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The Snellen terminology. What does it mean when we say someone sees 20/20? What do we mean when we say someone sees 20/40? The 20/20 line means that we are testing a particular person at 20 feet and that person is able to see what a so-called normal person can see 20 feet away.

Blepharitis is the most common inflammation of the eyelids. There are sebaceous glands which line the eyelid and they secrete glandular secretion which collects on the lashes and causes inflammation.

Chalazion. Very common to see bumps in the eyelids. Cystic inflammation of the meibomian glands of the eyelid, often staph related. Treatment is usually conservative: hot compresses, sometimes topical antibiotics, and topical steroids will really usually cool it down.

Ptosis. Ptosis can be congenital, it can be acquired. It can be involutional, it can be myogenic such as myasthenia gravis. It can be neurogenic such as third nerve palsy or Hornerís syndrome. It can be traumatic, it can be mechanical. Entropion on this slide here is the in-turning of the eyelash of the eyelid, with resulting irritation of the eye and ectropion here which is an out-pouching of the eyelid; can be involutional or it can be paralytic like a seventh nerve palsy.

Basal cell carcinoma, as you see on the left, is the most common malignant tumor of the eyelids. Usually on the lower lids. It has curly edges. Occasionally cystic and needs to be excised and clean margins. Here you have a squamous cell carcinoma, which is more invasive.

Herpes zoster. Herpes zoster is one of those unique conditions that can actually affect every part, from the eyelids going all the way back to the optic nerve and even further back. Herpes zoster involving the trigeminal branch can affect, of course, the forehead, can affect the eye. Hutchinsonís sign is when the tip of the nose is involved. Thatís the nasociliary branch of the trigeminal nerve. The tip with the side of the nose - and that is usually an indication that the eye will become involved and it can be involved, as you can see in this picture here on the right, with a dendrite involvement.

Conditions of the cornea. The cornea being like a crystal of a watch at the very front of the eye through which all our vision needs to pass through. The cornea has five layers. Epithelium, Bowmanís membrane, which is the basement membrane of the epithelium, the thick stroma, then you have the inner layer, single layer of endothelia cells and the basement membrane of the endothelium or Descemetís membrane. This is a speculum micrograph of the corneal endothelium, the single layer of cells and it is these cells that are responsible to keep the cornea relatively dehydrated.

Pterygium is a fibrovascular growth which is relatively common, particularly in tropical climates. Thought to be related to ultra-violet exposure. Requires excision. At least 30% of them re-grow. We now have various techniques to try to limit that with conjunctival grafts, mitomycin.

Corneal arcus, you are all familiar with that. Itís often a sign of ASHD or associated with ASHD possible with hyperlipidemia, although not always.

Herpes simplex. Dendrite lesions of the cornea occur with the recurrent form of Herpes simplex of the cornea. Herpes simplex is the most common cause of corneal blindness in this country. Fortunately we have topical antiviral medications which shorten the course of the individual attacks.

Conjunctiva. The conjunctiva is difficult to visualize. It is obviously a mucous membrane, clear cellophane-like which attaches at the limbus. The limbus being the junction between the cornea and the sclera and it actually forms a fornix and comes around and lines the inner side of the eyelid. So thatís what keeps contact lenses from going further backĖthey are trapped by the conjunctiva. But deep in the conjunctiva of course is the sclera, the other ocular structures. In this slide on the right you have a localized conjunctival inflammation. You would not likely call this a conjunctivitis.

Viral conjunctivitis and bacterial conjunctivitis. It is going to be hard to tell one from the other and if you are not sure, what you will end up doing is youíll treat the person with topical antibiotics, probably the favorites now are Ocuflox or Ciloxan. All you need to do is use them four or six times a day topically. Bacterial conjunctivitis is less likely in adults, more common in children. Viral conjunctivitis is often related.

Ciliary injection. Now in contrast to the pattern in conjunctivitis, this is reversed. Conjunctival inflammation here is around the cornea and yet deeper in the fornix area it tends to be whiter. What this is telling you is that this is not a straightforward conjunctivitis. This is just telling you that something is different. What is different here is this is telling you the inflammation is centered around the cornea or around the anterior segment.

Subconjunctival hemorrhage is just blood under the conjunctiva. You see again chemosis, which is swelling of the conjunctiva, and subconjunctival hemorrhage. Now this comes up in my office every single day of the week. Someone will call and say, "I have a blood spot on my eye. What do I do?" and what you have to know, and you have to deal with this too, if itís a spontaneous subconjunctival hemorrhage you can forget about it. Maybe they are on Coumadin, maybe there is no good reason, maybe the coughed, sneezed, rubbed their eye, whatever it is.

Glaucoma. Glaucoma is a condition in which the pressure in the eye is elevated. What happens is that when the pressure in the eye is elevated it causes micro-infarction and ischemia of the optic nerve in the back of the eye - because the blood supply is coming this way - and ultimately you have loss of vision. First peripheral vision then central vision. In the slide to the right, how do we check pressure?

Narrow-angle glaucoma can present as an acute emergency. Red-hot eye. In this case the pressure can often shoot up to 60 or 70 and the patients become acutely symptomatic. They come in with a red-hot eye. The redness would be similar to that ciliary flush that I showed you. The pupil is mid-dilated. They can be nauseous, they can have GI symptoms, and itís been known to happen - and Hermann in particular speaks of this - where people are on wards with GI symptoms and really no obvious cause found. Every once in awhile they will get an eye consult and the eye consult.

Now these are the various medications or treatments for glaucoma. Certainly the first line of treatment for glaucoma are eye drops. You know we have the beta-blockers, Timoptic, we have the new prostaglandin medications, Xalatan. We have the carbonic anhydrase inhibitors which are like Diamox and Dropform. We have Propine, we have alpha-adrenergic agonists and of course we have the old time miotics like pilocarpine. We usually have our favorites and depending upon the particular circumstances with the patient, such as can the patient tolerate beta-blockers or not, that dictates what medications will be the first line medications for someone with elevated pressure. After the eye drops we can go to oral medications such as the carbonic anhydrase inhibitors. Unfortunately they all are sulfa-based and if someone has a sulfa allergy we are not able to use them.

Uveitis. Uveitis is inflammation of the uvea, the pigmented layers of the eye. The uvea being the iris, the ciliary body and the choroid. Those are the three parts of the eye that belong to the uvea. The slide on the right here is supposed to show what we see when we look at a slit-lamp. A slit-lamp being a biomicroscope that allows us to examine the eye. When we look at the anterior chamber we project a beam from the front of the eye back.

Cataracts. Cataracts are very common. A cataract is when the lens inside the eye turns cloudy. A white pupil. Of course, light trying to pass through that lens is going to be relatively blocked. As you can see on the slide on the right, if someone were able to see the Snellen chart clearly they would see it as you see it on the left. Now with a cataract, you would see it as this projects on the right, very blurred. Because all light passing through that cataract is going to give them a blurred image. Now the buzz-words for cataract surgery now are phakoemulsification cataract extraction with insertion of small incision intraocular lens implant. Phakoemulsification is a technique that was developed over the last 20 years.

Laser corrective surgery. I put that in only because thatís what most people seem to be interested in nowadays. So weíll pass through this in about two minutes. Normally, to see clearly, light has to pass through the anterior structures of the eye and project sharply right on the retina. In myopia the rays come to focus anterior to the retina because the eye is a little bit too long. The slide on the right shows that any corrective lens, whether itís a spectacle lens or a contact lens on the front of the eye, will bend those rays so that they project further back.

Now you are all familiar with radial keratotomy, which used to be a way that we would correct refractive errors, in particular myopia. That was effective but it had a lot of Ö it wasnít that accurate and it had a lot of symptoms related to it. Then in 1995 the excimer laser was approved for photorefractive keratectomy. The excimer laser is the basis for all the laser corrective surgery. It was initially done as a photorefractive keratectomy, which simplistically meant that a laser beam was taken and it was projected right off to the surface of the cornea. If you look at the slide on the right, what was done for myopia was the excimer would flatten the central part of the cornea, removing tissue from the center of the cornea. Basically making the cornea flatter and reducing myopia. In PRK where you go right through the central epithelia, the epithelia has to grow over once again. What youíve done is youíve gone through Bowmanís membrane, which is the basement membrane of the epithelia. This procedure, PRK, is no longer as popular as some of the new procedures that Iíll show you in a second. A flattened cornea then is able to project light right on the surface of the retina. PRK - these are some results from 1993 - and you can see it was fairly successful; 96% of patients had vision of 20/40, 85% 20/25 and 73% actually showed 20/20. The problem with PRK was there was some regression and patients had a fair amount of haze, some of which developed a year or more after the procedure.

The newest procedure that you will all be hearing about is LASIK. And LASIK is laser assisted in situ keratomileusis. It was first approved for nearsightedness and the basic concept here is; you take a keratome, make a slice in the cornea, flap back the cornea, laser the bed and put the cornea back in. It heals very quickly. The benefit to LASIK is you donít have the anterior surface problems because all the lasering is done in the sandwich you created of the cornea. So you avoid a lot of the haze, a lot of the late complications you had with PRK and there is virtually no regression. This is just one of the keratomes we use to make the hinge in the cornea, and you can see in the slide on the right as it is coming across the cornea it will make that flap, which is so critical to the LASIK concept. LASIK will again remove and flatten the tissue in the center of the cornea, and then when you put the cornea back down youíll end up with an indentation and the surface cap will take that same contour and give you the flattening that you need to correct the myopia. The slide on the right will show you the final profile of the flattened cornea.

After LASIK was approved for nearsightedness it was approved for astigmatism. Similar concept but just giving you treatment in a particular axis to correct the astigmatism. Lastly, itís been approved recently for hyperopia and what we do in hyperopia, itís treating the mid-periphery not the center so you end up with effectively a steeper cornea and thatís what you need to bring that image, which is behind the retina, back on the surface of the retina. This is an eye after LASIK. Itís incredible because you can even fool ophthalmologists. Very often they wonít be able to tell that a person has had LASIK. That is how well the cornea is tolerating the LASIK procedures. Thatís not to say there arenít complications, and I havenít spent any time discussing the complications, but fortunately complications are rare and about 99% of the time there are none.

Hypertension. In the fundus of a patient with hypertension you notice the arteriolae are narrow. There is exudate, a little hemorrhage and itís an older patient and you suspect hypertension. How many of you see that at least twice a week? In other words, how many of you use the ophthalmoscope at least twice a week? Oh, thatís pretty good. More than last year. Of course it is important to classify it, hypertensive retinopathy, and it is classified in acute and chronic. The problem that sometimes arises is that patients age and you have to distinguish the changes.

Central retinal artery occlusion, also a complication of arteriosclerosis, mostly embolic, mostly embolic from the carotid arteries so you get carotid artery studies. These fundi are paler in contrast to vein occlusion which looks red. And there is a cherry-red spot. Incidentally, you also have central retinal artery occlusion in women, mostly age 40, who have migraines.

Diabetes. Here is selective peri-sight loss and in the retina may either leak or it may close off vessels. Thatís what it looks like on an angiogram. We call it background diabetic retinopathy. When they take it out of the retina then we call it proliferative diabetic retinopathy. Here is shown background diabetic retinopathy. It has these lipids in here, microaneurysms which leak and sometimes if you take the cholesterol or get a lipid profile and it is very high and you control the lipids and lower the blood pressure, the lipids may go away thereby the vision may get better.

Proliferative diabetic retinopathy has non-proliferative changes plus new vessels. These new vessels may be on the disc and they may be elsewhere. Iíll just show you an example. Here is the disc obscured by new vessels, and this is the macula with new vessels. The angiogram shows the new vessels. If it leaks the patient doesnít see and thereís a histological slide of these vessels starting to bleed.

Age-related macular degeneration. Most of your elderly patients have this fundus finding here, these whitish-tan spots, which are called drusen. The accumulation of basement membrane into the pigmented epithelial cell in Bruchís membrane. So what ages predominate in age-related macular degeneration? Is the inner choroid. It is not predominantly in the retina. What it looks like is that you have the choroid here and pigmented epithelium on top, the retina would be up towards the ceiling and there you have this kind of toxic waste dump that the pigmented epithelium has to sit on. Of course it doesnít function properly. It doesnít nourish the retina and that is why you have visual loss wherever these accumulations occur. There are two types of age-related macular degeneration; wet and dry. The wet kind is when new vessels grow from those drusen underneath the retina.