Ocular Emergencies (Mexico)
Adolfo Guandalini, DMV, Phd, DECVO
Ambulatorio Veterinario
Roma, Italy

We intend a patient to be in condition of ocular emergency when he shows sudden clinical signs of diseases that jeopardize irreversibly his vision.

Emergencies are mainly divided in traumatic and non-traumatic ones, although most of them have a traumatic origin.

Among non-traumatic emergencies we find: orbital cellulitis and abscesses, acute keratoconjunctivitis secca (KCS), corneal ulcers, acute glaucoma, acute uveitis, anterior lens luxation, retinal detachment, SARD (sudden acquired retinal degeneration), optic neuritis, centrally originated blindness and endophthalmitis.

Among traumatic urgencies we must identify those situations that we can consider true emergencies such as: globe prolapse, conjunctival and corneal foreign bodies, corneal chemical burns, corneal wounds and perforations, iris prolapses, and lens rupture with phacoclastic uveitis as a consequence.

Traumatic conditions which are not considered emergencies are eyelid and third eyelid wounds (TE). They cannot be treated immediately but only when post-traumatic edema is controlled with drugs and after conjunctival and scleral haemorrhages healed simply with medical therapy and time.

Proptosis of the eyeball consists in severe exophthalmos with eye protrusion out of its normal position inside orbit. Bites, contusions and car accidents are the most frequent reasons. Canine brachycephalic breeds, as a consequence of their non-deep orbit and a very large eyelid fissure, are naturally bent for this condition. However, it is rare in cats, with a bad prognosis for the maintenance of visual function. Clinically, in these cases we can find chemosis, subconjunctival and retrobulbar haemorrhage, hyphema and sometimes lens displacement. Proptosis can damage extraocular muscles (in particular the ventral oblique and medial rectus muscles) with a consequent divergent strabismus. We can observe keratitis due to exposure, still mydriasis (because of the optical nerve damaged). In case of prolapse, the ocular surface should be smoothed with ointments, saline solution, or simply a humid gauze, and the eyeball repositioned as soon as possible (within 15-30 minutes, to a maximum of 3-12 hours).

To help repositioning we can resort to lateral canthotomy. Then, a temporary tarsorrhaphy can be performed for 10-14 days and antibiotics are administered and NSAID systemically.

In the breeds which are bent to eyeball proptosis we can carry out medial and/or lateral canthoplasty.

The eyeball prolapse complications are: blindness caused by damage to the optic nerve, strabismus, chronic KCS, neurotrophic ulcer and atrophy of the globe.

Foreign bodies involving conjunctiva, TE and corneal bulbar surface can produce blepharospasm, photophoby, tearing and keratitis. The foreign bodies, most frequently found, are graminaceous awns or metal shot.

Foreign bodies involving TE can cause corneal trauma, while those penetrating the cornea can produce bacterial or mycotic intraocular infections. Removal is the only recommended therapy. Use a 25 G needle for the cornea.

Corneal chemical burns are treated irrigating with abundant saline solution or preferably lactated Ringer's solution or balanced salt solution (BSS). Acid elements usually do not penetrate through epithelium and superficial stroma because of the induced coagulation of proteins. Alkaline substances produce the worst damage destroying epithelium and stroma. Proteins do not clot and alkaline substances cannot be stopped from penetrating through the cornea. In this case, we recommend to administer a boric or acetic (0.5%) acid solution as soon as possible, for 2 hours, every 15 minutes.

Wounds, corneal perforations and iris prolapses are due to foreign bodies, bites, scratches, car accidents and lesions by shots. Clinically we observe, photophoby, tearing, blepharospasm and hyphema. In case of corneal wounds take into consideration the risk of perforation; in perforations we observe loss of aqueous humor and hypotonia as a consequence, iris prolapse, possible traumatic lens rupture followed by lens induced phacoclastic uveitis. In case of perforations and iris prolapses the patient risks intraocular infection with endophthalmitis and as a consequence loss of visual function and further loss of anatomic integrity of the eyeball. In case of wounds perforations and iris prolapses, the indicated therapies depend on the depth of the lesions: soft contact lens, cyanoacrylic glue, TE flap, direct corneal suture, pedicle or free conjunctival flap, corneo-conjunctival transposition, corneal graft, and, in case of severe infections, enucleation.

In case of corneal perforation it is extremely important to detect any possible anterior capsule rupture of the lens. In case of capsule laceration over 1.5 mm, lens removal is recommended through phacoemulsification. In fact, the exposure of a large amount of immunogenic lenticular proteins can overcome the normal condition of immunologic tolerance and cause a sudden intraocular inflammation with further secondary glaucoma. The eye involved must be treated with a topic and systemic antibiotic therapy, cycloplegic mydriatics and immune-suppressive steroid therapy.

Among non traumatic ocular emergencies we find first of all cellulitis or orbital abscess. It depends if the phlogistic material is diffused or tends to be accumulated into a sac. Clinical signs are: acute exophthalmos, mucous or mucopurulent discharge, TE protrusion, conjunctival hyperemia, pain evoked by retropulsion of the eyeball and while opening the mouth, fluctuating mass behind the last molar tooth, high temperature, general malaise and high neutrophilia. The most frequent reason are periapical dental abscesses. The most indicated therapy is the abscess drainage, placed through the retromolar space, and system administration of antibiotics.

Corneal ulcers are frequent emergencies caused by quantity and quality modifications alterations of the tear film, disorders of eyelashes (trichiasis, ectopic cilia, distichiasis) mycotic and bacterial infections.

The worst consequence of corneal ulcers is perforation. According to their depth, they can usually be treated with medical therapy (antibiotics, homologous serum, EDTA, acetylcysteine, tetracyclines, and cycloplegic mydriatics topically) or surgery (pedicle or free conjunctival flap, corneo-conjunctival transposition, corneal graft, etc.).

Acute glaucoma consists in a sudden increase of intraocular pressure (IOP). High IOP brings to irreversible damage to retinal ganglion cells within 24-48 hours.

Clinically we can notice severe pain, congestion of episcleral vessels, diffuse corneal edema, midriasis and sudden loss of vision. Glaucoma must be treated immediately with medical therapy, administering hyperosmotic agents, mannitol at 20% in particular, slow IV injection taking 20-30 minutes, 1-2 g per Kg of weight, and prostaglandins topically. The hypotensive effect is achieved after 15-30 minutes and lasts 4-6 hours.

The acute uveitis is distinguished by a possible temporary loss of vision or hypovision, aqueous flare, hypopyon, hyphema, extreme miosis. The most severe consequence is secondary glaucoma. The emergency must be treated topically and systemically with steroid and non-steroid therapy, cycloplegic mydriatics topically.

The lens luxation can be found in very elderly cats or old dogs (over 10 years) or in those breeds which are bent to (especially Terrier Breeds between 4 and 7 years old). The most frequent reason is the degeneration of zonular suspensory ligaments, because of hereditary predisposition in dogs or previous uveitis in cats. They can be uni- or bilateral. Clinical signs are: iridodonesis, phacodonesis, aphakic crescent, changes of depth in the anterior chamber and localized corneal edema. The most frequent complications are: uveitis, secondary glaucoma and cataract. The most indicated therapy is the intracapsular extraction of the lens, to be done as soon as possible (within 24-72 hours), with or without implanting a sulcus fixation intraocular lens (IOL).

Retinal detachment is another possible emergency. It can be rhegmatogenous (connected to retinal holes) or non rhegmatogenous (exudative or traditional). It is extremely important to identify any possible associated systemic disease (hypertension, infective diseases, etc.) that must be necessarily treated.

SARD (Sudden Acquired Retinal Degeneration) seems to be a toxic-origin disease. It presents sudden blindness, usually irreversible. It becomes evident in a short time (within 4 weeks) or even very quickly (within 12-24 hours). Diagnosis is carried out through electroretinography. There is no therapy.

Optic neuritis can be uni- or bilateral and it presents mydriasis, edema, optic disc haemorrhage and hyperemia and peripapillary retinal edema. If present, any possible infective systemic, neoplastic disease or GME must be detected. A neurologic consult is recommended. In case of infective disease the therapy will be specific while in case of immune-mediated or inflammatory disease therapy will be based on steroids, systemically administered.

Sudden centrally-originated blindness can be caused by an intracranial pressure increase (for ex. hydrocephalus) or by masses located at the optic chiasma level (ex: hypophisary macroadenoma). In this case a neurologic and oncologic consult is recommended.

Bacterial or mycotic originated endophthalmitis is a further severe condition of emergency to be faced quickly; due to its infective nature there is a high risk of embolic-metastatic blood spread, followed by septicemia. An aggressive antibiotic systemic therapy is recommended, although more frequently this condition requires enucleation.

REFERENCES

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Adolfo Guandalini, DMV, Phd, DECVO
Italy


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