PRESENTING SIGNS

The owner will present the patient due to an abnormal appearance – they notice that the affected eye is sunken with elevation of the nictitans membrane. They might think that the animal is holding its eye fully or partly closed. The condition might be present from a very early age but normally is acquired later. The patient may or may not show signs of ocular pain or systemic disease.

CASE HISTORY

In most cases there is no previous history of ocular disease or relevant systemic disease. Young animals might be presented with congenital lesions but adults are more frequently affected. In these cases there might be some history – for example, a recent traumatic event (e.g. a fight with another dog or cat), a previous episode of uveitis or chronic glaucoma with a recent change in appearance and apparent sinking of the eye. The patient might have recently been systemically ill and lost a lot of weight, resulting in a bilateral presentation, or might have undergone a surgical procedure to the head or neck. The owner (and indeed the veterinary surgeon) might not link the two episodes and therefore careful questioning is required along with examination of the patient.

CLINICAL EXAMINATION

On ophthalmic examination the first thing to determine is whether the eye is truly enophthalmic, i.e. sunken back into the socket, or whether it is just smaller than it should be. Comparison of the two eyes will assist, as will viewing the animal from above as well as from directly in front. A small eye can be present in young animals; sometimes it will be normally developed and visual, but just smaller than expected, but other ocular abnormalities, such as cataract, nystagmus and persistent pupillary membrane, might be present (Figure 54.1).

Figure 54.1 Microphthalmos in a young Old English sheepdog. The globe is small with the sclera more prominent, a prolapsed nictitans membrane plus cataract formation. Multiple ocular abnormalities such as these are currently being investigated by the BVA/KD/ISDS eye panel as the condition is suspected to be inherited in this breed.

One or both eyes can be affected. If bilateral, it might be a breed-related normal enophthalmos. For example, rough collies have very long noses, with small, deep set eyes, and some degree of enophthalmos is thus inevitable – even desired by breeders. The rest of the ophthalmic examination will be totally normal in such cases (unless they also have collie eye anomaly, but that’s another story!).

An acquired small globe develops following severe intraocular damage and is termed phthisis bulbi. It can follow severe trauma, uveitis or chronic glaucoma (Figure 54.2). A severely phthitic eye will usually be blind and grossly abnormal, with conjunctival hyperaemia, episcleral congestion and frequently severe keratitis such that detailed intraocular examination is not possible. Attempts at measuring intraocular pressure in such patients will be difficult since the globe becomes very soft such that obtaining accurate readings is problematical.

Figure 54.2 Shrunken right eye (phthisis bulbi) following a road traffic accident several months previously. Hyphaema and vitreal haemorrhage had occurred at the time and although the inflammation settled the eye gradually started to shrink.

The patient should be examined for evidence of ocular pain which can cause retraction of the globe. Thus a corneal lesion such as an ulcer or laceration, and severe uveitis or a lens luxation can all cause sufficient ocular pain to contract the retractor oculi muscle such that the globe sinks and the nictitans membrane becomes elevated. An ocular discharge is likely to be present in painful eyes – varying from serous epiphora to overt purulent material. This should be differentiated from the accumulation of mucus seen at the medial canthus in patients with deep set eyes (see Case example 12.1 on medial canthal pocket syndrome). Pupil size should be checked – a miotic pupil in an enophthalmic eye should suggest Horner’s syndrome, especially if the eye is not inflamed with no evidence of uveitis. The patient should be examined in bright and dim light, and the degree of anisocoria assessed. It will be more noticeable in the dark, as the affected pupil fails to dilate. The other signs of Horner’s syndrome, namely ptosis and elevation of the nictitans membrane, will usually be present, together with the enophthalmos and miosis, and all result from damage to the sympathetic supply to the eye.

General clinical examination might be normal in most cases of enophthalmos, but the patient should be checked thoroughly nonetheless. If Horner’s syndrome is suspected, a thorough aural examination should be performed. A neurological examination should also be undertaken.

CASE WORK-UP

For congenital cases of enophthalmos due to micro-phthalmia, or purely physiological due to breed, there is clearly no further work-up required. The same is true for cases of phthisis bulbi, where the previous history and clinical examination of the patient are diagnostic. If a source of ocular pain is identified, then the work-up will be directed at determining the cause of this – and is discussed in the case examples on corneal ulceration, uveitis, lens luxation, etc. Cases due to temporal muscle atrophy will similarly be obvious from the clinical examination and previous history. Thus the most frequent cases of enophthalmos which require significant further investigation is when they are due to Horner’s syndrome.

Signs of Horner’s syndrome include:

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