SAVA Wits 2019: “What to refer timeously?” – a look at ocular emergencies.The eye is a delicate organ and should a condition occur that is serious, or vision threatening then it should be attended to timeously. In essence the conditions requiring this type of action are your ocular emergencies.

What are they?

1. Eyelid disease [ectopic cilia]2. Corneal emergencies [melting stromal ulcer, chemical trauma, Descemetocele,

corneal laceration, iris prolapse, foreign body]3. Hyphaema4. Anterior lens Luxation5. Acute Glaucoma6. Diabetic cataracts7. Retrobulbar abscess8. Proptosis9. Acute onset blindness [optic neuritis]

Ectopic Cilia:Ectopic cilia originate from a Meibomian gland and grow through the palpebral conjunctiva. They emerge from the palpebral conjunctiva 2 - 6 mm from the eyelid margin. The most common site is the 12 ‘o clock position of the upper eyelid. In this position they then can cause severe trauma to the cornea surface resulting in deep ulcerations and descemetocoeles.

Diagnosis:

Evert the eyelid and examine with magnification. Cilia may be depigmented.

Treatment:

Resection of the cilium and gland under magnification [this is an older technique and likely to cause severe damage. It should only be considered when there are multiple nests of cilia.

Electroepilation of the cilium. Cryosurgery and epilation.

Corneal Emergencies:

Foreign Bodies:

The presence of any foreign body on the ocular surface or penetrating the eye should be removed immediately. In some cases superficial corneal foreign bodies

may be irrigated off the corneal surface after the application of a topical anaesthetic.

Corneal lacerations:

In companion animals the most common cause are cat scratches. Treatment:Non penetrating lacerations with minimal corneal damage will heal with topical medication (antibiotic and atropine). Lesions that extent up to descemet’s membrane or have perforated should be sutured using 8/0 Vicryl or 10/0 nylon.

Chemical trauma:

Caustic or basic chemical injuries result in progressive damage to the proteins of the cornea and damage is progressive whilst an acid chemical trauma will cause immediate damage to the ocular tissues. Corneal ulcers and secondary uveitis is the common presenting problem. Immediate irrigation of the eye is required followed by antibiotic drops, lubricants [viscoelastic] and oral NSAID. The intense corneal edema and subsequent ciliary flush may take weeks to resolve.

Melting Stromal Ulcers:

A corneal wound becomes complicated if healing is prevented by the persistence of the initial cause or by the invasion by microorganisms. If polymorphonuclear cells are unable to arrest bacterial multiplication, tissue destruction occurs. MMP’s released by bacteria (especially Pseudomonas), epithelial cells and leukocytes initiate melting by cleaving collagen fibrils. Once initiated the melting process can become autonomous and continues in spite of the eradication of microorganisms.

Treatment:Determine and treat the initiating cause if possible. The treatment of corneal ulcers requires one or more of these therapeutic influences:

Analgesic Antimicrobial Anticollagenase Protection Support

Analgesic therapy: Corneal ulcers are accompanied by pain, as a result of direct sensory nerve stimulation or through uveal stimulation. Parasympatholytic agents stop ciliary spasm by blocking the parasympathetic receptors of the iris and ciliary body leading to analgesia. Atropine eye drops bid for 5 to 10 days only. Morphine 10mg/ml can be used undiluted directly on the cornea tid. Never use topical ophthalmic anaesthetics as these are epitheliotoxic.

Antibiotic treatment: Topical antibiotics are indicated to prevent bacterial infection in superficial ulcers or to eradicate already established infections. Frequency of medication depend on the severity and etiology. Hourly with melting ulcers and qid for less severe. In uncomplicated ulcers a broad spectrum antibiotic drop like oflaxacin is used. If stromal melting is present an antibiotic is chosen whose spectrum includes activity against Pseudomonas. [moxifloxacin and aminoglycosides] . Tobramycin based products should always be the very last resort as these are potentially becoming the only available antibiotic world wide that may be able to manage otherwise resistant bacteria.

Anticollagenolytic drugs: EDTA and Tetracycline have been used, they are chelating agents preventing the breakdown of collagen. Oral Doxycycline is secreted in tears and by using this drug the cornea is constantly flushed by a chelating agent. The best anticollagenolytic agent is serum / plasma, because of this reason conjunctival flaps have an anti-collagenolytic effect. Blood can also be spun down and the plasma can be applied as a topical eye drop. Acetyl cysteine is less commonly used.

Surgical treatment: Surgical options include the careful surgical debriding of the affective tissue out of the cornea and then placement of a conjunctival pedical graft. Conjunctival flaps protect and support the cornea, provide analgesia and are anticollagenolitic. Other options include amnion grafts and crosslinking. Crosslinking stabilizers and strengthens the collagen of the cornea and assists in sterilizing the corneal tissue.

Descemetocole:

A descemetocoele will result when a stromal ulcer erodes down to the descemet’s membrane. In most cases it is infected and because it is a 4-7micron membrane, the globe can easily rupture and treatment is best managed with a conjunctival pedical graft or amnion graft.

Iris Prolapse:

Any perforation of the cornea or limbal sclera can result in the iris protruding out the globe. This will result in the iris desiccating. A prolapsed iris should be surgically managed as soon as possible should one aim at preserving the globe.

Hyphaema:Intraocular hemorrhage is a common finding in animals and can be due to:

Trauma - perforating wounds, blunt blow to the eye region, choking a dog with a leash.

Fragile iris blood vessel walls. Clotting disorders, platelet disturbances, dyscrasias, liver disease, DIC

Neovascularization of the iris or retina [CEA]. Vascularised tumours. Systemic hypertension Hyperviscosity syndrome Severe uveitis. Retinal dysplasia and rupture of vessels. Systemic disease [E canis], hypertension. Chronic glaucoma. Post cataract surgery [a few months later, following neovascularization and blood

vessel rupture]. Spontaneous.

In most cases it is not the presence of frank blood in the anterior chamber that causes problems but the sequelae that can occur following hyphaema. Most hyphaemas are minor and will be absorbed rapidly or over a few days. If the posterior segment of the eye cannot be visualised with a light source then it is mandatory to perform ocular ultrasound to image the posterior segment and retina. This can assist with a prognosis for the owner as retinal detachment with vitreal haemorrhage is frequently seen with hyphaema cases.

Complications following hyphaema include:

Glaucoma - the iridiocorneal angle is occluded by RBC’s. Fibrinous bands and synechiae development. Occlusion of the pupil. Cataract. Phthisis bulbi. Recurrent hyphaema. Corneal opacity.

Treatment:

Many different treatment regimes have been advocated.

Immediate and enforced cage rest and identify the cause of the hyphaema and treat appropriately.

Monitor for secondary glaucoma. Take a base line intraocular pressure when one is first presented with the patient.

Topical and systemic corticosteroids. Confirm the absence of corneal ulceration with fluorescein stain before topical corticosteroid medications.

Topical atropine drops to cause mydriasis. This causes cycloplegia and prevents synechiae and pupil block glaucoma as well as remove the pain due to iris and ciliary body muscle spasm. Atropine can also stabilize the blood aqueous barrier. This treatment may be controversial since mydriasis can further complicate a secondary glaucoma by further obstructing the drainage angle. It has also been shown that blood, inflammatory cells or cellular debris can further increase the hypertensive effects. Tropicamide [Mydriacyl, Mydriaticum], a short acting mydriaticum

could be used in an attempt to allow more regular movement of the iris. Phenylephrine can also be used to dilate the pupil.

Miotics such as pilocarpine have been used on the basis that by forcing miosis the drainage angle is more open and thus allows more RBC drainage. Also miosis will expose a greater surface area of the iris stroma which has fibrinolytic activity which can assist in breaking down the clot. Pilocarpine and phenylephrine can be used every second day to maintain iris movement.

Should a clot be persisting after the above treatments then one could consider opening the anterior chamber and flushing the clot or using an irrigation –aspiration port from the cataracts surgery module or even vitrector to remove the blood clot. This is a specialized procedure done under controlled conditions and requires magnification and specialized equipment.

Intra cameral tissue plasminogen activator [TPA] can be used in some cases to rapidly dissolve the fibrin and blood clot. Re-bleeds could also occur. It is mainly used when there is concern for the development of posterior synechiae.

Anterior lens luxation:

Lens luxation is the displacement of the lens from its normal position. It occurs due to a complete or partial breakdown of the zonnular attachments. Lens luxations can be classified as subluxation, anterior lens luxation and posterior lens luxation.

Anterior displacement of the lens without moving into the anterior chamber leads to the anterior displacement of the iris and a shallow anterior chamber. If the pupil dilates the lens can move into the anterior chamber, this may be partial or complete. Luxation into the anterior chamber will lead to contact between the lens and endothelial cells and permanent damage to the endothelial cells.

Etiology:

Primary lens luxations

o Congenital. It is most often seen in animals with multiple ocular anomalies, but can occur alone.

o Hereditary. These animals are born with an inherent zonnule weakness. Histologically these fibres have a bizarre reticulate formation. Hereditary primary lens luxation is seen often in Terriers [FT and JRT]. Boisterous behaviour may precipitate the condition. In Chinese Shar Pei’s it has been found to be a simple autosomal recessive trait [Vet Ophth 1998,1,2-3,101-107]

Secondary lens luxationo Traumatic. Usually seen with other ocular lesions for example hyphaema

and retinal detachments.o Glaucoma with buphthalmos. The stretching of the ocular tunics causes

physical stretching of the zonules and eventually zonnule rupture.o Chronic uveitis resulting in inflammation and weakened zonnules.o Cataracts. Advanced cataracts are associated with zonnular degeneration.o Intra ocular tumours.

Clinical signs:

Displacement of the lens is easily determined as long as the cornea remains clear. The lens can be seen in an abnormal position. If the cornea is not clear the globe should be imaged with ultrasound and the luxated lens will be visible in the anterior chamber or posterior segment of the globe if luxated caudally.

Iridodenesis/ phocodenesis. Abnormal vibration of the iris / lens when the patient move it’s eye.

Increased or decreased depth of the anterior chamber. Aphacic crescent. This is the area in the pupil where the lens is missing. Increased intra ocular pressure. This is caused by vitreous dragged into the

pupil and drainage angle. Vitreous situated in the pupil can block the pupil completely.

Corneal edema in the areas where the lens is in contact with the endothelial cells. Endothelial cell damage will lead to permanent corneal oedema.

Vitreous may be seen in the anterior chamber. Syneresis. Liquefaction of the vitreous is seen in posterior lens luxation.

Anterior lens luxation is the most hazardous form of displacement. In most cases it will lead to development of glaucoma and corneal edema. This condition is considered as an ocular emergency.

Treatment:

Trans-corneal reduction [TCR]: This procedure involves dilating the pupil with drops, intravenous mannitol drip to dehydrate the vitreous in the posterior segment of the eye, general anesthetic, fine needle aspirate of fluid from the anterior chamber of the eye, the application of a soft bandage contact lens and then gentle manual pressure applied to the eye to attempt to push the loose lens back through the pupil. The pupil is then medicated to constrict the pupil for life.

Trans corneal reduction followed by intracapsular lens extraction [TCR-ICLE]: As for the above but in some patients the lens cannot be manually pushed through the pupil as a result of adhesions or excessive vitreous present meaning that the next option to attempt to salvage vision is to open the eye surgically and deliver the loose lens from the eye and then close up the eye.

Trans-corneal reduction plus globe removal [enucleation]: Once again if the lens cannot be pushed caudally through the pupil [No 1 above] the owner may then decide not to consider the more invasive surgery [No 2 above] to salvage vision and decide to remove the globe.

Intracapsular lens extraction [ICLE]: No attempt is made to repulse the lens and the eye is opened through a 180 degree corneal incision, flapping the cornea open and then delivering the loose lens out the eye and finally closing up the eye with fine dissolvable sutures. This method means that the loose lens is no longer present in the eye to cause future problems. This is the direct first choice in patients that have cataracts and lens induced inflammation.

Watch this You Tube video: https://www.youtube.com/watch?v=tzajmhD0Tgw

Posterior lens luxationIf no glaucoma, the lens can be left in the vitreous. The owner should be warned about the possibility of anterior luxation as well as secondary glaucoma. Prostoglandin eyedrops / Demacurium Bromide can be used to induce miosis and keep the lens in the vitreous chamber.

It is suggested [Vet Ophth 2004, 7, 451] that prophylactic use of a miotic in the “normal” contralateral eye may improve outcomes.

Acute glaucoma:

Pain: Blepharospasm, epiphora and protrusion of the third eyelid. Red eye: Episcleral vessel congestion. These vessels appear as large, deep

straight veins coursing posteriorly from the limbus. The congestion occur secondary to a mechanical obstruction to scleral venous return secondary to globe enlargement.

Corneal edema Mydriasis Optic nerve cupping Increased size of the physiologic cup and reduced optic nerve diameter. The

increased intra ocular pressure cause mechanical compression of the axons and microcirculatory abnormalities in the area of the lamina cribrosa resulting in axoplasmic transport disruption, axon ischemia and atrophy. This is the primary cause for the loss of vision in animals with glaucoma.

Vision may be affected. Normal ERG. Glaucoma destroys the retinal ganglion cells first. In early

glaucoma the photoreceptor cells and inner nuclear layer of the retina remains normal, hence the normal ERG.

Medical treatment of acute glaucoma:Acute glaucoma is an ophthalmic emergency. A pressure of > 50 mmHg will lead to irreversible optic nerve damage.

Osmotic diureticsUsed to decrease intraocular pressure rapidly. It shifts fluid from the aqueous and vitreous to the adjacent vasculature, thus dehydrating the eye. These drugs should be used for emergency use only and are not practical or effective for long-term use.

Mannitol (2g /kg IV) is the drug of choice for dogs and cats. Mannitol should be administered through a blood administration set at body temperature over a period of 20 -30 minutes. Water should be withheld for 4 hours. The effect will last for 6 hours. If a patient does not respond during this time, it is considered refractory to medical treatment and surgical options should be considered.

Drugs that reduce aqueous production:Carbonic anhydrase inhibitors (CAI) are used for long-term maintenance of intraocular pressure. They prevent bicarbonate ions entering the posterior chamber. Dorzolamide (Trusopt / Glaucopress 1 drop tid). [This the current drug of choice for the treatment of glaucoma]

Drugs that increase aqueous outflowParasympathomimetics

Demecarium bromide is a potent, long acting cholinesterase-inhibitor used topically to treat acute glaucoma. Parasympathomimetic drugs cause contraction of the muscles associated with the ciliary body and of the iris sphincter. This allows increased outflow of aqueous humour by mechanically opening the iridocorneal angle. In dogs, demecarium bromide has been shown to decrease intra ocular pressure for up to 48 hours.

Prostaglandins. Increase uveoscleral outflow. It reduces intraocular pressure by 27-37 %. The drug should never be used in patients with uveitis. Patients should be examined regularly for the possible development of uveitis. Cats do not have the necessary receptors and therefore the drug is not that effective in the species.

Latanoprost (Xalatan 1 drop oid -bid) Travoprost (Travatan 1 drop oid) Bimatoprost (Lumigan 1 drop oid)

Prostoglandins lead to a very rapid decrease in intra ocular pressure and is the drug of choice [in dogs without uveitis] to decrease IOP in an emergency situation.

Diabetic cataracts:

The lens proteins are antigenic. There is a constant low level loss of lens proteins from a normal lens. This stimulates lens antibody production, but T suppressor cells prevent an inflammatory response. Cataracts and rupture of the lens capsule lead to excessive release of lens proteins with consequent uveitis, referred to as Lens Induced Uveitis [LIU]. Diabetic cataracts result in rapid influx of fluid into the lens, cause swelling of the lens fibers and subsequent increase in liquefaction of the lens proteins and their subsequent “leakage” through the lens capsule. This then drives the rapid onset LIU which then leads to secondary hypopyon and glaucoma. The globe then is destroyed and frequently may require enucleation.

The window of opportunity to perform cataract surgery and salvage vision is short so in essence all diabetic dogs should be evaluated for cataracts. It is interesting to note that basically all diabetic dogs will form cataracts:25% by D6050% by D170 (5mnths)75% by D360 (12mnths)80% by D470 (15mnths).The current literature indicates that there is a greater risk of losing the globe to uveitis / glaucoma if left unattended versus the potential complication risk following cataract surgery.

Retrobulbar abscess:Inflammatory orbital disease can be caused by bacteria [aerobes and anaerobes], fungi, parasites or other causes like eosinophilic myositis. The process usually begins as orbital cellulitis, which localizes, and at a later stage organizes and forms an abscess.

Agents causing inflammation may gain entrance to the orbit via; haematogenous route. wounds due to external caudal trauma. penetrating wounds in the oral cavity and retrobulbar space. infection in the adjacent paranasal sinuses and nasal cavity. sialoadenitis or abscess of the zygomatic salivary gland. secondary rupture of the proximal nasolacrimal duct in cases of

dacrocystorhinitis. foreign body from the oral cavity or those penetrating the orbital adnexa or

conjunctiva.Clinical signs:

Orbital cellulitis and abcessation is characterized most often by; Acute unilateral exophthalmos . Protrusion and congestion of the third eyelid. Decreased globe mobility. Serous to mucopurulent ocular discharge.

Periocular pain. Severe pain on opening the mouth. Lethargy and fever are common and assist in indicating an inflammatory cause. An inflammatory leucogram may also be present. A normotensive globe but scleral congestion may be present due to scleral

vessel occlusion and blood stasis

A differentiation between retrobulbar abscess and orbital cellulitis must be made. The latter generally has less pain, pyrexia and little or no exudate seen on drainage. Generally the eyelids are more discoloured, there may be severe chemosis and exophthalmos is substantially less. Both conditions are treated similarly.

Diagnosis and treatment:A definitive diagnosis and treatment of orbital disease requires a thorough investigation under general anaesthesia of all the possible routes of infection. Fluctuant swellings caudal to the upper molar should be probed for fistulous tracts or surgically prepared for lancing by incising only the buccal mucosa with a scalpel blade and then placing a curved haemostat into the hole and gently pushing it up into the retrobulbar region and opening the forceps points. Exudate should drain from the oral wound. Samples for culture could be taken at this point if required. By opening and closing the jaw more exudate can be “pumped” out of the wound. The retrobulbar space can be flushed with sterile fluids. Synulox is a good covering antibiotic to use following the surgical drainage. Oral non steroidal drugs may be indicated if the inflammation is severe and vision is threatened. The globe itself may require topical lubricants to protect the cornea from dessication.

GLOBE PROPTOSIS:

This is when a globe is displaced from the orbit and is usually associated with stretching and tearing of extraocular muscles and/or the optic nerve. Brachiocephalic breeds are predisposed because of their large eyes relative to the head as well as the shallow orbits. Severe fright, trauma, dog fights etc are frequent causes of proptosis. The table below indicates what are important prognostic signs for a prolapsed globe.

CLINICAL SIGN FAVOURABLE UNFAVOURABLEDuration Short LongDamage to extraocular muscles

No or mild muscle damage Muscle avulsion

Hyphaema None Present or obliterating pupilPupil size Miotic Mydriatic / NormalPupillary light response Present - direct pupil

response and a consensual response

Absent - direct pupil response and consensual response

Retrobulbar haemorrhage and edema

Minimal Extensive

Intraocular pressure Normal Hypotony [ruptured globe]Glaucomatous [Secondary glaucoma from hyphaema]

Table 15.4: Prognostic clinical signs for cases of proptosis

Proptosis is a condition that must be handled by the general practitioner. The clinical evaluation of the patient and globe is essential before the owner can be given a prognosis or treatment regimen is initiated.

Fig showing the proptosis

It is essential to perform the following steps:

Perform a thorough general clinical examination as frequently the proptosis is associated with other serious trauma. Check and see if the globe is viable. Is there a laceration of the sclera with vitreous leaking or the lens ruptured? These carry a zero prognosis and enucleation would be the treatment of choice. Check the degree of strabismus and extraocular muscle damage. Dorsolateral strabismus is most common as a result of the short medial rectus and ventral rectus muscles rupturing. The eye has a blood supply to the ciliary body via the rectus muscles and should more than two be ruptured then the blood supply could be affected. This alone would lead to phthisis bulbi over time. Check for hyphaema and secondary glaucoma. Hyphaema generally indicates damage to the ciliary body. Anterior lens luxation may also be present. Ultrasound would be a useful diagnostic tool in this case.Neurological assessment of the affected and fellow eye should be performed.

1] Miosis: is a normal response to pain - this is favourable.

2] Mydriatic: this indicates that sympathetic innervation is still present but damage to the oculomotor nerve or ciliary ganglion is present. The prognosis is guarded.

3] Normal, mid-dilated non-responsive pupil: This occurs when both sympathetic and parasympathetic innervation has been lost. The optic nerve is permanently damaged.

Check pupil responses. The direct pupil response is not of much use at the time of injury. A consensual response in the unaffected eye is a favourable response. If direct responses have not returned after about a week then the prognosis for vision to return is poor. Intraocular pressure. This is usually normal but will obviously be soft [hypotony] if the globe has ruptured.

Proptosis is a true ocular emergency and the eye should be replaced under general anaesthetic as soon as possible, providing the general health of the patient allows anaesthesia.

Surgical replacement of a proptosed eye:General anaesthetic is required. Clean the eye of debri, sand etc. use warm water and no detergents directly on the cornea. The hair at the lateral canthus could be clipped. Because the eyelids are holding the globe, it may be necessary to perform a lateral canthotomy. This is done by using scissors. The eyelids are grasped with forceps or by preplaced nylon sutures. The globe is lubricated liberally with topical ophthalmic antibiotic ointment before it is gently pushed back into the orbit so that it sits behind the eyelids again. This can be aided by lifting the preplaced nylon sutures. About three mattress sutures are placed through the eyelids. It is essential that the suture is passed through the tarsus and not through the bulbar conjunctiva. If the latter occurs the nylon could damage the cornea. Topical ophthalmic ointment is applied between the sutures. Postoperative antibiotics and corticosteroids / NSAID’s should be given. Sutures should be left until there is minimal tension between the eyelids [usually 1-3 weeks]. After removal of the sutures blepharoplastic surgeries may be required to reduce the palpebral fissure.

Acute onset blindness:Sudden Acquired Retinal Degeneration: Although the patient will go blind rapidly, the condition is not really in the category of an emergency as medical options may be consider after rather extensive medical work up, as the current thoughts are that SARD is an immune –mediate condition.

Rapid onset blindness may also be related to optic neuritis which would be considered an emergency as this condition could be resolved successfully with the immediate use of corticosteroid medications.

Optic Neuritis [papillitis]:This condition occurs in all species and can be unilateral or bilateral. It always causes blindness in the affected eye. Cause:Most cases occur as a primary disease whilst it may also be seen in association with CNS and systemic diseases. Any disease that may cause chorioretinitis could cause optic neuritis.

Infections Systemic disease, canine distemper,

Localized infections such as posterior episcleritis, retrobulbar abscess or cellulitis, guttural pouch infections.

Toxic: Ethyl and methyl alcohol, thallium, arsenic, lead, quinine and male fern ingestion in cattle.

Neoplasia: - Orbital neoplasia Immune-mediated conditions Granulomatous meningoencephalitis [GME] Traumatic:

Foreign bodies, trauma, orbital hemorrhage

Unknown – most cases of optic neuritis in dogs is in fact idiopathic.Signs:If bilateral involvement then the pupils will be mydriatic and there will be acute blindness. Fundoscopic examination will usually show papillitis [swelling of the optic nerve head and blurring of its border] There may be many small engorged blood vessels on the optic nerve as well as small hemorrhages. The physiological cup disappears when the nerve swells. The optic nerve head may also appear normal when only the retrobulbar portion of the optic nerve is affected. Circumpapillary retinal edema occurs and appears as though the blood vessels surrounding the nerve head are floating in space above the fundus. Small hemorrhages may also appear in this area. In horses there may be small blood clots in the vitreous. Exudate may also be seen on or around the optic disc. Papillitis is frequently associated with cells in the vitreous – hyalitis.There would be a normal ERG.

The differential diagnoses for this condition are: Papilledema SARD Severe retinal disease Cortical blindness [intact PLR, normal fundus]

Figs showing retinal blood vessel congestion [Colour Atlas, Barnett].

Treatment:Specific treatment if the cause is known. The basis of treatment is to relieve the inflammation and restore vision.

* Oral / injectable corticosteroid administration.* Systemic antibiotics if bacterial or fungal involvement is suspected.* GME patients respond best to Dexamethasone * Equine cases may be given Flunixin meglumine, oral NSAIDs

If sight is not restored within 2 weeks then the prognosis is poor. If anti-inflammatories are started soon after blindness is noticed then the prognosis is favourable and the results are dramatic. The main sequelae to this condition is optic nerve atrophy and circumpapillary scarring.