- As a result of its large size and relative lack of orbital protection, any form of cranial trauma frequently involves the eye and its associated structures.
- Common clinical findings in bird of prey with cranial trauma include eyelid or nictitating membrane laceration, retinal detachment, and hyphema, particularly massive hemorrhage into the vitreous body.
- The sequelae of lid defects are minimal if the nictitating membrane is functioning normally.
The large size of the raptor eye and its relative lack of orbital protection superiorly and laterally means any form of head trauma frequently involves the eye and its associated structures (Fig 1). In one report, ocular injuries were most commonly caused by vehicular collision, gunshot and leghold traps. The most common clinical finding in birds of prey presented for medical attention is hyphema. Trauma may also lead to conjunctivitis, eyelid lacerations, ciliary body detachment, hemorrhage of the ciliary processes, and chronic lesions such as non-healing corneal erosions or cataracts. Although anterior segment injury is more obvious, trauma can also cause more severe, often overlooked lesions in the posterior segment of the eye such as retinal detachment or extensive hemorrhage originating from the pecten.
Lesions of the eyelids
Disorders of the eyelid are relatively common in birds of prey. Avipoxvirus may cause eyelid lesions, but the chief problems seen are lid contusions and lacerations. When repairing an acute laceration surgically, gently debride and repair the defect using 5-0 to 7-0 absorbable suture material. Place split-thickness sutures to prevent corneal abrasion. Lid defects can result from improperly healed lacerations although sequelae will be minimal if the nictitans functions normally.
Lesions of the nictitating membrane
The primary cause of nictitating membrane lesions such as laceration is trauma. Apply topical broad-spectrum antibiotics for small or partial thickness lacerations, and carefully repair full thickness lacerations or lacerations involving the leading edge. Use 6-0 to 10-0 suture in a single layer closure and avoid corneal exposure to suture or knots.
Although the incidence of botulism in raptors is rare, clinical disease has been documented. Botulinum toxin inhibits the release of acetylcholine leading to paralysis of the pupillary sphincter muscle and the muscles that move the nictitans, the quadratus and pyramidalis. This in turn leads to delayed pupillary light response, mydriasis, and prolapse of the nictitans. Conjunctivitis is also observed in rare cases.
Lesions of the conjunctiva
Although conjunctival lesions are relatively uncommon in birds of prey, trauma is the most important cause of conjunctivitis. There are also numerous infectious causes of conjunctivitis that have been reported in birds, many of which are associated with systemic disease.
- Bacteria are the chief cause of infectious conjunctivitis. Conjunctival flora in raptors consists predominately of gram-positive microbes such as Staphylococcus and Corynebacterium, although gram-negative bacteria may make up 11% of normal flora. Reported causes of conjunctivitis include Pseudomonas, E. coli, Proteus, Staphylococcus, Streptococcus, Salmonella typhimurium, Chlamydophila psittaci, Mycoplasma, Micrococcus, Bordetella avium, Moraxella, Erysipleothrix rhusiopathiae, and Listeria monocytogenes. Bacterial conjunctivitis is frequently associated with upper respiratory tract infection (Fig. 2).
- Avipoxvirus is the most important viral infection of bird eyes causing unilateral or bilateral blepharitis, conjunctivitis, corneal edema, and corneal ulceration for 2-6 weeks. Sequelae to poxvirus may include periocular depigmentation, lid margin deformity, loss of filoplumes from the lid margin, and subepithelial corneal crystal formation. More serious sequelae may include epiphora after damage to the lacrimal system, corneal vascularization, ulcerating keratitis, panophthalmitis after perforating corneal ulcer, and symblepharon or a fibrous band that connects bulbar and eyelid conjunctiva.
- Fungal and parasitic conjunctivitis is quite rare in raptors. Candida albicans in conjunction with systemic mycoses can cause a chalky, grey-white residue to develop on the cornea and conjunctiva of young raptors as well as squabs, poults, and young psittacines. Parasites such as filaria may cause focal conjunctival lesions. Conjunctival edema has also been seen with Plasmodium.
Fluorescein stain the cornea of birds with conjunctivitis. Obtain cytologic samples by gently scraping the conjunctiva or swabbing the conjunctival sac. If the bird is fluorescein-negative and cytology does not suggest infection, begin a broad-spectrum antibiotic-steroid combination two to three times daily using ophthalmic drops or ointment in large birds. Small birds may suffer from systemic complications secondary to topical steroid use. Traumatic conjunctivitis usually responds to treatment within 3-5 days.
If cytology suggests infectious conjunctivitis, obtain a culture sample and begin topical broad-spectrum antibiotics 2-4 times daily. Popular choices for infectious conjunctivitis include triple antibiotic (Bausch & Lomb) ointment or drops, fluoroquinalones such as 0.3% ciprofloxacin (Ciloxan, Alcon) oxytetracycline (Terramycin, Pfizer) or tetracycline (Achromycin, Lederle), and. Consider gentamicin sulfate, tobramycin sulfate or 0.3% ciprofloxacin (Ciloxan, Alcon) for Gram-negative infections. Reevaluate birds at 5-7 days, although a 2-week course is usually required. Systemic antibiotic therapy may be indicated if infectious conjunctivitis recurs after the course of topical therapy is completed. Temporary tarsorrhaphy may aid severely irritated eyes.
Carefully evaluate the respiratory system including paranasal sinuses, as bacterial conjunctivitis is frequently associated with upper respiratory tract infection. If the respiratory tract is involved, obtain samples from the infraorbital sinus, choana, or even from the air sacs via laparoscopy and begin systemic antibiotics.
Lesions of the cornea
Corneal ulceration is a common lesion in the avian eye readily demonstrated with fluorescein dye. Treat ulcers with topical broad-spectrum antibiotics 3 times daily for 3-5 days. Most corneal ulcers heal rapidly, but re-stain the cornea periodically to monitor healing. In rare cases, chronic ulceration can result in superficial vascularization with pigmentation. Perform temporary tarsorrhaphy for a severely compromised cornea. Successful healing of severe, bilateral corneal damage has been described in a peregrine falcon (Falco peregrinus) after placement of bilateral 360º conjunctival flaps, and in two great horned owls (Bubo virginianus) with penetrating keratoplasties and conjunctival pedicle grafts. Routine use of a nictitans flap is not recommended due to the possibility of subsequently impairing function of this essential adnexal structure.
Corneal opacities are most commonly associated with ulceration and scarring. Focal corneal opacities may also develop as sequelae to keratic precipitates associated with uveitis, while diffuse corneal edema may result from lens luxation. Keratitis of unknown etiology has been described in a barred owl (Strix varia), tawny owls (Strix aluco), and eagle owls (Bubo lacteus). The clinical significance of corneal opacity depends on its density, size, and location. Corneal lacerations should be meticulously repaired using magnification with 9-0 or 10-0 nylon.
Scleral ossicle fractures
Ocular trauma can result in fracture of the scleral ring, which may be palpated digitally and confirmed radiographically. It is often very difficult to image ossicle fractures with the globe in situ.
Lesions of the anterior chamber
Hyphema is an extremely common finding in birds of prey (Fig 3). Blood usually organizes into a clot within a day or two and depending on its size, resolves over days to weeks. If uncomplicated by infection or persistent bleeding, resorption should occur regardless of the medication selected. Hyphema or fibrin strands that have not resorbed within 3 days may benefit from intracameral tissue plasminogen activator.
The principal cause of uveitis in raptors is trauma, although inflammation of the uvea may also develop with infection or corneal ulceration. Topical steroids (0.1% dexamethasone ophthalmic drops) may be cautiously applied every 4-8 hours in large raptors for severe uveitis without corneal ulceration.
Avoid steroids in small birds due to the danger of systemic absorption with subsequent morbidity and even death. For large raptors in which regular restraint is not feasible, one 0.1-0.25 ml subconjunctival injection of triamcinolone (Vetalog, Fort Dodge) has also been described. Common sequelae to severe uveitis and/or hyphema include anterior and posterior synechiae.
Topical or systemic non-steroidal anti-inflammatory drugs (NSAIDs) may be a practical alternative in some uveitis patients. Remember NSAIDs are not without potential adverse effects and they should never be used when there is hyphema present as they can also promote bleeding. Small birds will have more problems with systemic absorption of NSAIDs than large birds.
Other lesions that may be seen within the anterior chamber include iridic tears, which occur commonly with penetrating foreign bodies, disinsertion of the iris root with severe blunt trauma, hypopyon, and fibrin clots. Glaucoma in raptors is rare but may develop secondary to lens luxation or chronic inflammation associated with anterior synechiae or preiridal fibrovascular membrane formation.
Lesions of the lens
Head trauma may result in lens luxation, which in turn can lead to corneal opacity, anterior synechiae, and leakage of lens proteins with subsequent uveitis. A luxated lens has a pigmented ring around its equatorial region from avulsed tips of ciliary processes that fuse directly to the lens capsule. Completely luxated lenses should be surgically removed to reduce the likelihood of secondary complications (Figs 4a and 4b).
Cataracts seen in birds of prey may be divided into juvenile, senile, and traumatic types. In captive birds, most cataracts have been reported in diurnal raptors and appear to be senile in type. In free-ranging birds, most cataracts are traumatic in origin and are primarily seen in owls (Fig 5). Bilateral cataract surgery and intraocular lens implantation has been described in a great horned owl successfully released into the wild.
Lesions of the posterior segment
Because of the close fit of the globe with the orbit, the avian posterior segment is at risk for a variety of lesions caused by ocular contrecoup and compressive forces. Clinical signs suggestive of severe head trauma that may have associated posterior segment lesions include bleeding from the external ear in owls, nictitating membrane hematomas, and epistaxis.
Lesions of the pecten and vitreous
Hemorrhage into the vitreous body originating from the choroid and/or pecten occurs in approximately one-third of traumatized birds (Fig. 6). As in mammals, blood in the vitreous often persists for long periods of time. Pecten hemorrhage can result in organized clots surrounding the pectin obscuring complete visualization of this structure.
Intraocular inflammation may lead to lesions such as opaque vitreal strands, liquefaction of the vitreous, or small white opacities within the vitreous (asteroid hyalosis). Foreign bodies are also occasionally found within the vitreous.
Lesions of the choroid and/or retina
Lesions of the choroid and/or retina are extremely common in birds of prey. Traumatic injury can result in fluid and cells entering the subretinal space creating focal to complete retinal detachment which appears as raised, gray to white regions (Fig. 7 and Fig. 8). Retinal detachments block out details of the underlying choroidal vasculature, and extensive detachment with large tears may obscure the pecten during ophthalmic exam as the retina is draped across it.
Extensive retinal detachment generally results in total loss of vision. Unfortunately partial detachments can also progress so these lesions should be monitored over time. In some cases, portions of the detachment spontaneously reattach over 2-4 weeks, however these areas usually degenerate creating retinal scars. Retinal scars appears as flat, well demarcated, depigmented lesions sometimes with central and peripheral areas of hyperpigmentation (Fig 9). Retinal injury generally occurs at the time of trauma, and currently, there is collectively little experience with retinal reattachment surgery.
Chorioretinal lesions may also be caused by infectious disease. West Nile virus disease in red-tailed hawks (Buteo jamaicensis) and Cooper’s hawks (Accipiter cooperii) most commonly causes pectenitis, characterized by fibrinous material coating the pecten. Many birds also exhibit chorioretinal scarring and active chorioretinitis evidenced by variably sized, raised, white lesions with indistinct margins (Fig. 10). Some birds also had mild to moderate anterior uveitis.
Toxoplasmosis has also been linked to retinal lesions, particularly in owls. In a recent survey by Williams et al, retinal scars in tawny owls (Strix aluco) were not associated with high Toxoplasma gondii antibody titers.
Small, punctate, well-circumscribed bilateral retinal lesions are common in owls. These lesions are located in the ventral aspect of the fundus. Though very limited data are available, their size, location and histopathologic appearance make phototoxic changes caused by imaging the sun on the retina a possibility.
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