Ocular emergency

1. Ocular emergency

2. Ocular emergency • True emergency • Chemical burn • Central retinal artery occlusion • Rx should be instituted withinminutes

3. Urgent situations • Acute narrow angle glaucoma • Endophthalmitis • Penetrating injury of the globe • Orbital cellulitis , Preseptalcellulitis in children • Cavernous sinus thrombosis • Corneal ulcer • Gonococcal conjunctivitis • Giant cell arteritis with acute ischemic of optic nerve • Acute retinal detachment • Hyphema • Rx should be instituted within one to several hours

4. Semi-urgent situations • Optic neuritis • Ocular tumors • Acute exophthalmos • Old retinal detachment (involve macular >1 wk) • Strabismus in young children • Blow-out fracture of the orbit • Rx should be instituted withindays

5. CRAO • Unilateral, sudden, painless loss of vision • VA: FC (counting finger) to PL (light perception) in about 90% of cases • better vision in cases of cilio-retinal artery sparing (~ 15%)

6. NPL (no light perception) in cases of ophthalmic artery occlusion

7. Fundus finding • Cherry-red spot appearance • opaque or whitened and edematous retina, particularly in the posterior pole due to retinal ischemia

8. Causes • Emboli or thrombosis (mostly) • Connective tissue diseases -Giant cell arteritis - SLE - Rheumatoid arthritis • Others

9. Management • Treat without delay, before work up • irreversible damage within about 90 minutes of complete occlusion • Reduce intraocular pressure (IOP) - ocular massage - anterior chamber paracentesis - antiglaucoma drugs • Inhalation therapy: carbogen (mixture of 95% oxygen and 5% carbon dioxide)

10. Prognosis • Permanent severe loss of vision from retinal infarction despite reopening or recanalization of the central retinal artery • Irreversible damage within about 90 minutes of complete occlusion

11. Prognosis • Questionable efficacy of treatments • Cardiovascular disease is the leading cause of death in patients with CRAO!!

12. Chemical burn • The severity depends on • the volume and duration of contact • the pH • the inherent toxicity of the chemical

13. Alkali • Alkalis cause saponification of fatty acids in cell membranes and ultimately cellular disruption • lye (NaOH) • caustic potash (KOH) • fresh lime [Ca(OH)2]: plaster, cement • ammonia (NH3): househole cleaner, fertilizer, refrigerant

14. Acid • Acids denature and precipitate proteins in tissues they contact • battery acid (H2SO4) • bleach • fruit & vegetable preservatives • industrial solvents

15. Degree • Corneal haziness • Perilimbal blanching • Cells in anterior chamber

16. Mild degree • Erosion of corneal epithelium • Faint haziness of cornea • No ischemic necrosis of perilimbal conjunctiva and sclera (no blanching)

17. Moderate degree • Markedly hyperemic eye • Corneal opacity with blurring of iris detail • Corneal edema • Slight limbal ischemia (partial blanching) • Anterior uveitis

18. Severe degree • Marked corneal opacity with blurring of the pupillary outline • Marked corneal edema • Marked limbal ischemia (total blanching) • Whitening of the external eye • Severe uveitis

19. Ocular adnexa

20. Long term complications • Superficial neovascularization of the cornea • Persistent epithelial defect • Corneal thinning and perforation • Permanent visual impairment from corneal scar • Corneal transplantation

21. PKP (corneal transplantation)

22. Management • Immediate and copious irrigation • relief pain: topical anesthetic agent • at least 1,000-2,000 cc of NSS , test pH • avoid direct pressure if rupture suspected • remove any foreign bodies • careful examination after irrigation for other ocular injuries

24. Management • Decreasing inflammation • Topical steroid • Monitoring IOP • Antiglaucoma drugs • Limiting matrix degradation • Ascorbate, collagenase inhibitor • Promoting reepithelialization • Tear (non-preservatives) • Prophylaxis topical antibiotic

25. Acute glaucoma • Acute attack or acute angle-closure glaucoma • Unilateral, sudden, painful loss of vision • Risk factors: - elderly age, female>male - small, hyperopic eye - familial risk - previous attack of the fellow eye - dark environment

27. Sign & symptom • Aching pain, +/- nausea & vomiting • Decrease vision +/- halos due to corneal edema • Red eye (conjunctival congestion maybe ciliary injection or mixed injection) • Very tense eyeball (IOP often > 40-50 mmHg) • Sami dilated fixed pupil • Narrow angle in both eyes

28. Management • Rapidly lower high IOP by hyperosmotic agents(oral acetazolamide, 50%glycerine or 20%mannitol) • Other anti-glaucoma drugs: - b adrenergic antagonist - parasymmatomimetic agent - carbonic anhydrase inhibitor (CAI) - selective a 2 adrenergic agonist - prostaglandin analog

29. Management • Treatment of choice: peripheral iridectomy; PI, (laser or surgical PI) for both eyes • indicated when the cornea is clear enough

30. Other surgical treatments: • filtering surgery • tube implant surgery

31. Orbital cellulitis • Clinical appearance • eyelid edema and erythema • proptosis, chemosis , pain on eye movement , external ophthalmoplegia, decreased vision , RAPD + • malaise , headache , fever

32. Orbital cellulitis • Causes • Periorbital structures • most commonly from the paranasal sinuses • the face, the globe, and the lacrimal sac • Trauma or surgery • Hematogenous spread from bacteremia

33. Orbit: Infection • (Preseptalcellulitis) • Orbital cellulitis • Subperiosteal abscess • Orbital abscess • Cavernous sinus thrombosis

35. Management • Vision loss due to high orbital pressure : lateral cantholysis, rarely in very severe case, orbital decompression • Systemic ATB : 10-14 days, longer in severe case • Treat causes

36. Complication and sequelae • Corneal exposure with secondary ulcerative keratitis • Facial cellulitis, necrotizing fasciitis • Brain abscess, meningitis, osteomyelitis • Panophtalmitis • Sepsis

37. Endophthalmitis • Postoperative, posttraumatic, endogenous • Painful visual loss • Ciliary injection, chemosis, corneal edema, and eyelids edema • Cells in A/C, vitreous