16 Complicated keratoconjunctivitis sicca
The typical presenting signs of keratoconjunctivitis sicca (KCS) are well reported and generally the initial diagnosis is straightforward. Thus the dog presented with the slightly sticky mucoid or mucopurulent discharge and conjunctival hyperaemia should always have a Schirmer tear test (STT) performed. Readings of less than 10 mm are diagnostic for KCS but readings between 10 and 15 mm should be considered suspicious, particularly in large breed dogs (an association between higher STT readings in dogs of higher body weight has been demonstrated). Here we will discuss two complications of KCS: acute corneal ulceration and the poorly responsive case. The former will present with a suddenly painful eye – there will not be the increased lacrimation and ‘wet eye’ normally associated with an ulcer since the patient is unable to produce aqueous tears! Instead there will be a copious mucopurulent discharge, sometimes adhered to the cornea such that the patient cannot open its eye. Discomfort will be present and attempts at rubbing the eye are likely.
The presentation of the poorly responsive case of KCS is less dramatic. The dog will probably have been receiving treatment, but the owner might have discontinued this totally or become less meticulous with both medicating and cleaning the eye. Thus the tenacious ocular discharge will have gradually increased, some periorbital disease might have developed or the owner might present the dog again because they have become concerned that its vision has deteriorated.
As outlined above there is typically a previous ocular history. Keratoconjunctivitis sicca has probably already been diagnosed and treatment instigated. However, the condition has not responded as anticipated, or did initially respond such that the owner felt that the dog was better and stopped treatment, and a serious relapse has occurred. The condition is normally bilateral but one eye is often affected more severely and this might be the reason that the owner has returned for a follow-up consultation.
Unless the dog has a systemic disease which can exacerbate KCS, such as diabetes mellitus, hypothyroidism or hyperadrenocorticism, general clinical examination is usually unremarkable. On initial ophthalmic assessment the most striking problem is the copious mucopurulent discharge. A sample should be taken for culture and sensitivity before gently wiping this away. Conjunctival hyperaemia and hyperplasia will be apparent. Schirmer tear test readings are expected to be bilaterally low – probably less than 2 mm of wetting in a minute. The periorbital skin might be inflamed and thickened, or even slightly ulcerated if a chronic blepharitis has been present or the patient has self-traumatized (Figure 16.1). The cornea is likely to be pigmented either across the dorsal half or sometimes covering most of its surface (Figure 16.2). Many dogs can still see and retain a menace response despite significant pigmentary keratitis. Branching superficial blood vessels will also be present, and sometimes a slight granulation tissue reaction is also noted, particularly if previous ulceration has occurred. In poorly responsive or neglected cases of chronic KCS ulceration is not always a feature. Once the discharge is cleared away corneal examination will show a dull, lacklustre surface with some epithelial irregularity but not true ulceration. Careful irrigation of excess fluorescein dye is required to prevent false positives as the dye pools in the irregular surface or sticks to the mucus (Figure 16.3).
Acute ulceration associated with KCS is typically deep and central (Figure 16.4). Thus a facet is clearly visible in the central or subcentral cornea and surrounding corneal oedema can be present. If the secondary bacterial infection is severe then keratomalacia might be present such that the ‘melting’ cornea around the ulcer has a gelatinous appearance. Fluorescein staining will be positive, but it is not uncommon for a descemetocoele to be present such that only the sides of the ulcer retain dye with the central area remaining dark, representing Descemet’s membrane. Some peripheral corneal pigmentation and superficial vascularization might also be noted, reflecting the chronicity of the underlying KCS. A reflex uveitis and miotic pupil might also be noted.
The definitive diagnosis of keratoconjunctivitis sicca has already been made. However, other exacerbating factors such as entropion, lagophthalmos, blepharitis and systemic disease might be present and should be considered. A list of the possible causes of KCS is provided in Table 16.1.
|Possible causes for KCS||Comment|
|Immune-mediated lacrimal gland disease (most common)||Most common|
|Congenital lacrimal gland aplasia||E.g. Cavalier King Charles spaniels, Jack Russell terriers|
|Drug suppression of lacrimal gland||E.g. atropine drops|
|Drug toxicity and damage to lacrimal gland||E.g. sulfasalazine and sulphonamides|
|Lacrimal gland adenitis||Distemper virus and some cases of conjunctivitis and blepharitis will have lower Schirmer tear test readings|
|Traumatic injury to lacrimal gland||Road traffic accident with head trauma|
|Neurogenic||Lack of parasympathetic supply to lacrimal glands|
|Other neurological signs sometimes present|
|Prior removal of nictitans gland||Prolapsed nictitans glands are more common in the same breeds that are predisposed to KCS and gland removal is not recommended|
|Systemic disease||Hypothyroidism, hyperadrenocorticism, diabetes mellitus|
General clinical examination is important, and should any abnormalities be detected on this, further laboratory tests looking for diabetes mellitus, hypothyroidism and hyperadrenocorticism are indicated. All these conditions can exacerbate an underlying KCS and should be considered if the condition had previously been stable on medication but recently deteriorated.
Samples of the discharge should be taken for bacterial culture and sensitivity testing. In addition, conjunctival cytology or even eyelid biopsy in the case of suspected blepharitis might be warranted – particularly if the response to previous medical treatment has been poor.
Specific nursing of complicated cases of keratoconjunctivitis sicca will vary depending on whether ulceration is present or not and whether surgery is indicated. However, careful medical attention is required regardless. Frequent and thorough cleansing of the discharge is required – both to promote patient comfort and to reduce the risk of further secondary bacterial contamination. The eyes should be gently bathed with soft gauze swabs or cotton wool pads soaked in sterile saline before the application of any medication. Since frequent medication is necessary, nurses should ensure that owners are properly able to carry out the treatment at the desired intervals. Patients should be prevented from self-traumatizing – this is most common immediately after the application of topical medication and, as such, the patient should be distracted for a few minutes afterwards.
There are several causes for KCS in dogs (see Table 16.1) and its incidence is reported at about 1% of the population of dogs presented to North American Veterinary Colleges. Certainly a breed predisposition is noted with immune-mediated KCS, so a presumed inherited component is present, although details of this have not been elucidated, and many other factors are clearly involved. English bulldogs, West Highland white terriers, Cavalier King Charles spaniels, American and English cocker spaniels and pugs are among the many breeds commonly seen with the condition. A sex predisposition to females has been reported in West Highland white terriers.
Although these chronic, insidious, immune-mediated causes are the most common form of KCS seen in practice, various other aetiologies exist. Viral lacrimal gland adenitis occurs with canine distemper infection leading to KCS, which clearly can occur as outbreaks in unvaccinated dogs; congenital hypoplasia of the lacrimal tissue is recognized, sometimes as a unilateral problem in the Cavalier King Charles spaniel and some miniature breeds; drug-induced KCS following systemic sulphonamides, sulfasalazine and topical atropine occurs, and neurogenic KCS due to loss of the parasympathetic innervation to the salivary glands occurs occasionally. Some systemic diseases can also lead to reduced tear production and so patients with diabetes mellitus, hypothyroidism and hyperadrenocorticism in particular should have Schirmer tear tests performed regularly.