1. Ocular emergency

2. Ocular emergency True emergency Chemical burn
Central retinal artery occlusion
Rx should be instituted within minutes

3. Urgent situations Acute narrow angle glaucoma Endophthalmitis
Penetrating injury of the globe
Orbital cellulitis , Preseptal cellulitis 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 within days

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

9. Management Treat without delay, before work up - ocular massage
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 Monitoring IOP
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 > 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 Trauma or surgery
most commonly from the paranasal sinuses
the face, the globe, and the lacrimal sac
Trauma or surgery
Hematogenous spread from bacteremia

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

34. Preseptal
Orbital
Inflammation
Anterior to septum
Beyond septum
Fever
Mild ++
Lid edema +
+++
EOM limitation No
Yes
Proptosis
Hospitalization
Only children

35. Management
Vision loss due to high orbital pressure : lateral cantholysis, rarely in very severe case, orbital decompression
Systemic ATB : 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