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210

Acute Ocular Trauma

3.To control intraocular inflammation:

Corticosteroids: systemic (e.g., prednisolone, dexamethasone)

NSAIDs: topical (e.g., diclofenac [Voltaren], suprofen [Profenal], flurbiprofen [Ocufen])

Cycloplegic: topical (e.g., atropine, tropicamide)

13.What kinds of protection and support should be used?

Partial tarsorrhaphy decreases the palpebral fissure size and thus helps to protect the cornea

and maintain an adequate tear film. This is especially important in exophthalmic or lagophthalmic animals. A nictitans flap should be used with caution because it interferes with topical medication of the cornea and prevents observation of the wound. If self-trauma is a consideration, a protective collar should be used. Other methods of support include a conjunctival graft or flap, tissue adhesive, and collagen shields.

14. When should a corneal laceration be sutured?

Small corneal lacerations « 3--4 mm) of less than half thickness may be treated as a corneal ulcer with topical antibiotics and mechanical support (see Chapter 7). Larger or deeper lacerations should be closed with 7--D to 9--D suture. If the iris is incarcerated in the wound, it should be amputated or replaced into the anterior chamber before closure. A conjunctival graft placed over the sutured wound may be used for added support if necessary. Before suturing a laceration that has perforated the cornea. the integrity of the lens should be evaluated. Lens capsule perforation necessitates lens removal, preferably at the time of corneal repair. If this is not possible, referral for lens removal should be made as soon as possible to avoid severe uveitis associated with lens rupture (Fig. I).

Figure 1. Lacerated cornea sutured with 6-0 Vicryl. The sutures are not full thickness but rather two-thirds thickness. They will be rejected in approximately 3--4 weeks.

15. When should a conjunctival graft or flap be used?

Conjunctival flaps not only provide mechanical support and surface protection to the cornea but also furnish blood supply. Leukocytes, antibodies, anticollagenases, antiproteases, and nutrients for healing and wound repair are thus brought directly to the injury. Lacerations with loss of deep stromal tissue that prevent adequate primary closure and lacerations in which the viability of the sutured tissue is in question should be supported with a conjunctival flap (Figs. 2, 3, 4, and 5).

16.How can the collapsed anterior chamber be reformed?

In a healthy eye, the aqueous humor reforms at a rate of 2.5 ul/min in dogs and 15 p.l/min in

and cats. If the eye is not severely damaged, the aqueous production rate may be sufficient to reform the anterior chamber within several minutes afterthe eye has been sealed. Usually, however, the anterior chamber is reformed with lactated Ringer's or balanced salt solution. A 25or 27-

Acute Ocular Trauma

211

Figure 2. A free graft of Tenon's tissue taken from the dorsal area of the globe.

Figure 3. A pedicle graft covering a large ulcerative wound.

gauge needle is inserted at the limbus, parallel to the iris plane, and enough fluid is injected to restore the anterior chamber to its normal depth without creating high intraocular pressure (lOP). The lOP should be in the low-normal range (10-15 mmHg).

17.How and when should the entrapped iris be amputated or replaced?

When a prolapsed iris should be excised rather than repositioned is controversial. Recommen-

dations are based on the time it takes for the exposed iris to become sufficiently contaminated to cause infection if replaced. Recommended times range from I to 24 hours. It is safe to assume that smaller prolapses take longer to pose a threat of infection. Magnification is essential if iris amputation or replacement is attempted. Tissue to be excised should be grasped gently with fine forceps and cut flush with the cornea. A dilute solution of epinephrine (1: 10,000 in lactated Ringer's or balanced salt solution) aids hemostasis. To replace the iris, it is carefully freed from fibrinous corneal attachments with an iris spatula or irrigating cannula or dissected with viscoelastic material. After the iris is freed from the cornea, the anterior chamber is reformed with viscoelastic material (1% sodium hyaluronate or 2% hydroxypropylmethylcellulose). Care must be taken to avoid trauma to the corneal endothelium, iris, and lens. Just before placing the last suture, the viscoelastic material can be gently flushed from the anterior chamber or left in place. This procedure is difficult for inexperienced practitioners and preferably should be performed by a trained ophthalmologist.

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Acute Ocular Trauma

Figure 4. A healing corneal perforation covered with a conjunctival flap.

Figure 5. Corneal transplant into a degenerative cornea.

18.What type of suture pattern should be used in the cornea?

Simple interrupted sutures are the easiest to place correctly. If you experience a lot of ten-

sion, horizontal mattress sutures may be placed first, followed by interrupted sutures. Correct suture placement is important to avoid internal wound gape (too shallow), wound override (sutures of unequal depth and length on each side ofthe wound), and intraocular contamination (too deep). Sutures should be approximately 75-90% of corneal depth, 1.5-2 mm in length, of equal depth on each side of the wound, and 1-1.5 mm apart.

Acute Ocular Trauma

213

19.What are the common types of foreign body-related injuries?

Corneal and conjunctival foreign bodies from plant material and sand are frequently en-

countered in dogs, especially those used for hunting or field trials. Patients often present with an acutely red and painful eye. Linear abrasions of the cornea are an indication for eversion of the lid to examine for foreign material lodged in the upper palpebral conjunctiva. Superficial corneal foreign bodies may present with variable amounts of discomfort and usually can be detected with simple magnification (e.g., loupe or diagnostic otoscope head). Deeper corneal foreign bodies may have the appearance of a puncture wound and are harder to detect without the use of a slit lamp. Foreign body penetration into deeper ocular structures is often associated with Bls-pellet, bird shot, and glass. Involvement of orbital structures, iris, lens, retina, or vitreous humor is possible, and the prognosis is affected accordingly.

20.How should foreign bodies involving the ocular surface be treated?

Superficial foreign bodies can be removed with topical anesthesia in many cases, but some

animals may require sedation or general anesthesia. A spatula, corneal forceps, or hypodermic needle (25or 27-gauge) is used to elevate the foreign body from the ocular surface. If loosened foreign material remains on the eye, it can be picked up with a moistened cotton-tipped swab. Hypodermic needles should be held at a shallow angle to the cornea to avoid perforation. After removal, treat topically with a broad-spectrum antibiotic drop or ointment 3 times/day for 5-7 days. A single application of I % atropine sulfate is given if the pupil is miotic.

21. What should be done to manage an intraocular foreign body?

Management of intraocular foreign bodies depends on how long the foreign body has been in the eye, its location, and what it is made of. The potential for damage during removal should be compared with the potential for damage if it is left in the eye. Organic material leads to sepsis if not removed soon after penetration. Some metals and glass, however, may cause little reaction if left alone and eventually become anchored by fibrin or scar tissue. If the foreign body is recent and located in the anterior chamber, it should be removed through a limbal incision. Surgery to remove a foreign body from the posterior segment often results in complications leading to a blind eye and carries a poor prognosis. Broad-spectrum topical and systemic antibiotics should be used to control infection. Topical corticosteroids, cycloplegics, and oral corticosteroids (anti-inflam- matory dosages) or NSAIDs may be used to treat uveitis. Corticosteroids should be used with caution because of the potential for sepsis.

TYPE OF FOREIGN BODY

POTENTIAL FOR DAMAGE

REMOVAL NECESSARY?

 

 

 

Organic

Reactive; sepsis possible

Early removal essential

Nonferrous metal, glass,

Minimal; becomes walled off by fibrin

Removal not necessary

or plastic

and fibrous tissue

 

Ferrous metal

Highly reactive; toxic to intraocular tissue

Early removal recommended

 

 

 

BIBLIOGRAPHY

I. Featherstone HJ, Sansom J, Heinrich CL: The use of porcine small intestinal submucosa in 10 cases of feline comeal disease. Vet Ophthalmol 4: 147-153,2001.

2.Morgan RV: Ocular emergencies. Comp Cont Educ Vet 4:37-45,1982.

3.Roberts SR: Assessment and management of the ophthalmic emergency in cats and dogs. In The Compendium Collection: Ophthalmology in Small Animal Practice. Trenton, NJ, Veterinary Learning Systems, 1996, pp 252-267.

4.Wilkie DA, Whittaker C: Surgery of the cornea. Vet Clin North Am Small Anim Pract 27:1067-1107, 1997.

35. OCULAR HEMORRHAGE

Cynthia C. Powell, D.V.M., M.S.

1.Name the common causes of ocular hemorrhage.

Trauma, coagulopathies, thrombocytopenia, vasculitis, and neoplasia are potential causes for

ocular hemorrhage. Trauma-related hemorrhage is probably the most common cause of ocular hemorrhage presented as an emergency.

2.What forms of ocular hemorrhage have emergency significance?

All forms of ocular hemorrhage have the potential to be associated with life-threatening sys-

temic disease. If the cause of hemorrhage is not known, patients should be evaluated for systemic diseases, especially those causing clotting abnormalities and vasculitis. Although the ocular hemorrhage may not require emergency treatment, the disease associated with hemorrhage might. Intraocular hemorrhage alone or related to other diseases (e.g., uveitis or hypertension) can quickly become sight-threatening, and prompt medical management is important. Complications of intraocular hemorrhage that cause vision loss include glaucoma, cataract, retinal detachment, retinal degeneration, and phthisis bulbi.

3.Why is blunt trauma so potentially damaging to intraocular tissues?

Tremendous tissue distortion results from blunt ocular trauma. The four phases of blunt in-

jury that induce tissue damage are: I. Compression

2.Overshooting

3.Decompression

4.Oscillation

The initial anteroposterior globe compression at the cornea causes equatorial expansion and shortening of the globe along the anteroposterior axis so that the cornea may touch the iris and lens. As the momentary force of deformation is removed, the anteroposterior globe diameter increases, whereas the equatorial diameter decreases. The tissues overshoot so that the anteroposterior diameter becomes momentarily greater than normal and the equatorial diameter less than normal. The globe subsequently oscillates between these maximums and minimums with decreasing amplitude for a brief time. This extreme stretching of the ocular tissues causes injury to the choroid, lens, optic nerve, retina, and vitreous gel (Fig. 1).

Figure 1. Five days after blunt trauma to the eye of a German shepherd police dog. Clotting and resorption underway, but mild uveitis needs to be treated.

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Ocular Hemorrhage

215

4. Describe the implications of hyphema.

Hyphema is the presence of blood within the anterior chamber. Blunt or sharp trauma to the globe is the most common cause. However, hyphema may be due to thrombocytopenia, coagulopathies, iritis, intraocular neoplasia, congenital ocular anomalies, chronic glaucoma, and hypertension. Initial examination should determine whether the globe has been penetrated. Hyphema often causes little damage to the eye itself but may result in glaucoma, anterior uveitis, iris adhesions secondary to clot contraction, and capsular cataract formation. Anterior chamber bleeding may not clot completely because the iris produces fibrinolysin. Maximal clot integrity requires 4-7 days. Hyphema should be treated as a clinical sign, and its cause should be determined as soon as possible (Figs. 2 and 3).

Figure 2. Unclotted hyphema fills the anterior chamber in this dog with a clotting factor deficiency.

Figure 3. Recurring hyphema from constant barking following this dog's cataract extraction.

S.What clinical parameters should be evaluated in cases of hyphema?

A complete eye examination should be performed, and the entire animal must be evaluated

to assess concomitant injury or disease. In particular, globe rupture should be ruled out. Vision should be estimated based on the degree of menace when bright light is suddenly directed into the eye. Assuming that the examination light penetrates to the posterior part of the globe, the consensual pupillary light reflex indicates whether the retina and optic nerve are functional. If a globe rupture is not present, intraocular pressure should be measured. Finally, the hyphema should be graded by the anterior chamber volume occupied by the blood. The grading system is helpful prognostically because it indicates the severity of hemorrhage and the degree of intraocular tis-

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Ocular Hemorrhage

sue damage in trauma cases. Hyphema of grade I severity generally clears in less than I week. Grades 2 and 3 take several weeks or longer to resolve. Grade 4 hyphema often is associated with globe atrophy (phthisis bulbi).

GRADE

AMOUNT OF BLOOD IN ANTERIOR CHAMBER

 

 

I

Less than one-third

2

One-third to one-half

3

One-half to nearly total

4

Total

 

 

6. How should hyphema be treated?

If a primary cause other than trauma is determined, initial treatment must address the underlying problem. All animals with hyphema should be kept quiet and subdued, possibly by use of sedation. Many medical treatments have been proposed, but no studies have evaluated their effectiveness. Interest in some treatments continues, whereas others remain controversial. Basically the treatments can be separated into the following categories:

Cycloplegics Antifibrinolytic agents Miotics

Fibrinolytic agents Adrenergic agonists Surgical intervention Corticosteroids

7. What cycloplegics may be useful and why?

Cycloplegics are parasympatholytic drugs that cause paralysis of ciliary body and iris sphincter smooth muscles. Thus, the ocular accommodation by the ciliary body is prevented, and the pupil dilates. Prevention of smooth muscle spasm may enhance patient comfort and facilitate fundus examination. Topical atropine, I % solution once or twice daily, is sufficient. Once mydriasis (pupil dilation) occurs, the frequency of treatment may be reduced and the drug used to effect.

8.What miotics are useful and why?

Parasympathomimetic agents are miotics that induce spasm of the ciliary body and iris

sphincter smooth muscles. In theory, use of a miotic such as pilocarpine I % should open the filtration angle. However, miotics also tend to increase intraocular inflammation, so when pupil size is decreased, the chance of pupil obstruction by fibrin is increased. No scientific evidence suggests that they enhance the clearance of blood from the anterior chamber. Inthe author's opinion, miotics should not be used to treat hyphema.

9. What adrenergic agonists have been advocated and why?

Sympathomimetic agents such as topical epinephrine I % and phenylephrine 2.5% have been advocated to decrease anterior chamber hemorrhage by way of vasoconstriction. Such treatment may be helpful with evidence of ongoing hemorrhage but usually provides little effect. It is rarely considered an option in the treatment of hyphema in humans.

10.Which corticosteroids are best to use?

Invariably, traumatic hyphema is associated with anterior uveitis ranging from mild to se-

vere. Thus, topical steroids such as prednisolone acetate, prednisolone sodium phosphate, and dexamethasone ophthalmic drops are used 4 times/day. Their efficacy in improving outcome is unproved. Systemic steroids are more controversial but commonly used. Certainly any concurrent anterior uveitis will be lessened, and theoretical evidence suggests that steroids may enhance clot stabilization. Controlled studies, however, are lacking.

Ocular Hemorrhage

217

11.When is antifibrinolytic treatment indicated?

Agents such as aminocaproic acid have been proposed as a means of reducing rebleeding in

cases of traumatic hyphema. Rebleeding may result from premature clot lysis mediated by the fibrinolytic system. The theoretical rationale is that the reduced rate of clot lysis allows more time for the damaged blood vessels to heal. In humans, the current recommended dosage is 50 mg/kg orally every 4 hours for 5 days. Antifibrinolytic drugs are contraindicated in cases of intravascular clotting disorders, pregnancy, and cardiac, hepatic, or renal disease.

12.What is the purpose of fibrinolytic treatment?

Hyphema typically progresses from free blood to varying degrees of blood clot formation 1-7

days after injury. Once fibrin formation has occurred, clot lysis may be induced with fibrinolytic agents such as tissue plasminogen activator (tPA). Clinically, tPA is used by injecting 25 J..Lg in a 100 J..LI volume into the anterior chamber. Clot lysis typically occurs within 30-60 minutes of injection. As clot lysis occurs, red blood cell clearance is facilitated. Topical application of tPA is also promising.

13. What surgical interventions are used for hyphema?

If hyphema persists beyond 5-10 days or intraocular pressure increases, surgical removal may be necessary. An anterior chamber wash-out is the simplest and safest surgical procedure to clear free blood from the anterior chamber. Removal of the clotted blood is not required, only evacuation of loose blood cells and debris. A 3D-gauge needle or cannula is used to irrigate a balanced salt solution into the anterior chamber, and a second 2-mm incision is made to allow fluid egress. Removal of the entire clot is possible but may result in lens, iris, and corneal endothelial trauma. Other surgical procedures are available but should be performed by someone experienced and equipped for intraocular surgery.

14.What drugs may be contraindicated in cases ofhyphema?

Based on the antiplatelet effect ofthe cyclooxygenase inhibitors, nonsteroidal anti-inflammatory

drugs (NSAIDs) such as aspirin, flunixin megulamine, and topical ocular NSAIDs should be avoided. Although cycloplegics such as atropine are advocated for medical management of hyphema, a small percentage of patients develop glaucoma associated with use of atropine.

15. How can vitreous hemorrhage be recognized?

Disorders of the posterior segment (ocular tissues posterior to the lens) are more difficult to detect and characterize because direct examination must be performed through the pupil, or indirect imaging techniques such as ultrasound must be used. Direct examination is impaired with disease of the anterior segment and cornea. Dilation of the pupil, if possible, greatly facilitates evaluation of the posterior globe. If vitreous hemorrhage is near the lens, it may be visible with a penlight or transilluminator. Otherwise, an indirect ophthalmoscopic examination is the best way to evaluate the vitreous cavity. Vitreous hemorrhage appears as strands, sheets, or diffuse areas of blood accumulation. If the hemorrhage is preretinal (between the vitreous and retina), it may resemble a "boat keel" because of gravitational settling of the erythrocytes (Figs. 4 and 5).

16.Does vitreous hemorrhage have special implications?

The most common cause of vitreous hemorrhage is trauma-induced rupture of uveal or reti-

nal blood vessels. The animal should be evaluated closely for rupture of the cornea or sclera. Causes of vitreous hemorrhage may be grouped as follows (Fig. 6):

Tearing of a blood vessel in a congenital or acquired retinal detachment

Retention of the fetal hyaloid artery system

Widespread ocular disease (inflammation of the choroid and retina, optic neuritis, chronic glaucoma, and intraocular neoplasia)

Systemic disease (hypertension, coagulopathies, and thrombocytopenia)

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Ocular Hemorrhage

Figure 4. Vitreal hemorrhage from retinal vessels in the this domestic shorthair cat with a monoclonal gammopathy

Figure 5. Preretinal hemorrhage and focal retinal detachment in a dog following an automobile accident.

17. How is vitreous hemorrhage treated?

Other than dealing with the underlying ocular or systemic disorder associated with vitreous hemorrhage, no simple treatment is available. If hemorrhage occurs into the solid vitreous gel, clotting is rapidly activated because the gel matrix serves as a collagen framework for platelet adhesion. Infiltration of neutrophils and macrophages hasten clot removal but cause further vitreous gel breakdown and inflammation. Preretinal hemorrhage clots poorly. Concurrent use of topical and systemic corticosteroids is appropriate and may ameliorate the inflammatory reaction. If an-

Ocular Hemorrhage

219

Figure 6. Retinal hemorrhage in a dog with thrombocytopenia.

terior uveitis is present, the use of topical atropine as a cycloplegic is appropriate. Depending on the hemorrhage area and density, resolution may take many months.

18.What does retinal hemorrhage look like?

The appearance of retinal hemorrhage depends on the retinal layer involved. Because of the

relatively loose attachment between the retina and vitreous gel and the retina and retinal pigment epithelium, hemorrhage of large size may develop in either space. Preretinal hemorrhage (between the retina and vitreous) frequently has a boat keel shape because of gravitational settling of the erythrocytes. Intraretinal hemorrhages primarily are aligned vertically; their end on appearance is round, and the hemorrhages are small. Nerve fiber layer hemorrhages are typically feathered or striated and flat, because the hemorrhage follows the path of the nerve fibers. The retinal depth of a focal hemorrhage may be estimated based on which structures are positioned beneath and thus obscured or positioned above and thus visible (Fig. 7).

19.Explain the significance of retinal hemorrhage.

Retinal hemorrhage indicates disruption or inflammation of the vasculature. If there is no

clear history or physical evidence of trauma, systemic disorders must be considered. Infectious diseases capable of causing vasculitis or retinitis must be considered. Disorders that may be immediately life-threatening are coagulopathies, severe anemias, and blood dyscrasias. Chronic disorders such as hypertension, hyperviscosity syndromes, and neoplasia may cause retinal hemorrhage. Although not immediately life-threatening, such conditions may cause ocular signs that can be confused with a more acute process. The clinician should consider performing a complete blood count, serum chemistry profile, and clotting profile if retinal hemorrhage is noted. A portion of the serum should be saved for potential serologic testing (see Figures 2 and 3).