Published by Emily A. Latham, DVM
Uveitis, Phacoclastic in Dogs
Last updated on 7/15/2024.
Contributors:
Revised by Emily A. Latham MVB and Rachel L. Davis, DVM, MS, DACVO
Revised by Andrew Lewin BVM&S, MRCVS, DACVO, 4/2/2019
Revised by Ralph E. Hamor DVM, MS, DACVO, 9/28/2012
Original author was Heather Gray, DVM, DACVO, 10/23/2006
Synonyms:
Lens-induced iridocyclitis
Lens-induced iritis
Disease Description:
Definitions
Lens-induced uveitis (LIU) is intraocular inflammation affecting the anterior uveal tract that is associated with the release of lens proteins into the anterior chamber. In animals, LIU is divided into two types.
Phacolytic uveitis is anterior uveitis associated with cataract formation, especially rapidly-developing/progressing, longstanding, or hypermature cataracts.1,2 It occurs secondary to the leakage of soluble lens proteins through an intact lens capsule. When the term, LIU, is used most clinicians are referring to this form of uveitis.
Phacoclastic uveitis is generally a more severe anterior uveitis (Figure 1) that is associated with traumatic or spontaneous lens capsule rupture. It can result in vision-threatening anterior uveitis that requires aggressive medical and/or surgical management.
Etiology and Pathophysiology
Although the underlying etiology of lens capsule rupture is not defined in every case of phacoclastic uveitis, it occurs most often from penetrating ocular trauma.1 Cat-claw injuries are the most common cause.1,3,4 In dogs, diabetes mellitus can cause acute onset of bilateral cataract formation resulting in lenticular intumescence, which can lead to spontaneous lens capsule rupture (Figures 2A, 2B).11,12
Lens-induced uveitis is caused by the release of lens proteins through the lens capsule. Embryologically, the lens placode forms from ectoderm, whereas other ocular structures form from mesoderm. The lens and its proteins are sequestered from mesodermal tissue by the lens capsule. Leakage of lens proteins triggers an immune-mediated response because the proteins are recognized as “foreign”.1,2 The immune-mediated reaction causes secondary intraocular inflammation.
Diagnosis
Physical Examination Findings/History: Animals with traumatic injuries may be acutely painful, with blepharospasm, tearing, conjunctival hyperemia, and/or scleral injection. Clinical examination alone may be insufficient to determine if the anterior lens capsule has ruptured, especially if significant ocular abnormalities (e.g. anterior uveitis, miosis, hyphema, fibrinous aqueous flare, hypopyon, Figure 3A) prevent visualization of intraocular structures. In addition, clinical evidence of phacoclastic uveitis may be delayed for up to 2 weeks following initial lens capsule rupture. Other injuries may also be identified depending on the cause of trauma.
Spontaneous lens capsule rupture from diabetic cataracts is associated with rapid onset and progression of cataracts, and the rupture is typically equatorial.12
Ultrasonography: If the globe is stable, ocular ultrasonography may be done to determine if the lens capsule has ruptured and the extent of intraocular damage (e.g. retinal detachment).6 Ultrasonography is usually possible in conscious animals after the application of topical anesthesia. However, it should be avoided if significant corneal damage is present. It may not be possible to identify small tears in the lens capsule, and inflammatory debris or hemorrhage may mask a tear in the lens capsule. When available, high-resolution ultrasonography may detect smaller tears.6
Disease Description in This Species:
Signalment
Phacoclastic uveitis can occur in any breed, age, or sex of dog. Predispositions exist for penetrating ocular trauma and diabetes mellitus, which can influence the occurrence of phacoclastic uveitis.4,5 One study showed that diabetic Labrador retrievers may have a higher risk of spontaneous lens capsule ruptures.12
Clinical Signs
Signs associated with penetrating ocular trauma include acute onset of pain, with blepharospasm and tearing. If the cornea has been penetrated, generally a gray-white corneal opacity with a plug of fibrinous material and adjacent corneal edema are present. Hemorrhage from the site may also be noted. Foreign material that caused the penetration may or may not be visible. A foreign body may be hidden by corneal edema or ulceration, especially if the wound is not acute. The longer the corneal wound is present, the greater the vascular and/or stromal edematous response, and the more severe the anterior uveitis.
Signs of anterior uveitis include aqueous flare, fibrin and/or hypopyon in the anterior chamber, miosis, and focal or diffuse iritis. The anterior chamber may be shallow or collapsed. Collapse of the chamber may result in wrinkling of the cornea. Hyphema may be present. Wounds to the cornea may result in iris prolapse, with dyscoria and anterior synechia.7,8 Protrusion of lens material into the anterior chamber may be noted.
In cases of spontaneous lens capsule rupture from cataractous lens intumescence, vision is usually decreased, keratic precipitates, elevated intraocular pressure (Figure 4), intra-lenticular pigment deposition, retinal detachment, and posterior synechia may be noted.13 In some cases, the capsular tear can be directly visualized.12
Etiology:
Bite wound
Cat scratch
Cataract
Cataract, intumescent
Cataract, secondary
Diabetes mellitus
Explosions
Foreign body
Gunshot wounds
Hymenoptera sting (bees, wasps, hornets, ants)
Idiopathic, unknown
Penetrating wounds
Plant awns, burrs, splinters
Trauma
Trauma, abuse/malicious/non-accidental
Trauma, motor vehicle/automobile
Breed / Species Predilection:
None
Sex Predilection:
None
Age Predilection:
None
Clinical Findings:
AFEBRILE
Anisocoria, pupils unequal
Anterior lens capsule debris and/or pigment deposition
Blepharospasm, eye pain
BLINDNESS OR OTHER VISUAL DEFICIT
Blindness partial, visual deficit
Conjunctival congestion, hyperemia
Conjunctival hemorrhage
CONJUNCTIVITIS
Corneal laceration
Corneal ulcer, keratitis
Corneal vascularization
Edema conjunctiva, chemosis
Edema corneal
EDEMA or SWELLING
Epiphora, lacrimation increased
Glaucoma
HEMORRHAGE
Hypopyon
Iris bombe
Iris pigmentation abnormal
Iris prolapse
Keratic precipitates
Keratoconjunctivitis
Lens luxation, subluxation
Menace response absent or decreased
Miosis
OCULAR DISCHARGE
PAIN
PHOTOPHOBIA
Phthisis bulbi
Pupillary light reflex absent
Pupillary light reflex decreased
Rubeosis iridis, iris hyperemia
Scleral hemorrhage
Scleral laceration
Third eyelid, nictitating membrane prolapsed
ULCERS
UVEITIS
Uveitis, anterior
| Diagnostic Procedures: | Diagnostic Results: | |
| Ultrasonography of eye/orbit | Characterization and extent of the lesion | |
| Disruption or deformity of the lens capsule | ||
| Hyperechoic lens | ||
| Vitreal debris | ||
| Ocular examination | Aqueous flare | |
| Cataract, lens opacity | ||
| Hyphema, blood anterior chamber eye | ||
| Intraocular pressure increased on tonometry | ||
| Intraocular pressure normal or decreased on tonometry if uveitis present | ||
| Iris-to-cornea or iris-to-lens adhesion | ||
| Lens absent, small or deformed | ||
| Leukocoria, leukokoria | ||
| Preiridal fibrovascular membrane | ||
| Retinal detachment | ||
| Retinal hemorrhages | ||
| Scleral blood vessel congestion | ||
| Scleral penetration | ||
| Vitreal traction bands | ||
| Vitreous cloudy |
Images:
Treatment / Management:
SPECIFIC THERAPY
Treatment goals are to control intraocular inflammation, maintain vision, prevent infection, and reduce discomfort. Both medical and surgical management options are available and early referral to an ophthalmologist is recommended for an optimal outcome.
Surgical Therapy
When the anterior lens capsule has been lacerated, treatment recommendations become complicated. It was previously recommended that eyes with a lens capsular tear >1.5 mm, or with substantial herniation of lens cortex into the anterior chamber be taken immediately to surgery to remove the lens and repair the corneal laceration.1 Surgery involves phacoemulsification (Figure 3B) and aspiration of all visible lens material, which requires an operating microscope and micro-surgical instruments.4
If intumescent cataracts are present, prompt phacoemulsification is recommended.12 If a foreign body is present within the cornea and/or the globe, then surgery is required to remove it and repair the corneal wound. Enucleation may be warranted for eyes that are blind, unresponsive to therapy, chronically inflamed, and/or painful.5
Medical Therapy
Recently, two retrospective studies demonstrated that even large lens capsule lacerations may respond well to medical therapy alone.3,5 Factors that help determine the most appropriate method of management include corneal integrity; degree of intraocular inflammation; concurrent intraocular damage; potential for vision; and chronicity of uveitis. For details on medical therapy, see the Canine VINcyclopedia chapter on Lens-Induced Uveitis.
SUPPORTIVE THERAPY
Supportive medical therapy involves both topical and systemic medications. Topical bactericidal antibiotic solution (e.g. fluoroquinolone, gentamicin, tobramycin) is administered q 4-8 hrs. Ointments are contraindicated because the oil-based carrier is irritating to intraocular structures. A topical nonsteroidal anti-inflammatory (NSAID) agent may be administered if hyphema is not present. Topical atropine is given to dilate the pupil and help control pain. When glaucoma is present, medical therapy with topical beta blockers (e.g. timolol) and/or carbonic anhydrase inhibitors (e.g. dorzolamide) is started.
Broad-spectrum systemic antibiotics are indicated in many cases. Systemic NSAIDs may be considered once active hemorrhaging is controlled. Systemic pain medication is typically indicated. An Elizabethan collar is applied until the wound heals. Sedation may be needed to keep an anxious or overactive animal quiet for a few days.
Once the corneal wound has healed, topical steroids (e.g. dexamethasone, prednisolone acetate) may be substituted for topical NSAIDs, especially if severe, secondary uveitis and/or corneal inflammation is present. If intraocular inflammation is considered to be sterile and uncontaminated, oral steroids may also replace oral NSAIDs after an appropriate wash-out period.
MONITORING
Frequent, chronic monitoring is essential to evaluate response to therapy; monitor progression of the disease; and detect complications. Because IOP can change over time, it is commonly measured at each recheck examination. It is important to note that hypotonic (low IOP) eyes may not become normotensive again, even after all inflammation is clinically controlled. Hence, low IOP measurements cannot be used alone to determine whether continued anti-inflammatory therapy is needed. Long-term or permanent therapy may be required for LIU.
PROGNOSIS
Overall prognosis is fair based on published reports.1,4,5 Phacoclastic uveitis must be treated promptly via medical and/or surgical methods if vision is to be preserved.3 When bacterial implantation occurs in the lens prognosis may be poor, and the phenomenon may only be detected histologically after enucleation.10
Preventive Measures:
No direct preventive measures are available. Care should be taken when introducing a new puppy or young dog to a household with other animals, especially cats.
Special Considerations:
Other Resources
VIN Message board discussions on phacoclastic uveitis
Differential Diagnosis:
Other causes of uveitis
Lens-induced (phacolytic) uveitis
Penetrating ocular trauma without lens rupture
References:
- Davidson MG, Nasisse MP, Jamieson VE, et al: Traumatic anterior lens capsule disruption. J Am Anim Hosp Assoc 1991 Vol 27 (4) pp. 410-14.
- Fischer CA: Lens-induced uveitis and secondary glaucoma in a dog. J Am Vet Med Assoc 1971 Vol 158 (3) pp. 336-41.
- Paulsen ME, Kass PH: Traumatic corneal laceration with associated lens capsule disruption: a retrospective study of 77 clinical cases from 1999 to 2009. Vet Ophthalmol 2012 Vol 15 (6) pp. 355-68.
- Braus BK, Tichy A, Featherstone HJ, et al: Outcome of phacoemulsification following corneal and lens laceration in cats and dogs (2000-2010). Vet Ophthalmol 2017 Vol 20 (1) pp. 4-10.
- Pont RT, Riera MM, Newton R,et al: Corneal and anterior segment foreign body trauma in dogs: a review of 218 cases. Vet Ophthalmol 2016 Vol 19 (5) pp. 386-97.
- Perry JL: The evaluation of patients with traumatic cataracts by ultrasound technologies. Semin Ophthalmol 2012 Vol 27 (5-6) pp. 121-24.
- Ofri R: Lens. In: Maggs DJ, Miller PE, Ofri R (eds): Slatter’s Fundamentals of Veterinary Ophthalmology, 4 ed. Elsevier Saunders, St. Louis 2008 pp. 263-64.
- Miller PE: Uvea. In: Maggs DJ, Miller PE, Ofri R (eds): Slatter’s Fundamentals of Veterinary Ophthalmology, 4 ed. Elsevier, St. Louis 2008 pp. 203-29.
- Hersh PS, Rice BA, Baer JC, et al: Topical nonsteroidal agents and corneal wound healing. Arch Ophthalmol 1990 Vol 108 (4) pp. 577-83.
- Bell CM, Pot SA, Dubielzig RR: Septic implantation syndrome in dogs and cats: a distinct pattern of endophthalmitis with lenticular abscess. Vet Ophthalmol 2013 Vol 16 (3) pp. 180-85.
- Van Der Woerdt A: Lens-induced uveitis. Vet Ophthalmol 2000 Vol 3 (4) pp. 227-34.
- Wilkie DA, Gemensky-Metzler AJ, Colitz CMH, et al: Canine cataracts, diabetes mellitus and spontaneous lens capsule rupture: a retrospective study of 18 dogs. Vet Ophthalmol 2006 Vol 9 (5) pp. 328-34.
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