nerve severe loss of visual acuity.

PrognosisIn some cases, the complications described above are unavoidable despite well controlled blood pressure.Retinopati HT gr.III

Retinal detachment (ablasio retina)the separation of the neurosensory retina from the underlying retinal pigment epithelium, to which normally it is loosely attached. Rhegmatogenous retinal detachment results from a tearTractional retinal detachment results from tractionExudative retinal detachment is caused by fluid.Tumor-related retinal detachment.EpidemiologyRhegmatogenous retinal detachment (most frequent form) 7% of all adults have retinal breaks.The incidence with advanced age. The peak incidence is 5th -7th decades of life (PVD / posterior vitreous detachment (separation of the vitreous body from inner surface of the retina; also age-related)The annual incidence : 1/10 000 personsThe prevalence : 0.4% in the elderly. There is a known familial disposition, and retinal detachment also occurs in conjunction with myopia. The prevalence of retinal detachment with emmetropia : severe myopia > S-10D = 0.2 % : 7% EtiologyRhegmatogenous retinal detachment. This disorder develops from an existing break in the retina, usually in the peripheral retina Round breaks: A portion of the retina has been completely torn out due to a posterior vitreous detachment.Horseshoe tears: The retina is only slightly torn.Retinal break liquified vitreous body separates vitreous humor penetrates beneath the retina through the tear retinal detachment

Tractional retinal detachment. tensile forces exerted on the retina by preretinal fibrovascular strands especially in proliferative retinal diseases such as diabetic retinopathy.

Exudative retinal detachment. the breakdown of the inner or outer blood retina barrier, usually as a result of a vascular disorder. Subretinal fluid with or without hard exudate accumulates between the neurosensory retina and the retinal pigment epithelium.

Perdarahan vitreus

Tumor-related retinal detachment. Either the transudate from the tumor vasculature or the mass of the tumor separates the retina from its underlying tissue.Symptomsasymptomatic for a long time. acute stage posterior vitreous detachment: flashes of light (photopsia) and floaters, black points that move with the patients gaze. PVD a retinal tear avulsion of a retinal vessel Blood enter the vitreous body: black rain, dark shadow in the visual field: a falling curtain or a risingwallA break in the cente: sudden and significant loss of visual acuity, which will include metamorphopsia (image distortion) if the macula is involved.Diagnostic considerationsdiagnosed by ophtalmoscopy with the pupil dilated.

Differential diagnosisDegenerative retinoschisis choroidal detachment. TreatmentRetinal breaks with minimal circular retinal detachment argon laser coagulation Scleral buckleVitrectomy wih silicon oil tamponade or gas tamponadeTreatmentRetinal breaks with minimal circular retinal detachment argon laser coagulation Scleral buckleVitrectomy wih silicon oil tamponade or gas tamponadeargon laser photocoagulation

Vitrektomi pars plana

Penggunaan gas pada vitrektomi

Penggunaan minyak silikon pd vitrektomi

ProphylaxisHigh-risk patients:age > 40 with a positive family history and severe myopia examined once a year.

Clinical course and prognosisabout 95% of RRD : successfully with surgery. if macular involvement a loss of visual acuity will remain. The prognosis for the other forms of retinal detachment is usually poor, and they are often associated with significant loss of visual acuity.Central serous retinophathySerous detachment of the retina and/or retinal pigment epithelium

Etiologyphysical or psychological stressEpidemiologymen in the 3rd and 4th decade of life.

SymptomsA loss of visual acuity, a relative central scotoma (dark spot), image distortion (metamorphopsia), or perception of objects as larger or smaller than they are (macropsia or micropsia).

Diagnostic considerationsOphthalmoscopy : a serous retinal detachment, at the maculaHyperopiafluorescein angiographyTreatmentno treatment resolves spontaneously within a few weeks. Recurrences laser therapy Corticosteroid therapy is contraindicatedClinical course and prognosisThe prognosis is usually good. recurrences or chronic forms a permanent loss of visual acuity.Central serous retinophathy

Age-Related Macular DegenerationProgressive degeneration of the macula in elderly patients.

Epidemiologythe most frequent cause of blindness beyond the age of 65 years.

PathogenesisDrusen develop in the retinal pigment epithelium due to accumulation of metabolic products.

Symptomsa gradual loss of visual acuity. macular edema image distortion (metamorphopsia), macropsia, or micropsia.Findings and diagnostic considerationsOphthalmoscopic examination

Differential diagnosisBRVO Malignant melanoma

TreatmentNo effective medical therapy is available. Laser therapy : in exudative stage involving the fovea centralis. Use hand magnifier or binocular magnifier.Clinical course and prognosischronic progressive loss of visual acuity.Laser therapy: in exudative stageStages of age-related macular degeneration (ARM)

Age-related macular degeneration

Perdarahan subhialoid

Retinitis Pigmentosaa heterogeneous group of retinal disorders that lead to progressive loss of visual acuity, visual field defects, and night blindness.

EpidemiologyIncidence: 1/35000 1/70000 persons.incidence of mutated alleles: 1/80 persons.autosomal recessive (60%), autosomal dominant (up to 25%), X-linked (15%). Symptomsglare, night blindness, progressive visual field defects, loss of visual acuity, and color vision defects. Findings and diagnostic considerationsOphthalmoscopyBone-spiculegradually spread toward the center and farther peripherallyloss of visual acuity gradual progressive loss of visual fieldcolor vision defects disturbed contrast perceptionAtrophy of the optic nerveThe arteries will appear narrowedthe fundus reflex will be extremely muted Differential diagnosispseudoretinitis pigmentosaPosttraumatic changes.Postinflammatory or postinfectious changesTumors.Medications, such as chloroquine, Myambutol (ethambutol), and thioridazine.TreatmentThe causes of the disorder cannot be treated. Edge-filtered eyeglasses (eyeglasses with orange or blue colored lenses that filter out certain wavelengths)magnifying near vision aids

Prophylaxis No prophylaxis is possible.Clinical course and prognosischronically progressive.lead to blindness.

Posterior Uveitis Due to ToxoplasmosisFocal chorioretinal inflammation caused by infection

Epidemiologythis clinical syndrome is encountered frequently.

PathogenesisToxoplasma gondii, is transmitted by ingestion of tissue cysts in rawor undercooked meat or by oocysts from cat feces. In congenital toxoplasmosis, the child acquires the pathogen through transplacental transmission.Symptoms and diagnostic considerationsgrayish white chorioretinal focal lesions surrounded by vitreous infiltrationIn congenital toxoplasmosis: a macular scar that significantly impairs visual acuity secondary strabismus. Intracerebral involvement hydrocephalus and intracranial calcifications. acquired form: visual acuity is impaired only where the macula is involved. Differential diagnosisChorioretinitis with tuberculosis, sarcoidosis, borreliosis (Lyme disease), or syphilis

Treatmentcombination of pyrimethamine, sulfonamide, folinic acid, and steroids

ProphylaxisAvoid raw meat and cat feces.Clinical course and prognosisheals without severe loss of visual acuity where the macula is not involved.recur at any time. no cure for the congenital form.toksoplasmosis

AIDS-Related Retinal DisordersRetinal disorders in AIDS involve either AIDS-associated microangiopathy or infection.

Epidemiology Up to 80% of all AIDS patients have retinal disorders

PathogenesisThe pathogenesis of microangiopathy is still unclear. Opportunistic infections are frequently caused by viruses.Diagnostic considerationsOphthalmoscopic findings: hemorrhages, microaneurysms, telangiectasia, and cotton-wool spots.Cytomegalovirus retinitis occurs in 2040% of older patients. Peripheral retinal necrosis intraretinal bleedingVascular occlusion is rare. Secondary rhegmatogenous retinal detachmentAIDS is confirmed by positive serum cultures and by resistance testing.Differential diagnosisInflammatory retinal changes due to other causes should be excluded by serologic studies.

TreatmentMicroangiopathy does not require treatment. Viral retinitis is treated with ganciclovir or foscarnet.Herpes simplex and varicella-zoster viruses are treated with acyclovir.ProphylaxisOphthalmologic screening

Clinical course and prognosisThe prognosis for microangiopathy is very good. Infectious retinitis will lead to blindness if left untreated. Visual acuity can often be preserved if a prompt diagnosis is made.Korioretinitis CMV

TERIMA KASIH