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  2. VISION LOSS Visual loss is a common complaint among patients of different ages with variable presentations. Some patients describe it as a gray-black curtain that gradually descends or as blurring, fogging, or dimming of vision. It usually lasts a few minutes but can persist for hours. Frequency varies from a single episode to many episodes during a day; it may continue for years but more often lasts from seconds to hours. Ischemia is the most common mechanism of acute visual dysfunction, and it can affect any aspect of the visual system.

  3. CLASSIFICATION Multiple conditions are associated with transient visual loss. They can be classified according to origin or pathogenesis, but for the purpose of this article, they are outlined by source.

  4. Wray has classified TMVL into 3 groups based mostly on pathogenesis; they include the following: • Type 1 is characterized by loss of all or a portion of vision in one eye, lasting seconds to minutes, with full recovery. It is usually secondary to embolic phenomenon. Attacks have been correlated with vessels without critical narrowing but with ulceration. • Type 2 includes visual loss due to hemodynamically significant, occlusive, low-flow lesions in the ICAs or the ophthalmic arteries. Symptoms are brief but frequent, less rapid in onset, and longer in duration with gradual recovery. • Type 3 is believed to be due to vasoconstriction or vasospasm.

  5. Branch Retinal Artery Occlusion The central retinal artery, a branch of the ophthalmic artery, enters the eye through the optic disc and divides into multiple branches to perfuse the inner layers of the retina. A branch retinal artery occlusion (BRAO) occurs when one of these branches of the arterial supply to the retina becomes occluded.

  6. Causes • In elderly patients, embolic disease is the most common etiology of a BRAO. In a study of 70 patients with retinal emboli, 40 were found to have cholesterol emboli, 8 platelet-fibrin emboli, 6 calcific emboli, and 1 possible myxomatous embolus. These types of emboli can also be iatrogenically displaced during cardiac angiography, catheterization procedures, or any interventional embolization of any branch of the carotid artery.

  7. Types of emboli (endogenous and exogenous) include the following: • Cholesterol – Atheromatous plaques from the aorto-carotid system • Platelet-fibrin – Carotid or cardiac thrombosis • Calcific - Calcified cardiac valves and atheromatous plaques of the carotid artery • Leukoemboli - Vasculitis, Purtscher retinopathy, septic endocarditis • Fat emboli - Following long bone fractures • Amniotic fluid emboli - Complication of pregnancy • Tumors - Atrial myxoma, mitral valve papillary fibroelastoma • Talc emboli - Long-term intravenous drug abusers

  8. Corticosteroid emboli - Complication of intralesional or retrobulbar steroid injection  Air emboli – Following trauma or surgery Synthetic particles – From synthetic materials used in artificial cardiac valves and other vascular procedures; facial dermal filler (Restylane)

  9. Nonembolic causes of BRAO • Thrombosis - Atherosclerosis, chemotherapeutic agents, bone marrow transplants • Inflammatory conditions – Syphilis, toxoplasma, retinochoroiditis, Behçet disease, Lyme disease, pseudotumor cerebri, Bartonella infection, HIV infection, posterior scleritis, varicella-zoster infection, multifocal retinitis with optic nerve edema, West Nile virus infection • Vasospasm – Migraines, cocaine abuse, sildenafil citrate use • Coagulopathies - Sickle cell disease, Hodgkin disease, pregnancy, anemia, platelet and clotting factor abnormalities, protein C, protein S, antithrombin III, factor V Leiden deficiencies, oral contraceptives, homocystinuria, antiphospholipid syndrome, chelation therapy

  10. Autothrombosis- From a ruptured arteriolar macroaneurysm Compression - Preretinal arterial loops, vitrectomy surgery, trauma Idiopathic - A syndrome of recurrent episodes of multiple BRAOs in otherwise healthy individuals has been described. An association with Susac syndrome (microangiopathy of brain, retina, and cochlea) has been seen in some of these patients.

  11. Lab Studies • ESR • Antitreponemal antibody, antiphospholipid antibody,  antinuclear antibody, rheumatoid factor, serum protein electrophoresis, hemoglobin electrophoresis, prothrombin time/activated partial thromboplastin time (PT/aPTT), fibrinogen, protein C and S, antithrombin III, and factor V Leiden. • CBC to evaluate anemia, polycythemia, and platelet disorders • Fasting blood sugar, glycosylated hemoglobin, cholesterol, triglycerides, and lipid panel to evaluate for atherosclerotic disease • Blood cultures to evaluate for bacterial endocarditis and septic emboli

  12. Imaging Studies • Fluorescein angiography • Optical coherence tomography (OCT) • Electroretinogram (ERG) • Serial Humphrey visual field testing inferior branch retinal artery occlusion from a platelet-fibrin embolus. There is retinal whitening surrounding the occluded artery.

  13. Optical coherence tomography (OCT)

  14. Medical Care Considering the increased rate of mortality, patients with BRAO should receive a full medical workup with special attention to the cerebrovascular and cardiovascular system. Depending on the findings, carotid endarterectomy or anticoagulation may be indicated. Lab workup for coagulopathies should also be performed if no embolic source is found.

  15. Further Outpatient Care • Patients should initially be evaluated every 3-6 months to monitor progression. Ocular neovascularization after BRAO is rare. If neovascularization occurs, panretinal photocoagulation should be performed.

  16. Prognosis • Recovery from BRAO is usually very good without treatment; 80-90% of patients improve to a visual acuity of 20/40 or better. However, some degree of visual field deficit usually persists.

  17. Branch retinal vein occlusion • The Eye Disease Case-Control Study reported the following findings: • Systemic hypertension is a risk factor for BRVO. • Diabetes mellitus and open-angle glaucoma are not risk factors for BRVO. • Moderate alcohol consumption reduces the risk of BRVO. • Patients often complain of a sudden painless decrease of vision in the affected eye. • Some may complain of a scotoma.

  18. Causes • Most cases of BRVO are due to idiopathic factors. Usually, patients have an anatomical predisposing factor, such as an arteriovenous crossing where the artery compresses the vein. This compression leads to clot formation and subsequent BRVO. • Inflammatory conditions that affect the retinal veins may cause local damage that predisposes the individual to intravascular clot formation with subsequent BRVO. Some of the inflammatory conditions reported in the literature are the following: • Sarcoidosis • Lyme disease • Serpiginous choroiditis

  19. Thrombophilic conditions, such as the following, may also be involved: • Protein S deficiency • Protein C deficiency • Resistance to activated protein C (factor V Leiden) • Antithrombin III deficiency • Antiphospholipid antibody syndrome • Lupus erythematosus • Gammopathies

  20. Lab Studies • The authors of the Branch Vein Occlusion Study (BVOS) have recommended against extensive testing in patients with typical BRVO. • Certain laboratory studies may be useful in atypical cases (ie, bilateral cases, those in young patients, those in patients with a personal or family history for thromboembolism). Determinations of the following may be helpful:  • Prothrombin time (PT) and activated partial thromboplastin time (aPTT) • Protein C, protein S, factor V Leiden, and antithrombin III • Homocysteine • Antinuclear antibody (ANA), lupus anticoagulant, and anticardiolipin • Serum protein electrophoresis (SPEP) results

  21. Imaging Studies • Fluorescein angiography • A fluorescein angiogram is obtained as soon as the hemorrhages have cleared if the patient's vision is still depressed. The test is usually done 3 months after the event.

  22. The purpose is to determine the cause of the visual loss (eg, macular edema, macular ischemia). If the visual loss is secondary to macular edema, laser photocoagulation in a grid pattern may be of benefit. Conversely, if macular ischemia is responsible for the visual loss, laser photocoagulation should not be offered.

  23. Optical coherence tomography (OCT): Given its ability to measure retinal thickness in a quantitative fashion, OCT is a useful adjunct in the follow-up of patients with macular edema secondary to BRVO.

  24. Complications • Macular edema • Retinal neovascularization • Vitreous hemorrhage • Tractional retinal detachment • Rubeosis iridis • Epiretinal membrane

  25. Prognosis • An analysis of several series indicates that 53% of eyes obtain 20/40 or better visual acuity, 25% have a visual acuity between 20/50 and 20/100, and 22% have a visual acuity of 20/200 or worse. • The more distal the occlusion is from the optic disc, the better the visual prognosis.

  26. Central Retinal Artery Occlusion Background:In 1859, Van Graefe first described central retinal artery occlusion (CRAO) as an embolic event to the central retinal artery in a patient with endocarditis. In 1868, Mauthner suggested that spasmodic contractions could lead to retinal artery occlusion. There is a multitude of causes of CRAO, but patients typically present with sudden, severe, and painless loss of vision.

  27. History • The most common presenting complaint is an acute, persistent, painless loss of vision in the range of counting fingers to light perception in 90% of patients. Consider ophthalmic artery occlusion if visual acuity is worse. • Some patients may reveal a history of amaurosis fugax involving transient loss of vision lasting seconds to minutes but which may last up to 2 hours. The vision usually returns to baseline after an episode of amaurosis fugax. • Ask about symptoms of temporal arteritis in the older population. Patients complain of sudden, painless, nonprogressive vision loss in one eye. History of headaches, jaw claudication, scalp tenderness, proximal muscle and joint aches, anorexia, weight loss, or fever may be elicited.

  28. Ask about any medical problems that could predispose to embolus formation (eg, atrial fibrillation, endocarditis, coagulopathies, atherosclerotic disease, hypercoagulable state). • Prolonged direct pressure to the globe during drug-induced stupor or improper positioning during surgery may lead to CRAO. • Ask about drug history.

  29. Physical • Determine the degree of vision loss (eg, no light perception, hand movement, counting fingers). • Ocular examination includes the following: • Check for afferent pupillary defect. • Perform an optic nerve examination to look for signs of temporal arteritis. Critical signs include afferent pupillary defect, pale/swollen optic nerve with splinter hemorrhages. • Cherry-red spot and a ground-glass retina may take hours to develop. • The funduscopic findings typically resolve within days to weeks of the acute event, sometimes leaving a pale optic disc as the only physical finding. • Emboli can be seen in about 20% of patients with CRAO.

  30. Boxcar segmentation can be seen in both arteries and veins. This is a sign of severe obstruction. • Perform a cardiovascular examination for murmurs or carotid bruits. • Perform a systemic examination for temporal tenderness, jaw claudication, muscle weakness, and fever to evaluate for temporal arteritis.

  31. Causes • Causes of CRAO vary depending on the age of the patient. A detailed analysis of comorbid disease is necessary to elucidate the cause of the acute visual loss. • Systemic hypertension seen in two thirds of patients • Diabetes mellitus • Cardiac valvular disease seen in one fourth of patients • Cardiac anomalies such as patent foramen ovale

  32. Embolism • Most commonly cholesterol but can be calcific, bacterial, or talc from intravenous drug abuse • Associated with poorer visual acuity and higher morbidity and mortality • Emboli from the heart are the most common cause of CRAO in patients younger than 40 years. • Amaurosis fugax preceding persistent loss of vision suggests branch retinal artery occlusion (BRAO) or temporal arteritis and may represent emboli causing temporary occlusion of the retinal artery. • Coagulopathies from sickle cell anemia or antiphospholipid antibodies are more common etiologies for CRAO in patients younger than 30 years.

  33. Atherosclerotic changes • Carotid atherosclerosis is seen in 45% of cases of CRAO, with 60% or greater stenosis in 20% of cases. • Atherosclerotic disease is the leading cause of CRAO in patients aged 40-60 years. • Giant cell arteritis • Consider in patients older than 65 years, but do not ignore in younger patients • May produce CRAO or ischemic optic neuropathy • Treat to preserve fellow eye

  34. Hydrostatic arterial occlusion • Increased intraocular pressure from glaucoma or prolonged direct pressure to the globe in unconscious patients can precipitate CRAO. • Hypercoagulable state • Collagen vascular disease • Oral contraceptives • Polycythemia • Polyarteritis nodosa • Rare causes • Consider in younger patients • Behçet disease • Syphilis • Sickle cell disease • Migraine

  35. Lab Studies • Laboratory studies are helpful in determining the etiology of CRAO. • CBC to evaluate anemia, polycythemia, and platelet disorders • Erythrocyte sedimentation rate (ESR) evaluation for giant cell arteritis • Fibrinogen, antiphospholipid antibodies, prothrombin time/activated partial thromboplastin time (PT/aPTT), and serum protein electrophoresis to evaluate for coagulopathies • Fasting blood sugar, cholesterol, triglycerides, and lipid panel to evaluate for atherosclerotic disease • Blood cultures to evaluate for bacterial endocarditis and septic emboli

  36. Imaging StudiesImaging studies are helpful in determining the etiology of CRAO. • Carotid ultrasound imaging to evaluate atherosclerotic disease. This appears to be more sensitive than carotid Doppler, which only determines the flow. • Magnetic resonance angiogram may be more accurate in detecting obstruction. • Fluorescein angiogram • Delay in arteriovenous transit time (<11 seconds is normal). • Delay in retinal arterial filling • Arterial narrowing with normal fluorescein transit after recanalization

  37. Early filling of cilioretinal artery Non-filling of other vessels Late staining of vessel walls

  38. Imaging techniques of carotid artery Duplex scanning • High resolution real-time B-scan ultrasonography • with Doppler flow analysis Digital intravenous subtraction angiography Magnetic resonance angiography Intra-arterial angiography • Excellent visualization • Injection of contrast medium • into superior vena cava • Also images ischaemic • cerebral lesions • Potential morbidity • Images produced by computer- • assisted subtraction techniques • Seldom performed

  39. Treatment options for carotid disease Medical Surgical Antiplatelet therapy • Aspirin 75 mg daily • Aspirin + dipyridamole (Persantin) • Clopidorel (Plavix) 75 mg daily Anticoagulants - if antiplatelet therapy ineffective Carotid endarterectomy • Patients with other risk factors for stroke • Symptomatic carotid stenosis > 70%

  40. Central Retinal Vein Occlusion Central retinal vein occlusion (CRVO) is a common retinal vascular disorder. Clinically, CRVO presents with variable visual loss; the fundus may show retinal hemorrhages, dilated tortuous retinal veins, cotton-wool spots, macular edema, and optic disc edema. In view of the devastating complications associated with the severe form of CRVO, a number of classifications were described in the literature. All these classifications take into account the area of retinal capillary nonperfusion and development of neovascular complications.

  41. 2 clinical types ischemic and nonischemic Nonischemic CRVO is the milder form of the disease. It may present with good vision, few retinal hemorrhages and cotton-wool spots, no relative afferent pupillary defect, and good perfusion to the retina. Nonischemic CRVO may resolve fully with good visual outcome or may progress to the ischemic type.

  42. IschemicCRVO is the severe form of the disease. CRVO may present initially as the ischemic type, or it may progress from nonischemic. Usually, ischemic CRVO presents with severe visual loss, extensive retinal hemorrhages and cotton-wool spots, presence of relative afferent pupillary defect, poor perfusion to retina, and presence of severe electroretinographic changes. In addition, patients may end up with neovascular glaucoma and a painful blind eye.

  43. hemorrhages extending all over the fundus -same patient

  44. Clinical features Patients should undergo a complete eye examination, including visual acuity, pupillary reactions, slit lamp examination of the anterior and posterior segments, undilated examination of the iris, gonioscopy, fundus examination with indirect ophthalmoscope, and fundus contact lens.

  45. Visual acuity: Best-corrected vision always should be obtained. It is one of the important indicators of final visual prognosis. • Pupillary reactions may be normal and may present with relative afferent pupillary reflex. If iris has abnormal blood vessels, pupil may not react. • Conjunctiva: Advanced stages may show congestion on conjunctival and ciliary vessels. • Cornea: Advanced stages may show diffuse corneal edema obscuring the visibility of internal structures. • Iris may be normal. Advanced stages may show neovascularization. These vessels are detected best on an undilated iris. Initially, vessels may be seen around pupillary margins and peripheral iridectomy openings if present.

  46. Fundus examination • Retinal hemorrhages may present in all 4 quadrants. • Hemorrhages can be superficial, dot and blot, and/or deep. • In some patients, hemorrhages may be seen in peripheral fundus only. • Hemorrhages can be mild to severe, covering the whole fundus giving a "blood and thunder appearance." • Dilated tortuous veins: Veins may be dilated and tortuous.

  47. Optic disc edema: Optic disc may be swollen during early stage disease. • Cotton-wool spots are more common with nonischemic CRVO. Usually, they are concentrated around the posterior pole. Cotton-wool spots may resolve in 2-4 months.

  48. Neovascularization of the disc • Fine abnormal neovascularization on the disc (NVD) or within 1 disc diameter from the disc may be present. • NVD indicates severe ischemia of the retina. • Sometimes NVD is difficult to differentiate from optociliary shunt vessels. • NVD can lead to preretinal or vitreous hemorrhage.

  49. Neovascularization elsewhere • Neovascularization elsewhere (NVE) is not as common as NVD. • NVE indicates severe ischemia of the retina. • NVE can lead to preretinal or vitreous hemorrhage.

  50. Optociliary shunt vessels are abnormal blood vessels on the disc, directing blood from retinal circulation to choroidal circulation, which indicate good compensatory circulation. • Preretinal or vitreous hemorrhage • Macular edema with or without exudates • Cystoid macular edema • Lamellar or full-thickness macular hole • Optic atrophy • Pigmentary changes in the macula