Crao vs brao . by Dr.kausar ali

Lecture Notes:

Central Retinal artery .Occlusions.(CRAO)

Branch Retinal artery .Occlusions . (BRAO)

Prepared By .Dr. kausar Ali .

Doctor of optometry*At Pef university .

Prepared for .Doctor of optometry .

Professional level student .And coming juniors classes .

Lecture Include :

• Definition. • Etiology. • Signs.• Prognosis.• Treatment.• Epidemiology.

• Definition : • Central retinal artery occlusion is a

disease of the eye where flow of blood Through central retinal artery is blocked . Occlusion have different causes.

• Etiology : • Hypertension in old age .• Thrombosis due to atherosclerosis at the

level of lamina cribrosa is by far the most common cause accounts for about 75% of cases . • Embolism from atherosclerotic plaque of

carotid artery, aortic arch and cardiac origin accounts for about 20% of cases .

• Inflammation : retinal arteritis E.g giant cell arteritis.• Periarteritis e.g systemic lupus

erythematosus,, polyarteritis nodosa . • Angiospasm . • Raised intraocular pressure

(Glaucoma ) may occure after retinal surgery . • Clinical Features :

• Symptoms : • Amaurosis flug ( monocular repeated

trancient episodes of decreased vision blindness that may occurs before visual loss ) • Sudden painless loss of vision .

• Signs : • Visual acuity : profound loss of vision

even up to no perception of light .• Pupil : direct pupillary light reflex is

absent (total afferent pupillary conduction defect . • Fundus examination . • Whitish appearance (opaque) of retina as

a result of cloudy swelling caused by intracellular oedema.

• Retinal arteries are extremely thin. • Veins are almost normal. • Blood column within retinal veins may be

segmented ( cattle tracking sign ) • Retina become cloudy due to oedema

corresponding to ischemia . • The fovea centralis stands out as “cherry

red spot” due to choroidal vascular shining behind it.

• After few weeks oedema subsides, atropic changes occur arteries become thread like and optic atrophy occurs . • Prognosis : • The cause .• The degree of obstruction.• The artery can re-canalize over time and the

edema can clear. However, optic atrophy leads to permanent loss of vision. Irreversible damage to neural tissue occurs after only 90 minutes.

• Two thirds of patients experience 20/400 vision while only one in six will experience 20/40 vision or better.• Treatment : • Relief the spasm of vessel.• Dislodge and disintegrate and emboli . • Intraocular pressure is lowered

immediately to increase retinal perfusion by : Acetozolamide 500 mg IV .

Mannitol 20% IV 1g/kg . Paracentesis of anterior chamber.• Ocular massage to dislodge emboli and

lower the intraocular pressure . • Isosorbide nitrate sublingually to

increase circulation and dislodge the emboli by dilating the vessels . • Inhalation of mixture of 5 % carbon

dioxide and 95% oxygen may help to relive angiospasm .

• Streptokinase intravenously to disintegrate emboli .

• Retro bulbar tolazaline injection to decrase retro bulbar resistance to blood flow .

• Epidemiology: • Risk factors for CRAO include the following: being

between 60 and 65 years of age, being over the age of 40, male gender, hypertension, caucasian, smoking and diabetes mellitus.[2] Additional risk factors include endocarditis, atrial myxoma,inflammatory diseases of the blood vessels, and predisposition to forming blood clots

• Branch Retinal Artery occlusion : • It usually occur due to lodgment of emboli at

bifurcation of retinal artery .• Retina distal to occlusion become

edematous with narrowed arterioles .• Later on, the involved area is atrophied

leading to permanent sectorial visual field defect . • Investigation : • FFA shows nonperfusion of vascular

occlusion area .