Intro to Clinical Medicine - Angelfire



Intro to Clinical Medicine – 8:00 a.m. Scribes: Allison/Amber

April 12, 2001 Hire: Trey/ Kellie

Dr. Shami

Acute Visual Loss

We will talk about the following causes of acute visual loss today:

➢ Vitreous hemorrhage

➢ Central Retinal Artery Occlusion

➢ Branch Retinal Artery Occlusion

➢ Central Retinal Vein Occlusion

➢ Retinal Detachment

Vitreous Hemorrhage

➢ Bleeding into the vitreous cavity

➢ This can occur due to trauma or it can happen spontaneously.

• Trauma is usually blunt trauma or penetrating trauma, and hemorrhage results from rupture of a retinal vessel or tearing of the retina.

• There are many spontaneous causes of vitreous hemorrhage:

– The most important one is diabetic retinopathy, secondary to ischemia and neovascularization. The new vessels are abnormal and can bleed spontaneously.

– A branched retinal vein occlusion, again because of neovascularization.

– Posterior vitreous detachment: as we age, the vitreous gel tends to liquefy and has a tendency to collapse and separate from the surface of the retina. There are some spots in the back of the eye where the vitreous gel is extremely adherent to the retina (usually around blood vessels, the optic nerve, and the most peripheral part of the eyeball). As it separates from the retina, it tears the retina just like a piece of tape will tear a piece of paper as it is removed.

– Tearing of the retina along a blood vessel will also cause vitreous hemorrhage.

– Central retinal vein occlusion with neovascularization can cause vitreous hemorrhage.

– Any condition that causes capillary occlusion with ischemia will result in the secretion of growth factors that then cause new vessels to form. In a normal adult, there should be no angiogenesis in the eye.

– Sickle cell anemia

– Some patients who have undergone cataract extraction with a posterior chamber lens implant can also have vitreous hemorrhage from the lens rubbing against the retinal vessels.

➢ Vitreous hemorrhage is treated by telling the patient to avoid straining and lifting. If the retina cannot be seen on fundus examination, then the patient must remain in bed with his head elevated for 24 hours.

➢ The main concern is a retinal tear, and if one is seen then laser treatment is needed. If the blood does not clear up on its own, it can be cleared up surgically.

➢ Slide: Patient with vitreous hemorrhage secondary to diabetes mellitus

➢ Slide: Patient with vitreous hemorrhage – fluid level visible because posterior vitreous is still attached

➢ Slide: “Sea fan” lesion classically associated with sickle cell retinopathy

Central Retinal Artery Occlusion

➢ This is equivalent to a stroke in the eyeball. It is very important to recognize because it has systemic implications as well as the sudden loss of vision.

➢ It is rarely bilateral (1-2%), and the patient usually presents because of a sudden painless loss of vision.

➢ If the pupillary reflex is checked, the affected side will have an afferent pupillary defect.

➢ Retinal tissues are usually transparent, but this transparency is lost during central retinal artery occlusion and a cherry red spot is visible. This cherry red spot is a very typical sign for central retinal artery occlusion. The blood column in the vessel will be fragmented because of sluggish flow through the arteries, and you may see embolic plaques (usually at the head of the optic nerve, but occasionally seen peripherally as well).

➢ After 90 minutes of occlusion, there is irreversible damage to the retinal tissue.

➢ Cholesterol emboli are the most common (called Hollenhurst plaques), and patients with this should have their carotids worked up by a cardiologist to see where the plaque originated.

➢ A calcific embolus may be the result of acute pancreatitis, and emboli can also result from long bone injury such as that from car accidents.

➢ Vision loss will occur quickly unless the artery can be recanalized. Rarely (up to 20%), patients will have a branch from the choroidal artery called a semi-retinal artery(?) supplying the macula, so central vision is spared, but there is an extensive peripheral field loss.

➢ Etiology of central retinal artery occlusion:

• Hypertension – this is the most common cause

• Diabetes mellitus

• Cardiovascular disease

• Carotid artery disease

• Pancreatitis

• Trauma

• Collagen vascular diseases like lupus.

• Giant cell arteritis is a very important disease to recognize, because it can present with an acute central retinal artery occlusion, and within a week the patient will have occlusion in the other eye as well. This is a common medico legal liability issue. Erythrocyte sedimentation rate (ESR) and C reactive protein levels should always be obtained on every patient that presents will sudden visual loss to rule out giant cell arteritis. Start prednisone immediately, and refer the patient for a temporal artery biopsy.

➢ Treatment of a central retinal artery occlusion:

• This will involve anti-platelets or other anti-coagulation therapy if it can be started within 24 hours.

• Gentle massage of the eyeball in an attempt to dislodge the clot is another treatment, but you have to be careful about the oculocardiac reflex.

• Acetazolamide can be used to drop the intraocular pressure and improve blood flow.

• A needle can be inserted into the anterior chamber to accomplish a decrease in intraocular pressure as well.

➢ Slide: Angiogram of retinal vessels

Branch Retinal Artery Occlusion

➢ In some cases, instead of having obstruction of the central retinal artery, an embolus can wind up in a smaller branch, causing a branch retinal artery occlusion. The area of the retina that is perfused by the obstructed branch will lose its transparency and its function.

➢ The conditions predisposing to branch retinal artery occlusion are similar to those of central retinal artery occlusion, such as hypertension, diabetes mellitus, etc.

➢ We will attempt globe massage with these occlusions, but if it is not a main branch the massage is usually ineffective.

➢ Fibrinolytics have been tried, but the risk of bleeding in the brain is very high and they have not been shown to be effective. Selective canalization of the occluded branch vessel is tried in the lab, but there is a significant risk of nicking an artery and filling the posterior chamber with blood.

➢ It is also possible to have an ophthalmic artery occlusion, particularly in diabetics with mucormycosis, and in patients receiving a retrobulbar injection as part of cataract surgery. With occlusion of the ophthalmic artery, you will not see a cherry red spot because the choroidal artery is occluded as well. The patient will have no light perception, and intraocular pressure is also lower than normal because the ciliary body is not perfused, so it stops making aqueous fluid.

Central Retinal Vein Occlusion

➢ If the obstruction is complete, you will see diffuse hemorrhages in an arcuate pattern along the nerve fiber layer of the eye.

➢ In the ischemic subtype, you will see swelling in the macula.

➢ The main risk of this type of occlusion is neovascular glaucoma with vessels forming at the surface of the eye. If the neovascularization is severe enough, it will clog the channels in the trabecular meshwork that drain fluid from the anterior chamber. This is a quite aggressive type of glaucoma that doesn’t usually respond to medical therapy. If there is evidence of neovascularization that will lead to glaucoma, then a laser will be used to ablate the ischemic retina in an attempt to stop the production of vasoactive factors.

➢ The nonischemic subtype (about 70%) has a less severe obstruction. 30% of the patients will improve, 30% will progress to the ischemic type, and 30% will stay the same (hey, the math looked fishy to us, too). Laser therapy will not be used in this type unless neovascularization is prominent, but some patients will need their intraocular pressure lowered medically.

➢ Hemi-vein occlusion or branch vein occlusions are not as dramatic as the central retinal vein occlusion, but they can result in a significant decrease in vision.

• You see indentation of the vein where the hardened artery crosses it (AV nicking) in chronic hypertension. This nicking may create turbulence in the flow of blood, leading to thrombosis and then occlusion. It is most commonly caused by hypertension, but other causes (such as syphilis) occur as well.

• You will see cotton-wool spots and hard exudates, yellowish deposits in the macular area.

• The main complications of a branch retinal vein occlusion are the presence of swelling in the macular area and neovascularization as a result of ischemia. Again, if we do find neovascularization, then the ischemic areas should be treated with a laser. If the vision does not recover within 3-4 months, then a laser will be used to reduce macular edema.

Retinal Detachment

➢ The definition of a retinal detachment is the separation of the retina from its underlying pigmented epithelium. The retina captures light energy and converts it to electric, then sends it to the brain.

➢ There are three types of retinal detachments:

• Rhegmatogenous, where there is a hole or tear in the retina

• Traction detachment, which is usually due to diabetes mellitus, and is caused by scar tissue pulling on the retina

• Exudative detachment as a result of inflammatory diseases or sometimes hypertension.

➢ If a patient calls and says he is seeing black spots in his eyes (floaters) or flashes of light, he should have his eyes dilated because he is probably having a retinal detachment. In older patients, the vitreous is often liquefied and may dissect its way through the retina and hydrate the mucopolysaccharide bond between the photoreceptors and the pigmented epithelium. (The pigmented epithelium is supposed to pump fluid from under the retina to the choroid.) In this case, fluid builds up underneath the retina and causes it to pull away from the pigmented epithelium. A very specific sign is the patient will tell you there’s a curtain coming down over their vision.

➢ Treatment of the rhegmatogenous type of retinal detachment:

• Initial treatment is with laser or cryotherapy to create a scar and prevent further detachment.

• If that doesn’t work, then a gas bubble can be injected which will seal the tear internally and allow the retina to reattach spontaneously.

• A scleral buckle can be used where a suture is passed through the white of the eye and the sclera is then drawn in to indent the wall of the eye and seal the tear.

• Finally, a vitrectomy can be used where you remove the vitreous gel and replace it with a gas bubble.

➢ Folding of the retina on fundoscopic exam is a big clue that retinal detachment has occurred.

➢ Some people are predisposed to detachment:

•

• people with lattice degeneration

• trauma is the most common cause in young people

• family history of retinal detachment

• Marfan’s syndrome

➢ In an exudative type of detachment without tears, treatment is medical and not surgical. The underlying condition should be treated.

➢ In the traction type of detachment, treatment is surgical.

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