Ординатура / Офтальмология / Английские материалы / Notes on Veterinary Ophthalmology_Crispin_2005

OPHTHALMIC EMERGENCIES AND TRAUMA

Figure 2.24 Acute glaucoma in a dog. The eye is painful, there are conjunctival and episcleral congestion, panstromal corneal oedema, a clear anterior chamber of normal depth, apparently normal iris detail and a widely dilated pupil. The intraocular pressure measured with an applanation tonometer (Mackay Marg) was 55 mm of mercury.

Salient clinical signs of acute glaucoma in the dog

•Pain, photophobia, blepharospasm and lacrimation

•The patient may be head shy and reluctant to move because the pain is so severe. Affected animals may also lose their appetite and, occasionally, they vomit

•Ocular redness due to ciliary injection and conjunctival and episcleral congestion. A circumcorneal brush border of blood vessels may be apparent within a few days of onset, especially if there is marked corneal oedema

•Corneal oedema (if the intraocular pressure is greater than 40–50mmHg)

•Dilated (mydriatic), non-responsive pupil, but note that when a previous uveitis has caused extensive posterior synechiae (adhesions), the pupil will be immobile and constricted (miotic)

•There is no direct or consensual pupillary light response

•High intraocular pressure (in excess of 30mmHg)

•Abnormal anterior chamber depth – e.g. iris inflammation and iris bombé will cause the anterior chamber to be shallower than normal, posterior lens luxation will cause the anterior chamber to be deeper than normal. There may, however, be no change in the depth of the anterior chamber

•Reduced vision or blind: affected animals can become acutely blind within hours of the onset of glaucoma. Owners are unlikely to notice a partial unilateral reduction in vision, but may, if observant, pick up unilateral blindness

PRIMARY LENS LUXATION

Primary lens luxation is the commonest cause of acute glaucoma in terrier breeds and cases should be referred as a matter of urgency if the expertise and facilities for intraocular surgery are not available (see Section 3, pp 148–149) (Figure 2.25).

Figure 2.25 Primary lens luxation with secondary glaucoma in a Miniature Bull Terrier. The classical pain triad of lacrimation, blepharospasm and photophobia was present. The eye is reddened, the lens is lying in front of the iris and the dorsal lens equator is highlighted by the light source. Contact of the anteriorly luxated lens with the posterior cornea has caused localised corneal oedema. The intraocular pressure (Mackay Marg tonometer) was 65 mm Hg. Lens luxation occurred in the fellow eye some weeks later.

Clinical features of acute lens luxation (in addition to those of glaucoma outlined above)

•Local corneal oedema if the lens is, or has been, anterior. The anteriorly-luxated lens can cause mechanical damage to the endothelial cells of the posterior cornea

•The lens can be visualised in an abnormal position – in the anterior chamber, pupillary aperture, immediately posterior to the iris or within the vitreous. Part, or all, of the edge of the lens (equator) can be highlighted as a bright reflective rim with penlight illumination. If the lens has moved from an axial position, an aphakic crescent may be apparent. The lens moves with ocular movement (phacodenesis) and can change position within the eye, although an anterior position is commonest when intraocular pressure is high

•Anterior-chamber depth may be abnormal, e.g. deep, if the lens is in the anterior chamber, or has dropped back into a liquefied vitreous, shallow if the lens and vitreous are causing pupil block

•Trembling of the iris (iridodenesis) when the dog moves its head, as the iris has lost the support of the lens

•Vitreous may be apparent in the anterior chamber, visible as faint, cloudy opacities at the pupillary margin

SUDDEN LOSS OF VISION

If the cause is not obvious, it is sensible to seek early specialist help: some types of acute visual loss benefit from early intervention if sight is to be restored, and electroretinography (ERG) is a critical tool in the evaluation of vision loss. The causes can be empirically grouped into those that affect the normal transparency of the ocular media, those that affect retinal function and those that affect the central nervous system (optic nerve to visual cortex). In addition to local ocular insults as a cause of vision loss, many generalised diseases are associated with acute blindness.

OPHTHALMIC EMERGENCIES AND TRAUMA

OPHTHALMIC EMERGENCIES AND TRAUMA

Causes of sudden blindness

•Acute-onset pancorneal opacity (e.g. panstromal oedema)

•Lipaemic aqueous because of chylomicronaemia

•Uveitis (anterior, posterior and panuveitis)

•Acute glaucoma (mainly dog)

•Globe rupture

•Haemorrhage (intraocular haemorrhage, local intracranial and extracranial haemorrhage and generalised severe haemorrhage) can all be causes of sudden blindness

•Retinal detachment (e.g. systemic hypertensive disease – intraocular haemorrhage may also be present)

•Sudden acquired retinal degeneration (SARD) in the dog

•When the blood supply to the optic-nerve head is severely disrupted, ischaemic optic neuropathy can result. Acute blindness associated with ischaemic optic neuropathy is an occasional complication of both primary and secondary haemorrhage, septic emboli and the surgical ligation of arteries. In horses, arterial ligation (e.g. maxillary, greater palatine, internal, external carotid) is a treatment for epistaxis associated with guttural-pouch mycosis and an occasional cause of acute vision loss on the ipsilateral side

•Optic neuritis and retrobulbar neuritis (e.g. associated with distemper virus)

•Toxic damage (e.g. toxic hepatic encephalopathy, quinolone antibiotics, anthelmintics like ivermectin, salt poisoning and lead poisoning) (Figure 2.26)

•Severe ocular trauma (e.g. intraocular haemorrhage, globe prolapse) and head trauma (e.g. poll injuries in horses, as a result of rearing and falling over backwards, can cause partial or complete shearing of the optic nerve as it leaves the brain through the optic canal)

•Metabolic disease e.g. hypoglycaemia in all species

•Intracranial lesions such as brain tumours (e.g. optic chiasma compression by neoplasm), haemorrhage, hydrocephalus, tentorial herniation

•Consequence of hypoxia/anoxia (e.g. anaesthesia-associated and following cardiac arrest in all species)

•Feline ischaemic encephalopathy (cerebral vascular infarction)

•Post-ictal (epilepsy)

Clinical findings

•The history can be of crucial importance, but on occasions is misleading, particularly when the loss of vision is the result of non-accidental injury

•External signs of damage to the head or eye may be apparent

•Partial or complete unilateral or bilateral blindness

•Sudden bilateral loss of vision usually renders animals nervous, easily startled and unable to function normally, even in a familiar environment. Unilateral blindness may not be recognised as quickly, although affected animals may show a similar behaviour pattern when approached on the affected side

•Normal or abnormal pupillary light reflexes (usually abnormal)

•Intraocular haemorrhage, or other signs of intraocular damage

•Retinal detachment, or more subtle retinal changes

•Optic nerve head (ONH) oedema (papilloedema) ± peripapillary and retinal haemorrhage

•When the cause of blindness is central only, there will be no indication of intraocular abnormality

Management

•Accurate case assessment is crucial, as it helps to determine if the damage is reversible or irreversible

•Treatment regimes for common causes of vision loss are listed in the relevant sections under specific conditions

SUDDEN OCULAR PAIN

If the cause is not obvious after careful examination, and particularly if the pain is intractable, it is important to seek early specialist advice. Reduction of ocular pain after the application of topical local anaesthetic (e.g. proxymetacaine hydrochloride 0.5%) implies external eye disease (e.g. ocular surface disease, ulcerative keratitis) rather than an intraocular problem (e.g. uveitis, glaucoma). Successful treatment depends upon establishing and eliminating the cause and the treatment of common causes of ocular pain are listed in the relevant sections under specific conditions (Figure 2.27(a–c)).

•Traumatic damage to eye, adnexa, orbit (including foreign bodies)

•Retrobulbar (orbital) abscess and orbital cellulitis

•Endophthalmitis and panophthalmitis

•Allergic blepharoconjunctivitis (mainly horse): acute conjunctivitis in all species is usually uncomfortable, rather than frankly painful

•Ectopic cilia and, less commonly, distichiasis and other lash and hair problems (mainly dog) producing corneal irritation or frank ulceration

•Acute dry eye, particularly if there is accompanying corneal ulceration

•Ulcerative keratitis (superficial ulcers are often more painful than deeper ulcers)

•Acute uveitis

•Acute glaucoma (mainly dog)

OPHTHALMIC EMERGENCIES AND TRAUMA

OPHTHALMIC EMERGENCIES AND TRAUMA

(b)

Figure 2.27(a–c) Sudden ocular pain in a horse (a). This horse had sustained blunt trauma to the globe hours earlier. Sedation and an auriculopalpebral nerve block were administered and subsequent examination revealed intense miosis and hyphaema (b). Medical treatment with atropine 1% and prednisolone acetate 1% was instituted. The pain diminished within an hour of treatment commencing and recovery was uneventful. The haemorrhage had almost resorbed two days after initial presentation (c) and the horse went on to make a complete recovery.

Box 2.3 Ocular conditions for possible referral

•Acute proptosis and prolapse when the aetiology is not obvious*

•Orbital neoplasia (and other orbital problems for which surgery may be required)

•Complex adnexal and intraocular neoplasia

•Endophthalmitis and panophthalmitis*

•Complicated blunt and penetrating trauma, including complex foreign bodies*

•Complex eyelid problems, including cases which require revision because of previous failed eyelid surgery

•Parotid duct transposition, unless proficient and practised in the technique

•Deep corneal ulcers and penetrating corneal injuries*

•Liquefactive stromal necrosis including alkali burns*

•Corneal problems requiring keratectomy or keratoplasty

•Acute glaucoma*

•Lens luxation in the dog* and other species

•Cataract surgery (dogs with diabetic cataracts should be referred as soon as possible for assessment)

•Acute canine* and equine* uveitis and uveitis where the aetiology is complex or not obvious

•Sudden blindness*

•Unexplained ocular pain or redness (urgency of referral depends upon the degree of pain)

* Denotes urgent or emergency referral

OPHTHALMIC EMERGENCIES AND TRAUMA

INTRODUCTION

In this section, the basic principles of veterinary ophthalmology are described using the dog as the type species. Knowledge of normal ocular anatomy underpins the recognition of ocular abnormality (Figure 3.1(a–c)). Subsequent sections will highlight species differences, so as not to repeat much of the material outlined in this section. The common canine ocular and adnexal conditions and those that are important to recognise because of the serious implications of misdiagnosis are summarised in Box 3.1.

In many countries, dogs that are to be used for breeding are examined for inherited eye disease, and in some countries there is also a DNA testing scheme. In the USA, canine hereditary eye disease certification is run by the Canine Eye Registration Foundation (CERF) and for much of Europe the European College of Veterinary Ophthalmologists (ECVO) fulfils this function. In the UK, the ECVO plays a lesser role, and examination for hereditary eye disease comes under the auspices of the British Veterinary Association/Kennel Club/International Sheep Dog Society (BVA/KC/ISDS) Eye Scheme. An up-to-date list of the conditions and breeds covered by this scheme is published annually by the British Veterinary Association (In Practice Supplement on Hereditary Eye Disease) and the pamphlet is available free from the British Veterinary Association.

GENERAL AND CANINE OPHTHALMOLOGY