Equine Recurrent Uvei2s/ ERU. Equine Recurrent Uvei2s. Uvei2s. Uvea. Blood- ocular barrier. Uvea
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1 Equine Recurrent Uvei2s/ ERU Equine Recurrent Uvei2s Moon blindness Iridocycli2s Periodic ophthalmia Tijn J.P. Spoormakers dipl. ECVS, cert ISELP Most common cause of blindness Uvei2s Inflamma2on of uvea Iris, ciliary body (anterior uvea) and choroid (posterior uvea) Uvea Iris and ciliary body Large number of blood vessels Choroid (posterior uvea) Primary vascular supply for re2na It can involve the complete eye: panophthalmi2s Uvea Blood- ocular barrier Uvea in direct contact with peripheral vaculature and blood- ocular barrier: Blood- aqueous barrier Blood- re1nal barrier prevents large molecules and cells entering the eye Trauma and inflamma2on disrupt this barrier: Generate host immune responses An2body produc2on Self- an2gens Foreign an2gens 1
2 ERU Recurrent episodes of intraocular inflamma2on separated by periods with no signs of ac2ve intraocular inflamma2on Periods separated by weeks to some2mes years ERU develops from primary uvei2s Not all uvei2s become ERU General symptoms: Pain/ blepharospasm Photophobia ERU Miosis Altered corneal transparancy History First ERU reported 4 th century ad by Vege2us changes in the moon moon blindness Pathophysiology: History Infec2ous agents Bacterial, viral, protozoan, nand parasi2c Noninfec2ous e2ologies Pathophysiology ERU Mul2factorial related to Gene2c makeup of the individual Appaloosa Strongly autoimmune mediated Dysregulated immune response causes ERU Explains recurrence Posi2ve effect cor2costeroids Insufficient success of an2bio2cs 2
3 Physiology ERU Accumula2on noncellular exsudates uvea Dysfunc2on uvea: Nourish func2on uvea Ø Dysfunc2on re2na, lens, sclera, cornea Physiology ERU Transparency cornea No infiltrate nor extensive vascularisa2on Transparency anterior chamber Fibrin, cells, bloood, pus Obstruc2on trabecular meshwork: glaucoma Transparency lens: cataract (luxa2on) Transparency posterior segement Inflamma2on/ liquefica2on/trac2on Re2nal detachement Re2na: damage/ detachment Classifica2on of uvei2s Primary or ini2al uvei2s is not ERU Can become ERU Recurrent uvei2s: ERU is two or more episodes of uvei2s 3 types: 1. Classic ERU 2. Insidious ERU 3. Posterior ERU Classic ERU Most common type Ac2ve, painfull inflamma2on followed by no inflamma2on Iris, ciliary body, and choroid > cornea, anterior chamber, lens, re2na, vitreous Cataract, intraocular adhesions, phthisis bulbi and vision loss Glaucoma Classic ERU Classic ERU CAL1-13 Cabal 3
4 Classic ERU Classic ERU/ glaucoma Insidious ERU Insidious ERU Low- grade intraocular inflamma2on No painful episodes evident Gradual and cummula2ve destruc2ve effect Appaloosa and Drae breed horses WEE75-1 Indy Posterior ERU Inflamma2on in vitreous, re2na and choroid Clinical signs: Vitreal inflamma2on, cloudiness, re2nal detachment, vision loss Warmbloods, Drae breeds Posterior segment signs In acute ERU posterior not visible Fundoscopie: Choriore2nal scarring Bullet hole scarring Buherfly lesions Re2nal detachment 4
5 Recurrent episodes of inflamma2on/ constant low- grade discomfort Ocular structures become severly damaged Anterior synechiae Iris architecture lost Cataract/ lens luxa2on Re2nal detachment Phthisis bulbi Blindness Pathogenesis Strongly autoimmune mediated Dysregulated immune response causes ERU Ini2a2ng events remain obscure Triggering event in many autoimmune disorders: infec2ons Leptospiral infec2on?» Exact pathogenesis is poorly understood Vaccina2on: no equine registered vaccins Possible ac2va2on immune response! 5
6 Medical treatment ERU Aggressive: Reduce discomfort Atropine - > mydriasis 1dd to 4 dd (or more) Reduce inflamma2on Cor2costeroids and NSAIDs Reduce inflamma2on; topical Cor2costeroids: Prednisolone acetate 1%, dexamethasone HCl 0.1% 1dd to hourly No1ce: side effects 1ssue healing Triamcinolone 2mg subconjunc2val NSAIDs: Flurbiprofen 0.03%, bromfenac sodium 0.9%, diclofenac sodium 0.1% Less side effects Reduce inflamma2on; systemic Flunixin meglumine (0.5 mg/kg) Very potent for the eye Phenylbutazone (4.4 mg/kg) Less potent Ini2al therapy At least 1-2 weeks Treatment Aeer resolu2on of clinical signs tapered off over 2 weeks Treatment An2bio2cs Anecdotal effect Suspected leptospiral infec2ons: Doxycycline (12 mg/kg 2dd) 4- weeks course Strong evidence ERU : immune- mediated An6bio6cs unlikely to be successful Response to treatment Very variable Quick to very refrac2ve to therapy Recurrent inflamma2on More severe More refrac2ve to therapy NB: secondary glaucoma 6
7 1.Surgical treatment ERU Cyclsporine sustained release device MOA: Preven2on of T cell ac2va2on Slow release of cyclosporine directed to ciliary body Candidates: horses with frequent recurrences or early relapse of ac2ve ERU aeer stopping medica2on Horses with ac2ve inflamma2on and that can not be controlled are poor candidates 1. Surgical treatment ERU General anesthesia Conjunc2va incision 7 mm L- shapped scleral flap 8 mm posterior limbus Suprachoroidal implanta2on Device on uveal tract 1. Surgical treatment ERU Post- opera2ve Flunixin meglumine (5d) Topical an2bio2cs (10d) Atropine (7d) It takes days to reach adequate levels 1. Surgical treatment ERU Dura2on medica2on: 36 months Horses + cyclosporine implanta2on: No ERU Less frequent/ severe ERU 70-80% ERU No vision- threatening complica1ons! 2. Surgical treatment ERU Pars Plana Vitrectomy MOA: removal of resident inflammatory cells with the vitreous 2. Surgical treatment ERU Very specialis2c Sx Only touch vitreous - > complica2ons Complica1ons: transient hypoypon, vitreal and/ or re1nal hemorrhage, re1nal detachmene, catarct forma1on 7
8 2. Surgical treament ERU +/- 70% no recurrence ERU Serious complica2on: vision loss Beher outcome in horses with posi1ve Leptospiral serology in vitreous samples ERU Is ERU one disease or a syndrome with many causes? Further research is necessary! In daily prac2ce: Recognize ERU Aggressive treatment Medical/ surgery Inform your clients Severe complica2ons Ques2ons 8
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