Ocular Emergency

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OCULAR EMERGENCIES MANAOIS, RAFAEL S. JUNIOR INTERN DEPARTMENT OF OPTHALMOLOGY MCU-FTMF HOSPITAL

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Transcript of Ocular Emergency

OCULAR EMERGENCIES

MANAOIS, RAFAEL S.

JUNIOR INTERN

DEPARTMENT OF OPTHALMOLOGY

MCU-FTMF HOSPITAL

Central Retinal Artery Occlusion

• Causes painless catastrophic visual loss occurring over a period of seconds;

• Antecedent transient visual loss (amaurosis fugax) may be reported.

• Visual acuity ranges between counting fingers and light perception in 90% of eyes at initial examination.

Classic presentation:

• extremely sudden, acute unilateral nonpainful visual loss.

Causes: Branch retinal artery is usually embolic in origin and results in visual field loss and atherosclerosis.

Visual acuity is only reduced if there is foveal involvement.

Ocular exam: cherry red spot on fundoscopicexamination.

• Acute central retinal artery occlusion with cherry-red spot (arrow) and preserved retina due to cilioretinal arterial supply (arrowheads)

• superficial retina becomes opacified due to ischemia.

• A foveal cherry-red spot is evident as a result of visualization of the choroidal pigment and retinal pigment epithelium through the extremely thin retina overlying foveola.

• This resolves within 4–6 weeks,leaving a pale optic disk as the major ocular finding

Remember!!!

• Irreversible retinal damage occurs after 90 minutes of complete central retinal artery occlusion in the subhuman primate model, leaving little time in which to begin therapy.

Treatment

• Embolic central retinal artery occlusion - Sudden decrease in intraocular pressure resulting in increased retinal perfusion can be achieved with anterior chamber paracentesis and intravenous acetazolamide.

• nhaled oxygen–carbon dioxide mixture induces retinal vasodilation and increases the PO2 at the retinal surface.

• Thrombolytic therapy, infused directly into the ophthalmic artery or administered systemically, continues to be evaluated.

• Systemic anticoagulants are generally not employed.

Chemical Burns

AlkaliLiquifactive necrosis

Will denature collagen and destroy vessels

More common and worse than acid burns.

Require immediate ophthalmologic consultation.

Found in: household cleaners, fertilizers

Alkali burns more severe than acid

Rapidly penetrates through ocular tissues and will continue to cause damage long after the injury is sustained, prolonged lavage and repeated Ph checks are needed.

Acid

Coagulative necrosis

Found in: automobile batteries (sulfuric acid), industrial cleaners.

Acids form a barrier of precipitated necrotic tissue that tends to limit further penetration and damage.

Other ocular burns

• Thermal – usually local effect

• Electrical and Lighting – Systemic and wide spread effect coagulation of proteins (cataract)

Remember!!!

White eye is a bad eye!

If conjunctiva and cornea appears white, sign of very severe burn.

ACUTE MANAGEMENT

• pH determination • Immediate ocular irrigation: plain

NSS, lactated ringer’s or BSS sol. 2-3L in 1 hour

• Repeat pH determination after 5mins.

• Cul de sac cleaning and swabbing • Repeat irrigation

THANK YOU FOR LISTENING!!!