Southwood and Wilkins Chapter 8: Eye and Associated Structures

Blepharospasm

Squinting

Iridocyclitis

Inflammation of the iris and ciliary body, also called anterior uveitis

Keratomalacia

‘Melting’ or collagenolysis of the cornea

Photophobia

Greater than normal sensitivity to light

Epiphora

Excessive lacrimation or tearing

Endophthalmitis

Inflammation of the internal structures within the globe, often caused by infection; can be a complication of intraocular surgery

Hyphema

RBCs within the anterior chamber

Hypopyon

WBCs within the anterior chamber

Synechia

Adhesion between the cornea and iris (anterior) or the iris and lens (posterior)

Seidel Test

Application of concentration fluorescein, which appears orange, to the corneal surface to detect a perforation. A perforation, or leak, appears as dilute fluorescein (fluorescent green with a cobalt blue light) at the site of the leak, surrounded by the concentration fluorescein

Uveitis

Inflammation of the uvea, which is the middle layer of the eye between the sclera and retina, including the iris, the choroid of the eye, and the ciliary body

Indications for Auriculopalpebral Nerve Block

• Provides akinesia of the orbicularis oculi muscle

• Used to prevent eyelid closure

Indications for Supraorbital (Frontal) Nerve Block

• Frontal nerve innervates the medial and central upper lid

• Can be blocked at the supraorbital foramen, a depression medial to the narrowest aspect of the supraorbital process of the frontal bone

• Performed prior to placement of an upper lid SPL

Auriculopalpebral Nerve Block Technique

• Palpated just latera to the dorsal most border of the zygomatic arch and on the zygomatic arch caudal to the bony process of the frontal bone

• Can also be blocked just anterior to the base of the ear where the nerve cannot be palpated

Supraorbital (Frontal) Nerve Block Technique

Insert the needle into or just over the supraorbital foramen

What innervates the lateral upper lid?

Lacrimal nerve

Where can the lacrimal nerve be blocked?

Along the lateral aspect of the orbital rim

What innervates the medial aspect of the lower lid and the medial canthus?

Infratrochlear nerve

Where can the infratrochlear nerve be blocked?

At the palpable trochlear notch, on the medial aspect of the orbital rim

What innervates the lower lid?

Zygomatic nerve

Where can the zygomatic nerve be blocked?

Along the ventrolateral orbital rim

Indications for a Conjunctival Graft

• Used for deep corneal ulcers and other corneal wounds when the lesion extends to or close to Descemet's membrane

• Grafts provide blood supply, fibroblasts, anticollagenases, and support for weakened corneal stroma

Complications of a Conjunctival Graft

• Dehiscence and infection

• If the conjunctiva used for the graft is too thick, extensive scarring can cause loss of vision

Indications for Tarsorrhaphy

• Surgical closure of the eyelid

  • Can be partial or complete and temporary or permanent

• Temporary tarsorrhaphy is most commonly performed to facilitate corneal wound healing, to protect the cornea, during recovery from anesthesia following corneal surgery, and to support the surgical site during healing following corneal surgery

• A partial temporary tarsorrhaphy may also be performed to prevent corneal dessication in cases of facial nerve paralysis

Complications of Tarsorrhaphy

• An improperly placed tarsorrhaphy can cause corneal injury with ulceration as a consequence of the suture material rubbing against the cornea

Indications for Enucleation

Severe ocular trauma, infection, and endophthalmitis

Surgical Approach for Enucleation

• Transpalpebral - indicated for infectious or neoplastic disease

• Transconjunctivals - may be preferred for glacomatous or uveitic globes

• Conjunctiva, globe, and nictitating membrane are completely removed

Complications of Enucleation

• Most common complication is swelling, which may be associated with hemorrhage

• Infection can occur and is managed with drainage

• Complications associated with prosthesis placement include prosthesis shifting, surgical wound dehiscence, and prosthesis extrusion

Management/Treatment of Eyelid Laceration

• The wound should be minimally debrided without excising tissue

• If the eyelid margin and palpebral fissure cannot be restored with available tissue, blepharoplastic procedures such as sliding skin grafts are warranted

• Wounds should be closed in two layers to prevent dehiscence of the deep conjunctival layer and subsequent cornea ulceration from mechanical trauma

• A figure of eight suture pattern at the eyelid margin is critical to achieve perfect apposition and prevent cicatricial entropion, secondary corneal damage, and potential globe loss

• Suture placement should begin at the eyelid margin or the base of the wound and work toward the apex of the laceration to ensure perfect eyelid apposition

• The use of topical antimicrobials can be associated with excessive granulation tissue and wound dehiscence if the upper eyelid is manipulated and in particular forced open when medication is applied so use of topical antimicrobials is discouraged

• Prognosis for retention of lid function is typically good but lid margin irregularities and mechanical or exposure keratitis may result

Etiology/Pathogenesis of Entropion

• Most common in the lower lid in recumbent neonatal foals with systemic disease that typically have impaired corneal sensitivity and enophthalmos secondary to dehydration, insufficient body fat, or abnormal globe position

• Can occur as a primary anatomic disease but this is uncommon

Management/Treatment of Entropion

• Temporary surgical imbrication of the lower lid in foals with entropion secondary to systemic disease is typically all that is warranted

• Entropion in these foals is generally self-correcting with the resolution of systemic disease

• Imbrication is best performed using interrupted sutures in a vertical mattress pattern entirely on the lower lid

• Cicatricial entropion should be corrected with blepharoplastic procedures as dictated by the lid conformation

  • Improper repair can be associated with impaired lid function, persistent corneal ulceration, and loss of the globe

Orbital Fracture Management/Treatment

• Minor orbital rim fractures rarely require surgical treatment

• Open fractures should be debrided and lavaged

  • Small bone fragments should be removed to avoid sequestrum formation

• Large fractures causing extensive facial deformity and/or impinging or entrapping the globe should be surgically repaired

  • Should be performed within days of injury because fibrous union occurs within 1 week

  • Involves elevating the fragments into the normal position and stabilizing the fracture with monofilament stainless steel, cerclage wire, small pins, or orthopedic bone plates

• Ophthalmic complications include corneal ulcers, iridocyclitis, entrapment of the globe by bone fragments, and blindness

Corneal Ulceration

Loss of corneal epithelium resulting in exposed corneal stroma

Corneal Ulceration Etiology/Pathogenesis

• Conjunctiva and cornea are constantly bathed in bacteria and fungus which quickly adhere to exposed stroma

  • Consider secondary infection in ulcers that do not improve or worsen within a few days

• Microbial and ubiquitous tear film proteinases may contribute to the progression of the corneal injury, resulting in keratomalacia characterized by a 'melting' cornea

Corneal Ulceration Clinical Features

• Nonspecific signs: epiphora, ocular discharge, conjunctival hyperemia, blepharospasm, photophobia, and corneal edema

• Ulcer depth can range from superficial abrasions to extremely deep erosions

• A descemetocele is the result of complete stroma loss and exposure of the thin Descemet's membrane

• Keratomalacia and corneal neovascularization may also be apparent

Corneal Ulcer Diagnosis

• Positive uptake of fluorescein stain is diagnostic for a corneal ulcer and will appear green in the exposed stroma with a cobalt blue light

• Rose Bengal dye positively stains degenerate or dead epithelial cells and can be used to identify early disease

• Descemet's membrane does not stain with fluorescein so a descemetocele will have a fluorescein-stained outer ring of exposed stroma with a non-staining center

• A corneal scraping should be obtained with a cotton swab or the blunt end of a scalpel blade and submitted for

  • Bacterial culture

  • Fungal culture

  • Cytology

Healing of Uncomplicated Superficial Ulcers

Occurs by migration and mitosis of epithelial cells and is completed in 5-7 days

Medical Therapy for Corneal Ulcers

• Antimicrobial drugs (broad spectrum) such as triple antibiotics

• Antifungal chosen based on geography

• Atropine is used to treat uveitis by reducing ciliary spasm and preventing iris to lens adhesions, which can occur with prolonged miosis

• Autologous serum is a broad-spectrum anticollagenase that should be used to inhibit proteinases released by infectious organisms and WBCs and in the tear film

• Systemic NSAIDs

• Topical antimicrobials should be continued until the cornea has completely epithelialized

Surgical Therapy for Corneal Ulcers

• Corneal grafts are indicated in cases of severe and deep ulcers and those not responding to medical therapy

  • Biomaterial indicated in each case is determined by the reason for the graft

    • Optical, to restore or improve vision

    • Therapeutic, to control medically refractory corneal disease

    • Tectonic, to preserve or restore the structural integrity of the globe when tissue is missing

    • Cosmetic, to improve the appearance of the globe without necessarily improving vision

• Conjunctival grafts are indicated to bring blood supply to the ulcerated cornea for therapeutic and tectonic reasons, but can be associated with significant scarring

  • Pedicle conjunctival grafts are the most commonly used

  • Hood or bipedicle (bridge) conjunctival grafts may be used to bring a blood supply to larger ulcers

  • When the stromal defect is deep or an iris prolapse has developed, a corneal graft (fresh or frozen) may be used underneath the conjunctival graft to replace missing tissue

• In cases of extreme keratomalacia or for ulcers with a large surface area, an amniotic membrane transplant may be warranted

  • Amniotic membrane can provide significant structural support

  • Amnion has antiangiogenic, anti-inflammatory, and antimicrobial properties that contribute to healing

  • Amnion typically sloughs off as the underlying cornea heals

• Treatment should be continued until the cornea is completely epithelialized and the graft material (conjunctiva, cornea, or amnion) has become incorporated into or sloughed from the recipient cornea

  • Usually at least 2 weeks postoperatively

  • Anti-inflammatory therapy is sometimes required longer term (weeks to months) to control keratitis and uveitis associated with grafting procedures

Prognosis for Corneal Ulcers

• Prognosis for retention of vision depends on the resulting corneal scar as well as the presence of a pupillary opening

• Prognosis for retention of the globe depends on maintenance of structure integrity of the globe

Corneal Burn

• A corneal burn occurs with corneal exposure to a chemical or naturally occurring substance, including ultraviolet light, which causes a corneal ulcer

Corneal Burn Etiology/Pathogenesis

• Can occur following corneal exposure to any substance that is irritating, an acid or base (chemical burn) or to ultraviolet light (i.e. flash burn)

• Severity depends on the cause, the cornea, and the initial treatment

• Alkali burns caused by a substance with a pH >7 are the most dangerous because these substances react with fat in the cornea to form soap and so the damage can rapidly progress to Descemet's membrane and result in perforation

• Acids with a pH <7, precipitate with stromal proteins so these burns are typically self-limiting

• Irritants with a neutral pH tend to cause more discomfort to the eye than actual damage

• Can also occur as a result of thermal injury (e.g. barn fires)

Corneal Burns Clinical Features

• Damage typically limited to the cornea and conjunctiva but in severe cases the globe may rupture

• Signs of a corneal burn include blepharospasm, blepharitis, conjunctival hyperemia and chemosis, and epiphora

Corneal Burns Diagnosis

• Use fluorescein stain to determine if an ulcer is present and if so evaluate the depth

Corneal Burns Management/Treatment

• Immediate copious lavage with sterile saline or clean water if saline isn't available, is critical to stop chemical degradation of the cornea

• Medical treatment includes a topical broad-spectrum antimicrobial, a mydriatic, and anti-collagenase therapy

• Systemic NSAIDs

Do sharp force or blunt force corneal injuries have a better prognosis?

Sharp force corneal injuries have a better prognosis than blunt force injuries and injuries involving the sclera

Corneal Laceration Clinical Features

• Affected eye is frequently cloudy, red and painful

• Blepharospasm, lacrimation, and corneal edema at the wound margins

• With a full-thickness laceration or corneal perforation, iris prolapse, anterior chamber collapse, and severe iridocyclitis (i.e. anterior uveitis) will be present

Corneal Laceration Management/Treatment

• Superficial corneal lacerations can be managed with medical treatment

• Surgical repair is indicated for deep lacerations or corneal perforation and should be performed as soon as possible

  • Primary closure of the cornea is recommended and covering the laceration with a conjunctival graft may be warranted

  • If the iris is prolapsed, the necrotic tissue should be sharply removed and the remaining iris pushed back into the eye

  • The anterior chamber may be re-established with sodium hyluronate, irrigation solution, or an air bubble

• In severely infected or severely traumatized eyes, enucleation should be considered

• Prognosis depends on the chronicity, size, and location of the laceration

• Full-thickness wounds >15 mm, corneal ulcers older than 2 weeks, and lacerations that extend along or past the limbus carry a poorer prognosis

Corneal Stromal Abscess

• A corneal stromal abscess is a focal abscess in the stroma covered by epithelial cells

Corneal Stromal Abscess Etiology/Pathogenesis

• A corneal stromal abscess is formed by the migration of epithelial cells over a corneal injury, which seals infected material in the corneal stroma

• The lack of blood vessels and lymphatics within the cornea slows the recognition and removal of foreign material by the immune system

• The abscess may be bacterial, fungal, or sterile; however, epithelial cells are more likely to cover fungal hyphae and 56% of stromal abscesses are fungal in origin

• Treatment of an epithelialized ulcer with topical corticosteroids to reduce the resultant scar is a risk factor for the development of a stromal abscess because even though the epithelium may have completely migrated over an ulcer, infectious organisms may still be present within the stroma and infection can be exacerbated by corticosteroid treatment

Corneal Stromal Abscess Clinical Features

• A focal white or yellow opacity within the corneal stroma is highly suggestive of stroma abscessation

• Stromal abscesses are typically disproportionately painful relative to the apparent severity of the lesion

• Abscess is commonly singular and centrally or paracentrally located, but multiple and peripheral lesions have also been noted

• Clinical signs include corneal edema, blepharospasm, epiphora, photophobia, aqueous flare, and anterior uveitis

• Variable corneal vascularization is noted in chronic lesions

Corneal Stromal Abscess Diagnosis

• Fluorescein dye retention will typically be negative

• Sampling of a deep abscess tissue is only achieved with surgery

Medical Management of Corneal Stromal Abscess

• Broad-spectrum antimicrobials

• Antifungals

• Atropine

• There has been concern regarding the ability of topical antimicrobial drugs to penetrate the corneal epithelium, but the inflamed cornea may allow adequate penetration even through an intact epithelium so debridement may not be necessary

• Most abscesses are centrally located and healing is not complete until vascularization, the duration of treatment can be long

• Systemic antimicrobial or antifungal drugs may be useful if there is good corneal blood supply

• Systemic NSAIDs

Surgical Therapy of a Corneal Stromal Abscess

• Corneal debridement with or without a conjunctival graft can be successful in cases of superficial lesions

• With deep lesions, abscess removal and replacement with donor cornea using a penetrating keratoplasty, posterior lamellar keratoplasty, or deep endothelial lamellar keratoplasty is recommended

Immune Mediated Keratitis

• Defined by corneal opacity or infiltrate that is typically non-infectious, not associated with severe pain or uveitis, and responds to varying degrees, based on the depth of the infiltrate, to anti-inflammatory therapy

Immune Mediated Keratitis Etiology/Pathogenesis

• Inciting cause not known, but may be a self-antigen or a foreign protein that stimulates an immune response

• Histology reveals lymphoplasmacytic inflammation, stromal fibrosis, and vascularization, with neutrophils also evident in more acute (i.e. <12 months) cases and mineralization identified in more chronic (i.e. >24 months) cases

Immune-Mediated Keratitis Clinical Features

• Manifests as a white or yellowish-white corneal opacity at varying depths in the stroma which may or may not be accompanied by corneal edema and vascularization

• Blepharospasm, epiphora, aqueous flare, and miosis, are typically not seen

Immune Mediated Keratitis Diagnosis

• Based on clinical signs including measurement of IOP as well as by response to anti-inflammatory therapy

Immune Mediated Keratitis Management/Treatment

• Topical anti-inflammatories including corticosteroids and immunosuppressive drugs such as cyclosporine

• Superficial and mid-stromal lesions are more likely to respond to topical therapy than deep endothelial lesions

• Surgical intervention via keratectomy to remove the infiltrate may be curative

Equine Recurrent Uveitis

• Characterized by multiple episodes of intraocular inflammation

Equine Recurrent Uveitis Etiology/Pathogenesis

• Inciting cause often unknown

• Preponderance of T lymphocytes suggests that ERU is an immune-mediated delayed-type hypersensitivity reaction

• Leptospira are commonly incriminated, but other bacteria and EHV have been implicated as possible causes

• Appaloosas are 8.3 times more likely than other breeds to develop ERU

Clinical Features of Equine Recurrent Uveitis

• Blepharospasm, miosis, and excessive lacrimation are common

• In acute episodes, corneal edema, conjunctival hyperemia, and ciliary injection may be noted

  • Aqueous flare (cloudy anterior chamber) and hypopyon or hyphema may also be present

• In chronic cases, corneal scarring, corpra nigra atrophy, posterior synechia, and cataract formation can be noted

Diagnosis of Equine Recurrent Uveitis

• Based on clinical signs and recurrence of uveitis

• Fluorescein dye retention is typically negative but secondary corneal disease, such as calcific band keratopathy, can complicate ERU and IOP is typically low, but secondary glaucoma can develop if cells and protein accumulate in the iridocorneal angle

• Leptospiral serology is useful for assessment of previous exposure to this risk factor

Management/Treatment of Equine Recurrent Uveitis

• Goals of therapy are to reduce pain, preserve vision, and minimize recurrence

• Topical atropine and corticosteroids and systemic NSAIDs are typically indicated

• Cyclosporine implants decrease the frequency and severity of uveitis flare-ups

  • Tend to have the best results when placed in a quiet eye

  • May need repeat implants after depletion of the drug, ~4 years

Hyphema Etiology/Pathogenesis

• Causes include causes of third compartment bleeds elsewhere in the body, most notably trauma, inflammation, coagulopathy, and neoplasia

• Traumatic hyphema and hyphema secondary to severe uveitis are most common in the horse

Hyphema Clinical Features

• Red appearance behind the cornea which may be partial or complete

• Often accompanied by corneal edema associated with inflammation of and damage to the corneal endothelium

• Secondary glaucoma is a concern as red cells can occlude the iridocorneal angle

  • Measurement of IOP is critical to direct medical therapy

Hyphema Diagnosis

• Evaluation of the indirect PLR can help establish the potential for return of vision once the hyphema resolves, but absence of an indirect pupillary light reflex can be the result of failure of light to reach the retina due to obstruction by dense anterior chamber blood

• If corneal edema or hyphema precludes evaluation of structures posterior to the cornea, ocular ultrasound should be performed

  • Retinal detachment, lens luxation, or intraocular neoplasia may be underlying etiologies for hyphema and can potentially be identified ultrasonographically

Hyphema Management/Treatment

• Stopping the bleeding for sources that are amenable to therapy, reducing inflammation associated with frank blood in the anterior chamber, and facilitating resorption of blood

• Topical and systemic anti-inflammatory drugs are the primary medical therapies

• Caution in use of topical corticosteroids as corneal ulceration is potentially associated with hyphema

• Caution with the use of mydriatics because IOP can increase rapidly as RBCs occlude the iridocorneal drainage angle

• Anti-inflammatory and mydriatic therapy may need to be continued long term, even after hyphema has apparently resolved, to reduce synechia formation and decrease the likelihood of cataract formation

Retinal Detachment

• Separation of the neurosensory retina from the pigmented epithelium

Retinal Detachment Etiology/Pathogenesis

• Occurs when the interface between the retinal pigmented epithelium and the neurosensory retina is disrupted

• May be accomplished by fluid accumulation, hemorrhage, or during blunt force trauma

  • Also a complication of ERU

Retinal Detachment Clinical Features

• Evaluation of the fundus will reveal an elevated hazy area in the retina in partial tears or a gray, floating veil of tissue extending into the vitreous in complete tears

• Acute blindness or slowly progressing loss of vision may be appreciated

Retinal Detachment Diagnosis

• If the cornea is opaque, the vitreous is cloudy or bloody, or a cataract is present, ultrasonographic examination may be necessary to obtain a diagnosis

  • Seagull sign may be noted on ultrasonographic examination in a complete detachment

Retinal Detachment Management/Treatment

• Treatment of the underlying source of inflammation is indicated

• Prognosis for retinal reattachment and return of vision in the detached area is poor

Glaucoma

• Optic neuropathy associated with abnormal aqueous outflow resulting in elevated IOP

Glaucoma Etiology/Pathogenesis

• Results when outflow of aqueous humor is impaired

  • Can occur as primary disease associated with abnormal conformation of the iridocorneal angle, or as secondary disease

    • Primary disease not well described in horses

    • Secondary glaucoma has numerous mechanisms including contraction of preiridial fibrovascular membranes (which form as a result of uveitis), occlusion of the iridocorneal angle by cellular debris or protein (as with uveitis or hyphema), posterior synechia (adhesion of the iris to the cornea) causing pupillary block, or mechanical obstruction as with lens luxation, intraocular tumor (e.g. melanoma), or infectious endophthalmitis

Glaucoma Clinical Features

• Associated with increased IOP, but pressure in a uveitic eye with secondary glaucoma may be normal

• Normal range of IOP in horses is generally 18-28 mmHg

• Typically manifests clinically as corneal edema with a dilated pupil, but may be accompanied by signs of uveitis such as corneal vascularization, aqueous flare, and miosis

• Bupthalmos develops with very high IOPs in horses

  • Once it develops it typically doesn't resolve

• On evaluation of the iridocorneal angle, the pectinate ligament appears abnormal

Glaucoma Diagnosis

• Measurement of IOP is necessary but not sufficient to diagnose glaucoma

  • IOP must be interpreted in the context of the remainder of the ocular examination including globe size, globe position, and pupil size

• Examine the iridocorneal angle

  • Additional diagnostics that may provide more information about visual prognosis include ocular ultrasound and electroretinography

Glaucoma Management/Treatment

• Management is directed at decreasing IOP and controlling any associated primary disease process that underlies secondary glaucoma

• Medical therapy is generally directed at one of two mechanisms

  • Decrease in the rate of aqueous production

  • Increase in the rate of aqueous outflow

• Drugs that decrease aqueous production in horses: beta blockers (timolol) and carbonic anhydrase inhibitors (dorzolamide)

  • Prostaglandin analogs (latanoprost) don't work in horses

• Surgical therapy includes procedures targeted towards decreasing aqueous production and those intended to increase aqueous outflow

  • Aqueous production can be decreased by damaging the ciliary body, either with cryotherapy or laser therapy

    • Cryotherapy is associated with severe postoperative inflammation and is best reserved for use in permanently blind eyes

  • Transcleral cyclophotocoagulation with a diode laser is used but topical therapy must also be used after

  • Increased aqueous drainage from the eye can be accomplished via a gonioimplant, which bypasses the obstructed iridocorneal angle and directs aqueous humor to the subconjunctival space where it is absorbed into the bloodstream

    • Experimental in horses

Acute Bilndness Etiology/Pathogenesis

• Often traumatic

• Many causes

  • An obstruction in the normally clear ocular media

  • Bullous separation of, or a tear in, the neurosensory retina from the outer retinal pigmented epithelium

  • Acute glaucoma

  • Optic nerve ischemia related to acute blood loss

  • Optic neuritis

• Surgical ligation of the internal or external carotid artery can cause ischemic optic neuropathy and acute, permanent blindness

• Optic neuritis can be caused by parasites, recurrent uveitis, encephalomyelitis, and neoplasia

Acute Blindness Clinical Features

• In cases where blindness is retinal in origin, or involves structures involved in the PLR including the optic nerve, mydriasis is the hallmark

• Horses with central or cortical blindness but normal retinas and optic nerves will typically have intact PLRS, but still be blind

Acute Blindness Diagnosis

• Electroretinography can be used to evaluate retinal function and differentiate between retinal and non-retinal blindness

• Ocular ultrasound examination for retinal detachment

Acute Blindness Management/Treatment

• Directed at the underlying disease process

• Optic neuritis - treatment with systemic corticosteroids

• Prognosis for return of vision depends on the nature of the underlying disease and response to treatment