1. A CUTE AND C HRONIC VISUAL LOSS Dr Mahmood Fauzi ASSIST PROF OPHTHALMOLOGY AL MAAREFA COLLEGE

2. O BJECTIVES Define visual loss Differentiate between acute and chronic visual loss Formulate differential diagnoses for acute and chronic visual loss Take history and Outline the examination procedure for case presenting with visual loss Recognize the Danger signs while history taking. Recognize chief ocular conditions presenting with visual loss,understand their systemic associations, their etiology, clinical presentation and management.

3. V ISION L OSS Categorization Total or Partial One or Both eyes Sudden/ Acute or Gradual / Chronic Painful or Painless

4. D EFINING A CUTE In medicine, an acute disease is a disease with a rapid onset and/or a short course. minutes up to few weeks

5. DD X OF ACUTE VISION LOSS Corneal Abrasion Corneal ulcer Acute angle closure glaucoma Acute uveitis (sometimes painless) Endophthalmitis Hyphema Vitreous hemorrhage. Retinal Artery Occlusion Retinal Vein Occlusion Retinal Detachment Optic Neuritis (can be associated with ocular pain on eye movement) Painful (usually)Painless (usually)

6. D EFINING CHRONIC CHRONIC A chronic condition is a human health condition or disease that is persistent or otherwise long – lasting in its effects. The term chronic is usually applied when the course of the disease lasts for more than three months

7. DDX OF C HRONIC VISION LOSS 1- Amblyopia 2- Corneal opacities 3- Cataract 4- Glaucoma 5- Retinal vascular diseases 6- Macular degeneration 7- Chronic uveitis 8- Refractive error 9-Neglected or persistent cause of acute visual loss

8. H ISTORY Questions Danger Signs How long ago? Recent How sudden? Sudden: ischemia or bleed Course? Worsening

9. H ISTORY What do they see? Flashes or floaters “Curtain” rising or falling Central patch or distortion Key symptoms Pain or headache Nausea / Vomiting

10. H ISTORY In addition to general Hx/Px: Usual corrective glasses / contacts? Still in? Previous transient episodes? Trauma?

11. E XAMINING A PATIENT WITH LOSS OF VISION Visual acuity Visual field testing Swinging light test Direct ophthalmoscopy Dilating the eye Tropicamide 1% Especially important for suspected Intraocular FB Central retinal artery occlusion Retinal detachment Tonometry Tonopen Contraindicated if suspected ruptured globe T tono = 10 – 21 mm Hg (N) False elevation IOP - Blepharospasm (“squeezers”) - Avoid pressure on the eye by holding eyelids only against bony orbital rim

12. C ORNEAL ULCER OR MICROBIAL KERATITIS History of (trauma, CL wear) Need urgent referral to ophthalmologist Need samples for microbiology Might need hospitalization Treated with frequent application of topical broad spectrum antibiotics. If neglected can lead to corneal perforation and endophthalmitis

14. Corneal Epithelial Defect (CED) or Corneal Abrasion

15. A CUTE A NGLE C LOSURE G LAUCOMA Aqueous humor produced in posterior chamber Blockage of normal drainage and circulation to anterior chamber Increasing IOP worsens outflow as iris pushed forward Often 40-80 mm Hg

16. A CUTE ANGLE CLOSURE G LAUCOMA C/O acute vision loss, pain, headache, vomiting Corneal edema Mid-dilated non-reactive pupil Ciliary injection High IOP (around 50s) Optic disc swelling Systemic IOP lowering medications YAG laser peripheral iridotomy ASAP

17. A CUTE A NGLE C LOSURE G LAUCOMA E XAM Anterior chamber Shallow “Shadow sign” Cells and flare www.hypertension-consult.com/Secure/textbookarticles/Primary_Care_Book/126.htm www.opt.indiana.edu/riley/HomePage/Direct_Oscope/Text_Direct_Oscopt.html

18. A CUTE UVEITIS Most commonly idiopathic can be associated with pain and high IOP Characterized by: ciliary injection, keratic precipitates (KPs), iris nodules, synechia, vitritis, vasculitis, chorioretinitis and/or papillitis. Any type of uveitis (anterior, intermediate and posterior) can cause acute loss of vision but usually posterior (toxoplasmosis retinitis) Rule out infection and malignancy Treatment is usually with Local or systemic immunosuppression

19. E NDOPHTHALMITIS Painful loss of vision Usually Recent intraocular surgery. Usually unilateral (except septicemia) Need urgent referral to ophthalmologist. Need vitreous samples for microbiology Need intravitreal antibiotic injections Might need retina surgery.

20. H YPHEMA History of trauma (usually) Medical illness (DM, HTN) Painless loss of vision Rubiosis (NVI) due to CRVO or PDR High IOP Treat the cause Steroids and cycloplegic topical drops. Might need surgery (AC washout)

21. V ITREOUS HEMORRHAGE History of trauma Medical illness (DM, HTN) Painless loss of vision Rubiosis (NVI) due to CRVO or PDR Retinal Hrg, NVD, NVE Treat the cause Might need surgery (PPV)

22. C ENTRAL R ETINAL A RTERY O CCLUSION Sudden painless monocular loss of vision May have history of previous transient episodes. “Amaurosis fugax” Causes Embolic (carotid, cardiac) Thrombosis Temporal arteritis Vasculitis (eg. lupus) Sickle cell disease Trauma Treatment Attempt moving embolus distally: Digital massage Firm steady pressure x 15 seconds, release, repeat IOP lowering drugs Beta-blockers/CAI/alpha-agonists… +/- Vasodilation techniques Re-breathing to increase PaCO2

23. R ETINAL A RTERY O CCLUSION BRAO CRAO

24. C ENTRAL R ETINAL A RTERY O CCLUSION Macula, thinnest portion, remains visible Cherry red spot may take 24 h to develop Visual acuity may be normal if sparing by cilioretinal vessel patent cilioretinal

25. R ETINAL V EIN O CCLUSION BRVO CRVO

26. C ENTRAL R ETINAL V EIN O CCLUSION Key facts 10 times more common than CRAO Painless monocular loss of vision over hours to days Vision may improve through the day ? CRV impingement by lamina or atherosclerosis of CRA Ischemic vs. non-ischemic types

27. C ENTRAL R ETINAL V EIN O CCLUSION Treatment No known effective treatment or prevention Ophthalmology may consider: ASA Anti-coagulation Fibrinolytics Corticosteroids Anti-inflammatories

28. CRVO Non-ischemic Good vision RAPD absent Fewer retinal hemorrhages Cotton-wool spots May resolve fully or progress to ischemic type Ischemic Severe visual loss RAPD+ Extensive retinal hemorrhage and cotton- wool spots

29. R ETINAL D ETACHMENT Separation of inner sensory layers from underlying RPE Tear in retina Traction Subretinal fluid Mechanical stimulation of retinal tissue.

30. R ETINAL D ETACHMENT Risk Factors Severe myopia (eg. –12 to –15) Advanced age Previous cataract surgery Blunt trauma Family history

31. R ETINAL D ETACHMENT Typical black curtain complaint Shower of black spots or floaters Flashing lights (photopsia) From a “shadow” in periphery to “dark curtain” Wavy distortion of objects (metamorphopsia)

32. R ETINAL D ETACHMENT - MANAGEMENT Transient floaters not as urgent Full exam in clinic likely needed Home with ophtho call and follow-up WARNING: RT ED if FURTHER flashing lights or floaters, LASTING more than seconds

33. O PTIC N EURITIS Key Points Relatively common and important cause of visual loss Usually in young adults, esp. caucasian women Commonly first manifestation of MS Examination- Marcus-Gunn Pupil Presumably autoimmune reaction with demyelinating inflammation of optic nerve

34. O PTIC N EURITIS RAPD Color vision VF Management Consult ophtho and neurology Steroids?

35. I SCHEMIC O PTIC N EUROPATHY Usually painless – Vascular - embolic or thrombotic Signs – Acutely - hyperemic, swollen nerve - sometimes sectoral – Later - pallid nerve Treatment – Little can be done – Consider: Checking carotids Checking heart +/- Aspirin

36. O PTIC N ERVE E DEMA Papilledema is a term reserved for optic nerve edema, usually bilateral, caused by elevated intracranial pressure A definite ophthalmologic or life emergency

37. M ACULAR DEGENERATION Loss of central vision Reading, recognising faces impaired Peripheral (navigational) vision preserved Leading cause of legal blindness in developed world Multifactorial Age Smoking, vascular disease, UV light, diet, FHx, … Atrophic (dry, 90%) or exudative (wet, 10%)

38. Geographic atrophy – Dry AMDMacular scarring – Wet AMD

39. M ANAGEMENT Dry AMD Lifestyle Stop smoking, reduce UV exposure, Zinc & antioxidants Low vision aids Legal blindness and driving Monitoring with Amsler chart Wet AMD Observation Laser photocoagulation Verteporfin photodynamic therapy (PDT) Anti-VEGF

40. C ORNEAL OPACITIES Corneal scars (Trachoma, old trauma, old infection, advanced keratoconus) Corneal dystrophies (macular stromal corneal dystrophy, congenital hereditary corneal dystrophy CHED, Fuchs corneal dystrophy) Corneal degenerations (band keratopathy, CDK)

41. T REATMENT OF CORNEAL OPACITIES Refraction Laser (if superficial opacity) Corneal transplant

42. A CUTE DISCOVERY OF CHRONIC VISUAL LOSS Catract Can develop or worsen quickly – Usually in association with trauma metabolic Imbalances

45. R ESOURCES http://cme.medcomasia.com/cme_symposium/han dout.asp?id=433&yr=2006&m=8&d=20 http://www.patient.co.uk/doctor/gradual-loss-of- vision

46. Q UIZ TIME http://www.studyblue.com/notes/note/n/02- chronic-visual-loss/deck/2322409