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Ocular emergency.  True emergency Chemical burn Chemical burn Central retinal artery occlusion Central retinal artery occlusion  Rx should be instituted.

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Presentation on theme: "Ocular emergency.  True emergency Chemical burn Chemical burn Central retinal artery occlusion Central retinal artery occlusion  Rx should be instituted."— Presentation transcript:

1 Ocular emergency

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

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

4  Semi-urgent situations Optic neuritis Optic neuritis Ocular tumors Ocular tumors Acute exophthalmos Acute exophthalmos Old retinal detachment (involve macular >1 wk) Old retinal detachment (involve macular >1 wk) Strabismus in young children Strabismus in young children Blow-out fracture of the orbit 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 Emboli or thrombosis (mostly) Connective tissue diseases - Giant cell arteritis - Giant cell arteritis - SLE - SLE - Rheumatoid arthritis - Rheumatoid arthritisOthers

9 Management Treat without delay, before work up irreversible damage within about 90 minutes of complete occlusion Reduce intraocular pressure (IOP) - ocular massage - ocular massage - anterior chamber paracentesis - anterior chamber paracentesis - antiglaucoma drugs - 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 the leading cause of death in patients with CRAO!! in patients with CRAO!!

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

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24 Management  Decreasing inflammation Topical steroid Topical steroid  Monitoring IOP Antiglaucoma drugs Antiglaucoma drugs  Limiting matrix degradation Ascorbate, collagenase inhibitor Ascorbate, collagenase inhibitor  Promoting reepithelialization Tear (non-preservatives) 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 - elderly age, female>male - small, hyperopic eye - small, hyperopic eye - familial risk - familial risk - previous attack of the fellow eye - previous attack of the fellow eye - dark environment - dark environment

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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: -  adrenergic antagonist -  adrenergic antagonist - parasymmatomimetic agent - parasymmatomimetic agent - carbonic anhydrase inhibitor (CAI) - carbonic anhydrase inhibitor (CAI) - selective  adrenergic agonist - selective  adrenergic agonist - prostaglandin analog - 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 filtering surgery tube implant surgery tube implant surgery

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

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

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

34 PreseptalOrbital InflammationAnterior to septum Beyond septum FeverMild++ Lid edema++++ EOM limitationNoYes ProptosisNoYes HospitalizationOnly childrenYes

35 Management Vision loss due to high orbital pressure : lateral cantholysis, rarely in very severe case, orbital decompression Vision loss due to high orbital pressure : lateral cantholysis, rarely in very severe case, orbital decompression Systemic ATB : days, longer in severe case Systemic ATB : days, longer in severe case Treat causes 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 Painful visual loss Ciliary injection, chemosis, corneal edema, and eyelids edema Ciliary injection, chemosis, corneal edema, and eyelids edema Cells in A/C, vitreous Cells in A/C, vitreous

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