----start----- rubin medsurg 5/8/98 LAST DAY OF CLASS so we were talking about the lens, the nomenclature of lens opacities, etc. remember that lens is made of only lens epithelium and its immediate derivatives. so there is a very limited variety of reactions to injury. the most common by far reaction to injury is the production of an opacity, and that is called a cataract. any opacity of the lens is called a cataract. position has to be determined to make an accuate prognosis. you have to look in, see it, and know where it is. this is simple provided you keep in mind that the lens is located for all practical purposes in the center of the eye, and the center of the lens is the center of rotation of the eye. so if an opacity is in front of that, the opacity moves in the same direction as the eye, and if it is posterior to the center, the opacity moves in opposite direction from direction of eye movement. if it is in the center, it will stay still when the eye moves. so by moving your head or the animal eye, you can see which way the opacity goes and you can localize it. this is important. opacities in posterior portion of lens are progressive and may spread and blind animal. the ones in nucleus or anterior subcapsular ones are usually not progressive. before, we talked about nuclear sclerosis. a grey haze to the lens, if you were to look at it by reflected light, it would be bluish grey. but if you transilluminate it, it will transmit light. this is not a cataract per se. it isn't an opacity. it interferes with only some wavelengths of liht. cataracts depending on their position will vary in their effect on the animal. here we see a nuclear cataract in center of the lens. this animal was sick at birth and then got better - the lens was affected. this is going to produce visual difficulty in bright light - when pupil constricts, opacity in central area blocks light but when pupil is dilated animal can see around it. animals with nuclear or axial cataracts have visual problems in bright light. animals with retinal dz, esp hereditary kind, have visual problems in dim light. the usual cataracts - most common ones are inherited ones forming at suture lines in form of triangles, in posterior subcapsular area, that spread peripherally. spread varies with breed, type of gene. most of these animals never really have visual difficulty. if they do, you can refer them to an ophthalmologist or, for nonsurgical tx, dilate pupil so they can see around the cataract. then they may not need surgery. same thing here, another siberian husky with posterior subcapsular cataract in triangular form. problems seeing in bright light. same thing, closer up, we see suture lines, upside down Y, with opacification going outward from it. if progresses, can blind animal. exception to this - cataract of posterior capsular/subcapsular area with blood vessels in it. this is always result of congenital anomaly. those blood vessels come from a vessel emanating from optic disk - the hyaloid artery. this is supposed to atrophy at/shortly after birth, without any consequences, but it may persist, and then you see vessels in the lens. you should know that this is a nonprogressive cataract. as animal grows, the effect will be minimized because lens gets bigger but vascular area stays the same size. on the other hand, the other major progressive cataract is that which occurs in the rapidly dividing area aroudn the lens equator - equatorial cataract. when lens epi divides at equator, if mitosis is interfered with or something, it will opacify. this cataract starts peripherally and goes centrally - blindness occurs later - when it reaches the middle and involves the pupil, blindness is sudden. commmon with diabetes. if you see bilateral equatorial cataracts, check for diabetes mellitus. opacity starts forming bubbles and vacuoles, moves in toward center, eventually filling pupil, and when it becomes complete, animal is blind. when it becomes complete, and animal is blind, or shortly before that, certain things take place that you should be aware of. the lens capsule is a very efficient separator of lens protein from general circulation. that lens protein is foreign material to the body. when the cells die in there, the protein underoes hydrolysis and forms smaller peptides which may leak out through the capsule. this may be able to set up a foreign protein inflammatory repsonse. this can cause a secondary uveitis. this is called phacogenic uveitis. it is a sterile process. expect low pressure in eye. treat with antiinflammatories, but really this is a surgical case - need to remove FB. if you minimize uveitis, as peptides leak out, volume of material in lens gets smaller - you get hydrolysis, the peptides cause swelling of lens but as osmotic difference changes, you get stuff leaking out and nothing coming in and lens shrivels. if it shrivels enough and you have already minimized inflammation, the animal may be able to see around the cataract. so the lens resorption process may allow the animal to avoid surgery and regain vision. this young dog had rapid cataract development - lens cortex has become liquid. nucleus has slid down. in a few months, the liquid slurry will leak out the capsule and animal will regain vision. when you dilate the eye and look - you see the periphery is clear, and you can see some retina behind it - so in light, the dog is blind, but can see in dim light or if you dilate pupil. decision for cataract surgery has to be personal. you can refer for cataract removal =- ophthalmologists will say b/c of uveitis you have to get the lens out - but if you can control uveitis and keep pressure up, you may allow animal to regain vision. dr rubin did cataract surgery on one eye of a cocker spaniel here - he really screwed it up, it had tons of complications, he sent it home. two weeks later they called and said the dog was doing great. the eye he had operated on was a mess, but the other eye was dilated from meds, and the animal could see out of it since the cataract was being resorbed. so you too may want to wait and see if the animal regains vision on his own. sometimes there will be some calcification and cholesterol deposits showing up. slide - some clear areas of lens, some messed up areas. the clear areas are where there is just capsule, and the other areas are wrinkles, deposits. resorption occurs in animals with young, soft lenses more than in old animals. so what do you do when the lens is opaque and animal is blind or nearly so? send it to ophthalmologist who will remove the lens. this is done by a process called phacoemulsification. uses a computer controlled probe with three concentric tubes. the middle piece vibrates as a - about 20,000 times/sec, sets up ultrasonic field, and slurries the lens proteins. immeidately around that is a controlled input of salt solution to help slurry it up. around that is a vacuum that takes it all away. so you stick that in there and lens gets slurped out. it's a nice procedure. quite successful with minimal postop copmlications. it's expensive though. ACVO ad video on phacoemulsification--- a state of the art sx procedure, derived from greek phaco, lens; and emulsification, shattering. advantages: small incision and only 2 sutures eye structure maintained less postop inflammation faster healing, visual restoration bilateral cataracts removed at the same surgery [nuclear sclerosis is not cataract] causes of cataract inherited, metabolic dz, trauma, inflammatory, nutritional preop - complete evaluation, PE, bloodwork, full eye exam, electrodiagnostic testing (ERG) to ensure success, eye meds are used several days before and after sx - requires good temperament of patient and compliant owner. machine does: irrigation aspiration emulsification operated by foot pedal. --end video-- --start other video-- incision = 3.2 mm incision made parallel to iris so anterior chamber is reached. after aqueous starts leaking out, anterior chamber will be reformed by some viscoelasto material (?) lens capsule is broken, hole in center of it is made - but not involving whole anterior lens capsule. cellulose sponges are used to soak up gooey stuff that leaks out. apparently, you are required to listen to muzak during the procedure. the probe is put into the lens. it sucks stuff out. doo doo do do do do doo doo, doo doo do do do do doo doo.... waaaaaaaaaaahhhhhh, doobee doo waaaaaaaaaaaaah. waaaaaaaaaaahhhhhh, doobee doo waaaaaaaaaaaaah. anterior chamber remains formed. large chunks of stuff are seen, probe is liquefying it and sucking it out. lens in animals is huge. in people, it is much smaller. as more material is removed we start to see reflection of light from retina. this is often done as a one day procedure. in people it is an outpatient procedure. doo doo doo doo, doo doo doo doo, doobee doo doo, doobee doo doo... waaah, doobee doo waaaaaah. --end video --continuation of ad video-- use foot pedal to control stuff.... prepare surgical site. make incision. inject stuff to protect corneal endothelium and maintain eye shape. remove anterior lens capsule and insert probe. emulsify! once lens nucleus is gone, aspirate peripheral capsule. in this case they are inserting a fake lens. close with 8-0 to 10-0 sutures. postop give topical and systemic antiinflammatories and monitor for glaucoma, inflammation. pet the dog a lot so the owner is happy. --end-- so that is the normal cataract surgery as is done in animals and humans. in humans, invariably a lens is implanted in the eye so patient has normal refraction; in animals that may or may not occur, doesn't seem to make too much difference but physiologically one would hope for better vision with the implant. that's lens and lens surgery. the only other problem associated with the lens that you will see is a disease called lens luxation in which the lens suspensory apparatus, the zonules, become weak, loosen, and lens floats free in the eye. this can cause problems by itself. if the lens is not attached and able to move, if it moves forward into anterior chamber, and pupil is behind it, it will produce an impediment to aqueous flow, and will cause secondary rise in intraocular pressure; secondary glaucoma. if it goes back into the vitreous, the vitreous may prolapse forward and again may block pupil and cause seconadary glaucoma. so when lens luxation occurs we generally remove the lens in its entirety either as above or via a large incision and removal of lens. technique is a bit different. --video: sutures to anchor lens are placed 180 degrees from each other - limbus is marked to ensure this. conjunctival flaps are made near the marks. a 2/3 depth corneal groove is made using the marks as landmarks. the anterior chamber is entered, pigment deposits from persistent pupillary membranes are noted on anterior lens capsule. incision here is large so lens will fit through. now a freezing tip is used to touch lens - "cryoextraction" - brush vitreous from posterior lens capsule. gently. lens is pulled out. vitreous body stays in eye. now he is putting in this fake lens. etc. -end to diagnose lens luxation is not difficult. generally the signs are pretty self evident. with this big glob of material in the eye, when the eye moves, this thing moves by inertia a bit later, then when eye stops moving, it bounces off nearest surface and shakes it, so vitreous or iris will be tremulous. if you see the iris shaking like it is in a bowl of jello, that is pathognomonic for lens luxation. the tremulousness is called iridodenesis. the other diagnostic thin is that the lesn will tend to refract or tend to handle light somewhat more differently, so if lens is clear and you shine light in eye, there will be internal reflection as normally plus bounceback from the equator - like sparkle in diamond. as you wave light in front of eye, you will see arcs of bright light - you will see equator of lens - that means, it isn't behind the iris. so red, irritated eye and arcs of bright light are diagnostic of anterior lens luxation. slide: this is what it looks like. in wire haired fox terrier, is genetic dz. we see the equator of the lens as a white arc around periphery of eye - this means lens is in front of iris. another diagnostic feature is presence of an area where there is no lens. if lens luxates medially or laterally - there is a zone where you can see edge of lens and edge of iris and nothing b/w them. this crescent shaped zone is called an aphacic crescent. this means lens has luxated away from normal position. questions on lens? ---break--- moving on.... glaucoma: increase in intraocular pressure beyond the bounds of health, causing ocular damage. when pressure in eye goes up (btw glaucoma affects about 2% of humans over 40), it will cause irreversible blindness if it isn't controlled. the blindness is a blindness that affects the retina and optic nerve. pressure goes up, it goes up in all directions equally, and eye expands. in early stages, though, the weakest part of eye is where the wall is partly perforated and this is where the optic nerve comes to the eye - this is the lamina cribosa, and it is through the lamina cribosa that the eye is innervated. when pressure in eye goes up, the lamina cribosa bulges out, axons going through there are functionally transected. there is impeded axonal flow, and it is as though you have cut the axons there with scissors. the transection starts to occur early, well before clinical signs, both in animals and people. usually in animals by the time you see it it is very advanced and eye is almost always irretrievably blind. your effort has to be directed in preventing the occurence of advanced glaucoma in opposite eye. no matter what stage the animal comes in with - the animal must be on preventive tx in other eye for life. you must measure intraocular pressure and you must monitor it. intraocular pressure is usually about 20 mmHg, glaucoma is usually 25+ mmHg. in clinical cases, it is usually 50-60 mmHg. when pressure rises, there are some specific signs - first, the endothelial pump that dehydrates the cornea will fail, so there will be corneal edema. then nerves to iris are impeded, and iris is dilated and nonresponsive to light. later eye expands in size. finally you see a cup at the base of the optic nerve - cupping of the optic disk. pressure is measured with a number of devices. these are called tonometers. those are necessary to go ahead and monitor progress of tx. you can feel a glaucomatous eye if pressure is up - eye will feel hard. but, if you need to know difference b/w 20 and 25 you need an instrument. prices go from 150 to 2500 bucks. also a classic sign of glaucoma is related to capability or incapability of blood to get into the eye. when pressure is elevated and pupil is dilated, you see large blood vessels in the conjunctiva, penetrating the eye. these are normal vessels trying to pump against a high pressure head, being dilated b/c they need more pressure to get into the eye. large congested vessels with white areas b/w them strongly suggest high intraocular pressure. with uveitis, you would have vessels that had no white in b/w them - would see all redness, overall diffuse conjunctival congestion. there are three types of glaucoma. two we already know. one is that which is associated with impaired venous return - proptosis, blood can't get from eye back to body, pressure goes up - this is glaucoma secondary to venous impediment, is treated by fixing the venous impairment. two is pupil block glaucoma - as with uveitis where pupil sticks to lens, iris bulges forward. also seen with lens luxation where lens or vitreous blocks the pupil. we already know tx for this - treat uveitis, dilate pupil, remove lens. three is basically an outflow block of obscure etiology - essential glaucoma is what we call it b/c we don't know the real cause. in most cases block is somewhere from drainage angle out, most common one we'll see is drainage angle blockade. if you can unblock the angle, you can control the glaucoma but if not, you can not control the glaucoma. you have to know if the drainage angle is permanently or impermantently blocked. think of the eye as a sink with a spigot and a drain. if the drain is partly closed, but not always closed, you can cut down on fluid going in to control overflow. if it's totally closed, unless you turn off faucet totally, sink will eventually overflow. tx: directed toward either cutting down fluid into eye or assisting outflow. cutting down fluid coming in is associated with giving carbonic anhydrase inhibitors like acetazolamide, dichlorphenamide. these are also diuretics which cut back on carbonic anhydrase in kidney. they are not bad diuretics either, animals will pee a lot on these meds. nowadays, in past year, a topical one called dorzolamide has been developed, that will probably replace the systemic ones for glaucoma tx with fewer side effects. so for animals w/partly open trabecular meshwork (drainage angle) fluid input is decreased as above. the treatment if topical is used in both eyes, and animal is on it for life. other compounds to open drainage angle by contracting ciliary muscles: classic one is pilocarpine. this causes miosis and increased aqueous outflow. this is a directly acting cholinergic drug. kind of irritating and not good for longterm use so other drugs like ACHesterase inhibitors were developed - these are far less irritating, more powerful, more effective. these include echothiophate and phospholine iodide - nerve gas type things, sarin derivatives. used infrequently to avoid severe systemic cholinergic signs. these txs generally are most effective in the as yet unaffected eye, the early diseased eye, rather than the eye presented with obvious signs. b/c of complications efficacy in badly affected eye is poor, and many times we put all the effort in saving the less sick eye, and we take out the bad eye or kill the ciliary body in the bad eye to stop aqueous humor production, or whatever. slides: here's a cat with glaucoma secondary to uveitis. iris bombe is seen, iris is coming forward and sticking to cornea, blocking drainage angle. if you catch this early and you can't dilate pupil, tx will be to put a hole in the iris so fluid can drain through it. if drainage angle is blocked, may have to enucleate. drainage angle - meshwork of iris connecting to posterior cornea through which filtration occurs. you can see that area indirectly and not directly by putting a lens over it - a goneo lens (?) and you can look in there and see if angle is open or closed. if you see a lot of ophthalmic cases, this lens also lets you see if drainage angle is there or not and to tailor your tx accordingly. closed angle shows up as plain heavily pigmented band. new development - ophthalmologists are implanting valves and drains in the eye that avoid having to remove the eye by acting as one way valves when pressure in eye rises - allows fluid out. at U of FL they have used them for a while and they are becoming clinically efficacious. video of human case.... so, in this procedure, they put a tube in the eye to drain fluid into this bag which will collect fluid and then let it out through a semipermeable membrane into the subconjunctival sac, for absorption into circulation. this is available for people and they are starting to make some for animals, which have different properties of the aqueal humor to consider. so you have to lower intraocular pressure or remove the eye. you must must must treat the other eye preventatively. you will overtreat some animals but this will be outweighed by the number of animals you help. you should know a bit about glaucoma meds, how to use them, and how to use them if angle is open vs closed and stuff. glaucoma is complex. you should probably refer to ophthalmologist for the care of the remaining eye. losing the other eye is a real bummer. slide: retina last thing we're going to discuss (woo) there are only 4 things to see - optic disk, blood vessels, tapetal membrane, and nonreflecting heavily pigmented nontapetal area. tapetum is part of choroid, is under retina, acts like photomultiplier. animals with tapetums are night vision animals. all but rabbit and pig of animals we deal with do have them. if you see rather even reflection with lots of bvs and nerve, you can pretty much be sure that the retina is normal. if you don't, the animal is in big trouble. here, optic nerve looks small, sharply defined, blood vessels seen. little myelin. here - lots of myelin, lots of bvs, even reflections, this is ok too, though there is lots of myelin. normal retina. another retina - optic nerve has lots of vessels coming in, tapetum is somewhat pigmented but relatively evenly reflecting - also normal. animals w/o pigment - husky, weimaraner, blue eyed animals - no tapetum, no pigmented retinal epi - you see dense choroidal circulation and more sparse retinal circulation. notice choroidal vessels are fuzzy and ill defined, retinal ones are sharper. cat with no tapetum - nerve small but normal; blood vessels look good. this one reflected red at night. still normal. when retina gets screwed up, what happens is retina gets thinner and reflection changes, gets more intense, blood vessels go away. the general diffuse retinal disease that is most common in animals is a syndrome called progressive retinal atrophy. lots of research being done on PRA. in animals and man. in man, they call it retinitis pigmentosa, RP. there are blood tests to ID carriers and affecteds. PRA no matter what the cause, what the mutation is, is always characterized initially by degeneration of rods. rods are used for night vision. so in animals with early PRA< they present with history of night blindness. owner takes dog out for walk at night and she walks into something, falls in pool, whatever. pretty diagnostic. cows in winter - one gets lost in field at night... in most cases, PRA is inherited as simple autosomal recessive. only one exception and we're not going to mention it. for our purposes, it is always autosomal recessive, and breeding implications are obvious. PRA occurs in different breeds at different ages. as it goes on, as you see it clinically, these animals will present and have totally degenerate retinas. in advanced stages, when you look in, there are few blood vessels, and very brightly reflecting tapetum that will dazzle you. you don't really need to look. good history can be diagnostic. PRA in lab - no vessels seen - if you determine that ophthalmoscope is turned on, you know retina is screwed up. tapetal reflection varies - not consistant - parts are dull, parts are bright. animal is night blind. eventually progresses to total blindness, cones are lost as well. long term sign is night blindness. last thing to talk about (he said that once already...) is a disease that is a dog disease mainly in collies. this is collie eye anomaly. this is the most prevalent eye disease in a breed that exists. collie people have in some way not being able to see the retina selected and bred a simple autosomal recessive trait so that 90% of collies are homozygous recessive. it is rare to see a typey collie with normal eyes. this is theoretically impossible, to breed for this, since they can't see what they are selecting for... this anomaly is dangerous in that it results in detached retinas in some animals. this causes immediate blindness. so about 5% of collies at any one time when you examine them will have retinal detachment in one or both eyes. but the 90% prevalence rate is of a portion of the syndrome called "choroidal hypoplasia" which means there are fewer vessels in the choroid than normal. that area of fewer vessels occurs in an area initially lateral to optic disk, where there is no pigment. you find nerve, and if you see pink spot near there, animal has choroidal hypoplasia. this part of the syndrome occurs with 90% prevalence at any age of collie. if choroidal hypoplasia is extensive enough, if vascular coat is poorly developed enough, the area is a weak point in the eye, and if that occurs, at normal pressures, the weak point bulges out, and that is called coloboma of the choroid, or staphyloma. that occurs in about 25% of collie dogs. incidence doesn't vary with age either. all animals that have coloboma also have choroidal hypoplasia, but not all animals with CH hae coloboma. the other thing, think about long nose of collie, and what you are looking for is area lateral to optic nerve. to look there, you have to scrunch around the nose to look laterally. it's easily dxed if you're prepared, though. retinal detachment tends to occur at a decreasing rate with age. so in young puppies, incidence of retinal detachment is much higher than in two year olds. each day the animal lives, the likelihood of detachment decreases. so follow them for 6 mos to a year and if they don't detach, they are probably ok as far as that goes. tracy asks, is the pink spot where the choroid is or where it isn't? he says funny you should ask. when you look in the eye, you see blood vessels and nerves, but lateral to disk you see area of choroidal hypoplasia - pink area with fewer vessels than normal and no pigment. this doesn't mean there is no retina. retina is thinner, maybe, but is still there and has enough capillary supply. in normally pigmented area there is normal underlying choroid. problem occurs when there are funny merle coat colors - then there is no pigmentaton of the entire area and it is hard to dx. in this animal, the choroidal vessels do look less extensive with lots of space b/w them. but you woudln't be faulted for missing this case of collie eye anomaly. and in areas of choroidal hypoplasia, when you see the retinal vessels and the fuzzy nerve, looking out of focus, you can figure that this is coloboma or staphyloma - the area is bulging. later on, retina tends to elevate, some dull spots show up with different reflectivity - early retinal detachment - will blind animal unless it is stopped. eventually you see nothing in retina at all - that is diagnostic of extensive retinal detachment. you should know about collie eye anomaly, about PRA as a common degenerative dz of the eye. it would be very very prudent of you to review the last three years of test questions. in fact, that is mandatory (almost) b/c everything important is in those questions. have a nice summer. ----end-----