Neutered female Pekingese dog (Canis familiaris), 9.5-years-oldThe dog developed a right-sided corneal ulcer five months previously. The eye became cloudy five days
ago, and severe periocular swelling and pain developed two days ago. The right globe was enucleated, fixed and submitted for microscopic examination.
A perforation of the cornea is present, with debris in the defect connecting the outer
aspects of the cornea and the chambers of the eye.Â Iridal tissue is herniated into the defect, protruding through an
often fragmented Descemets membrane, but inflammation and hemorrhage affect both the anterior and posterior
chambers and the uvea, and the inflammation extends around the periphery of the eye to involve the extra-ocular
muscle.Â Lens liquefaction (cataractous change) is present, and neutrophils occur within the abnormal lens matrix
and beneath the detaching capsule.Â Lenticular fibrovascular membranes are not observed.Â The cornea peripheral to
the perforation contains embedded hemorrhage and full-thickness edema.Â The filtration angle is minimally visible
but contains hemorrhage and debris as well.Â Widespread corneal ulceration is associated with a superficial infiltrate
of neutrophils, and remaining corneal epithelium is undergoing squamous metaplasia and melanization.Â Well
defined clusters of cornified material are suspended in inflammation at the surface of the cornea, along with
microabscesses.Â Central and superficial corneal vascularization is apparent, along with localized melanin.Â Colonies
of coccoid bacteria are most easily seen in fibrin deposits in the anterior chamber but occur throughout the eye.Â The
iris is adhered to the posterior aspect of the cornea, and a long stretch of fibrovascular membrane extends down part
of its anterior surface.Â Neutrophils infiltrate the iris stroma and the posterior epithelial layer is incomplete.Â Much of
the ciliary apparatus and remaining retinal and choroidal structures are obliterated by inflammation.Â Neutrophils
diffusely infiltrate the sclera and separate the episcleral fascia.Â Evidence of neovascularization and early fibroblast
proliferation are seen in the latter.
Eye: Chronic suppurative panophthalmitis with corneal perforation,
staphyloma, lens liquefaction and bacteria
The microscopic lesions in this eye are exemplary of traumatic perforation with
continued inflammation.Â In the absence of infection, the minimal lesions associated with canine lens trauma are
characterized by breaks in the anterior lens capsule and uveitis of the anterior segment.Â In one study, 36/40 cases of
traumatic eye injury resulted in extrusion of lens material into the anterior chamber.(5) Of these cases, 12/14 were
related to direct lens trauma.Â The result was endophthalmitis with or without glaucoma.
The presence of corneal perforation and associated lens inflammation point to the likelihood of a penetrating foreign body.Â Although the history is vague in this case, and while younger animals are more often affected, a cat claw wound was deemed most likely.Â These wounds cause (6) corneal and lens capsule perforation with ensuing phacoclastic uveitis.Â Phthisis or glaucoma resulted in 50% of the cases.Â Grass awns and porcupine quills are also frequently cited as sources of ocular or orbital foreign bodies in dogs.(2-4,6)
In 20 cases of lens rupture that excluded animals with intractable intraocular infection, lens-induced uveitis was characterized by capsular rupture, cataract, lymphoplasmacytic iridocyclitis, and perilenticular inflammation.(8) Moreover, capsule defects were in line with breaks in the Descemets membrane similar to the one in this case. Even in the absence of infection, the affected lens will become invested with neutrophils, lens epithelium and/or metaplastic fibroblasts.Â In 13/20 cases in this study, the vitreous and posterior uvea were also inflamed.Â Four dogs with recent perforations had fibrinopurulent inflammation surrounding the lens.
Phacoclastic uveitis is distinguished from phacolytic uveitis in that the latter is a result of reaction to protein leakage from a cataractous lens and without other associated causes of uveal inflammation.(7) In both conditions, normal low dose tolerance to lens proteins is thought to be overwhelmed by rupture of the lens and release of high dose antigen.Â When lens lysis occurs, lens membrane proteins are also released, and this results in a more powerful presentation of antigens to the systemic immune system that is likely to overwhelm tolerance.
This case demonstrates the potentially catastrophic results of intraocular inflammation, which had at the time of enucleation involved every structure of the eye.Â Panophthalmitis, defined as inflammation of all the tunics of the eye, is much less common than endophthalmitis, defined as inflammation of the uvea, retina, and ocular cavities. The acute changes near the site of corneal rupture contrast with those inside the eye.Â These are of longer duration based on the presence of an anterior fibrovascular membrane, corneal vascularity, and the neovascularization at the back of the eye.Â Wilcock points out that many cases of traumatic lens laceration are detected by a lack of response to treatment, (8) and in his cases, the interval between injury and uveitis onset (when known) was 4-20 days.
Eye: Panophthalmitis, fibrinosuppurative, diffuse, severe, with corneal rupture, iridal prolapse,
phacoclasia, and intralesional bacteria.
This case of ocular trauma had lesions involving almost every part of the eye.Â The ocular
anatomys relationship to eye injury was discussed during the conference, and this review will briefly discuss
anatomy of the cornea and its response to superficial ulceration.
The cornea is avascular and covered by nonkeratinized, nonpigmented stratified squamous epithelium.Â This thin, non-pigmented epithelium allows for clarity of vision.(9) The stroma also maintains a state of relative dehydration aided by numerous epithelial and endothelial tight junctions in combination with a Na-K-dependent ATP-ase pump in the cell membrane of the corneal endothelium.(9) Bowmans layer is just below the squamous epithelium. Bowmans layer was discussed during the conference because it is a distinctive membrane in humans, but is not distinct in mammals.Â Underlying Bowmans layer, and compromising 90% of the thickness of the cornea, is the corneal stroma and layers of collagen interspersed with fibroblasts.Â Descemets membrane, distinct in domestic animals, lies between the corneal stroma and the corneal endothelium.(1)
The cornea is a highly specialized area of the body; therefore, it is protected from damage by numerous mechanisms including an antibacterial tear film and a physically movable barrier known as the eyelid.Â After damage, the cornea often quickly takes on water.Â Water enters from the eye's anterior aspect via lacrimal secretions and the posterior aspect via fluid from the anterior chamber.Â Even more water enters the cornea if the electrolyte pump is compromised because of corneal damage.
If injury to the cornea is superficial and only involves the epithelium, this defect heals by epithelial cells sliding over the defect, followed by mitosis after approximately 24 hours.(9) Chronic ulcers often require additional resources to heal.Â These resources are drawn from the epithelium of the corneoscleral junction where permanent populations of cells available for replication reside.Â Cells recruited from the corneoscleral junction tend to retain phenotypic characteristics of conjunctiva including pigmentation and rete ridges.Â This is an easy way to recognize a chronic ulcer.Â This is referred to as conjunctival (or cutaneous) metaplasia.
If the underlying stroma of the cornea is damaged in addition to the epithelium, rebuilding of the damaged stroma may be required before epithelial repair can occur.Â Within a few hours of the initial insult, neutrophils enter the wound and begin to kill bacteria, degrade damaged collagen, and stimulate fibroplasia and vascularization.Â Stromal cells at the edge of the defect and fibroblasts recruited from the limbus produce new stroma and cover the defect.(9) New blood vessels begin to form approximately 4 days after an extensive injury, and this ingrowth is from the limbus and progresses at a rate of about 1 mm a day.Â This lag time is important because superficial wounds can heal in less than 4 days without the help of vascularization.Â If vascularization occurs during healing, visual impairment from stromal fibroplasia is often the result.(9)
1.Â Bacha WJ, Wood LM: Eye.Â In: Color Atlas of Veterinary Histology, ed.Â Bacha WJ, Wood LM, pp.Â 231-233.
Williams & Wilkens, Media, PA, 1990
2.Â Brennan KE, Ihrke PJ: Grass awn migration in dogs and cats: A retrospective study of 182 cases.Â J Amer Vet Med Assoc 182:1201-1204, 1983
3.Â Bussanich MN, Rootman J: Intraocular foreign body in a dog.Â Can Vet J 22:207-210, 1981
4.Â Grahn BH, Szentimrey D, Pharr JW, Farrow CS, Fowler D: Ocular and orbital porcupine quills in the dogs: A review and case series.Â Can Vet J 36:488-893, 1995
5.Â Pfleghaar S, Sch+ï¿½-ï¿½ffer EH: Die linseninduzierte Uveitis (Endophthalmitis phakoanaphylactica) beim Haustier. Tierd Prax 20:7-18, 1992
6.Â Spiess BM, R+ï¿½-+hli MB, Bollinger J.Â Augenverletzungen durch Katzenkrallen beim Hund.Â Schweiz Arch Tierheilk 138:429-433, 1996
7.Â Van der Woerdt A, Nasisse MP, Davidson MG: Lens-induced uveitis in dogs: 151 cases (1985-1990).Â J Amer Vet Med Assoc 201:923-926, 1992
8.Â Wilcock BP, Peiffer RL, Jr: The pathology of lens-induced uveitis.Â Vet Pathol 24:549-553, 1987
9.Â Wilcock BP: Eye and ear.Â In: Jubb, Kennedy and Palmers Pathology of Domestic Animals, ed.Â Maxie MG, 5th ed., vol 1, pp.481-485.Â Elsevier Limited, Philadelphia, PA, 2007