OCULAR EMERGENCIES

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

Central Retinal Artery Occlusion .

• Antecedent transient visual loss (amaurosis fugax) may be reported.• Causes painless catastrophic visual loss occurring over a period of seconds. . • 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.

Visual acuity is only reduced if there is foveal involvement.Causes: Branch retinal artery is usually embolic in origin and results in visual field loss and atherosclerosis. .

.Ocular exam: cherry red spot on fundoscopic examination.

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

• This resolves within 4–6 weeks.• superficial retina becomes opacified due to ischemia.leaving a pale optic disk as the major ocular finding . • 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.

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.

Sudden decrease in intraocular pressure resulting in increased retinal perfusion can be achieved with anterior chamber paracentesis and intravenous acetazolamide. • Thrombolytic therapy. infused directly into the ophthalmic artery or administered systemically. continues to be evaluated. • nhaled oxygen–carbon dioxide mixture induces retinal vasodilation and increases the PO2 at the retinal surface. .Treatment • Embolic central retinal artery occlusion . • Systemic anticoagulants are generally not employed.

Chemical Burns .

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. Found in: household cleaners. Require immediate ophthalmologic consultation.Alkali Liquifactive necrosis Will denature collagen and destroy vessels More common and worse than acid burns. .

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.

• Cul de sac cleaning and swabbing • Repeat irrigation . lactated ringer’s or BSS sol.ACUTE MANAGEMENT • pH determination • Immediate ocular irrigation: plain NSS. 2-3L in 1 hour • Repeat pH determination after 5mins.

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