A Clinical Case from the Archives : 26/05/2006

Posted on May 26, 2006 by davidwilliams

[tab name=”The Case”]Today this Akita turns up in the clinic with erosive lesions around its eyes and muzzle and an anterior uveitis, not with miosis particularly but with a muddy looking iris and intraocular pressures below 10mmHg. What might this be and how would you treat it?[/tab][tab name=”David’s view”]My suspicion is that this is Vogt-Koyanagi-Harada-like syndrome seen in the Japanese Akita, although normally the periocular disease is poliosis and vitiligo (whitening of the hair and skin) rather than these erosive lesions and the uveitis is posterior with a blinding choroiditis and retinal detachment not anterior with keratitis as here. Tom Kern was I think the first person to report several dogs with the problem back in the 1980s (Uveitis associated with poliosis and vitiligo in six dogs. Journal American Veterinary Medical Association 187:408-14. ) but two more recent papers which might interest you include one linking the disease to a specific dog leucocyte antigen haplotype (Angles et al (2005)Uveodermatologic (VKH-like) syndrome in American Akita dogs is associated with an increased frequency of DQA1*00201. Tissue Antigens 66:656-65). Another group experimentally induced the disease, showing that Akitas immunised with tyrosinase related protein 1 developed the condition (Yamaki et al (2005)Experimentally induced Vogt-Koyanagi-Harada disease in two Akita dogs. Exp Eye Res. 80:273-80) showing the similarity to the condition in man where this molecule has been found to be the key autoantigen in the disease. To get back to our case, we have treated the dog with oral prednisolone and azathioprine to reduce the inflammatory lesions: the condition normally needs a substantial immunosupressive onslaught to resolve it.[/tab][end_tabset] 

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A Clinical Case from the Archives : 25/05/2006

Posted on May 25, 2006 by davidwilliams

[tab name=”The Case”]This five year old cocker spaniel came to me this morning with a history of gradually failing vision. I asked the students, before we saw the dog, what the likely diagnosis could be. My resident replied PRA, a possible diagnosis with which I agreed. But I didn’t ask what sort of PRA she meant and was surprised to see this retina. What is this disease? The dog is getting clumsier, which could be because of visual deficient – or could it be something else?[/tab][tab name=”David’s view”]Here’s the dog – a rather lovely working cocker spaniel (note the ‘working’ bit!). This is retinal pigment epithelial dystrophy (RPED) or central PRA (note not generalised!) The brown spots in the retina are lipofuscin, deposited because the rpe isn’t adequately dealing with the photoreceptor debris its meant to be phagocytosing. There is also gradually increasing tapetal hyper-reflectivity with the retinal degeneration. Gill Mclellan has done some wonderful detective work uncovering the fact that these dogs are vitamin E deficient, not because of insufficient dietary intake but from a metabolic problem. Read her two papers in the Veterinary Record (Clinical and pathological observations in English cocker spaniels with primary metabolic vitamin E deficiency and retinal pigment epithelial dystrophy. Vet Rec 153:287-92 and Vitamin E deficiency in dogs with retinal pigment epithelial dystrophy.
Vet Rec. 151:663-7). The clumsiness may be because of neurological licofuscinosis and while the retinal changes can only be halted by supplemental vitamin E, we are hoping that the neurological sequelae may be reversed to some extent with the vitamin given orally.[/tab][end_tabset] 

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A Clinical Case from the Archives : 24/05/2006

Posted on May 24, 2006 by davidwilliams

[tab name=”The Case”]This little Siamese has esotropia – its cross-eyed if you want it in normal language! When you look at its retina with an ophthalmoscope its always moving around. Why cross-eyed and why the nystagmus?[/tab][tab name=”David’s view”]The answer lies in the weird projections of the retina ganglion cell axons in these sub-albinotic animals. The key paper is Hubert and Weisel back in 1971 (Aberrant visual projections in the Siamese cat. J Physiol. 1971 218:33-62). If you think that you would never be able to access this, it is online at http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=5130620! (Exclamation mark mine not part of the web address!) Even the structured abstract takes me half an hour to read and understand, so here I’ve drawn a simplified diagram of what I think is happening. The most lateral portions of retina, rather than sending axons which stay ipsilateral, send fibres which aberrantly decussate (drawn in red). Basically by being cross-eyed, the cat is avoiding using the lateral portions of its retinas to look forward at all. The nystagmus is caused by the poor retina not knowing quite where to look![/tab][end_tabset] 

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A Clinical Case from the Archives : 24/05/2006

Posted on May 24, 2006 by davidwilliams

[tab name=”The Case”]This eight year old Siamese cat has had differently sized pupils for some time but since the cat is not in any discomfort and can see, nobody was very worried. Today you are asked to see it, just for interest I guess. What might your differentials be and what tests would you do to come to a conclusion?[/tab][tab name=”David’s view”]This large a pupil concerns me. The cat has no pupillary light reflex, direct or consesual when light is shon into the eye and no consensual when the light is shon into the normal eye, though the direct is present and correct! My first thought was glaucoma. The intraocular pressure was indeed staggeringly high at 85mmHg but not normal in the sighted eye either, at 35mmHg. While glaucoma in the cat is normally secondary to uveitis there were no inflammatory signs in the eye. In the Siamese glaucoma can be seen as an inherited condition, as noted by Dr Glaze (Congenital and hereditary ocular abnormalities in cats.
Clin Tech Small Anim Pract 2005;20:74-82). The condition is generally considered as an open-angle glaucoma but gonioscopy in this cat showed closed angles in both eyes. I’m not particularly worried about the dilated eye – its blind and always will be. But if we can prevent progression in the other eye we will stop the cat going bilaterally blind. We used Trusopt, a topical carbonic anhydrase inhibitor tid for treatment in the first instance. Latanoprost, my favourite glaucoma medication in dogs doesn’t work in cats as they lack the key prostaglandin receptor.[/tab][end_tabset] 

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A Clinical Case from the Archives : 23/05/2006

Posted on May 23, 2006 by davidwilliams

[tab name=”The Case”]This eight year old cat has rapidly lost her vision. She is being treated for cystitis – could that have anything to do with the changes you see here?[/tab][tab name=”David’s view”]The cat has been treated with enrofloxacin and while the veterinary surgeon asked for 15mg tablets to be dispensed the nurse misheard and counted out 50mg tablets. Even at a little over three times the recommended dose, enrofloxacin can be retinotoxic, giving this tapetal hyper-reflectivity, vessel attenuation and irreversible blindness. The key paper here is Kirk Gelatt’s from a few years ago: Enrofloxacin-associated retinal degeneration in cats.
Veterinary Ophthalmology 2001;4:99-106. Baytril is fine to use in cats as long as one sticks to the recommended dose of 5mg/kg and goes no higher![/tab][end_tabset] 

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A Clinical Case from the Archives : 23/05/2006

Posted on May 23, 2006 by davidwilliams

[tab name=”The Case”]This week old mianture horse foal has been having quite considerable ocular irritation. What is the problem and what might you suggest to the owners?[/tab][tab name=”David’s view”]The cause of the irritationis likely to be trichiasis with these amazingly long eyelashes abrading the cornea. We thought of tacking the eyelid as with a congenital entropion or even performing a Stades procedure, but the easiest thing is to get the owners to roll back the lids even few hours so that the lashes do not abrade the ocular surface. In a few weeks the rather bulbous appearance of the eye will reduce and the irritation from the lashes will reduce.[/tab][end_tabset] 

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A Clinical Case from the Archives : 23/05/2006

Posted on May 23, 2006 by davidwilliams

[tab name=”The Case”]What is this strange hairy lesionin this young Dachshund’s eye? Is it infectious? Is it inherited? What should we do about it?[/tab][tab name=”David’s view”]Its a corneal dermoid, that’s to say an area where instead of transparent cornea there is skin; sometimes, as in this case, hairy. It isn’t directly heritable although some breeds such as dachshunds are said to be predisposed. Superficial keratectomy removes it as can be seen here – the ulcer left will heal in a few days. Looking in the literature its surprising how little information there is on the condition in dogs which, while not seen every day, is not rare. A recent Japanese paper is available online at http://www.vetsci.org/2005/pdf/369.pdf for those wanting to know more.[/tab][end_tabset] 

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A Clinical Case from the Archives : 17/05/2006

Posted on May 17, 2006 by davidwilliams

[tab name=”The Case”]This little cat was presented to me today having come out of a bush yesterday with its two pupils different sizes. What might be the cause of this and how might we verify our diagnosis?[/tab][tab name=”David’s view”]This anisocoria is probably caused by some mild uveitis associated with trauma. Tonometry would be a useful tool to investigate this, as uveitis leads to a lower intraocular pressure, probably because released prostaglandins open up the unconventional outflow pathway for increased aqueous drainage from the eye, thus causing mild hypotony. The intraocular pressure was indeed lower, being 11mmHg compared with 16mmHg in the normal right eye. We used a mydriatic to ensure that no synechiae formation occured and left the eye to sort out the inflammation on its own, given that it was mild – we could have prescribed some topical steroid drops as well I guess.[/tab][end_tabset] 

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A Clinical Case from the Archives : 17/05/2006

Posted on May 17, 2006 by davidwilliams

[tab name=”The Case”]This 5 year old Cavalier King Charles spaniel presents with blood in the anterior chamber of an eye which the owner reports has been blind since birth. What might your differentials for the hyphaema in such a case be?[/tab][tab name=”David’s view”]Trauma, a systemic coagulopathy or uveitis could be potential differentials as could an intraocular tumour. I used an ultrasound scan to look for the latter and was surprised to find this appearance. Interestingly the normal fellow eye has a persistent hyaloid remnant and the likelihood is that this has haemorrhaged in the affected eye giuving the hyphaema. This cause of hyphaema has been reported in three dogs in the last few years (Bayon et al (2001)Ocular complications of persistent hyperplastic primary vitreous in three dogs. Veterinary Ophthalmology 4:35-40)[/tab][end_tabset] 

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A Clinical Case from the Archives : 07/05/2006

Posted on May 7, 2006 by davidwilliams

[tab name=”The Case”]This two year old chihuahua presents with a somewhat protruding left eye with lateral strabismus. With a forced duction test it is possible to move the globe normally and there is no pain on opening the mouth. What is your diagnosis likely to be and what would you do to confirm it?[/tab][tab name=”David’s view”]Well this is an orbital space-occupying lesion and given the lack of pain on mouth opening its likely to be a tumour. I broke this news to the owner who then surprised me by asking why the same had occured in the right eye but completely resolved! Here is an orbital ultrasound which, because of its heterogenous echogenicity looks more like inflammation than neoplasm. If we were being strictly scientific we should have done an ultrasound-guided biopsy but understandably (given the dog is not at all bothered by the problem at present)we’ve chosen to treat with systemic NSAIDs and see what happens![/tab][end_tabset] 

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