Proceedings of the Southern European Veterinary Conference and Congreso Nacional de AVEPA

Transcription

1 Proceedings of the Southern European Veterinary Conference and Congreso Nacional de AVEPA Oct , Barcelona, Spain Next Conference: Oct , Barcelona, Spain Reprinted in the IVIS website with the permission of the SEVC - AVEPA

2 NON ULCERATIVE KERATITIS Christine Heinrich DVOphthal DipECVO MRCVS Willows Referral Service Highlands Road Shirley, Solihull, B90 4NH KERATOCONJUNCTIVITIS SICCA (KCS, DRY EYE) the tear film is vital for the health and normal function of the ocular surface it is a tri-laminar structure comprising a superficial lipid layer, a middle aqueous layer and an inner mucin layer the aqueous phase constitutes the bulk of the tear film, and underproduction of this component is the major cause of the signs associated with keratoconjunctivitis sicca aqueous tears are produced by the lacrimal gland (which lies within the orbit) and the nictitans gland (located behind the third eyelid) Clinical signs KCS is generally an insidious condition although occasionally it may be of acute onset (especially in neurogenic cases or those associated with drug toxicity). The signs listed may be subtle initially, but usually advance with time and ultimately may lead to blindness: conjunctivitis - thickening may develop with chronicity ocular discharge usually tenacious and mucopurulent uneven corneal surface leading to a lack-lustre appearance and an irregular corneal reflex corneal vascularisation / pigmentation often commences dorsally corneal epithelial thickening ulceration ulcers are often small and rapidly deepening, especially in acute cases pain more often in acute cases, less so in chronic disease dry ipsilateral nostril in some cases o due to involvement of the lateral nasal gland, either due to neurogenic disease or involvement in the same disease process as that of the The causes of KCS include: congenital due to aplasia or hypoplasia of the lacrimal and nictitans glands. The author has seen this most often in Yorkshire Terriers drug-induced e.g. sulphur drugs sulphasalazine/diazine and phenazopyridine (a urinary analgesic) canine distemper virus neurogenic disruption of the parasympathetic nerve supply e.g. after trauma, secondary to otitis (may be associated with facial nerve palsy) exogenous damage to the lacrimal + nictitans glands as a result of e.g. radiation therapy

3 immune-mediated West Highland White Terrier, spaniels, English Bulldog, Shih Tzu, Lhasa Apso "idiopathic" most are probably immune-mediated Of those causes listed immune-mediated disease is the most commonly encountered in dogs. These cases are essentially bilateral, although they may initially present with disease in one eye. Diagnosis Diagnosis is based upon signalment, history, clinical signs and the performance of the Schirmer tear test the Schirmer tear test is carried out prior to applying any drops to the eye. In dogs, a reading of less than 12 mm/min is suspicious of keratoconjunctivitis sicca, whilst a reading of less than 5 mm/min can be taken as diagnostic (N.B. ensure that no drying agents, such as atropine, have been administered) cats generally have lower Schirmer tear test readings than dogs. High stress levels can result in Schirmer tear test readings as low as 2 or 3 mm/minute interpret results with caution! it is important to measure the tear production in both eyes and interpret the findings in the light of signs of pathology remove the cause if possible, e.g. stop sulphonamide therapy nursing care bathe the eye with sterile water or saline as often as is required to remove excessive mucus aqueous phase replacement (medical): o this can be achieved in a number of ways: artificial tears e.g. carbomer 940 (polyacrylic acid) e.g. Viscotears. These should be applied 4 to 6 times daily or more often if required. Artificial tears do not adequately substitute for endogenous tears, however o in suspected immune-mediated cases stimulate endogenous tear production and control immune-mediated dacryoadenitis topical cyclosporine (Optimmune ) b.i.d. Cyclosporine is an immunosuppressive agent which also has lacrimogenic properties. The response to cyclosporine is generally best in cases which have been diagnosed early in the course of the disease and which have not suffered extensive loss of nictitans and lacrimal gland tissue. Need to use for up to 6 weeks to assess whether adequate response is being gained. Refractory cases my need higher concentrations of cyclosporine or may benefit from the use of topical tacrolimus (no ocular product available in the UK) o in suspected neurogenic cases stimulate endogenous tear production oral 1 to 4% pilocarpine drops depending on size of patient (starting at 1 drop 1% per 10 kg bid gradually increasing dose until either tear production is noted or until signs of systemic toxicity (salivation, vomiting, diarrhoea) occur. Clients need to be carefully educated about the process of the gradual dose increase and must stop treatment if signs of toxicity occur. The treatment is then halted for 24 hours (or until the clinical signs have resolved) and treatment is re-started at the last lower dose. aqueous phase replacement (surgical): o parotid duct transposition this involves translocation of duct papilla from the mouth to the lower conjunctival fornix. It is reserved for cases which do not respond to medical therapy and is most often required in cases with a zero Schirmer tear test

4 reading. Complications include iatrogenic damage to the parotid duct and papilla, failure of saliva production (must be assessed pre-operatively), salivary epiphora (especially when eating) with resulting facial dermatitis/pyoderma, excessive alkalinity of saliva, calcium crystal deposition which can be associated with irritation and blepharitis Summary Keratoconjunctivitis sicca is generally a lifelong condition which is essentially bilateral in most cases. It requires lifelong management, even when parotid duct transposition has been carried out. Considerable client education is required when a diagnosis of keratoconjunctivitis sicca is made PIGMENTARY KERATITIS Pigmentary keratitis is a chronic condition seen especially in brachycephalic dogs. The cause of pigmentary keratitis is usually a combination of some or all of the following: drying of the cornea, especially centrally, due to: o globe prominence o poor blink (lagophthalmos) o low corneal sensitivity (which has been demonstrated in brachycephalics) nasal fold trichiasis distichiasis hair at the medial canthus medial entropion These problems lead to low grade irritation, vascularisation (usually) and pigmentation which may be so severe as to cause blindness. The pigmentation often commences at the medial limbus and progresses across the cornea Therapy in this condition can be difficult and may involve the correction of a number of underlying problems. Once corrected the progression of the condition may be halted, but pigment tends to remain in the cornea after it has been deposited. trim nasal folds shorten eyelids (preferably by medial canthoplasty) correct any keratoconjunctivitis sicca (see above) topical steroids or cyclosporine (even in the absence of frank keratoconjunctivitis sicca) may be beneficial in some cases superficial keratectomy may be indicated as a last resort in severe cases, but all the predisposing factors should be corrected prior to undertaking surgery there is a marked tendency for pigment and vessels to return post-operatively

5 CHRONIC SUPERFICIAL KERATITIS (CSK, PANNUS) CSK is an immune-mediated disease seen only in dogs a genetic component is suggested by a breed incidence CSK primarily affects the German Shepherd Dog (and occasionally other breeds e.g. Greyhound, Lurcher, Border Collie, Dachshund, Belgian Shepherd) it is exacerbated / triggered by UV light (therefore more commonly seen at higher altitude) Clinical signs CSK is generally bilateral but not necessarily symmetrical commonly starts at 3 to 5 years of age starts at the pigment patch (in the conjunctiva at the ventro-lateral limbus) as a red, raised, vascularised conjunctival lesion which then progresses over the corneal surface (pathology comprises a sub-epithelial fibrovascular infiltrate with a predominance of lymphocytes and plasma cells). Pigmentation may be slight to very marked, and the combination of vessels and pigment makes CSK a potentially blinding disease. Lesions often progress more rapidly in younger dogs. the third eyelid may be involved (sometimes without corneal involvement) follicular hyperplasia is manifested as multi-focal depigmentation with red, raised nodules on the third eyelid surface; this is known as plasma cell infiltration of the nictitating membrane or plasmoma. cyclosporine used twice daily has been shown to be effective in many cases commonly used for long-term maintenance topical steroid therapy (e.g. fluorometholone [FML, Allergan], prednisolone, dexamethasone etc) may be used initially, sometimes in combination with cyclosporine. Start at 6 times daily and reduce with resolution control not cure is achieved in CSK treatment is often for life and, at the very least, longterm supervision and considerable client education and co-operation is required to optimise control of the condition pigmentation may persist despite long-term treatment. Superficial keratectomy can be performed in these cases, although rapid recurrence may follow surgery FELINE EOSINOPHILIC KERATOCONJUNCTIVITIS The cause of this condition is unknown. It does not occur in dogs but is not dissimilar to vernal disease in humans. Approximately 76% of cases in one series were reported as being associated with FHV-1 infection it is not clear if this is a causal relationship, however. Clinical signs the condition is often unilateral initially, becoming bilateral in time usually presents as a proliferative pink / white lesion spreading across the cornea from the conjunctiva at the nasal or temporal limbus. The surface is irregular and exhibits associated oedema / vessels. The dorsal palpebral conjunctiva is often involved "cottage cheese" type deposit may be present on the corneal surface the third eyelid(s) may be thickened.

6 Diagnosis on appearance scrapings / biopsy eosinophils are often present in patients with clinical signs suggestive of an acute FHV 1 infection, treatment should be started with a course of Famciclovir orally, which in some patients my result in resolution of clinical signs topical prednisolone, dexamethasone or fluorometholone are often effective start 6 times daily and reduce the dose gradually over several weeks (remember FHV-1 infection may be present and the concurrent use of Famciclovir may have to be considered) topical cyclosporine twice daily may be efficacious, but probably best used longer-term (if required) once the condition is resolving systemic therapy may be required in patients where (possibly frequent!) topical medication is not an option o o oral prednisolone (0.5 mg/kg once or twice daily) is preferable to megestrol acetate (Ovarid ) can have a dramatic effect on the condition but carries the risk of inducing diabetes mellitus relapse may occur in some cats