Diagnostic Ophthalmology

History and clinical signs

A 9-year-old, male Quarter horse was examined at the ophthalmology service at the Western College of Veterinary Medicine for evaluation of a suspected traumatic injury of the right eye. He had been found several hours earlier with a laceration of the right forelimb and a painful right eye. The menace response was present in the left eye but absent in the right eye. Palpebral and occulocephalic reflexes were present bilaterally. The direct and consensual pupillary light reflexes were present on the left side, but could not be evaluated in the right due to opacity of the anterior chamber. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 20 and 15 mm/min in the right and left eye, respectively. The intraocular pressures were estimated with a rebound tonometer (Tonvet; Tiolat, Helsinki, Finland) and were 12 and 21 mmHg in the right and left eye, respectively. Fluorescein staining (Fluorets; Bausch & Lomb Canada, Markham, Ontario) was positive in the central right cornea surrounding a 4-mm corneal defect associated with protruding pigmented tissue. On direct examination there was moderate blepharospasm, conjunctival hyperemia, and mucopurulent ocular discharge in the right eye. The cornea surrounding the defect was moderately and diffusely edematous and the anterior chamber appeared opaque and yellow. Biomicroscopic examination (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) revealed the right pupil was miotic and anterior synechia was present. Following application of 0.5% tropicamide (Mydriacyl; Alcon Canada, Mississauga, Ontario) indirect ophthalmoscopic (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) examination was completed on the left eye and was normal. The fundus could not be examined in the right eye due to the anterior segment abnormalities. A photograph of the right eye at presentation is provided for your assessment (Figure 1).

Figure 1.

Photograph of the right eye of a 9-year-old Quarter horse.

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Discussion

Our clinical diagnosis was a corneal perforation with iris prolapse and anterior uveitis in the right eye. Corneal perforations may occur due to penetrating or blunt trauma or from progression of a deep or melting corneal ulcer (1,2). In this case a penetrating injury was considered to be most likely based on the history and concurrent suggestive physical examination findings.

The clinical manifestations of a corneal perforation include blepharospasm, serous or purulent ocular discharge, corneal defect, corneal edema, a shallow anterior chamber, and iris prolapse. Iris prolapse appears as a protrusion from the corneal surface which may be brown (due to pigmentation of the iris) or tan/pink (due to fibrin accumulation on the iris surface). Aqueous humor may leak from the corneal defect, or more commonly, will be sealed by fibrin and iris tissue.

The diagnosis of a corneal perforation is made based on the clinical signs, and fluorescein staining. A Seidel test for aqueous leakage can be performed by placing concentrated fluorescein dye on the eye and watching for dilute riverlets of fluorescein flowing from the perforation. However, this test may be negative if the corneal wound is sealed by iris tissue and fibrin, and is not necessary if there is presence of uveal tissue within the corneal defect as this confirms perforation. It is important to evaluate the integrity of the lens in cases of traumatic ocular perforation. This requires dilation of the pupil and careful examination of the lens surface. When the lens is not clearly visible due to anterior segment opacities, an ocular ultrasound can aid in this evaluation. Penetration of the lens will cause extrusion of lens material, an irregular lens contour, and rapid cataract development. Fibrin in the anterior chamber often obscures the lens and it may be difficult to differentiate from extruded lens material. Therefore, examination of the lens at the time of surgery may be required in some cases. Further diagnostic testing in the case of corneal perforation should include aerobic and anaerobic bacterial and fungal culture and sensitivity and cytology. These samples are taken from the corneal wound carefully to avoid exacerbating wound leakage, and may be completed at the time of surgery.

Ocular trauma and corneal injuries are usually accompanied by anterior uveitis. Manifestations of anterior uveitis include miosis, ciliary spasm causing pain and photophobia, lacrimation, aqueous flare, and a lowered intraocular pressure. Fibrin may appear in the anterior chamber as a yellow Web-like mass. Leakage of white and red blood cells may occur from uveal blood vessels into the anterior chamber; resulting in hypopyon and hyphema, respectively.

Treatment of a corneal perforation requires a combination of medical and surgical therapy (1–3). Prompt referral to an ophthalmologist for surgery is essential. However, appropriate medical therapy should be initiated prior to referral. Medical treatment should include broad-spectrum topical antibiotic drops administered at least four times daily. Ointments are contraindicated in cases of corneal perforation as they exacerbate uveitis. Systemic antibiotics are indicated as the full-thickness defect in the cornea exposes the anterior chamber to the environment and potential pathogens. Systemic non-steroidal anti-inflammatory drugs (NSAIDs) should be administered to reduce pain and control secondary uveitis. Topical NSAIDs applied up to 4 times daily are also recommended to reduce anterior uveitis. Topically applied anticholinergics (1% to 2% atropine) are essential for 3 reasons: i) they reduce proteinaceous and cellular leakage from inflamed uveal blood vessels, ii) they dilate the pupil which protects the eye from development of posterior synechia, and iii) they relax ciliary muscle spasm, which is a major factor in discomfort associated with uveitis (2). Topical anticholinergic medications may be applied up to 4 times daily. Surgical therapy may include primary closure of the corneal wound, and/or corneal or conjunctival grafting procedures. Traumatic injuries with lens capsule disruption warrant phacoemulsification to remove the damaged lens and prevent phacoclastic uveitis (3).

Treatment of this horse was initiated with sulfamethoxazole and trimethoprim 800 and 160 mg (Apo-Sulfatrim-DS; Apotex, Toronto, Ontario), 15 tabs, PO, q12h in addition to a topical fluoroquinolone antibiotic (ofloxacin 0.3%; Pharmascience, Montreal, Quebec), q6h. A topical non-steroidal anti-inflammatory drug (NSAID), diclofenac sodium 0.1% (Voltaren; Novartis, Mississauga, Ontario), q6h and a systemic NSAID, flunixin meglumine (Flunazin; Vétoquinol Canada, Lavaltrie, Quebec), 1.1 mg/kg body weight (BW), q12h, IV were initiated to reduce intraocular inflammation. Topical atropine sulphate 1% (Isopto-atropine; Alcon Canada, Mississauga, Ontario) was administered q6h. Ocular mediations were delivered through a subpalpebral lavage system (Mila International, Florence, Kentucky, USA). Tetanus antitoxin (Tetanus Toxoid; Fort Dodge Animal Health, Fort Dodge, Iowa, USA) was administered IM and the limb laceration was cleaned and bandaged.

The eye was treated medically for 2 days to reduce inflammation and potential infection prior to surgery. The opacity within the anterior chamber began to clear; however, a mass of opaque material, most consistent with a fibrin clot obscured the lens. Ocular ultrasound showed no evidence of a lens capsule rupture. Because the retina could not be visualized by ophthalmoscopy, electroretinography (ERG) was used to investigate retinal function, which was found to be within the reference range. During surgery, the entrapped iris was amputated from the corneal wound and the fibrin was removed from the anterior chamber. The lens was carefully examined and appeared to be normal. The corneal laceration was sutured primarily and then covered with a conjunctival pedicle graft to ensure a proper seal and support for healing of the wound. Bacterial and fungal cultures were obtained from the corneal wound at the time of surgery and these were negative for microbes. Topical and systemic medical therapy was continued for the next 3 wk. Wound care for the limb laceration was continued daily until it had healed.

At re-evaluation 3 wk later, the eye was comfortable and sighted. The conjunctival graft was healing and incorporated into the cornea. There was no evidence of uveitis, the lens was clear, and ophthalmoscopic examination was normal. The subpalpebral lavage system was removed and all ocular medications were discontinued.

The prognosis for a corneal perforation is guarded and depends on the cause, size, and location of the lesion, concurrent intraocular injury, and duration between injury and appropriate therapy (1–4). Perforating corneal wounds induced by sharp objects have a better prognosis than wounds produced by blunt trauma (4). A perforation secondary to penetrating or blunt trauma may have concurrent lens rupture which can lead to severe blinding inflammation (phacoclastic uveitis) if lens removal is not completed promptly (3). Blunt trauma may also result in severe uveal injury and hyphema. Hyphema that involves more than 50% of the anterior chamber is associated with a poor prognosis (1,4). Corneal lacerations longer than 15 mm and those that extend to or beyond the limbus are also associated with a poor visual prognosis (1). Full-thickness corneal wounds expose the interior of the globe to potential pathogens and may result in bacterial or fungal endophthalmitis which is devastating to the eye. In general, the longer the duration between injury and initiation of therapy the more difficult it may be to achieve therapeutic success. Therefore, prompt referral to a veterinary ophthalmologist is recommended for assessment and therapy in all horses with perforating corneal ulceration.