Ординатура / Офтальмология / Английские материалы / Veterinary Ocular Pathology A Comparative Review_Dubielzig, Ketring, McLellan_2010

Ocular complications following radiotherapy where the eye is in the irradiation field (Fig. 4.23)

Eyelid margin and haired skin of the eyelid

•Necrosis followed by atrophy of the pilosebaceous unit

•Vasculopathy

•Atrophy of the Meibomian glands, contributing to ocular surface disease (keratoconjunctivitis).

Lacrimal or nictitans glands

•Necrosis followed by atrophy

•Can be responsible for reduced tear production, leading to signs of keratoconjunctivitis sicca.

Lens

•Necrosis of the proliferative layer of the lens epithelial cells leads to equatorial cortical cataract.

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Retina

•Retinal vasculopathy is recognized as a relatively common, chronic, long-term adverse effect:

■Retinal hemorrhage

■Retinal edema

■Regional retinal ischemia.

Comparative Comments

Ocular complications of radiation therapy in humans, in which the eye is in the irradiation field, usually involve retinal vasculopathy, although dry eye, loss of lashes and eyebrow, and chronic erythema are all encountered.

Intraoperative complications

Chu, T.G., Green, R.L., 1999. Suprachoroidal hemorrhage. Surv. Ophthalmol. 43, 471–486.

Intraoperative inflammation: toxins and infection

Moore, D.L., McLellan, G.J., Dubielzig, R.R., 2003. A study of the morphology of canine eyes enucleated or eviscerated due to complications following phacoemulsification. Vet. Ophthalmol. 6, 219–226.

Olivero, D.K., Davidson, M.G., Nasisse, M.P., et al., 1993. Canine intraocular lens quality control: light and scanning electron microscopic evaluation. Prog. Vet. Comp. Ophthalmol. 3, 98–104.

Taban, M., Behrens, A., Newcomb, R.L., et al., 2005. Acute endophthalmitis following cataract surgery: a systematic review of the literature 10.1001/archopht.123.5.613. Arch. Ophthalmol. 123, 613–620.

Mamalis, N., Edelhauser, H.F., Dawson, D.G., et al., 2006. Toxic anterior segment syndrome. J. Cataract Refract. Surg. 32, 324–333.

Holland, S.P., Morck, D.W., Lee, T.L., 2007. Update on toxic anterior segment syndrome. Curr. Opin. Ophthalmol. 18, 4–8.

Taylor, M.M., Kern, T.J., Riis, R.C., et al., 1995. Intraocular bacterial contamination during cataract surgery in dogs. J. Am. Vet. Med.

Assoc. 206, 1716–1720.

Ledbetter, E.C., Millichamp, N.J., Dziezyc, J., 2004. Microbial contamination of the anterior chamber during cataract phacoemulsification and intraocular lens implantation in dogs. Vet. Ophthalmol. 7, 327–334.

Epithelial inclusion cysts and epithelial down-growth

Koch, S.A., Langloss, J.M., Schmidt, G., 1974. Corneal epithelial inclusion cysts in four dogs. J. Am. Vet. Med. Assoc. 164, 1190–1191.

Schmidt, G.M., Prasse, K.W., 1976. Corneal epithelial inclusion cyst associated with keratectomy in a dog. J. Am. Vet. Med.

Assoc. 168, 144.

Bedford, P.G.C., Grierson, I., McKechnie, N.M., 1990. Corneal epithelial inclusion cyst in the dog. J. Small Anim. Pract. 31, 64–68.

Kostuik, H., 2007. Intraocular epithelial downgrowth in a dog. Can. Vet. J. 48, 943–945.

Endothelial damage

Gwin, R.M., Lerner, I., Warren, J.K., et al., 1982. Decrease in canine corneal endothelial cell density and increase in corneal thickness as functions of age. Invest. Ophthalmol. Vis. Sci. 22, 267–271.

Gwin, R., Warren, J., Samuelson, D., et al., 1983. Effects of phacoemulsification and extracapsular lens removal on corneal thickness and endothelial cell density in the dog. Invest. Ophthalmol. Vis. Sci. 24, 227–236.

Nasisse, M.P., Cook, C.S., Harling, D.E., 1986. Response of the canine corneal endothelium to intraocular irrigation with saline solution, balanced salt solution, and balanced salt solution with glutathione. Am. J. Vet. Res. 47, 2261–2265.

Gerding Jr., P.A., McLaughlin, S.A., Brightman, A.H., et al., 1990. Effects of intracameral injection of viscoelastic solutions on corneal endothelium in dogs. Am. J. Vet. Res. 51, 1086–1088.

Hyndiuk, R.A., Schultz, R.O., 1992. Overview of the corneal toxicity of surgical solutions and drugs: and clinical concepts in corneal edema. Lens Eye Toxic. Res. 9, 331–350.

Glasser, D.B., Schultz, R.O., Hyndiuk, R.A., 1992. The role of viscoelastics, cannulas, and irrigating solution additives in post-cataract surgery corneal edema: a brief review. Lens Eye Toxic. Res. 9, 351–359.

Postoperative glaucoma

Miller, P.E., Stanz, K.M., Dubielzig, R.R., et al., 1997. Mechanisms of acute intraocular pressure increases after phacoemulsification lens extraction in dogs. Am. J. Vet. Res. 58, 1159–1165.

Biros, D.J., Gelatt, K.N., Brooks, D.E., et al., 2000. Development of glaucoma after cataract surgery in dogs: 220 cases (1987– 1998). J. Am. Vet. Med. Assoc. 216, 1780–1786.

Lannek, E.B., Miller, P.E., 2001. Development of glaucoma after phacoemulsification for removal of cataracts in dogs: 22 cases (1987–1997). J. Am. Vet. Med. Assoc. 218, 70–76.

Johnsen, D.A., Maggs, D.J., Kass, P.H., 2006. Evaluation of risk factors for development of secondary glaucoma in dogs: 156 cases (1999–2004). J. Am. Vet. Med. Assoc. 229, 1270–1274.

Strubbe, T., 2002. Uveitis and pupillary block glaucoma in an aphakic dog. Vet. Ophthalmol. 5, 3–7.

Denis, H.M., 2002. Anterior lens capsule disruption and suspected malignant glaucoma in a dog. Vet. Ophthalmol. 5, 79–83.

Corneal incision: normal healing and complications

van Ee, R.T., Nasisse, M.P., Helman, G., et al., 1986. Effects of Nylon and Polyglactin 910 suture material on perilimbal corneal wound healing in the dog. Vet. Surg. 15, 435–

440.

Gilger, B.C., 2007. Diseases and surgery of the canine cornea and sclera. In: Gelatt, K.N.

(Ed.), Veterinary ophthalmology, 4th edn. Blackwell, Ames, pp. 690–752.

Effects of electrocautery, cryosurgical and laser application

Edmonds, C., De Roetth Jr., A., Howard, G.M., 1970. Histopathologic changes following cryosurgery and diathermy of the rabbit ciliary body. Am. J. Ophthalmol. 69, 65–72.

Howard, G.M., De Roetth Jr., A., 1967. Histopathologic changes following cryosurgery of the rabbit ciliary body. Am. J. Ophthalmol. 64, 700–707.

Rosenberg, L.F., Karalekas, D.P., Krupin, T., et al., 1996. Cyclocryotherapy and noncontact Nd:YAG laser cyclophotocoagulation in cats. Invest. Ophthalmol. Vis. Sci. 37, 2029–2036.

Merideth, R.E., Gelatt, K.N., 1980. Cryotherapy in veterinary ophthalmology. Vet. Clin. North Am. Small Anim. Pract. 10, 837–846.

Vestre, W.A., Brightman 2nd., A.H., 1983. Effects of cyclocryosurgery on the clinically normal canine eye. Am. J. Vet. Res. 44, 187–194.

West, C.S., Barrie, K., 1988. The use of cryosurgery in veterinary ophthalmology practice. Semin. Vet. Med. Surg. (Small Anim.) 3, 77–82.

Gilmour, M.A., 2002. Lasers in ophthalmology. Vet. Clin. North Am. Small Anim. Pract. 32, 649–672.

Chandler, M.J., Moore, P.A., Dietrich, U.M., et al., 2003. Effects of transcorneal iridal photocoagulation on the canine corneal endothelium using a diode laser. Vet.

Ophthalmol. 6, 197–203.

Cook, C.S., 1997. Surgery for glaucoma. Vet. Clin. North Am. Small Anim. Pract. 27, 1109–1129.

Cook, C., Davidson, M., Brinkmann, M., et al., 1997. Diode laser transscleral cyclophotocoagulation for the treatment of glaucoma in dogs: results of six and twelve month follow-up. Vet. Comp. Ophthalmol. 7, 148–154.

Nadelstein, B., Wilcock, B., Cook, C., et al., 1997. Clinical and histopathologic effects of diode laser transscleral cyclophotocoagulation in the normal canine eye. Vet. Comp. Ophthalmol. 7, 155–162.

Hardman, C., Stanley, R.G., 2001. Diode laser transscleral cyclophotocoagulation for the treatment of primary glaucoma in 18 dogs: a retrospective study. Vet. Ophthalmol. 4, 209–215.

O’Reilly, A., Hardman, C., Stanley, R.G., 2003. The use of transscleral cyclophotocoagulation with a diode laser for the treatment of glaucoma occurring post intracapsular extraction of displaced lenses: a retrospective study of 15 dogs (1995–2000). Vet. Ophthalmol. 6, 113–119.

Bras, I.D., Robbin, T.E., Wyman, M., et al., 2005. Diode endoscopic

cyclophotocoagulation in canine and feline glaucoma. 36th Annual Conference American College of Veterinary Ophthalmologists, Nashville, TN, p. 50.

Morreale, R.J., Wilkie, D.A., Gemensky-Metzler, A.J., et al., 2007. Histologic effect of semiconductor diode laser transscleral cyclophotocoagulation on the normal equine eye. Vet. Ophthalmol. 10, 84–92.

Sullivan, T.C., Davidson, M.G., Nasisse, M.P., et al., 1997. Canine retinopexy – a determination of surgical landmarks, and a comparison of cryoapplication and diode

laser methods. Vet. Comp. Ophthalmol. 7, 89– 95.

Pizzirani, S., Davidson, M.G., Gilger, B.C., 2003. Transpupillary diode laser retinopexy in dogs: ophthalmoscopic, fluorescein angiographic and histopathologic study. Vet. Ophthalmol. 6, 227–235.

Cook, C.S., Wilkie, D.A., 1999. Treatment of presumed iris melanoma in dogs by diode laser photocoagulation: 23 cases. Vet. Ophthalmol. 2, 217–225.

McCally, R.L., Bargeron, C.B., Green, W.R., et al., 1983. Stromal damage in rabbit

corneas exposed to CO2 laser radiation. Exp. Eye Res. 37, 543–550.

English, R.V., Nasisse, M.P., Davidson, M.G., 1990. Carbon dioxide laser ablation for treatment of limbal squamous cell carcinoma in horses. J. Am. Vet. Med. Assoc. 196, 439–442.

Bussieres, M., Krohne, S.G., Stiles, J., et al., 2005. The use of carbon dioxide laser for the ablation of meibomian gland adenomas in dogs. J. Am. Anim. Hosp. Assoc. 41, 227–234.

Nasisse, M.P., Davidson, M.G., MacLachlan, N.J., et al., 1988. Neodymium:yttrium, aluminum, and garnet laser energy delivered transsclerally to the ciliary body of dogs. Am. J. Vet. Res. 49, 1972–1978.

Nasisse, M.P., Davidson, M.G., English, R.V., et al., 1990. Treatment of glaucoma by use of transscleral neodymium:yttrium aluminum garnet laser cyclocoagulation in

dogs. J. Am. Vet. Med. Assoc. 197, 350–354.

Nasisse, M.P., Davidson, M.G., Olivero, D.K., et al., 1993. Neodymium:YAG laser treatment of primary canine intraocular tumors. Prog. Vet. Comp. Ophthalmol. 3, 152–157.

Sapienza, J.S., Miller, T.R., Gum, G.G., et al., 1992. Contact transscleral cyclophotocoagulation using neodymium:yttrium aluminum garnet laser in normal dogs. Prog. Vet. Comp. Ophthalmol. 2, 147.

Rosenberg, L.F., Burchfield, J.C., Krupin, T., et al., 1995. Cat model for intraocular

pressure reduction after transscleral Nd:YAG cyclophotocoagulation. Curr. Eye Res. 14, 255–261.

Sullivan, T.C., Nasisse, M.P., Davidson, M.G., et al., 1996. Photocoagulation of limbal melanoma in dogs and cats: 15 cases (1989–1993). J. Am. Vet. Med. Assoc. 208, 891–894.

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Weigt, A.K., Herring, I.P., Marfurt, C.F., et al., 2002. Effects of cyclophotocoagulation with a neodymium:yttrium-aluminum-garnet laser on corneal sensitivity, intraocular pressure, aqueous tear production, and corneal nerve morphology in eyes of dogs. Am. J. Vet. Res. 63, 906–915.

Peiffer Jr., R.L., Nobles, R.D., Carter, J., et al., 1997. Internal sclerostomy with a mechanical trephine versus the neodymium:YAG laser in dogs. Ophthalmic. Surg. Lasers. 28, 223–230.

Beale, A.B., Salmon, J., Michau, T.M., et al., 2006. Effect of ophthalmic Nd:YAG laser energy on intraocular lenses after posterior capsulotomy in normal dog eyes. Vet. Ophthalmol. 9, 335–340.

Gilger, B.C., Davidson, M.G., Nadelstein, B.,

et al., 1997. Neodymium-yttrium-aluminum- garnet laser treatment of cystic granula iridica in horses: eight cases (1988–1996). J. Am. Vet. Med. Assoc. 211, 341–343.

Photodynamic therapy

Giuliano, E.A., Ota, J., Tucker, S.A., 2007. Photodynamic therapy: basic principles and potential uses for the veterinary ophthalmologist. Vet. Ophthalmol. 10, 337–343.

Lens surgery

Moore, D.L., McLellan, G.J., Dubielzig, R.R., 2003. A study of the morphology of canine eyes enucleated or eviscerated due

to complications following phacoemulsification. Vet. Ophthalmol. 6, 219–226.

Davidson, M.G., Nasisse, M.P., Rusnak, I.M., et al., 1990. Success rates of unilateral vs. bilateral cataract extraction in dogs. Vet.

Surg. 19, 232–236.

Peiffer Jr., R.L., Gaiddon, J., 1991. Posterior chamber intraocular lens implantation in the dog: results of 65 implants in 61 patients. J. Am. Anim. Hosp. Assoc. 27, 453–462.

Collinson, P.N., Peiffer Jr., R.L., 2002. Pathology of canine cataract surgery complications. New Zealand Vet. J. 50, 26–31.

Glover, T.L., Davidson, M.G., Nasisse, M.P.,

et al., 1995. The intracapsular extraction of displaced lenses in dogs: a retrospective study of 57 cases (1984–1990). J. Am. Anim. Hosp. Assoc. 31, 77–81.

Nasisse, M.P., Glover, T.L., 1997. Surgery for lens instability. Vet. Clin. North Am. Small Anim. Pract. 27, 1175–1192.

Nasisse, M.P., Glover, T.L., Davidson, M.G.,

et al., 1995. Technique for the suture fixation of intraocular lenses in dogs. Vet. Comp. Ophthalmol. 5, 146–150.

Wilkie, D.A., Gemensky-Metzler, A.J., Stone, S.G., et al., 2008. A modified ab externo approach for suture fixation of an intraocular lens implant in the dog. Vet. Ophthalmol. 11, 43–48.

Bagley 2nd., L.H., Lavach, J.D., 1994. Comparison of postoperative phacoemulsification results in dogs with

and without diabetes mellitus: 153 cases (1991–1992). J. Am. Vet. Med. Assoc. 205, 1165–1169.

Johnstone, N., Ward, D.A., 2005. The incidence of posterior capsule disruption during phacoemulsification and associated postoperative complication rates in dogs: 244 eyes (1995–2002). Vet. Ophthalmol. 8, 47–50.

Sigle, K.J., Nasisse, M.P., 2006. Long-term complications after phacoemulsification for cataract removal in dogs: 172 cases (1995–2002). J. Am. Vet. Med. Assoc. 228, 74–79.

Fife, T.M., Gemensky-Metzler, A.J., Wilkie, D.A., et al., 2006. Clinical features and outcomes of phacoemulsification in 39 horses: a retrospective study (1993–2003). Vet. Ophthalmol. 9, 361–368.

Capsular opacification, lens epithelial metaplasia, proliferation and migration

Bras, I.D., Colitz, C.M., Saville, W.J., et al., 2006. Posterior capsular opacification in diabetic and nondiabetic canine patients following cataract surgery. Vet. Ophthalmol. 9, 317–327.

Gerardi, J.G., Colitz, C.M., Dubielzig, R.R.,

et al., 1999. Immunohistochemical analysis of lens epithelial-derived membranes following cataract extraction in the dog. Vet. Ophthalmol. 2, 163–168.

Bernays, M.E., Peiffer, R.L., 2000. Morphologic alterations in the anterior lens capsule of canine eyes with cataracts. Am. J. Vet. Res. 61, 1517–1519.

Colitz, C.M., Malarkey, D., Dykstra, M.J., et al., 2000. Histologic and immunohistochemical characterization of lens capsular plaques in dogs with cataracts. Am. J. Vet. Res. 61, 139–143.

Davidson, M.G., Morgan, D.K., McGahan, M.C., 2000. Effect of surgical technique on in vitro posterior capsule opacification. J. Cataract Refract. Surg. 26, 1550–1554.

Davidson, M.G., Wormstone, M., Morgan, D., et al., 2000. Ex vivo canine lens capsular sac explants. Graefes Arch. Clin. Exp. Ophthalmol. 238, 708–714.

Glaucoma drainage implant surgery

Gelatt, K.N., Gum, G.G., Samuelson, D.A., et al., 1987. Evaluation of the Krupin-Denver valve implant in normotensive and glaucomatous beagles. J. Am. Vet. Med. Assoc. 191, 1404–1409.

Bedford, P.G.C., 1989. A clinical evaluation of a one-piece drainage system in the treatment of canine glaucoma. J. Small Anim. Pract. 30, 68–75.

Tinsley, D.M., Betts, D.M., 1994. Clinical experience with a glaucoma drainage device in dogs. Vet. Comp. Ophthalmol. 4, 77–83.

Bentley, E., Nasisse, M.P., Glover, T., et al., 1996. Implantation of filtering devices in dogs with glaucoma: preliminary results in 13 eyes. Vet. Comp. Ophthalmol. 6, 243.

Bentley, E., Miller, P.E., Murphy, C.J., et al., 1999. Combined cycloablation and gonioimplantation for treatment of glaucoma in dogs: 18 cases (1992–1998). J. Am. Vet. Med. Assoc. 215, 1469–1472.

Cullen, C.L., 2004. Cullen frontal sinus valved glaucoma shunt: preliminary findings in dogs with primary glaucoma. Vet. Ophthalmol. 7, 311–318.

Sapienza, J.S., van der Woerdt, A., 2005. Combined transscleral diode laser cyclophotocoagulation and Ahmed gonioimplantation in dogs with primary glaucoma: 51 cases (1996–2004). Vet. Ophthalmol. 8, 121–127.

Evisceration and intrascleral prosthesis placement

Brightman, A.H., Magrane, W.G., Huff, R.W., et al., 1977. Intraocular prosthesis in the

CHAPTER CONTENTS

The relative importance of ocular trauma in a mail-in pathology practice

General post-traumatic response of ocular tissues, regardless of the type of trauma

Non-specific proliferative reaction

Intraocular hemorrhage

Blood in the anterior chamber (hemophthalmos)

Non-penetrating (blunt) ocular trauma

Corneal effects Uveal effects Lens effects

Cataract

Lens capsule rupture

Traumatic lens subluxation or luxation

Retinal effects

Scleral effects, scleral rupture

Penetrating injuries

Corneal penetrating injury Scleral penetrating injury Suppurative endophthalmitis

Septic implantation syndrome (‘cat scratch’ injuries)

Chemical injury

Acid burn Alkali burn Snake bite

Proptosis and optic nerve trauma

End-stage disease (atrophy of the globe and phthisis bulbi)

Feline post-traumatic ocular sarcoma (FPTOS)

Spindle cell variant FPTOS Round-cell variant FPTOS

Post-traumatic osteosarcoma and/or chondrosarcoma Prophylactic enucleation of traumatized feline globes

THE RELATIVE IMPORTANCE OF OCULAR TRAUMA IN A MAIL-IN

81 PATHOLOGY PRACTICE

83• It is estimated that 20% of canine submissions to COPLOW are

84related to non-surgical trauma.

A B

C

■Posterior iridal neovascular membrane

–Which may lead to posterior synechiae

■Cyclitic membrane

–This can lead to traction resulting in retinal detachment

Retinal detachment and subsequent hypoxia leads to the release of growth factors which further stimulate neovascular proliferation

■Choroidal neovascular membranes (Fig. 5.3)

–This can lead to subretinal hemorrhage or serous exudation, with subsequent retinal detachment

■Neovascular membranes extending from the optic disk into the vitreous in dogs

–This can lead to traction and retinal detachment, with retinal hypoxia contributing to further neovascular proliferation

■Retinal neovascular membranes rarely occur in domestic animal species

Comparative Comments

Proliferative vitreoretinopathy occurs in humans secondary to trauma, or can be secondary to retinal detachment, and is rare in domestic species

Figure 5.3  Fibrovascular proliferation in the globe. (A) Photomicrograph showing a choroidal neovascular proliferation in a traumatized canine globe. (B) Photomicrograph showing a fibrovascular membrane extending from the optic nerve head into the vitreous

body in a traumatized dog globe (arrow).

(C) Low magnification photomicrograph of a canine globe showing extensive intravitreal hemorrhage and neovascular proliferation near the optic nerve head.

■The general absence of granulation tissue formation within the tissues of the uveal tract is quite striking

–If fibrosis is observed within the uvea, it is important to look for evidence of scleral rupture, which provides a portal for fibrosis originating within the episcleral tissues to enter the globe.

Comparative Comments

The post-traumatic reaction of ocular tissues described for animal eyes applies also for human eyes.

INTRAOCULAR HEMORRHAGE

Blood in the anterior chamber (hemophthalmos) (Fig. 5.4)

•May result from blunt or penetrating trauma, but has many other potential causes; including intraocular inflammation, neoplasia, fibrovascular membranes, retinal detachment, systemic hypertension or disorders of hemostasis

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•Hemophthalmos (blood in the anterior chamber) can contribute directly to the pathogenesis of glaucoma by obstructing conventional aqueous outflow via the drainage angle

•Hemophthalmos may play a role in stimulating a neo-vascular proliferative response which can lead to anterior or posterior synechiae, as well as predisposing to further episodes of intraocular hemorrhage

•In its aftermath, hemophthalmos can lead to secondary hemosiderosis

■Blood pigment staining of the cornea, after traumatic hemorrhage, can involve hemoglobin, hemosiderin, or hematoidin. Staining is seen most often in the peripheral cornea and the tissues of the iridocorneal angle. A Prussian blue stain is useful to distinguish hemosiderin from melanin

•Continued hemorrhage can fill the globe (hemophthalmos)

■Recurrent episodes of intraocular hemorrhage may reflect underlying disease; vicious cycles of hemorrhage associated with clotting and subsequent activation of the fibrinolytic pathway, or leakage from new vessels formed as part of a fibrovascular response

•Cholesterolosis bulbi (synchysis scintillans, cholesterol granuloma)

■Blood which pools within the globe and is not resorbed will eventually be broken down to hemosiderin and cholesterol, stimulating a profound phagocytic response. Frequently, free cholesterol crystals are identifiable within the globe as

acicular cholesterol clefts in tissues or free in the chambers of the globe. Cholesterol crystals are birefringent when viewed with polarized light, but only if the tissues are unprocessed.

Comparative Comments

The occurrence and sequelae of intraocular hemorrhages are little different in humans from those described in animal eyes.

NON-PENETRATING (BLUNT)

OCULAR TRAUMA

Corneal effects

•Abrasion – not often a feature of a pathology submission

•Ruptures in Descemet’s membrane

■May lead to striate keratopathy

■Relatively common clinical presentation in horses and may follow blunt trauma, such as whip or rope injuries to eye, although a history of trauma is often lacking

■Careful evaluation is required to exclude glaucoma, which may cause of ruptures in Descemet’s membrane related to globe stretching (see Ch. 13)

Limbus

Iris

Figure 5.5  Acute cyclodialysis. Photomicrograph of a feline iridocorneal angle within hours of blunt trauma showing hemorrhage in the anterior chamber and iridocorneal angle, as well as tearing away of the iris and ciliary body from the sclera (cyclodialysis).

•Retrocorneal membrane; duplication of Descemet’s membrane, and extension of Descemet’s membrane over the iridocorneal angle:

■These changes can be focal or diffuse and can be associated with corneal edema, causing corneal opacity

■Traumatic changes to the endothelium and Descemet’s membrane are characterized by the following:

–Spindle cell metaplasia of the endothelium

–Deposition of a cell-poor collagen posterior to the cornea even if the endothelium is still present

–Duplication of Descemet’s membrane

Most often the secondary Descemet’s membrane is about the same thickness as the original

Multiple thin membranes are often seen

Extension of Descemet’s membrane and extension of endothelium over the iridocorneal angle is sometimes seen.

Uveal effects (Figs 5.5, 5.6)

•Cyclodialysis, the tearing and separation of the ciliary body and iris base from the sclera creating an opening into the suprachoroidal space (Fig. 5.5)

■Cyclodialysis is relatively more likely to occur in cats than dogs

–This is because of the absence of a robust primary pectinate ligament structure in the feline iridocorneal angle

■Cyclodialysis is relatively even more likely to occur in birds for the following reasons:

–The rigid scleral ossicles of the avian eye magnify shearing forces, which act to strip the soft tissues of the ciliary body away from the sclera

–The attachment apparatus at the iridocorneal angle is delicate

■Cyclodialysis is recognized in the acutely traumatized eye by paying close attention to the loss of integrity of the ciliary cleft and the tissues around the ciliary cleft

–However, years after the traumatic event, ‘angle recession’ may still be observed as evidence of prior trauma to the structures of the irido-corneal angle (Fig. 5.6)

•Angle recession is characterized by the dramatically increased distance between the end of Descemet’s membrane and the anatomic irido-corneal angle. Angle recession has implications in aqueous drainage and is a risk factor in the development of glaucoma (see Ch. 13)

■In some cases, Descemet’s membrane extends over the inner sclera beyond the limbus and, in those cases, angle recession is recognized by the increased distance between the anatomic angle and the limbus.

•Rupture or avulsion of corpora nigra is often seen after blunt trauma in horses.

Lens effects (see also Ch. 10)

Cataract (Fig. 5.7)

Cataract is a common consequence of blunt trauma. Cataract can be prominent within days of trauma (Fig. 5.7).

•Anterior or posterior subcapsular cataract

•Cortical cataract, focal or complete, is often seen and it is good to search for other morphologic indicators of trauma such as retinal detachment or retinal necrosis/atrophy.

Lens capsule rupture (Figs 5.8–5.10)

Lens capsule rupture is a commonly observed consequence of nonpenetrating injury to the globe, in submissions to the pathology laboratory.

Pathologic lens capsule rupture

Pathologic lens capsule rupture is differentiated from artifact by the following findings (in descending order of diagnostic value) (Fig. 5.8):

•Presence of inflammatory cells such as macrophages or neutrophils, or blood vessels, inside the lens capsule

■This feature may be encountered, even if the actual lens capsule defect has not been sampled in the section

•Presence of a cellular reaction at the severed margins of the lens capsule

■This reaction can involve proliferating lens epithelial cells, inflammatory cells, or spindle cells and may be associated with synechiae

•Recoil or scrolling of the severed ends of the lens capsule.

Inflammation

Inflammation (phacoclastic uveitis) is an important consequence of lens capsule rupture (Fig. 5.9).

•Immediately adjacent to the released lens material, there will be a foreign body granulomatous reaction

■Some authors assert that lens proteins released following capsule rupture frequently elicit a robust pyogenic or pyogranulomatous response. However, one must be cautious in distinguishing the effects of sepsis; which would be expected to elicit a pyogenic reaction, and may be introduced by a penetrating injury; from the response induced solely by exposure of the lens proteins, which is typically a relatively ‘bland’ foreign body, granulomatous reaction

•Away from the immediate area of exposed lens protein, a lymphocytic and plasmacytic uveitis develops, that may be associated with synechiae or neovascular membrane formation

•Phacoclastic uveitis often results in secondary glaucoma, due to the formation of synechiae or neovascular membranes.

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Spindle cell metaplasia of lens epithelial cells and migration of lens epithelial cells (Fig. 5.10)

•Spindle cell metaplasia of lens epithelial cells is the first step in the formation of subcapsular cataract in response to trauma, and is associated with posterior capsular opacification after cataract surgery. It is an important feature of the intraocular reaction to lens capsule rupture in domestic animals

•Metaplastic lens epithelial cells express vimentin and smooth muscle actin, and they proliferate and migrate. They also produce collagen and secrete a thick basement membrane reminiscent of lens capsule

■Lens epithelial cells of dogs and cats appear to have a greater tendency to proliferate and migrate in response to injury than those of humans

–Metaplastic lens epithelial cells in damaged human lenses may migrate, but they seldom migrate away from the lens capsule

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–In dogs and cats, metaplastic lens epithelial cells often migrate along the surface topography of the inner aspect of the globe, including:

The outer surface of the lens

The anterior and posterior surfaces of the iris

The surfaces of the detached retina

The inner choroid, within the sub-retinal space

–In cats, metaplastic lens epithelial cells may give rise to post-traumatic sarcoma

This neoplasm is discussed in detail later in this chapter.

Comparative Comments

A significant difference seen in the response to non-penetrating (blunt) ocular trauma in humans is a less aggressive spindle cell metaplasia and migration of lens epithelial cells after the lens capsule is ruptured.