September 2001

Update on Veterinary Ophthalmology

J. Phillip Pickett, DVM, Diplomate, A.C.V.O.
Associate Professor, Ophthalmology
Virginia-Maryland Regional College of Veterinary Medicine
  1. Reference texts and instrumentation

    1. Information sources

      1. Severin's Veterinary Ophthalmology Notes, 3rd ed. G.A. Severin
        ~$50 direct from Dr. Severin
        Veterinary Ophthalmology Notes
        Box 272390, Fort Collins, CO 80527-2390
        Fax/voice mail 970-490-5954

      2. Small Animal Ophthalmology, A Problem-Oriented Approach, 2nd ed., Peiffer and Peterson-Jones
        W.B. Saunders Company Ltd. (Bill Larimore, 800-358-4643)

      3. Fundamentals of Veterinary Ophthalmology, 3rd ed., D. Slatter, ed.
        W.B. Saunders Company Ltd. (Bill Larimore)

      4. Atlas of Feline Ophthalmology, Ketring and Glaze
        Veterinary Learning Systems
        Trenton, New Jersey
        800-426-9119

      5. Color Atlas of Veterinary Ophthalmology, K. C. Barnett
        Mosby-Wolfe (Bill Larimore)

      6. Veterinary Ophthalmology, 3rd ed., K. N. Gelatt, ed.
        "The Bible" of veterinary ophthalmology
        Lippincott, Williams & Wilkins (Robert Johnson, 540-364-9239)

      7. Essentials of Veterinary Ophthalmology, K. N. Gelatt
        Much more "user friendly" to practitioners
        Lippincott, Williams & Wilkins (Robert Johnson)

      8. Color Atlas of Veterinary Ophthalmology, K. N. Gelatt
        Lippincott, Williams & Wilkins (Robert Johnson)

      9. Veterinary Clinics of North America, Small Animal Practice. Surgical Management of Ocular Disease, 27:5, Sept. 1997 M. P. Nasisse, ed.
        W.B. Saunders Company Ltd. (Bill Larimore)

      10. Veterinary Clinics of North America, Small Animal Practice. Infectious Disease and the Eye, 30:5, Sept. 2000 J. Stiles, ed.
        W.B. Saunders Company Ltd. (Bill Larimore)

      11. Veterinary Ophthalmology (official journal of the ACVO)
        Blackwell Science, +44(0)1865 206180
        http://www.blackwell-science.com/cservices

    2. "New toys" and ophthalmic uses for things you already may have in your practice

      1. Magnification - for diagnostic and surgical use

        1. single lens systems (OptiVisors, clip on loupes (Bausch & Lomb), "reading glasses" ; diopter numbers give relative magnification and focal distance)

          1. 2D, 1 1/2X @ 20 inches

          2. 3D, 1 3/4X @ ~14 inches

          3. 4D, 2X @ 10 inches

          4. 5D, 2 1/2X @ 8 inches

          5. 7D, 2 3/4X @ ~ 6 inches

          6. 10D, 3 1/2X @ 4 inches (standard veterinary otoscope head)

          7. 20D, 5X @ 2 inches

        2. "Galilean loupes" (Zeiss, Keeler, SurgiTel, Dan Scott, and others)

          1. more versatility in magnification and focal distances

          2. 2.5X - 5X

          3. focal distances 12 inches to 20 inches

      2. Slitlamp biomicroscope

        1. for examination of adnexa, external eye, anterior chamber, lens, and anterior vitreous

        2. Kowa SL-14 (Lombart Instruments), Clement Clarke Haag Streit
          904 (Lombart), Zeiss HSO-10 (Lombart), Eidolon (Dan Scott), Heine XHL (Lombart)

        3. The "Aggie Slitlamp" (I-Slit pen light (XOMED) and Opti-Visor, clip on loupes, or "reading glasses")

      3. Indirect ophthalmoscopy

        1. for examination of the posterior segment and fundus

        2. indirect headset and condensing lens or light source and lens

        3. Keeler, Welch Allyn, Heine, Proper, Topcon, and others

        4. lens sizes

          1. 40D - small exotics

          2. 28-30D - small exotics, cats, small dogs, undilated pupils

          3. 2.2 PanRetinal lens (Volk) - cat, dog

          4. 20D - dog, cat

      4. WelchAllyn PanOptic Ophthalmoscope (new, Dan Scott, Lombart)

          1. similar to old American Optical monocular indirect

          2. fits on standard WelchAllyn halogen light source handle

          3. has diopter setting to allow focusing at different levels of the eye like a direct ophthalmoscope

          4. fundic magnification is about 5X (about half that of direct scope)

          5. "wider view" than direct ophthalmoscope (~25 degrees)

          6. image is right side up and real

      5. TonoPen applanation tonometer (Dan Scott)

        1. the most accurate, dependable measurement of intraocular pressure (IOP) in veterinary species

        2. common causes of "poor readings"

          1. not cleaning and calibrating instrument daily

          2. latex tip too tight

          3. touching cornea "too hard" or at wrong angle

          4. blepharospasm

          5. excited patient or overzealous restraint

          6. batteries low

          7. ointment or viscous material on cornea

      6. Ultrasonography

        1. use 7.5 mHz probe (or 10 mHz if available)

        2. abdominal setting will give more "grays", less contrast

        3. cardiac setting will give less "grey", more "black and white" contrast

        4. can apply probe directly to cornea (use topical anesthetic and K-Y jelly vs. regular U/S gel) or through closed lid (still use K-Y jelly)

        5. silicon offset (or glove filled with water) will allow some anterior segment enhancement

        6. uses

          1. identifying iris/ciliary body masses

          2. cataractic lenses/luxated lenses

          3. vitreous abnormalities (hyaloid remnants, asteroid hyalosis, vitreous degeneration, foreign bodies, masses)

          4. retinal/choroidal abnormalities (detachments, subretinal exudate, choroidal masses)

          5. optic nerve disease (optic neuritis, neoplasia)

          6. orbital disease (retrobulbar masses, cysts, extraocular myositis)

      7. Sources - instrumentation

        1. Lombart Instruments, Norfolk, VA (Pete Leadem, 800-446-8092)

        2. Dan Scott & Assoc. Westerville, OH (Dan Scott, 614-890-0370)

        3. Carl Zeiss, Inc. 800-442-4020

        4. Welch Allyn, Skaneateles Falls, NY (Dave Manley, 800-769-4014 ext. 2563)

        5. XOMED, Jacksonville, FL (Rick Morton, 800-888-7978 ext. 3404)

        6. Bausch & Lomb 800-637-8586

        7. SurgiTel 800-959-0153

        8. Keeler Instruments 800-523-5620, e-mail - keeler@keelerusa.com summer clearance sale through September 29, 2001

        9. Diagnostic Instruments Group, Inc., Tampa, FL (Roger Sill, 813-926-3447) (used equipment)

  2. Glaucoma

    1. Review of aqueous humor dynamics

      1. production

        1. "passive" production due to vascular leakage within ciliary body

        2. "active" production by ciliary body epithelium

          1. regulated by sympathetic nervous system (beta stimulation)

          2. also regulated by the enzyme carbonic anhydrase

      2. drainage

        1. trabecular meshwork/iridocorneal filtration angle outflow; main outflow mechanism in dogs and especially cats

        2. uveoscleral outflow

          1. a minor outflow mechanism in dogs and especially cats

          2. has become important in veterinary ophthalmology due to development of prostaglandin analogs for treatment of human glaucoma

    2. "Primary" vs. "secondary" glaucoma

      1. "narrow/closed angle glaucoma" - diagnosed via gonioscopy

        1. most common type of glaucoma seen in the dog

        2. progressive "closure" of iridocorneal filtration angle with age

        3. high breed predisposition (American Cocker Spaniel, Chows, Shar Peis, and others)

        4. almost all end stage glaucoma angles will have a closed angle

      2. "goniodysgenesis"

        1. breed related malformation of iridocorneal filtration angle ("mesodermal sheets" and "flow holes")

        2. classically described in the Basset Hound, also seen in Arctic circle breeds, Bouvier des Flandres, Chows, Shar Peis, and spaniels

        3. acute attacks seen in association with low grade anterior uveitis (?)

      3. "open angle glaucoma" of the University of Florida Beagle

        1. an animal model for a human disease

        2. colony developed and maintained at the University of Florida

        3. not a common type of glaucoma seen in canine patients

        4. in past 5 years, Beagle glaucoma cases that I have seen a VMRCVM have had angle anomalies as well as apparent primary lens luxation

      4. "secondary glaucoma" causes

        1. uveitis - fibrin, RBC's, WBC's occlude iridocorneal filtration angle, or posterior synechia causes iris bombe

        2. primary lens luxations occlude pupil or lead to vitreous in iridocorneal filtration angle

        3. exfoliated pigment from iris or ciliary body occlude iridocorneal filtration angle (Cairn terrier)

        4. uveal cysts collapse and fill iridocorneal filtration angle with debris (Golden Retriever)

        5. exfoliated cells from iris/ciliary body tumors (melanomas and primary ciliary body adenocarcinomas) occlude iridocorneal filtration angle

        6. "swollen" or intumescent cataracts in diabetics (especially in those dogs prone to have narrow angles anyway, e.g. Cocker Spaniels)

    3. Clinical signs of glaucoma

      1. acute glaucoma

        1. "red eye" - usually episcleral injection vs. simple conjunctival hyperemia

        2. "cloudy eye" - initially not true corneal edema, but rather "stretching" of corneal stromal lamellae due to elevated IOP

        3. "painful eye" - deep corneal nerve fibers are pressure sensitive

        4. mydriasis - when IOP 40 mm Hg+, iris sphincter muscle cannot work, iris "mechanically" is opened

        5. elevated intraocular pressure - occasionally angle closure glaucoma "waxes and wanes" with intermittent elevations of IOP. Usually IOP goes up and stays up. IOP with a TonoPen of greater than 25 mm Hg (when performed properly) should be considered glaucoma. If using a Schiotz tonometer, use calibration chart that comes with instrument (Friedenwald calibration chart, 1955) and take into consideration how much struggling was needed to take reading. It is not uncommon for acute glaucoma cases to be seen with IOP's in the 50-60 mm Hg range.

        6. vision loss (?) - check for direct and consensual pupillary light reflex (PLR)

      2. chronic glaucoma

        1. buphthalmos - stretching of corneal/scleral tunic occurs with chronic elevated IOP. USUALLY is a bad prognostic sign for vision (except in Shar Peis). May be accompanied by insensitive cornea with secondary axial ulcerative keratitis.

        2. corneal edema - as corneal endothelial cells are "crushed" by elevated IOP, true corneal edema occurs with thickening of stroma.

        3. "perilimbal flush" - in conjunction with episcleral injection, deep corneal neovascular injection is seen as a "red ring" around circumference of cornea.

        4. Haab's striae - stretching of the globe leads to tears in Descemet's membrane with subsequent "grey tracts" seen on endothelial surface of the cornea

        5. aphakic crescent - stretching of the globe results in tearing of lens zonules. Unlike in primary lens luxations, globe is usually buphthalmic and lens is usually not freely moveable.

        6. optic disc degeneration/ "cupping" - elevated IOP causes death of optic nerve fibers with resulting pale (or hyperpigmented), shrunken disc. Peripapillary hyperpigmentation or hyper-reflectivity is usually also seen. Lack of vascularity of the disc is also seen.

        7. vision loss - lack of menace response, dazzle response, and a total afferent PLR deficit (Marcus-Gunn sign)

    4. Medical therapy

      1. carbonic anhydrase inhibitor (CAI) diuretics - decreases production of aqueous humor

        1. oral - methazolamide, 1-2 mg/lb, bid-tid (Neptazane or generic (Zoptic) from Effcon, Inc. 800-722-2428 or from Bindley Western, NC 800-445-9976) and dichlorphenamide, 1-2 mg/lb, bid-tid (Daranide liquid- Wedgewood Pharmacy
          800-331-8272)

        2. adverse side effects of oral CAI

          1. metabolic acidosis seen as panting

          2. hypokalemia, hyponatremia, hyperchloridemia seen as weakness and potential cardiac arrhythmia

          3. disorientation, confusion, irritability

          4. vomition, diarrhea, polyuria, alkaline urine

          5. tingling of extremities seen as foot licking

        3. topical - 2% dorzolamide (TruSopt - Merck) 1 drop, tid (not usually as effective as oral, can be locally irritating)

      2. miotics - miosis enhances outflow of aqueous humor through iridocorneal filtration angle

        1. demecarium bromide, 0.125% or .25% (Wedgewood Pharmacy)

          1. usually less irritating and longer lasting than pilocarpine

          2. any miotic may worsen uveitis, so do not use with uveitis induced glaucoma

          3. therapeutically - 1 drop, bid

          4. prophylactically (see below) - 1 drop once daily in evening

        2. 2% pilocarpine - much more irritating than demecarium bromide, I do not use this drug much any more

      3. hyperosmotic agents - these drugs stay in the vascular space and pull extravascular fluid into the vascular space (dehydrate vitreous and anterior chamber space to lower IOP)

        1. mannitol - intravenous, 1/2 to 1 g/lb (give over 20-30 minute period)

        2. glycerin - oral, 1/2 to 1 ml/lb

        3. mannitol works quickly, glycerin must be absorbed and metabolized

        4. mannitol usually given once as an emergency drug, glycerin can be given tid (but effective for only 3-5 days)

        5. following administration of mannitol, withhold water for ~3 hours, not as important with glycerin

        6. these drugs are contraindicated in cases of congestive heart failure

        7. glycerine is in a sugary, sweet syrup base, most dogs do not like the taste, makes some dogs vomit. Mixed with a little chocolate milk, seems to go down/stay down well. Will greatly complicate diabetic regulation.

      4. beta blockers - 0.5% timolol (Timoptic, Merck) is main drug used, 1 drop, bid

        1. beta adrenergic blockade reduces active production of aqueous humor

        2. in small dogs, can cause very noticeable bradycardia

        3. with lower airway obstructive disorders, can cause respiratory distress

      5. prostaglandin analogs - 0.005% latanoprost (Xalatan, Pharmacia & Upjohn)

        1. newest and greatest antiglaucoma drug in human medicine

        2. prostaglandins enhance uveoscleral outflow of aqueous humor

        3. prostaglandins also cause significant miosis (but enhanced iridocorneal filtration angle outflow is apparently not the mechanism of this drug's IOP lowering effect)

        4. is very effective in some dogs (Cocker Spaniels) and not as effective in others

        5. do not use systemic NSAID's (carprofen) with Xalatan

        6. Xalatan will worsen anterior uveitis

        7. 1 drop, bid

      6. combination drug - CoSopt (2% dorzolamide, 0.5% timolol) 1 drop, tid

      7. systemic corticosteroids (?) - to reduce inflammation to optic nerve from acute pressure spike

      8. therapy protocols

        1. primary glaucoma

          1. demecarium bromide OR pilocarpine OR Xalatan

          2. methazolamide

          3. timolol

          4. mannitol or glycerin

          5. +/- systemic corticosteroids

        2. anterior lens luxation induced glaucoma

          1. NO miotics

          2. methazolamide

          3. timolol

          4. mannitol or glycerin

          5. +/- systemic and topical corticosteroids

        3. uveitis induced glaucoma

          1. NO miotics

          2. methazolamide

          3. timolol

          4. +/- mannitol or glycerin

          5. topical corticosteroids

          6. systemic NSAID's

          7. IDENTIFY THE UNDERLYING CAUSE OF UVEITIS

      9. long-term efficacy of medical therapy alone

        1. most cases of primary glaucoma will not control with medical therapy alone (one study done years ago at CSU showed about 10% primary glaucoma cases were still visual at one year post diagnosis)

        2. in my hands, uveitis induced glaucoma has the best chance of long-term medical management with retention of a visual eye

        3. in my hands, anterior lens luxation induced glaucoma has better long-term medical management (after removing luxated lens) than does primary glaucoma

    5. F. Surgical therapy for glaucoma

      1. visual eye

        1. cyclodestructive procedures - decrease production of aqueous humor (enhance uveoscleral outflow??)

          1. N2O cyclocryosurgery

            1. freeze ciliary body directly through sclera

            2. lots of post-operative inflammation (conjunctival chemosis, blepharoedema, anterior uveitis, fair number of retinal detachments)

            3. incidence of post-op "pressure spikes" is high

          2. Nd:YAG laser cyclophotocoaggulation

            1. the most "successful" glaucoma surgery that I have seen over the past 20 years

            2. laser through sclera (energy absorbed by ciliary body pigment)

            3. less incidence of post-op "pressure spikes", hyphema, uveitis, and retinal detachments

            4. fair incidence of post-op corneal anesthesia with secondary neurotropic keratitis (axial ulcers that heal very slowly)

            5. I quote the following results to clients: at the end of 6 months, 2/3 of visual dogs will still be visual, at end of one year, about 1/2 will still be visual. I have kept some dogs visual for 5 years or more (the lucky ones).

          3. Diode laser cyclophotocoaggulation

            1. similar to Nd:YAG laser technique

            2. published results (Comp Vet Ophth: 1997;7:148-154) not as good as my experience with Nd:YAG laser therapy (37% visual at six months)

          4. the afore mentioned neurotropic keratitis, chronic anterior uveitis, and potential for retinal detachments are seen with all cyclodestructive procedures. In addition, secondary cataract formation and phthisis bulbi can also be seen as complications.

        2. anterior chamber "shunts" (enhance outflow of aqueous humor)

          1. a "tube" is placed into the anterior chamber that passes into the subconjunctival space

          2. aqueous humor supposedly passes into the subconjunctival space and is "removed" by conjunctival vasculature

          3. used by some as primary surgical intervention, others use as a "last resort"

          4. very high incidence of fibrosis of filter bleb over the tube implant with return to the glaucomatous state

      2. blind eye

        1. enucleation (orbital silicone prosthesis, 25 mm diameter ball can be trimmed to fit most dogs (Jardon Eye Prosthetics, Inc. Southfield, MI 313-424-8560)

        2. evisceration and intraocular silicone prosthesis implantation

          1. under a conjunctival flap, through a sclerotomy incision, globe contents eviscerated, leaving a corneoscleral "shell"

          2. a silicon prosthetic ball is placed into "shell"

          3. total vascularization of avascular cornea occurs, followed by "clearing" (over ~ 6 week period)

          4. resulting "eye" moves with other eye, may or may not be cosmetically pleasing

          5. usually have decreased corneal sensitivity, may have decreased tear production

          6. for this to work, must have intact corneoscleral shell, good surface ocular health (including adequate tear production and normal blink)

        3. intravitreal gentamicin injection

          1. approximately 7 mm posterior to corneoscleral limbus, use 27 or 30 ga. needle to inject 10-25 mg of 100 mg/ml gentamicin into vitreous space (be careful to not hit the lens)

          2. gentamicin chemically "ablates" ciliary body to decrease production of aqueous humor

          3. incidence of secondary cataract is high ( 50+% in my hands)

          4. ~ 50% of cases will result in a calm, soft, comfortable eye needing no further therapy

          5. other 50% will either do nothing (eye still glaucomatous), will become phthisical, or will have chronic uveitis/hyphema, etc.

          6. if intravitreal injection of gentamicin does not "work", can usually go back and eviscerate (provided eye not phthisical and other criteria are met)

    6. Prophylaxis for the "at risk" second eye (JAAHA: 36:431-438, Sept-Oct. 2000)

      1. incidence of second eye becoming glaucomatous with primary closed angle glaucoma in the dog is high

      2. in the above study, median time to 2nd eye developing glaucoma was 8 months

      3. prophylactic therapy with 0.25% demecarium bromide (Wedgewood Pharmacy) in conjunction with a topical steroid, once daily medication resulted in a median time of onset of glaucoma in second eye of 31 months

      4. prophylactic therapy with 0.5% betaxolol (selective beta-1-adrenergic antagonist), twice daily medication resulted in a median time of onset of glaucoma in the second eye of 30.7 months

    7. Feline glaucoma (Vet Ophth :4(2):81-85, June 2001)

      1. rarely seen as a primary disease, usually is secondary to chronic anterior uveitis, occasionally secondary to intraocular neoplasia (iris melanoma or lymphosarcoma)

      2. usually seen in older (9+ years) cats as insidious buphthalmos, mydriasis, vision loss. Rarely appears to be painful with an "acute" attack as is the usual case with glaucoma in dogs.

      3. few cats will have detectable underlying diseases (FIV, FIP, toxoplasmosis, FeLV) associated with uveitis

      4. short-term "control" of IOP may be had with various protocols using anti-glaucoma medications used in dogs (topical dorzolamide, topical timolol, topical pilocarpine, topical latanoprost, oral dichlorphenamide [Wedgewood pharmacy, 2.2mg/kg sid- bid], and topical corticosteroid therapy [prednisolone acetate, 1%, bid-qid]). Most cats are more "sensitive" to adverse side effects of these drugs than are dogs.

      5. "long-term" control of IOP and vision restoration/retention is poor with medical or surgical (Nd:YAG cyclophotocoaggulation or N2O cyclocryotherapy) therapy

  3. Keratoconjunctivitis sicca ("KCS")

    1. Causes

      1. breed related, "immune mediated" (idiopathic ?) lacrimoadenitis (Vet Clin No Amer 20(3), 583-614, May 1990)

        1. most common cause of KCS in dogs

        2. association with atopy and other allergic phenomena ?

        3. breeds over-represented : Cavalier King Charles Spaniel, English Bulldog, American Cocker Spaniel, Lhasa Apso, Shih Tzu, West Highland White Terrier, Pug, Pekingese, Boston Terrier, Yorkshire Terriers

      2. secondary to previous or chronic herpes virus infection in cats

      3. secondary to active bacterial or viral (distemper) conjunctivitis

      4. secondary to neonatal ophthalmia

      5. congenital atresia of lacrimal glands/ductules (Yorkshire Terriers, Miniature Dachshunds, Miniature Schnauzers, Pugs)

      6. parasympathetic denervation to the lacrimal glands (facial injury, otitis, etc.)

      7. iatrogenic sicca

        1. excision of third eyelid gland ("cherry eye" removal) (JAAHA 29: 56-60, Jan-Feb, 1993)

          1. in this 10 year retrospective study, ~68% of dogs with KCS had excised "cherry eye" (48% of dogs with amputated glands developed KCS)

          2. ~16% of dogs with KCS had non-replaced "cherry eye" (~43% of dogs with longterm prolapsed glands developed KCS)

          3. ~11% of KCS dogs had replaced "cherry eye"(~14% of dogs with prolapsed glands replaced developed KCS)

        2. chronic sulfonamide usage (JAAHA 31:236-241, Mar-Apr, 1995)

          1. less than 2% of trimethoprim-sulfa treated cases develop KCS

          2. pyrimidine ring causes toxic necrosis of lacrimal acinar cells

          3. if caught early and discontinued, lacrimation can return

          4. once total necrosis occurs, irreversible

        3. topical atropine usage (usually reversible)

        4. general anesthesia (both during and post-op, can take up to 48 hours for some normal dogs to regain normal tear production)

    2. Clinical signs

      1. decreased Schirmer tear test

        1. some dogs do fine with STT value of 12 mm/min

        2. some dogs (brachycephalics) show clinical signs with STT values over 15 mm/min

      2. mucoid/mucopurulent ocular discharge (due to lack of "flushing" of mucous portion of precorneal tear film)

      3. recurrent "eye infection" (due to overgrowth of normal flora and pathogens, as the Corps of Engineers say…"the solution to pollution is dilution….")

      4. "melting ulcers" (secondary to infection, but also due to poor rinsing away of proteolytic enzymes)

      5. keratitis

        1. neovascularization due to low oxygen levels and dryness

        2. pigmentation (pigment from limbus migrates with corneal vascularization)

    3. Therapy for KCS (medical)

      1. cyclosporine A (Optimmune, Schering-Plough) (JAVMA 199(8):1039-1042, 1991 and JAVMA 199(8):1043-1046, 1991)

        1. for treatment of immume mediated lacrimoadenitis cases

        2. ~82%and 75% effective in restoring tears, respectively

      2. parasympathomimetics

        1. topically applied, diluted pilocarpine (1/8 to 1/4% in artificial tears bid-qid) may help some cases of KCS due to parasympathetic denervation of glands (otitis and ear ablation Cockers)

        2. oral pilocarpine (titrated, beginning at 1 drop 2% pilocarpine in food bid) may help some denervation cases. Watch for systemic toxicity: salivation, vomiting, diarrhea)

      3. symptomatic therapy

        1. artificial tear supplements

          1. methylcellulose containing drops more viscous

          2. add Adequan to regular artificial tears (2.5 ml added to 10 ml)

          3. Genteal by Sigma is a new OTC "gel/liquid" that seems to work well

          4. use lubricant ointments at bedtime, when owner gone for more than 3-4 hours

        2. "KCS mixtures"

          1. my favorite, 15 ml saline based artificial tear, 2-4 ml of 20% acetylcysteine, 2 ml of 100 mg/ml injectable chloramphenicol or gentamicin, and 2 ml of 2% pilocarpine (can mix without antibiotic, too)

          2. chronic antibiotic use can lead to resistant bacteria

    4. Therapy for KCS (surgical)

      1. "cherry eye" replacement (to "prevent" KCS, see JAAHA reference above)

        1. the "excuse" that replacement surgery is too costly is a lame one

        2. over 3 times more dogs with amputated "cherry eyes" develop KCS than dogs with replaced glands

        3. cost of cyclosporine A alone is over $200/eye/year, not to mention office calls, additional drugs, cultures, etc.

        4. it is a "bargain" to have this awful, vision threatening and costly disease potentially prevented by a surgical procedure in a puppy

      2. shortening palpebral fissures (to reduce evaporative surface of globe)

      3. parotid duct transposition (in my opinion, "spit" in the eye is a "last ditch" effort in the treatment of KCS)

  4. Diseases of the cornea and sclera

    1. Pigmentary keratitis

      1. causes

        1. brachycephalic facial conformation

          1. medial entropion

          2. nasal fold trichiasis

          3. exposure

        2. KCS

      2. therapy

        1. medical

          1. tear supplements, liquid and ointment

          2. cyclosporine A

            1. for KCS

            2. even non-KCS cases will improve (pigment "break up") with cyclosporine A usage

            topical corticosteroids are a "double edged sword"

            1. reduce vascularization, but help "break up" pigmentation minimally

            2. can lead to "melting ulcers" and overgrowth of surface bacteria

        2. surgical

          1. medial (best) or lateral canthoplasty in brachycephalic breeds

            1. Wyman or "pocket-flap" technique to close medial canthus and reduce frictional irritation from medial trichiasis/nasal folds

            2. lateral canthal closure to reduce evaporative surface

          2. superficial keratectomy

            1. "last ditch" effort in the treatment of pigmentary keratitis

            2. very high incidence of poor healing/recurrence

            3. potential for post-op "melting ulcers"

    2. Lipid keratopathy

      1. causes

        1. genetic predisposition

          1. axial, subepithelial dystrophy, usually bilateral

            1. Arctic circle breeds, Cocker Spaniels, poodles, Bichons, others

            2. usually not vision threatening, painful, etc.

          2. multifocal, punctate keratopathy ("Sheltie dystrophy")

            1. can cause keratitis, ulcers

            2. responds well to cyclosporine A

        2. metabolic disease, usually (but not always) bilateral

          1. hypothyroidism

          2. Cushing's syndrome

          3. diabetes mellitus

          4. hypercholesterolemia, elevated triglycerides, etc

          5. may be axial or peripheral

        3. local corneal disease

          1. episcleritis

          2. German shepherd pannus

          3. chronic topical corticosteroid usage

      2. therapy

        1. identify the underlying cause and treat accordingly

        2. low fat diets (even in "genetic predisposed" breeds ?)

        3. topical cyclosporine A for "Sheltie dystrophy"

        4. topical cyclosporine A for other surface eye disease (pannus, keratitis due to sicca, etc.) instead of topical corticosteroids

    3. Superficial erosion complex ("Boxer ulcers")

      1. clinical signs

        1. superficial erosion (not into corneal stroma)

        2. loose "lip" of epithelium around ulcer

        3. no contributing cause (e.g. distichia, entropion, etc.)

        4. signalment (not just Boxers, also Goldens, Poodles, Lhasas, older dogs)

      2. cause

        1. usually nebulous history of trauma initiates

        2. lesion just does not heal (epithelium slides across, but does not bond down)

        3. epithelial basement membrane disorder

      3. therapy

        1. remove abnormal basement membrane

          1. striate keratotomy (Vet Med 90:561-572, 1995)

          2. multifocal punctate keratotomy (JAAHA 28:213-216, 1992)

          3. superficial keratectomy

          4. cyanoacrylate glue (Nexaban or Superglue)

        2. enhance epithelial binding to underlying stroma

          1. topical 5% NaCl drops or ointment

          2. extended wear soft contact lenses or collagen shields

          3. application of 5% polysulphated glycosaminoglycan solution (2.5 ml of 100mg/ml Adequan IM, Luitpold Pharmaceuticals with 10 ml of saline base artificial tears, Vet Med: 916-922, Oct 1996)

          4. oral tetracycline?

        3. expect exuberant corneal neovascularization in the Boxer, possibly no corneal neovascularization at all in other breeds

    4. Proteolytic enzyme ulcerative keratitis ("melting ulcers")

      1. clinical signs

        1. rapidly deteriorating corneal ulcerations ("well holes" or "hot wax")

        2. usually axially located, may or may not be horizontally ovoid

        3. signalment (usually brachycephalic breeds of dogs)

      2. causes (usually a combination of factors)

        1. bacterial enzymes (Pseudomonas sp., other Gram negatives and positives, too)

        2. neutrophil lysosomal enzymes

        3. stromal proteolytic enzymes (remember osteoblasts and osteoclasts in healing bone)

        4. decreased corneal sensitivity (sensation, sympathetic, parasympathetic innervation and a lack of other neuropeptides)

        5. decreased amounts or poor distribution of precorneal tear film

      3. therapy

        1. reduce proteolytic enzyme activity

          1. serum (alpha macroglobulin from platelets)

          2. acetylcysteine ("ulcer mix" - 15 ml saline base artificial tear, 2-4 ml 20% acetylcysteine (Mucomyst), 2-4 ml of 100 mg/ml injectable gentamicin or chloramphenicol)

          3. Na EDTA (1 ml of saline in large purple top, apply to eye)

          4. tetracycline?

        2. enhance vascular response and epithelialization (serum)

        3. appropriate antibiotics

          1. scrapings and cytology/Gram's stain - immediate return

          2. culture and sensitivity - 3 to 7 days for result

          3. chloramphenicol, Gram positives

          4. gentamicin, Gram negatives

          5. ciprofloxacin - Ciloxan, high dollar, very broad spectrum

          6. go by results of culture and sensitivity

        4. surgical therapy

          1. conjunctival grafts

            1. immediate blood supply for healing and support

            2. does not inhibit drug penetration

            3. depending on technique done, animal can see with graft in place

            4. time consuming, requires expertise and equipment, and heals with a scar

          2. third eyelid flap

            1. bandage, helps distribute tearfilm and supports

            2. inhibits medication of cornea

            3. with third eyelid up, cannot examine eye, animal cannot see

    5. Episcleritis

      1. "breed related", fairly benign

        1. poodles, bichons, beagles

        2. pink, raised area adjacent to limbus, minimal surface inflammation, no intraocular inflammation

        3. responds well to topical corticosteroids, sometimes goes away on its own

        4. some cases do not respond to topical corticosteroids, see tetracycline/niacinamide therapy below for collie NGE

      2. Nodular Granulomatous Episclerokeratitis (NGE, "collie granuloma")

        1. seen in collies and collie crosses

        2. usually bilateral

        3. pink, fleshy mass extends beyond lateral, or sometimes medial, limbus

        4. may progress to cover the entire cornea

        5. granulomatous masses may also be seen on third eyelid and lid margins (can affect skin of entire body)

        6. diagnosis based on breed, lesion appearance, and histopathologic confirmation

        7. therapy

          1. topical or intralesional corticosteroids (low yield in my hands)

          2. topical cyclosporine A (low yield in my hands)

          3. oral tetracycline and niacinamide (JAAHA 33:540-543, Nov-Dec 1997 and JAAHA 29:403-409, Sept-Oct 1993)

            1. 500 mg tetracycline tid (or doxycycline, 2.5-5 mg/lb, sid) and 500 mg niacinamide tid

            2. I have seen some dramatic improvements in not only collie NGE cases, but also resistant episcleritis cases in other breeds

          4. oral interferon 2 alpha (Roferon A - Roche)

            1. 3 million IU per vial, diluted in 1 liter saline (3000IU/ml), divide into 1 ml aliquots and freeze. Dispense 99 ml sterile water and 1 ml interferon diluted in 4 oz. brown bottle (30 IU/ml), keeps refrigerated for one month.

            2. work at Cornell University has shown 5 dogs successfully treated that were refractory to all other therapy

            3. dosage, 80 IU per day, per os for six months

            4. I have no experience with this therapy

          5. azathioprine (Imuran)

            1. 1 mg/lb sid for 10 days followed by tapering dose until lesions gone. "Maintanence dose" can be as little as 12.5 mg 2 times per week

            2. I have used this treatment with good success in dogs who can tolerate drug

            3. can cause hepatotoxicity and bone marrow suppression, need to monitor patients, especially when dose is high

          6. superficial keratectomy and N2O cryotherapy

            1. has been somewhat successful in my hands

            2. is useful therapy for localized episcleritis cases in other breeds than the collie

      3. episcleritis with panuveitis

        1. seen mostly in our practice in American Cocker Spaniels

        2. young adult to middle aged dogs present blind with massive perilimbal episcleritis and panuveitis, sometimes with retinal detachments

        3. dogs usually have history of immune mediated skin disease as well

        4. usually respond well to immunosuppressive doses of systemic prednisolone along with topical prednisolone

        5. some dogs can be weaned off with no recurrence, some are switched to oral azathioprine

  5. Update on cataracts ( Vet Med Jan 2001, 14-38) and other disease of the lens

    1. Definition: cataract - an opacity of the crystalline lens of the eye or its capsule

    2. In the "civilized world", what is usually termed a "cataract", in man, is actually the equivalent of old dog nuclear sclerosis.

    3. Young dog cataracts ("juvenile cataracts")

      1. lots of breed predisposition (Poodles, Cocker Spaniels, Miniature Schnauzers, Lhasa Apsos, Shi Tzus, Golden Retrievers, Labrador Retrievers, Arctic circle breeds, Beagles, Bichon Frise, Boston Terriers, other small terriers, Pomeranians, others as well as mixes)

      2. at an early age (6 months to 7+ years) dogs develop unilateral or bilateral cataracts

      3. usually quite rapid in onset

      4. usually cortical if evaluated via slit lamp biomicroscopy

      5. lens cells degenerate rapidly, liquefy, and may release antigenic material through intact lens capsule into anterior chamber fluid with subsequent "lens induced uveitis"

      6. if young enough dog, lens may "clear", and animal become visual again

    4. Old dog cataracts ("senile cataracts")

      1. lots of old dogs will have "nuclear sclerosis" that does not seem to affect the dog's functional vision

      2. a combination of nuclear sclerosis and cortical opacity may combine to affect an older dog's functional vision

      3. senile cataracts are usually slower in onset than juvenile cataracts

      4. older, predisposed breeds for juvenile cataracts (Cockers and Poodles) may develop rapid onset cortical lens opacities ("old age onset juvenile cataracts"??)

    5. Diabetic cataracts

      1. almost all diabetic dogs will develop cataracts if they live long enough (diabetic cats SELDOM develop cataracts)

      2. usually very rapid, bilateral onset of cortical cataract formation

      3. may or may not cause lens induced uveitis

      4. anterior chamber may be very shallow due to swelling of the lens ("intumescent cataract")

      5. diabetic cataracts may be "inhibited" or at least "postponed" by aldose reductase inhibitor drugs (experimental drug Sorbinil or even aspirin)

    6. Therapy for cataracts

      1. medical therapy

        1. NOTHING has been proven to medically resolve cataracts

        2. topical mydriatic agents may enhance vision "around" a nuclear opacity. Can be especially useful in immature juvenile cataracts and in some senile cataracts

        3. topical/systemic anti-inflammatory agents will reduce inflammation of lens induced uveitis, while a juvenile cataract is "resolving"

      2. cataract extraction surgery

        1. phacoemulsification and aspiration

          1. small hole procedure

          2. best done EARLY while lens is somewhat soft, no uveitis seen

          3. less corneal scarring, better removal of residual lens cells and fibers, so postoperative uveitis is less, and potential for lens "regrowth" or "after cataract" is less (a REAL problem in the young dog)

          4. if capsular bag is left intact, artificial lens (IOL) may be implanted (without IOL, average dog is 8D-15D "far sighted". To show client what dog sees, have them look through -8D to -15D lens on your direct ophthalmoscope.)

          5. success rate claimed by some of 95% (at 6 months)

        2. extracapsular extraction

          1. 160-180 degree incision ("open sky")

          2. if no irrigation-aspiration available, surgeon may wait until lens dehydrates or "ripens" to aid in removal of entire lens. This may allow for further degenerative changes to occur within the eye (smoldering uveitis, vitreous liquefaction, lens zonule rupture, retinal detachment, secondary glaucoma, etc.) which may lower percentage for long-term success.

          3. rarely will extracapsular extraction surgeons implant IOLs

        3. intracapsular extraction

          1. usually reserved for removal of luxated lenses

          2. whole lens, capsule and all, removed

          3. has higher incidence of post-operative retinal detachment, glaucoma, and other vision robbing complications

          4. some ophthalmologists will sew an IOL into the ciliary sulcus following intracapsular lens removal

    7. Primary lens luxation

      1. breed predisposition

        1. small terrier breeds (Bostons, Jack Russells, Fox, Yorkies, Cairns, Westies)

        2. Shar Peis (seen in conjunction with glaucoma)

        3. rarely in other small breeds (Poodles, Cockers, etc.)

      2. also seen in old dogs and in dogs with hyper-mature cataracts

      3. clinical signs

        1. acute corneal edema, episcleral injection, pain

        2. glaucoma +/-

        3. lens in anterior chamber or deep in vitreous

        4. vitreous in anterior chamber

        5. iridodenesis

        6. a bilateral condition, although not always symmetrical

      4. therapy

        1. if lens in anterior chamber and eye visual, remove lens (intracapsular extraction)

        2. if lens in anterior chamber and eye blind due to glaucoma or detached retina, salvage procedure (evisceration and prosthesis or enucleation)

        3. if lens in posterior chamber and eye visual

          1. intracapsular extraction

          2. medical management (miotic therapy, demecarium bromide, 0.125-0.25%, bid, to "trap" lens in posterior chamber)

      5. long-term outlook

        1. IS a bilateral disease, if one luxates, other one will probably go, too (especially in young, predisposed breeds)

        2. even if it does not occur with initial luxation, glaucoma is a probable long-term sequela

    8. Feline lens disorders

      1. cataracts

        1. uncommonly seen as breed related/inherited juvenile onset like in the dog

        2. dense nuclear sclerosis seen commonly in OLD (high teens) cats. Usually are not a threat to vision.

        3. most common cause of feline cataracts in our practice is chronic uveitis (see below). Surgery to remove lens and restore vision has low yield.

      2. lens luxation

        1. occasionally seen as congenital defect (also cataract, glaucoma, etc.)

        2. most commonly seen due to chronic uveitis and glaucoma

        3. usually pretty low yield for extraction and vision retention

      3. post-traumatic undifferentiated sarcoma in the cat

        1. history of puncture wound to eye as youngster, followed by phthisis bulbi

        2. as old cat, pink to tan mass appears in eye, eye slowly enlarges

        3. undifferentiated sarcoma, probably from lens cells

        4. tumor can grow out of eye along optic nerve, to brain, and cause death

        5. a good reason to enucleate cats with traumatically induced phthisis bulbi (especially if a lens rupture could have occurred)

  6. Feline surface ocular inflammation

    1. THE most common feline ocular disease seen by veterinary practitioners

    2. Acute conjunctivitis - causes:

      1. chlamydia

        1. many times unilateral onset that becomes bilateral

        2. chemosis, lymphoid follicle hyperplasia

        3. no keratitis

        4. +/- systemic disease (respiratory, gastroenteritis)

        5. characteristic basophilic perinuclear, intracytoplasmic inclusion bodies seen in epithelial cells from conjunctival scrapings (best seen when done within first 1-2 weeks of infection)

        6. PCR testing available from Colorado State University (970-491-1281)

        7. IFA testing available from University of Tennessee (865-974-5643)

        8. therapy - DO NOT USE TOPICAL CORTICOSTEROIDS

          1. topical tetracycline ointment, qid, OU (irritating)

          2. topical chloramphenicol or erythromycin ointments, qid, OU ( if tetracycline too irritating)

          3. oral doxycycline, 5 mg/lb or 50 mg tablet, once daily (only if adult)

          4. oral azithromycin (Zithromax - Pfizer), 25 mg/cat, 2 days on , 2 days off for 3-5 treatments (either 200mg/5ml powder or 250 mg tablets dissolved in 10 ml tuna oil, can be gotten from Wedgewood Pharmacy)

        9. potential "carrier state", need to treat all cats in household

      2. ACUTE herpes virus keratoconjunctivitis

        1. usually bilateral ocular disease with systemic signs (upper respiratory signs)

        2. very common cause of neonatal ophthalmia

        3. supposedly only infectious, upper respiratory disease causing keratitis (ulcerative or interstitial)

          1. dendritic ulcerative keratitis

          2. geographic ulcerative keratitis

        4. diagnosis

          1. IFA test (Univ Tenn Knoxville ) - low yield test; if comes back positive, probably is, high number of "false negatives". False positives seen if animal's cornea stained with fluorescein prior to doing scraping.

          2. PCR testing - looking for amplified viral DNA, Colorado State Univ (a lot lower numbers of positive tests than when Univ. Missouri was doing PCR). Scraping put in transport media or biopsy specimen.

          3. antibody titers - felt by most to be useless in vaccinated cats

          4. virus isolation - considered "gold standard", but only useful if media can be immediately inoculated.

        5. therapy - DO NOT USE TOPICAL CORTICOSTEROIDS

          1. symptomatic therapy includes topical broad spectrum antibiotics

          2. acute disease usually runs its course in immune competent animals

          3. Betadine solution diluted in saline 1:10 (1% final concentration)

          4. Interferon (Roferon A, Roche) 30-100 (up to 1000) IU daily per os, one week on, one week off. Make up stock and dispense as above for NGE in collies. Can also dilute in saline to 3 mg/ml and use qid in the eye.

          5. idoxuridine topically (Herplex, Allergan or compounded by Wedgewood Pharmacy) q2-3h (usually well tolerated by cats)

          6. trifluorothymidine (Viroptic, Burroughs Wellcome or trifluridine, Schein). Q1h first day, then 5x/day (usually not tolerated well by cats, Wedgewood Pharmacy has 2 ml "trial size" bottles available since is so expensive)

          7. adenine arabinoside (Vira-A, Parke-Davis) 4-5x/day (not always tolerated well by cats)

          8. acyclovir (Zovirax, Glaxo Wellcome) 200 and 400 mg capsules, banana flavored elixir(?). Either 200mg per os bid-tid or 5 mg/lb bid-tid. Zovirax skin ointment is not to be used in the eye. Work at University of Missouri a few years ago claimed that cats could not maintain a therapeautic level at tolerated doses, so most ophthalmologists no longer use. Other anti-viral, anti-AIDS drugs (valacyclovir) are extremely hepatotoxic to cats, and can cause death.

          9. l-lysine - amino acid supplement, comes in 500 mg tablets. 250- 500 mg/cat bid per os. Work at Purdue University showed that l-lysine therapy early in course of disease reduces duration of illness, viral shedding, and incidence of recrudescence.

        6. if topical or systemic corticosteroids used, increases viral shedding, incidence of corneal sequestration, interstitial keratitis

        7. recurrent herpes viral conjunctivitis/keratitis seen with immunosuppression (see chronic herpes virus associated disease below)

      3. mycoplasmal conjunctivitis

        1. felt by some to not be a primary entity (only seen in association with herpes)

        2. can start unilateral and become bilateral

        3. +/- systemic disease (respiratory)

        4. supposedly no keratitis (but I have seen two cases of severe ulcerative keratitis that were culture positive for mycoplasma only)

        5. diphtheritic membrane on conjunctival surface is supposedly pathognomonic

        6. therapy

          1. topical tetracycline, chloramphenicol, or erythromycin (like treatment for chlamydia)

          2. oral doxycycline or Zithromax (like therapy for chlamydia)

      4. reovirus and calicivirus conjunctivitis

        1. reovirus causes a serous ocular discharge associated with conjunctivitis. There appears to be no long-term significance with reovirus infections in cats. Therapy is symptomatic.

        2. calicivirus has been for years associated with the upper respiratory disease/conjunctivitis complex in cats, but some studies have shown that calici virus infection only rarely causes conjunctivitis in cats.

    3. Chronic/recurrent surface eye disease in cats - causes:

      1. chlamydia

        1. supposedly a carrier state for chlamydia can occur, therefore the need to treat all animals in a household when an active case of chlamydial conjunctivitis is diagnosed.

        2. supposedly recovery from chlamydial infection does not incur long-term protective immunity. Animals may get recurrent episodes of chlamydial conjunctivitis with re-exposure.

        3. therapy is the same as for acute chlamydial conjunctivitis

      2. recrudescent herpes virus disease

        1. a very common clinical entity

        2. 80% of cats infected with FHV-1 will be latently infected, and 45% will have spontaneous recurrences of clinical disease (and potential viral shedding).

        3. stress (boarding, travel, new cat in household) and immunosuppression (FeLV or FIV, iatrogenic use of corticosteroids, other disease, aging) may cause acute recrudescence and clinical disease.

        4. the virus lays dormant in sensory nerve ganglia (trigeminal ganglia with distribution to the conjunctiva and cornea), so recrudescence results in localized disease (much like "shingles" in humans associated with prior "chicken pox" infection and "cold sores").

        5. a common clinical history is a cat that has recurrent conjunctivitis when boarded, when travels, etc. This may be bilateral, or many times is unilateral in the same eye repeatedly.

        6. therapy is the same as for acute disease. DO NOT USE TOPICAL CORTICOSTEROIDS (see stromal keratitis and corneal sequestration below). In an attempt to PREVENT recurrent episodes, some will treat with l-lysine prior to an anticipated stressful event or indefinitely treat with l-lysine.

        7. because of the association between herpes recrudescence and immunosuppression, afflicted cats should be screened for presence of FeLV or FIV.

    4. Other disorders associated with herpes virus infection in cats

      1. without a doubt, FHV-1 is the leading underlying cause of surface ocular disease in cats. Just about every surface ocular disorder in cats has been scientifically or anecdotally linked to herpes virus infection. Because immunosuppression is important in the pathophysiology of herpetic eye disease, testing for FeLV and FIV should be done in all cases of suspected FHV-1 ocular disease.

      2. corneal sequestration ("corneal nigrans")

        1. clinical entity seen only in cats

        2. axial pigmentation of the corneal surface, may extend into stroma

        3. may be painful and elicit diffuse keratitis, or may be rather benign, non- painful.

        4. seen in all cats, but commonly seen in brachycephalic breeds. Frictional irritation ("dry eye", entropion, exposure keratitis) seems to be contributory.

        5. in the research lab, inoculation with FHV-1 followed by topical and/or systemic corticosteroids will result in sequestrum formation, as well as interstitial keratitis (Investigative Ophthalmology and Visual Science 30:1758-1768, 1989). Many clinical cases of corneal sequestration have a history of conjunctivitis treated with topical corticosteroids.

        6. different studies (JAAHA 30:24-28, Jan-Feb 1994 and AJVR 59(7):856-858 July 1998) have shown sequestrum samples to be positive via IFA (17%) and PCR testing for FHV-1 DNA (AJVR study that showed overall 55% PCR positive sequestra, brachycephalic breeds had a significantly lower incidence of positive FHV-1 DNA, 43% for Persian and 58% for Himalayan vs DSH/DLH at 80% FHV-1 positive).

        7. therapy

          1. benign neglect, some will "fall off" with time

          2. topical and systemic antivirals to hasten "natural course"

          3. superficial keratectomy and other supportive surgery (third eyelid flap, conjunctival graft, partial thickness keratoplasty) and supportive medical therapy (topical and systemic antivirals and antibiotics).

          4. some will put post-op sequestrum patients on indefinite l-lysine

          5. do NOT use topical corticosteroids post-operatively to "reduce scar", incidence of sequestrum recurrence is high under this circumstance.

      3. eosinophilic keratoconjunctivitis

        1. two clinical syndromes that I have seen :

          1. bilateral disorder, no other history of eye disease (i.e. consistent with FHV-1)

          2. unilateral (occasionally bilateral) disorder with history consistent with previous FHV-1

        2. bilateral disease

          1. young mature to middle aged cats (3-8 years old)

          2. bilateral, but not necessarily symmetrical, disease

          3. appears at lateral limbus as neovascularization and surface corneal white to grey "plaque"

          4. +/- painful

          5. fairly seasonal in occurrence (summer months)

          6. scrapings and cytology show eosinophils and eosinophilic granules

          7. association with eosinophilic granuloma complex (???), rare

          8. responds well to topical and/or systemic corticosteroids (wean back to minimum therapy to control disorder, seasonal therapy in summer months)

          9. has been treated in the past with megostrol acetate (OvaBan)


        3. unilateral disease or bilateral disease with history of previous FHV-1

          1. any age cat

          2. may be bilateral or unilateral

          3. distribution not always lateral to begin with

          4. may have other prior signs (keratitis, conjunctivitis, sequestra, symblepharon)

          5. will see eosinophils on cytology of corneal/conjunctival scrapings

          6. may respond well to topical/systemic steroids, or may worsen!!

          7. probably is a manifestation of FHV-1 (AJVR 59(7):856-858, 1998)this study showed 76% of cases of eosinophilic keratitis tested for FHV-1 via PCR were positive for FHV-1

          8. therapy

            1. systemic and topical antivirals

            2. systemic steroids in conjunction with antivirals (???)

            3. OvaBan (???) 5 mg per day for first 7-10 days, should see marked improvement, followed by weaning to a final dose sometimes as low as 1.25 mg every third week (personal communication, Dr. Kerry Ketring, Cincinnatti, OH)

            4. topical (3 IU/ml) and oral (30 IU/day) Interferon therapy

      4. stromal keratitis

        1. usually "painful" infiltration of cornea with inflammatory cells and neovascularization

        2. can be reproduced in laboratory (Invest Ophth study listed above and AJVR 56(1):51-55, Jan 1995) by inoculating cats with FHV-1 followed by steroid therapy

        3. seen clinically in cats with history of conjunctivitis and steroid use

        4. many times seen in conjunction with sequestra and eosinophilic keratitis

        5. in man, herpes induced stromal keratitis is felt to be due to hypersensitivity reaction to stromal viral antigen (histopathology shows high numbers of mononuclear inflammatory cells). Antiviral therapy alone or along with JUDICIOUS use of topical steroids can help control this painful condition. Steroid therapy is a "double edged sword".

        6. therapy may involve antivirals along with systemic steroids or OvaBan.

      5. symblepharon

        1. lack of palpebral/bulbar cul-de-sacs due to scarring of lid to eyeball, maybe even a total membrane covering corneal surface.

        2. seen secondary to early FHV-1 infections and/or neonatal ophthalmia

        3. can cause chronic epiphora (nasolacrimal duct system scarred over) or may cause blindness if severe enough

        4. if cat visual, no therapy

        5. if cat nonvisual, can try to "peel" membrane from cornea (not that hard to do) and attempt to reconstruct cul-de-sacs (hard to do successfully) followed by long-term antiviral therapy

      6. neonatal ophthalmia

        1. infection under closed eyelids prior to opening of physiologic ankyloblepharon

        2. in cats, usually associated with neonatal FHV-1 infection

        3. therapy

          1. open lids and drain ASAP

          2. topical antibiotic ointment (kittens and puppies produce no tears until after lids open)

          3. topical dilute Betadine (1:10 in saline) as antiviral agent

          4. l-lysine therapy, 25-50 mg bid depending on size of kitten

        4. incidence of symblepharon, epiphora due to lacrimal duct punctal scarring, and KCS due to lacrimal gland/duct scarring is great

      7. feline keratoconjunctivitis sicca

        1. not near the clinical entity in cats that it is in dogs

        2. STT is difficult to interpret in cats (sympathetic nervous system can cause STT values to be very low in normal cats)

        3. diagnosis made based on other clinical signs (lackluster cornea, horizontal axial band of exposure keratitis, corneal neovascularization)

        4. history in most cats consistent with previous FHV-1 infection

        5. many times unilateral

        6. therapy

          1. some use cyclosporine A with success; some say cyclosporine A causes herpes recrudescence

          2. topical or systemic pilocarpine seems to do little good

          3. supportive lubrication works well in some cats (especially if not brachycephalic)

          4. parotid duct transpositions sometimes work well, sometimes not, technically very difficult in cats and have to work at making cats salivate continuously.

      8. idiopathic anterior uveitis

        1. a recent report (AJVR 60:932-936,1999) indicates that some cats with chronic anterior uveitis have FHV-1 antigen in aqueous humor as well as intraocular production of antibody against FHV-1.

        2. these new results may indicate that some previously diagnosed "idiopathic uveitis" cases may have FHV-1 as an underlying cause.

        3. possibly systemic therapy with antivirals and judicious use of topical steroids may be useful in treating these previously frustrating cases.

        4. some ophthalmologists treat all of their "idiopathic" anterior uveitis cases with NSAID's for fear of causing FHV-1 recrudescence

      9. recurrent erosions in cats

        1. some believe that all "superficial erosion complex" cases in cats are a form of FHV-1 infection

        2. some ophthalmologists treat these with topical antvirals as well as topical antibiotics

        3. many ophthalmologists shun cross hatch or punctate keratopathy on these cats for fear of inducing stromal keratitis or sequestra

  7. Uveitis, the "can of worms"

    1. Anatomy and physiology

      1. the "uvea" is the vascular portions of the eye: the iris, cilary body, and choriod

      2. the ciliary body makes the aqueous humor, and the choroid nourishes the outer retinal layers (rods and cones and bipolar cells)

      3. the "blood-eye barrier" prevents blood components (albumin and other proteins, RBC's and WBC's) from getting into the aqueous humor and between the retinal pigment epithelium and the neuroretina.

      4. the "blood-eye barrier" at the level of the iris is the tight junctions between the vascular endothelial cells, at the level of the ciliary body is the tight junctions between the ciliary body epithelial cells, at the level of the retinal vessels is the endothelial tight junctions, and at the choroid is the tight junctions of the retinal pigment epithelium.

      5. when inflammatory mediators or mechanical forces cause "breakdown" of this "blood-eye barrier", large protein molecules ("plasmoid aqueous" or "aqueous flare"), RBC's (hyphema), and WBC's (hypopyon) may appear in the aqeuous humor and vitreous or in the subretinal space (seen as subretinal exudate or detachment of the retina)

      6. the "stability" of this "blood-eye barrier" varies with the species. From "toughest" to "weakest" is as follows: primates (man), ruminants, cats, dogs, horses, rabbits.

    2. Clinical signs of acute uveitis

      1. "anterior uveitis" (iritis, cyclitis, iridocyclitis)

        1. a "red eye"

          1. usually due to episcleral injection seen as individual engorged vessels, not diffuse conjunctival redness (although some animals will have diffuse conjunctival hyperemia and chemosis with the episcleral injection)

          2. dogs typically have much more dramatic episcleral injection than do
            cats with anterior uveitis

        2. a "painful eye"

          1. along with breakdown of the "blood-eye barrier", inflammatory medicators (prostaglandins, etc.) cause spasming of the iris sphincter and ciliary body muscles

          2. seen clinically as blepharospasm, photophobia, and serous (+/- seromucoid) ocular discharge

        3. a "cloudy eye"

          1. diffuse corneal edema and "aqueous flare" make intraocular structures difficult to see

          2. vision is usually poor for the patient as well, especially if bilateral

          3. since the corneal endothelial cells that are responsible for keeping the cornea "dehydrated" get their nourishment from the aqueous humor, when the aqueous humor is pathological, the cornea will be as well

        4. miosis due to prostaglandin activity on iris sphincter muscles and the parasympathetic nervous system's effect on the iris sphincter muscles

        5. hypotony due to poor active production of aqueous humor and prostaglandin enhancement (?) of aqueous humor outflow

      2. "posterior uveitis" (chorioretinitis, retinochoroiditis, hard to separate because of the proximity of the choroid and the retina)

        1. poor recognition of fundic structures, due to vitreal debris, retinal edema, and subretinal fluids

        2. focal retinal/subretinal fluids/exudates seen as poorly demarcated areas of tapetal hyporeflectivity or "fuzzy" areas of white, tan, or grey discoloration over the nontapetal portion of the fundus

        3. retinal detachment

        4. retinal vascular hemorrhage or perivascular exudates

        5. swelling or lack of clarity of the optic disc

    3. Clinical signs of chronic uveitis (seen after a few days to weeks)

      1. cloudy cornea/keratic precipitates and "perilimbal flush" or "ciliary flush"

        1. keratic precipitates are accumulations of inflammatory cells, fibrin, and blood that settle inferiorly on the corneal endothelial surface

        2. especially seen in chronic uveitis in cats (may be tough to visualize because of third eyelid protrusion)

      2. synechia

        1. adhesion of iris to the lens (posterior synechia) or cornea (anterior synechia)

        2. if iris has been adherred to lens, but has pulled loose, may leave blotches of pigment on anterior lens capsule surface ("pigment rests")

        3. if pupil stuck to lens capsule 360 degrees, aqueous humor cannot get out of posterior chamber into anterior chamber, causing bulging forward of peripheral iris ("iris bombe") and potentilly secondary glaucoma

      3. iris color change

        1. chronic prostaglandin stimulation to iris melanocytes causes iris hyperpigmentation (especially seen in dogs)

        2. iris surface neovascularization ("rubiosis irides") seen especially in light colored eyed cats

      4. cataract formation

        1. "unhealthy" aqueous humor leads to poor lens metabolism and subsequent cataract formation

        2. the most common cause of cataract formation in adult cats (horses, too)

        3. because of the underlying pathology, lens removal and vision restoration in cats usually carries a poor prognosis

      5. phthisis bulbi due to chronic ocular hypotension. There is a high association with phthisis bulbi and retinal detachment

      6. secondary glaucoma due to occlusion of outflow pathways. The most common cause of feline glaucoma

      7. chorioretinal scars

        1. in tapetal region of the fundus, seen as sharply demarcated focal areas of hyper-reflectivity, areas of hyperpigmentation, and areas of hyperpigmentation surrounded by tapetal hyper-reflectivity.

        2. in the nontapetal fundus, seen as sharply demarcated areas of depigmentation or hyperpigmentation

    4. Classifications of uveitis

      1. exogenous uveitis

        1. direct trauma to the globe, surgery, penetrating wounds that directly damage parts of the uvea such as the iris and ciliary body will cause uveitis.

        2. external ocular disease - such as a corneal ulcer ("the corneal- uveal reflex") The afferent arm of the corneal-uveal reflex is the ophthalmic branch of the trigeminal nerve (CN V), the efferent arm of the corneal-uveal reflex is parasympathetic innervation to the ciliary body and iris through the parasympathetic branch of the oculomotor nerve (CN III). This causes miosis, ciliary spasm, and breakdown of the blood-aqueous barrier with production of aqueous flare and cells, and conjunctival and episcleral vasodilation. This corneal-uveal reflex is especially strong in horses, rabbits, and to some extent dogs, and is not as much of a clinical entity in cats, cattle, and primates.

        3. extension of infection per se via hematogenous spread or spread of inflammatory mediators to the eye via the blood stream (such as cyclooxygenase, prostaglandins, leukotrienes, or histamines). This may include nonspecific entities such as septicemias, abscesses, pneumonia, pyometra, etc.

          Some common systemic diseases associated with uveitis:

          1. FELINE DISEASES

            FeLV associated, some say that with the exception of lymphosarcoma, FeLV has nothing to do with feline uveitis. There is an association with immunosuppression caused by FeLV and uveitis due to toxoplasmosis, FIP, and FHV-1. All cases of feline uveitis should be screened for FeLV.

            FIV associated, "pars planitis" is considered by some a pathognomonic sign of FIV. Seen as mild anterior uveitis, the distinctive clinical signs include inflammatory precipitates on the posterior lens capsule, anterior vitreal inflammatory debris, and "snow banking" along the pars plana near the ciliary body (JAVMA 196:1116-1119, 1990). Like FeLV infection, FIV can cause immuno-suppression, and therefore all cases of feline uveitis should be screened for FIV.

            FIP, feline infectious peritonitis in the eye is usually seen as a bilateral anterior uveitis. Perivascular retinal hemorrhages and exudates may be seen, and retinal detachments also occur. Dramatic keratic precipitates and rubiosis irides may be seen in kittens with FIP.

            toxoplasmosis, some would have us believe that all cases of feline anterior uveitis are due to toxoplasmosis, and that treatment with clindamicin would make them all better and we could live happily ever after. Toxoplasmosis in the eye may be unilateral or bilateral, can involve the anterior segment or posterior segment. Anterior uveitis can be acute or chronic. Flare, rubiosis, and K.P. are seen much like FIP. Chronic uveitis can lead to cataract formation and/or glaucoma. Posterior segment infection may be seen as multifocal areas of inactive chorioretinitis potentially surrounded by active inflammation.

            FHV-1, some think is a cause of "idiopathic" anterior uveitis in older cats as well as lymphocytic-plasmacytic iritis (see below)

            systemic mycoses, rare in cats in this area with exception of cryptococcosis. See clinical signs below as dogs and cats are similar.

          2. CANINE DISEASES

            brucellosis, seen as an anterior uveitis or chorioretinitis or both, usually due to bacteria within the eye itself.

            leptospirosis, usually anterior uveitis, is probably not due to bacteria in the eye itself but due to inflammatory mediators from inflammation elsewhere in the body.

            toxoplasmosis, not as big a problem in dogs as in cats, can cause anterior uveitis or chorioretinitis, and is due to the organism being within the eye.

            ehrlichiosis, fairly common problem in the eastern United States, can cause a panuveitis, and can cause tremendous inflammation within the eye, retinal detachments, and glaucoma.

            Rocky Mountain Spotted Fever, uveitis does occur, but usually is not as much inflammation in the eye as with ehrlichiosis. Can also see retinal vasculitis.

            cryptococcosis, mostly a posterior segment disease, subretinal abscesses and optic neuritis.

            histoplasmosis, seen in the Missouri River Valley, Oklahoma, Texas, and other western and Midwestern states as a mild anterior uveitis, mild chorioretinitis.

            blastomycosis, seen in the Ohio River Valley and Mississippi River Valley. Can cause severe chorioretinitis, anterior uveitis, endophthalmitis, and secondary glaucoma.

            coccidioidomycosis, seen in the desert southwest, and looks very similar to blastomycosis in the eye.

            infectious canine hepatitis, "blue eye", seen as an anterior uveitis, severe corneal edema, and sometimes secondary glaucoma. This is due to a Type III Ag-Ab immune hypersensitivity response, can be seen with clinical disease or vaccine reaction.

            Lyme disease, has been described to cause anterior uveitis in dogs, but is rare.

            lymphosarcoma, seen as hyphema, chorioretinitis, anterior uveitis, hypopyon. Ocular lymphosarcoma is usually associated with Stage V lymphosarcoma with bone marrow involvement. We see a lot of Rottweillers with panuveitis and secondary glaucoma.

      2. endogenous causes of uveitis

        1. less well defined and less well understood as a whole compared to exogenous causes.

        2. the source of the antigen responsible for the inflammatory response is a portion of the eye itself. Although some trauma and infection may have initially triggered the body's immune system to begin attacking some portion of the eye, the eye (or some component of the eye) is now the target of the body's immune response. Some examples of endogenous uveitis may include:

          1. Uveodermatologic Syndrome (VKH - like syndrome)- This is seen in dogs, swine, poultry, and humans. In this disorder, the body's immune system attacks neuroectodermal and cutaneous derived pigmented cells of the body. Described as being "common" in the Akita, I have seen this entity in Samoyeds, Irish Setters, Shetland sheepdogs, and mixed breeds. Seen as a severe anterior uveitis with lots of pigmented cells in the aqueous humor, secondary glaucoma and cataract formation is common. Retinal detachment and depigmentation of the fundus occurs routinely. Dermatitis and skin depigmentation (vitaligo) with depigmentation of the hair (poliosis) also occurs.

          2. lens induced uveitis - lens material is not considered "self" by the immune system since the developing lens cells were sequestered from the developing immune system during embryogeneiisis. A very common cause of uveitis in the dog, especially seen in breeds of dogs that develop hypermature juvenile cataracts. This is also part of what causes uveitis when there is a ruptured lens in any species of animal.

      3. idiopathic causes of uveitis

        1. a very high percentage of uveitis cases in animals never reach a conclusive diagnosis. Examples include old cats with idiopathic uveitis and many dogs with acute uveitis that resolves.

        2. lymphocytic-plasmacytic iritis in cats - seen as "lumps" within the iris stroma, differential diagnoses should include lymphosarcoma and all the above listed diseases causing uveitis in cats. Many think this represents an FHV-1 induced disease.

        3. steroid responsive retinal detachments in the dog - initially described by Andrews and Abrams, this entity is usully seen in large breeds of dogs with the German Shepherd dog and Labrador retrievers being over-represented (especially shepherds). Dogs present with bilateral retinal detachments with a minimum of anterior segment inflammation. Diagnostic workup is usually unrewarding as far as a diagnosis of underlying disease, and the retinas re-attach with systemic corticosteroid therapy.

    5. Sources for diagnostic testing

      1. University of Georgia, 706-542-5812
        ehrlichia, Rocky Mountain Spotted Fever, Lyme disease, toxoplasmosis, cryptococcosis (antibody titers)

      2. DyNAgenics Veterinary Diagnostics, 417-451-0201
        FIV, FeHV-1, toxo, FIP, ehrlichia, RMSF, Lyme, and others (PCR)

    6. Therapy for uveits - LOOK FOR AN UNDERLYING DISEASE AND TREAT APPROPRIATELY!!

      1. corticosteroids

        1. topical administration for anterior uveitis (topical administration will do little for chorioretinitis/posterior uveitis)

          1. will need a drug with good penetration and potency

          2. 1% prednisolone acetate (Pred Forte, EconoPred, others) my choice

          3. 0.1% dexamethasone alcohol (Maxitrol - Alcon, AkTrol - Akorn, Neoplybac-dex products, numerous suppliers) my second choice

        2. oral administration can be used to augment topical administration in treatment of anterior segment disease. Is mandatory to treat posterior segment disease.

          1. for suspected "immune mediated disease", I will use 1 mg/lb dose or higher

          2. lower doses used for suspected non-immune mediated disease

          3. the "double edged sword" of corticosteroid therapy. Be careful with potential cases of infectious disease.

      2. mydriatic/cyloplegics

        1. counteract the iris sphincter and ciliary muscle spasming and pain

        2. helps restore the integrity of the blood-aqueous barrier in anterior uveitis

        3. agents available

          1. atropine, 1% solution or ointment

            1. "old standby", used for decades

            2. long lasting (can last for up to 3+ days in a normal cat or dog)

            3. use "to effect" (overzealous use can cause acute angle closure glaucoma in predisposed canine breeds)

            4. bitter taste can cause drooling/vomiting in some cats and dogs (use ointment or feed patient when drug administered to minimize effect)

            5. occasionally will cause sicca (especially with chronic use and in older patients)

          2. tropicamide 1% solution (Mydriacyl - expen$ive - and others)

            1. shorter lasting and less "potent" than atropine

            2. tid-qid administration

            3. can cause drooling (but seldom sicca) like atropine

      3. NSAID's

        1. since prostaglandins are important inflammatory mediators for intraocular inflammation, these drugs are especially effective

          1. oral medications

            1. aspirin, 5-10 mg/lg sid-bid (watch for gastric upset)

            2. carprofen

            3. etodolac

          2. topicals


            1. I use these infrequently, I have not been impressed with their "potency". Some ophthalmologists use them a lot, especially in herpes prone cats on long-term anti-inflammatory therapy.

            2. diclofenac (Voltaren - CIBA Vision), qid

            3. flurbiprofen (Ocufen - Alcon), qid

  8. Disease of the fundus

    1. Progressive retinal atrophy in dogs

      1. inherited disorder of the neuroretina commonly seen in dogs, occasionally in cats, sometimes in man.

      2. retinal development and function is normal early on, but a genetically programmed "death" of first the rods and cones followed ultimately by the entire neuroretina leads to eventual blindness.

      3. described in almost every pure bred dog (as well as many "mutts"), the disorder is especially prevalent in the Miniature poodle, the Labrador retriever, American and English Cocker Spaniels, English Springer spaniels

      4. "new blood test" for PRA

        1. DNA-based test to identify dogs that will develop PRA, are carriers of the gene, or are "clear" of defective PRA gene

        2. marker-based test, not able to test for single gene itself

        3. developed at James A. Baker Institute for Animal Health, Cornell University, Drs. Gustavo Aguirre and Gregory M. Acland

        4. able to test for bred related PRA in the following breeds: Portuguese Water dogs, Chesapeake Bay Retrievers, English Cocker Spaniels, Labrador Retrievers Poodles, Cardigan Welsh Corgis, Irish Setters, Mastiffs, Miniature Schnauzers, Samoyeds, and Siberian Huskies

        5. commercially available testing

          1. OptiGen LCC http://www.optigen.com
            Jeanette S. Felix, Ph.D.
            President and Manager
            OptiGen, LLC
            Cornell Business & Technology Park
            Phone: 607-257-0301
            Fax: 607-257-0353
            e-mail: genetest@optigen.com

    2. Sudden Acquired Retinal Degeneration Syndrome (SARDS) (JAAHA 28:199-202, May-June 1992, Prog Vet & Comp Ophth 1(1):11-18, 1991, AJVR 59(2): 149-152, 1998)

      1. originally described as "toxic metabolic retinopathy" and "silent retina syndrome", this syndrome was first described in 1983, and we have little more information about the disease since those early reports

      2. the disease is characterized by apparent acute vision loss (although observant owners have described "a problem" with vision that may have been going on for up to 4 weeks prior to blindness)

      3. the acute vision loss is accompanied by normal funduscopic findings and extinguished electroretinographic tracings indicating no electrical activity of the neuroretina

      4. most dogs are middle age or older, one report listed 70+% of the cases to be females or spayed females

      5. upon physical examination and questioning, most dogs show one or more of the following clinical signs:

        1. polyuria/polydipsia/polyphagia

        2. history of weight gain/obesity

        3. hepatomegaly

      6. ophthalmic examination may reveal fixed, dilated pupils or slow, incomplete pupillary light reflexes. Funduscopic examination is usually normal early in the disease, but later, tapetal hyper-reflectivity and vascular attenuation typical of retinal death may be seen

      7. most dogs have normal CBC's (some reported to have abnormalities consistent with a stress leukogram)

      8. serum biochemistry profiles reveal many dogs having elevation of some hepatoenzymes (Alk Phos and ALT), and many dogs have low elevations of resting serum cortisols

      9. some dogs will have urinalysis results consistent with isosthenuria

      10. many dogs look Cushingoid ("pot bellied", thin skinned and hair coat)

      11. some (a minority) of dogs are diagnosed as being Cushingoid based on ACTH stimulation or dexamethasone suppression studies

      12. at our practice, we see the majority of cases between August and November. Other ophthalmologists have described the condition as being seen more frequently in the summer, while some see more cases in the winter.

      13. with time, most dogs will return to normal eating/drinking habits from the initial PU/PD. Some dogs continue to have a voracious appetite.

      14. "adaptation" to vision loss occurs in most dogs with time

      15. currently there is a study being conducted by Dr. Ken Abrams of the A.C.V.O. to look at epidemiologic factors of SARDS cases

      16. as of yet, we do not know the cause of this disorder, and there is no effective treatment

    3. Enrofloxacin-associated retinal degeneration in the cat (JAAHA 35:511-514, Nov-Dec1999 and Veterinary Ophthalmology 4(2):99-106, 2001)

      1. first seen approximately 4 years ago, enroflaxacin-associated retinal toxicity has become a clinical entity in some cats

      2. afflicted cats have been treated with varying doses of enrofloxacin for varying periods of time before onset of apparent blindness and fixed, dilated pupils


        1. in Veterinary Ophthalmology report above, dosages ranged from as little as 4.6 mg/kg PO once daily for 8 days to 15mg/kg PO twice daily for 14 days

        2. afflicted cats on lower dosages were usually older (13-16 years of age)

      3. clinical signs seen as acute onset of nonpainful vision loss, mydriasis, with fairly rapid onset of fundic signs consistent with retinal degeneration:

        1. tapetal hyper-reflectivity

        2. retinal vascular attenuation

        3. large gold to rust-colored foci scattered throughout the tapetal fundus

        4. irregular pigment loss and pigment clumping within the nontapetal fundus

      4. electroretinography revealled flat ERG tracings indicating photoreceptor (rod and cone) cell death

      5. return of some vision occurred in those cats who were taken off the drug as soon as mydriasis and blindness were noted (although retinal degeneration and eventual blindness occurred in some cats despite being taken off the drug in a timely manner)

      6. current dosage recommendations by the manufacturer are for 5 mg/kg once daily (different from the previous dosage of 11 mg/kg once daily that was recommended for the cat and is still recommended for the dog)

      7. if dosages higher than those recommended by the manufacturer are used, it is recommended that periodic ophthalmoscopy be performed looking for tapetal hyper-reflectivity and vascular attenuation

      8. onset of mydriasis and/or blindness should cause prompt cessation of parenteral enrofloxacin.

      9. histopathology shows outer retinal layer (rods and cones) death followed by death of remainder of retinal layers

      10. retinal necrosis appears to be eventually total with little chance of functional "regeneration"

    4. Ophthalmic manifestations of systemic hypertension (Veterinary Ophthalmology 4(2):131-140, 2001 and Vet Med Feb 2001: 134-158)

      1. the most commonly recognized ophthalmic manifestation of systemic hypertension is "acute" blindness due to retinal detachments or retinal degeneration

        1. most often seen in old cats, occasionally in dogs

        2. animals are hesitant, bump into objects

        3. pupillary light responses may range from normal to slow to nonexistent

        4. animals may or may not have a positive menace or dazzle response to appropriate stimuli

        5. funduscopic examination may reveal total vitreal hemorrhage, "sails in the wind" total retinal detachment, or large areas of preretinal or subretinal hemmorhage

        6. diffuse subretinal effusion may not be easily recognized via direct ophthalmoscopy

        7. generalized retinal degeneration seen as diffuse tapetal hyper-reflectivity

      2. "early" (prior to total blindness due to retinal detachment or total retinal degeneration) funduscopic signs may include:


        1. posterior segment hemorrhage

          1. intra-, sub-, or pre-retinal

          2. vitreal

        2. subretinal or intraretinal effusion (seen as tapetal hypo-reflectivity or fuzzy, gray discoloration of the nontapetal fundus)

        3. multifocal hyperpigmented foci of RPE proliferation in the tapetal fundus(sites of healed previous hemorrhages or retinal effusions)

        4. multifocal, sharply demarcated hypopigmented foci of RPE degeneration in the nontapetal fundus (sites of healed previous hemorrhages or retinal effusions)

        5. retinal vascular dilation/tortuosity (although this is commonly reported, it has been my personal experience that this is uncommon, especially in cats. Many cats actually have attenuation of retinal vasculature, especially arterioles. I have seen retinal vascular dilation and tortuosity in dogs, but this is not consistent.)

      3. other ocular signs (not as commonly seen as fundic changes)

        1. episcleral vessel engorgement

        2. corneal stromal/subepithelial hemorrhage from corneal neovascularization

        3. hyphema

        4. iris "aneurisms"/iris stromal hemorrhage

      4. differential diagnoses include:

        1. toxic coaggulopathies

        2. autoimmune coaggulopathies

        3. neoplasia (lymphosarcoma, hemangiosarcoma, etc.)

      5. diagnosis - blood pressure measurement (Vet Med Feb 2001:135-143)

        1. Doppler ultrasonography

          1. probably simplest, most cost effective method

          2. good for getting a systolic pressure, much more difficult for diastolic

          3. need unit, transmitting-receiving transducer, and appropriate cuff

        2. oscillometry

          1. old Dinamap units and similar units

          2. transducer and cuff are in one unit

          3. good for systolic, diastolic, and mean arterial pressure

        3. photoplethysmography

          1. used on man, infrared light transmission measures arterial volume through a cuff on a finger

          2. limited to use in small patients

          3. difficult to get readings in darkly pigmented or furry patients

        4. direct measurement

          1. the "gold standard" for blood pressure measurement

          2. requires use of an intra-arterial catheter attached to a pressure transducer

          3. used a lot to measure intra-operative continuous blood pressure

          4. is not practical for repeated monitoring of blood pressure

        5. normal readings at our practice using Doppler ultrasonography

          1. canine - over ~180 mm Hg systolic considered "hypertensive"

          2. feline - over ~170 mm Hg systolic considered "hypertensive"

          3. repeated readings are obtained to avoid "white coat hypertension"

          4. the older the patient, the expected higher the systolic blood pressure

      6. primary diseases associated with secondary systemic hypertension

        1. renal disease

          1. pyelonephritis

          2. chronic interstitial nephritis

          3. polycystic kidney disease

          4. glomerulonephritis

          5. amyloidosis

          6. glomerulosclerosis

        2. thyroid disease

          1. hyperthyroidism

          2. hypothyroidism

        3. adrenal disease

          1. hyperadrenocorticism

          2. pheochromocytoma

          3. hyperaldosteronism

        4. miscellaneous

          1. anemia

          2. polycythemia

          3. hyperestrogenism

          4. diabetes mellitus

        5. most common cause of secondary hypertension in cats

          1. chronic renal disease (of cats with chronic renal disease, 61% are hypertensive)

          2. hyperthyroidism

        6. most common cause of secondary hypertension in dogs

          1. chronic renal disease

          2. hyperadrenocorticism

        7. essential hypertension (?) - 54% of cats in two studies that had retinal lesions and elevated blood pressure were not afflicted with renal failure or hyperthyroidism

      7. therapy - CONSULT WITH AN INTERNIST OR A CARDIOLOGIST!1

        1. amlodipine (Norvasc - Pfizer)

          1. calcium channel blocker

          2. causes peripheral vasodilation with minimal decrease in cardiac muscle contractility

          3. gradual onset of action, making hypotension unlikely

          4. long duration, once daily medication possible

          5. dosage

            1. cats - 0.18 mg/kg (1/4 of a 2.5 mg tablet) once daily to 1/2 of a 2.5 mg tablet daily

            2. dogs - 0.13-2.2 mg/kg once daily

        2. enalopril (Enacard - Merial (888)637-4251)

          1. angiotensin converting enzyme inhibitor

          2. decreases peripheral arterial and venous resistance

          3. increases renal perfusion

          4. dosage - dogs and cats - 0.5 mg/kg once or twice a day

      8. prognosis

        1. good with minor retinal hemorrhage, minor intra- or subretinal effusionif can control blood pressure

        2. guarded if large mass of intravitreal hemorrhage or acute retinal detachment. The sooner subretinal fluid resolves, the more likely retina will "reattach" and photo receptors will still be viable.

        3. poor if retinal degeneration has already occurred (as seen by diffuse tapetal hyper-reflectivity, RPE proliferation, and RPE degeneration)

© 2001 - J. Phillip Pickett, DVM, Diplomate, A.C.V.O. - All rights reserved