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Ocular emergency.

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Presentation on theme: "Ocular emergency."— Presentation transcript:

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


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