Sistema Circulatório

CASEBOOK
FOR THE CERTIFICATE IN

VETERINARY
OPHTHALMOLOGY
Contents
Meibomian Adenoma In A Dog (Updated) ............................................................................... 3
Lipogranulomatous Conjunctivitis In A Cat (Updated)........................................................... 12
Cherry Eye in a Bulldog (New) ............................................................................................... 23
Corneal Ulceration In An Alpaca (Updated) ........................................................................... 30
Herpetic Keratitis In A Cat (Updated) ..................................................................................... 40
Corneal Sequestrum In a Cat (New) ........................................................................................ 50
Ocular Melanosis In A Dog (New) .......................................................................................... 61
Lens Opacities In A Horse (Updated) ...................................................................................... 74
Presumed Congenital Ocular Defects in a Dog (New) ............................................................ 81
Hypertensive Ocular Disease In A Cat (Updated) ................................................................... 88
Appendix 1 ............................................................................................................................... 98
Appendix 2 ............................................................................................................................. 105
Meibomian Adenoma In A Dog

(Word count 997)
Case history
A 9 year old, female, crossbred, neutered bitch (32kg), presented with a firm swelling over the right
eye. The mass did not appear to cause discomfort and had gradually increased in size over 2-3
months.
Clinical examination
General clinical and ophthalmic exams were performed (Appendix-1). The ophthalmic examination
showed the following ocular abnormalities:
Firm swelling of the upper right eyelid involving 1/3-1/2 of the lid length (Figure-1).
A small pigmented mass at the lid margin (Figure-2), extending into the palpebral
conjunctiva forming a larger pink mass 1x2cm diameter (Figure-3).
Conjunctival hyperaemia associated with the lesion (Figure-3).
Figure 1. Swelling of the upper right eyelid.
Page 3
Figure 2. Small pigmented mass at the lid margin.
Figure 3. Palpebral extension of mass. Conjunctival hyperaemia.
Differential diagnosis
Sebaceous/meibomian adenoma
Sebaceous/meibomian adenocarcinoma
Benign melanoma
Papilloma (squamous/fibro benign epithelial neoplasm)
Malignant melanoma
Page 4
Less common eyelid neoplasms include histiocytoma, keratocanthoma, mastocytoma/mast cell

tumour, basal cell carcinoma, squamous cell carcinoma, fibroma, myoblastoma, haemangiosarcoma,
lipoma and meibomian gland epithelioma (1).
Other non-neoplastic, and in this case less likely, differentials would include granuloma formation
due to foreign body or chronic irritation, bacterial/mycotic/parasitic blepharitis or trauma.
Diagnosis
Sebaceous adenoma, confirmed on histopathology (Table-1)
Treatment and outcome

Surgical excision of the eyelid mass was performed, removing approximately 1/3 of the eyelid,
combined with lateral canthoplasty to correct the resulting lid defect. The mass was sent for
histopathology.
Surgical procedure
A standard anaesthetic protocol, and surgical preparation, was used (Appendix-1).
A four-sided wedge resection was used to remove the eyelid mass, leaving approximately
2mmnormal tissue margins (Figure-4a). The wound was closed in two layers, using 6-0 Polyglactin
910(coated Vicryl, Ethicon) absorbable suture. A simple continuous pattern, with buried knots, was
used in the conjunctiva. The skin was closed using simple interrupted pattern, starting at the lid
margin with a figure of eight suture (Figure-4b).
(a)
(b)
Figure 4 (a) Four-sided wedge resection to remove eyelid mass.
(b) Figure of eight suture to reform the eyelid margin.
Page 5
A sliding lateral canthoplasty was used for tension relief and correction of the lid defect created by
excising the mass (Figure-5). A skin incision was made at the lateral canthus continuing from the
upper eyelid laterally in a full thickness incision. A triangle of skin was excised at the lateral end,
allowing the skin to slide medially to lengthening the upper eyelid. The resulting defect was closed
routinely in 2 layers using 6-0 Polyglactin 910(coated Vicryl, Ethicon).
Figure 5. Sliding lateral canthoplasty.

Post-operative treatment
Fucidic Acid ointment(Fucithalmic Vet, Leo Laboratories) twice daily for 10 days
Meloxicam(Metacam, Boehringer Ingelheim) 0.1mg/kg once daily for 7 days
Buster collar
Results
3 days. Small amount of dried discharge adhering to the sutures. Mild lateral canthal pyoderma
associated with pre-surgical clipping (Figure-6 & Figure-7)
2 weeks. Satisfactory healing of the wound with good lid positions. Sutures left to dissolve.
21 months. A new smaller lesion, causing no sign of discomfort, seen at the lower right lid margin
(Figure-8 & Figure-9). Surgical removal has been advised, especially if cause discomfort or increase in
size.
Page 6
Figure 6, 3 days post-operatively
Figure 7, 3 days post-operatively.
Page 7
Figure 8. A comfortable eye 21 months after initial surgery
Figure 9. Small mass at lower lid margin 21 months after initial surgery
Page 8
Prognosis
Good. No further clinical problem expected after complete excision of the original mass. Further
surgery may be required to remove the more recent growth, regular examinations have been
advised.
Discussion
Eyelid neoplasms are the most frequently seen ophthalmic tumours in dogs (1). Most eyelid
neoplasms are benign (73-87%) (2, 3) and, when malignant, do not typically metastasize and rarely
recur (2). Sebaceous gland adenomas are the most frequently reported eyelid neoplasms and usually
associated with meibomian glands. Sebaceous adenocarcinoma, papillomas and melanomas are also
commonly seen (1,2).
Sebaceous gland adenomas occur in older dogs, with an age average of 8-10 years (2,3), tend to
grow slowly, vary greatly in size, and may extend posteriorly into the palpebral conjunctiva (1). They
appear to be slightly more frequent on upper eyelids versus lower (2), and usually presents as an
outward papillary growth of the eyelid margin. Various breed predispositions have been reported
with mixed breeds having a lower risk (2,3).
Eyelid neoplasms do not tend to cause corneal irritation (1). However, lid masses may ulcerate, get
inflamed and bleed. Local irritation resulting in blepharospasm, epiphora, conjunctival hyperaemia,
corneal vascularisation/pigmentationneal/ulceration may potentially occur (12/L), either directly
from contact by the mass (1), or secondary to functional alterations of the eyelids (3).
Early treatment is required to preserve normal eyelid function and prevent complications, especially
when eyelid margin is involved (3). Early treatment will also give better cosmetic results. Best
prognosis is attained by surgical excision (1).
Size and shape of normal eyelids is highly variable in animals. Tight fitting eyelid fissure is present in
most cat and dog breeds e.g. Miniature Poodle and Collie. A much larger palpebral fissure is present
in dog breeds such as Labrador Retrievers or American Cocker Spaniels. The amount of eyelid length
lost before reconstruction is necessary therefore vary between breeds.(5) In general, a simple fullthickness wedge resections, using a V or four-sided excisions, are sufficient to remove smaller
lesions involving up to 1/3 of lid margins. Simple closure of larger defects cannot be achieved
without interfering with optimal eyelid function (6). Lesions involving more than 1/3 of the eyelid
margin require more extensive reconstructive blepharoplasty to replace some of the lid defect
formed, avoid tension and notching and achieve a good lid corneal apposition (1). Different
techniques described include; rotational flap and sliding skin grafts e.g. rhomboid-flap and z-plasty
Page 9
(5), bridge-flap (8), lip-to-lid procedure (Pavletic graft) (8), lid-splitting (10), sharing of eyelid margins
(Mustarde flap) (6) and opposing lid graft (Cutler-Beard graft)(6). Cryosurgery may also be used and
has been reported to have the same success rate as excision of malignant forms of tumours, whilst
electrocautery causes too much tissue destruction (3). Radiotherapy may also be appropriate for
certain types of tumours (11).
Although eyelid neoplasms are generally benign, malignancy and metastasis may occur (2).
Malignant tumours tend to be locally invasive and histopathology is advisable to check excision
margins as well as tumour type (1).
Macroscopic
1cm portion of tissue.
Microscopic
The sample shows a portion of haired skin containing multi-lobular mass composed of well
differentiated sebaceous epithelial cells. There are central ducts containing keratin. The
mass is partly disrupted and surrounded by a marked inflammatory reaction composed of
epithelioid macrophages and multinucleate giant cells with lower numbers of lymphocytes
and plasma cells. The affected area appears excised with an adequate margin.
Diagnosis
Meibomian adenoma with secondary granulomatous inflammation.
Comment
The eyelid mass is a meibomian adenoma. This is a benign lesion. It is quite large due to the
accompanying inflammation but the affected area is now excised and this should not
constitute a further clinical problem.
Axiom Veterinary Laboratories Ltd
Table-1. Histopathology
References
1. Gwin R.M., Gelatt K.N., Williams L.W. Ophthalmic neoplasms in the dog. Journal of
the American Animal Hospital Association. 1982;18,853-865.
2. Krehbiel J.D., Langham R.F. Eyelid Neoplasms of Dogs. American Journal of
Veterinary Research. 1975;36,115-119.
3. Roberts S.M., Severin G.A., Lavach J. D. Prevalence and treatment of palpebral
neoplasms in the dog: 200 cases (1975-1983). Journal of American Veterinary
Medicine Association. 1986;189,1355-1359.
4. Bedford P.G.C. Diseases and Surgery of the Canine Eyelids. In: Gelatt KN, ed.
Veterinary Ophthalmology. Lippincott Williams & Wilkins. 3rd edition. 1999, 535-568.
5. Van der Woerdt A. Adnexal surgery in dogs and cats. Veterinary Ophthalmology.
2004;7,(5), 284290.
Page 10
6. Munger R.J., Gourley I.M. Cross Lid Flap for Repair of Large Upper Eyelid Defects.
Journal of American Veterinary Medicine Association. 1981;178,45-48.
7. Blanchard G.L., Keller W.F. The Rhomboid Graft-Flap for the Repair of Extensive
Ocular Adnexal Defects. Journal of the American Animal Hospital Association.
1976;12,576-580.
8. Pavletic M.M., Nafe L.A., Confer A.W. Mucocutaneous subdermal flap from the lip
for lower eyelid restoration in the dog. Journal of American Veterinary Medicine
Association. 1982;180,921-926.
9. Doherty M.J. A Bridge-Flap Blepharorrhaphy Method for Eyelid reconstruction in the
Cat. Journal of the American Animal Hospital Association. 1973;9,238-241.
10. Buyukmihci N., Karpinski L.G. Cosmetic removal of a sebaceous adenocarcinoma of
the eyelid. Veterinary medicine Small animal clinician. 1975,1091-1093.
11. Crispin S.M., notes on Veterinary Ophthalmology, Blackwell Science Ltd. 2005. pp9394. Gelatt K.N., et All. Veterinary Ophthalmology. 4th Edition. Blackwell Publishing.
2007;608-614.
Page 11
Lipogranulomatous Conjunctivitis In A Cat

(Word count 998)
Case history
A 13-year-old, female neutered, domestic short haired cat (4.5kg) was presented with an
increasingly red and uncomfortable right eye of 6-8 months duration. The lesions had been
unresponsive to topical treatment with fucidic acid 1% ointment (Fucithalmic Vet, Leo
Laboratories), and polymixin/neomycin/dexamethasone 0.1% solution (Maxitrol, Alcon). The
cat was vaccinated for feline herpes virus, feline calicivirus and feline panleucopenia.
General clinical and ophthalmic examinations were performed (Appendix 1).
Examination of the right eye showed the following abnormalities;
Blepharospasm (Figure-1)
Mucoid discharge at medial canthus (Figure-2)
Hyperaemic lid margins (Figure-2)
Hyperaemia and mild chemosis of the palpebral conjunctiva (Figure-3)
Multiple smooth, non-ulcerated, nodular, white-pink lesions, 0.5-1mm in diameter,

within the upper and lower palpebral conjunctiva, adjacent to the eyelid margins
(Figure-3). The bulbar conjunctiva appeared normal. The affected lids where nonpigmented.
No abnormalities were detected in the left eye. Schirmer tear test were 10mm/min
bilaterally and fluorescein staining were negative.
General examination;
Dermatitis of bilateral pinnae i.e. alopecia, ulceration and crusting of the nonpigmented tips of the ears (Figure-1).
Page 12
Figure-1. Dermatitis of bilateral pinnae and ocular blepharospasm.
Figure-2. Hyperaemic non-pigmented lids and mucoid ocular discharge.
Page 13
Figure-3. Nodular lesions of the upper lower palpebral conjunctiva.

Further tests:
Cytology from Conjunctival swab- epithelial cells and small number of lymphocytes
(in-house Diff-Quick stain examination)
Conjunctival swab for Chlamydophila felis, feline herpes virus(FHV-1) PCR and feline
calicivirus - all negative (Langford Veterinary Diagnostic Laboratories)
Conjunctival biopsy for histopathology a small sample including nodular lesions

were taken, using small dissecting forceps and tonotomy scissors, after application
of proxymetacaine 0.5% (Minims Proxymetacaine, Chauvin Pharmaceuticals)
showing lipogranulomatous conjunctivitis (Axiom Veterinary Laboratories Ltd)
(Table-1)
Differentials diagnosis
Conjunctival masses
Lipogranulomatous conjunctivitis
Neoplasia e.g. Squamous cell carcinoma, Lymphosarcoma
Chalazion
Nodular/chronic/eosinophilic conjunctivitis
Scar tissue
Conjunctival inflammation
Page 14
Infectious conjunctivitis e.g. Chlamydiophilia felis, Feline herpes virus-1, Feline,

Calicivirus, Mycoplasma, other bacteria, Reovirus, Thelazia Californiensis
Foreign body/dust reaction
Trauma
Allergy
Drug hypersensitivity
Diagnosis
Lipogranulomatous conjunctivitis was diagnosed on clinical signs, lack of response to
treatment and histopathology.
Prognosis
Good prognosis for excision of affected conjunctiva, with recurrence rare. Guarded with
regards to tear production, with potential reduction of volume or change in composition,
due to meibomian gland involvement.
Fucidic acid 1% (Fucithalmic Vet, Leo Laboratories) ophthalmic ointment twice daily,
whilst awaiting biopsy results
Amoxicillin trihydrate/clavulanic acid (Synulox Palatable Tablets, Pfizer) 50mg twice

daily for 7 days before surgery, due to aural pyoderma
Surgical excision of the affected conjunctiva (Figure-4), and bilateral aural resections,
were carried out
Surgical procedure for conjunctival excision

A routine anaesthetic procedure was followed (Appendix 1). Pre-anaesthetic blood test and
urine analysis were unremarkable. Routine preparation of the surgical site was used, with
the cat in a lateral recumbency and the lateral canthal region clipped for a canthotomy.
A lateral canthal incision allowed access to the palpebral conjunctiva. Conjunctival excision
was made by two incisions in the palpebral conjunctiva, parallel to the eyelid margin, on
either side of the lesions i.e. 1-2mm and 6-7mm below the lid margin. A strip of conjunctival
and subconjunctival tissue containing the lesions was then excised (Figure-4). Surgical sites
Page 15
of conjunctiva were not sutured. Canthotomy site closed in routine two layers, including
figure-of-eight pattern at lid margin, 6/0 Polyglactin 910 (Coated Vicryl, Ethicon).
Figure-4. Conjunctival excision.

The cat had an uneventful recovery and the postoperative management was as follows:
Fucidic acid 1% (Fucithalmic Vet, Leo Laboratories) ophthalmic ointment twice daily
for 10 days
Amoxicillin trihydrate/clavulanic acid (Synulox Palatable Tablets, Pfizer) 50mg twice

daily for 5 days
Buster collar fitted
Histopathology was repeated to ensure no neoplastic changes had occurred in the resected
area of conjunctiva and also to check for neoplastic changes of the resected ears. No
neoplastic changes were detected from either site (Table-2).
Outcome:
3 days. Mild haemorrhagic discharge after cleaning the eye. Mild conjunctival hyperaemia
and swelling. No apparent discomfort
6 days. No discharge, mild conjunctival inflammation, comfortable
10 days. No discharge or inflammation, comfortable
4 weeks and 6 months. No discharge, no conjunctival inflammation, comfortable.
STT=13mm/min bilaterally at 4 weeks, and 14mm/min bilaterally at 6 months (Figure-5)
No signs of complications or recurrence was detected on re-examinations in the 12 months
following surgery. The cat was euthanised 2 years later due to unrelated problems.
Page 16
Figure-5. Comfortable eye 4 weeks post-surgery.
Discussion
Lipogranulomatous conjunctivitis in cats is a conjunctival disease consisting of large amounts
of deposited lipid, with an associated granulomatous inflammatory reaction. The
histopathology of the affected conjunctival in this case contained numerous, discrete
colourless vacuoles caused by lipid, surrounded by numerous clusters of macrophages, with
lesser numbers of admixed neutrophils (Figure-6).
Lipogranulomatous conjunctivitis appears to be associated with the meibomian glands,
which have been identified in excised lesions, and may represent a form of chalazion.
Previously, adipocytes of the connective tissue and mucosal goblet cells and have also been
suggested as possible sources of the lipids, possibly in association with trauma and
inflammation (1). In humans, lipogranulomas have been associated with circulatory lipids
e.g. in hyperlipidaemia or hypercholesterolaemia or as a reaction to mineral oils which may
gain access to tissues by therapeutic, cosmetic or accidental means (2).
The condition often occur in middle-aged or older cats with depigmented or minimal eyelid
pigmentation suggests a possible role of solar ultraviolet radiation damage in the
etiopathogenesis of this disease. Chronic actinic radiation damage may cause obstruction of
meibomian gland ducts, leading to accumulation of secretions, gland rupture and associated
inflammation. Trauma and inflammation causing lysis of lipid-containing cells with leakage of
lipid-rich secretion into surrounding tissues have also been suggested as possible causes (1).
The lesions are found in the palpebral conjunctiva adjacent to the eyelid margin, as single or
multiple lesions in overlapping rows, with nodules of varied size from 1mm-5 mm in
diameter. Smaller, multiple lesions were seen in the above case. The condition appears to
Page 17
affect upper and/or lower lids and can be unilateral or bilateral. The condition is refractory
to medical therapy (1). Surgical escission, by conjunctival resection (3), of the lesions is the
optimal treatment and lead to resolution of the associated irritation and recurrence does
not appear to occur. Excision of the majority of meibomian glandular tissue might be
expected to alter the qualitative tear film properties, with an inadequate lipid component of
the precorneal tear film. Qualitative tear film instability, may predispose to the development
of conjunctivitis and may also be associated with ocular surface disease (1). Smaller or more
defined lesions may respond to treatment by curettage (4,5).
An association between lipogranulomatous conjunctivitis and eyelid neoplasia has been
suggested (1). This might only reflect the typical occurrence of both conditions in
depigmented tissues, rather than a neoplastic change as a direct effect of the
lipogranulomatous conjunctivitis. Histopathology should however be carried out to ensure
no neoplastic changes has occurred (6).
Solar radiation has been suggested as a possible cause of damage to the meibomian glands
(1). Lack of melanin and protective hair, genetic predisposition and hypersensitivity to
sunlight with repeated sunburns are also predisposing factors to dermatitis of the pinnae in
cats. Initial mild erythema may develop into a more severe dermatitis, and later squamous
cell carcinoma. Persistent ulceration being the most consistent indicator of malignant
transformation. Amputation of both pinnae, is the surgical therapy of choice (3,7).
Page 18
Figure-6. Histopathology - A focally extensive area of the conjunctival

submucosa containing numerous, discrete colourless vacuoles (lipid) surrounded
by numerous clusters of macrophages with lesser numbers of admixed
neutrophils.
Page 19
Macroscopic
2 x 2-4mm pale tissue, all tissue processed.
Microscopic
Upper eyelid, conjunctiva: A focally extensive area of the conjunctival submucosa is
infiltrated by vast numbers of macrophages and multinucleate giant cells with
abundant often finely vacuolated cytoplasm. Inflammatory infiltrates are centred upon
and interspersed by numerous large lipid vacuoles. Occasional lymphocytes and
plasma cells and rare neutrophils are admixed.
Diagnosis
Lipogranulomatous conjunctivitis.
Comment
Lipogranulomatous conjunctivitis in cats presents as smooth, non-ulcerated creamy
white nodules within the palpebral conjunctivae. Middle aged and older cats that
have minimal eyelid pigmentation seem to be predisposed, suggesting that solar
ultraviolet radiation damage may play a role in aetiopathogenesis. The lesions are
apparently sterile, non-responsive to medication, and cured by excision.
Table-1. Histopathology - Conjunctival biopsy.
Page 20
Macroscopic
1. 2 x 1.2cm pale tissue. All tissue processed.
2. 2 x 4cm ear.
Microscopic
1. Conjunctiva: A focally extensive area of the conjunctival submucosa contains
numerous, discrete colourless vacuoles (lipid) surrounded by numerous clusters of
macrophages with lesser numbers of admixed neutrophils.
2. Pinnae, haired skin: Multiple sections are examined. The auricular cartilage is
multifocally discontinuous and these regions are associated with abundant reactive
fibrosis occasionally containing small numbers of lymphocytes and plasma cells.
Diagnosis
1. Conjunctiva: Lipogranulomatous conjunctivitis.
2. Pinnae, haired skin: Multiple sections are examined. The auricular cartilage is
multifocally discontinuous and these regions are associated with abundant reactive
fibrosis occasionally containing small numbers of lymphocytes and plasma cells.
Comment
1. As in the previous submission from this cat the lesion present was consistent with
lipogranulomatous conjunctivitis although in the current case neutrophils were rather
more prominent than the previous submission.
2. I examined multiple sections from the ear. In none was there any evidence of
neoplasia. In several areas the cartilage had undergone degeneration and necrosis
with subsequent repair by fibrous tissue. This may have given the ear an uneven
appearance and possibly represented the site of prior now resolved haematomas.
These regions were occasionally associated with mild chronic inflammation.
Table-2. Histopathology conjunctival excision.
Page 21
References
1. Read R.A. and Lucas J. Lipogranulomatous conjunctivitis: clinical findings from
21 eyes in 13 cats. Veterinary Ophthalmology. 2001; 4 (2), 9398.
2. Kerlin RL, Dubielzig RR. Lipogranulomatous conjunctivitis in cats. Veterinary
and Comparative Ophthalmology. 1997; 7, 177179.
3. Long R.D. Treatment of distichiasis by conjunctival resection. Journal of Small
Animal Practice. 1991; 32,146-148.
4. Crispin, S M, notes on Veterinary Ophthalmology, Blackwell Science Ltd.
2005.
5. Glaze M.B., Gelatt K.N. Feline Ophthalmology. In: Gelatt KN, ed. Veterinary
Ophthalmology. Lippincott Williams & Wilkins. 3rd edition. 1999, 997-1053.
6. Williams D. Case Study. Small Animal Ophthalmology. 2004; 9:37-38.
7. Scott, D.W. Feline dermatology 190078: a monograph. Journal of the
American Animal Hospital Association 1980; 16,394-400.
Page 22
Cherry Eye in a Bulldog

(Word count 998)
Case history
A 6 months old Bull dog (22.5kg) was presented with a sudden onset pink mass at the medial
canthus of the left eye. On further questioning of the breeder, after the initial consultation,
it was revealed that the dog had had treatment for cherry eye before purchase, details of
which were not given.
General clinical and ophthalmic examinations were performed (Appedix-1). The general
examination was unremarkable. The ophthalmic examination showed the following
abnormalities;
Mild lower medial entropion bilaterally, but more marked in the right eye. The right eye also
showed mild lower lateral lid ectropion (Figure-1), complete absent of third eyelid and mild
keratitis of the lower medial cornea. A pink fleshy mass, follicular conjunctivitis and mucoid
ocular discharge was seen at the left medial canthus (Figure-2a&b).
Schirmer tear test was 16mm/min left eye and 18mm/min right eye. The corneas were
fluorescein negative. Tear break-up time appeared normal. Corneal sensation and blink was
normal. There were no further lid abnormalities, distichiasis or ectopic cilia present and no
other ocular surface irritants were identified.
Figure-1. Ectropion mid to lateral lower lid. Entropin medial lower lid.
Page 23
Figure-2a. Fleshy mass and thick mucoid ocular discharge.
Figure-2b. Mass still evident after third eyelid turned back towards normal
position.
Diagnosis
A diagnosis of prolapsed nictitans gland was made on clinical examination.
There was also mild bilateral medial lower lid entropion, exaggerated on the right eye (with
associated keratitis) due to lack of support from the third eyelid, which was assumed to have
been surgically removed prior to purchase.
The main differential of prolapsed nictitans gland include:
Primary/secondary neoplasia
Chronic inflammation
Page 24
Cyst formation
Differential diagnosis of third eylid prominence also include:
Bent, everted, third eyelid cartilage
Hyperplasia/hypertrophy of glandular tissue
Anatomical protrusion of the third eyelid
Enophthalmos e.g. ocular pain/debilitating disease/horners syndrome
Exophthalmos, retrobulbar space occupying lesion e.g. neoplasia, inflammation,

abscess
Microphthalmos
Trauma
Foreign body reaction
Abscessation
Orbital fat prolapse
Emphysema
Haematoma
Granuloma
Seroma
Plasmoma
Iatrogenic
Treatment
Surgical correction of the prolapsed third eyelid gland was carried out using Morgan mucosal
pocket technique. A bilateral modified Hotz-Celsus was used to correct the medial lower
eyelid entropion (Appedix-2). The ectropion did not warrant surgical correction.
Page 25
Pre-surgical Procedures
Routine anaesthetic procedures (Appendix-1).
Pre-anaesthetic bloods unremarkable
Routine surgical preparation, no clipping required
Stay sutures, 3 metric nylon, placed at either end of the free border of the third eyelid to
hold the lid in an everted position, and aid manipulation, during surgery.
Morgan mucosal pocket technique

Two incisions, 1-1.5 cm wide, where made on the posterior surface of the third eyelid, one
on either side of the prolapsed gland, parallel to the globe. Blunt dissection, using small
metzenbaum scissors, was used to extend the depths of the incisions. The two mucosal flaps
formed, where sutured together over the gland using 6/0 Polyglactin 910 (Coated Vicryl,
Ethicon), pushing the gland down into the submucosal pocket created. A simple continuous
suture pattern was used, and the knots placed on the palpebral aspect of the nictitating
membrane. A small opening of 1-2mm was left on either side of the suture line to allow
nictitans gland secretions to reach the conjunctival sac and avoid cyst formation (Figure-3-5).
Figure-3. Morgan mucosal pocket technique.
Page 26
Figure-4. Gland sutured in place.
Figure-5. Third eyelid gland prolapse corrected. Immediate post-operative

chemosis and hyperaemia present.
Post-operative treatment
Post-operative recovery was uneventful. Post-operative care;
Meloxicam (Metacam, Boehringer Ingelheim) 0.1 mg/kg daily by mouth, 5 days
Fucidic acid 1% (Fucithalmic Vet) topically twice daily, 7 days
Buster collar
Page 27
Outcome
Day 3; Mild third eyelid hyperaemia and chemosis. Good lid-corneal apposition bilaterally.
Day 14; Normal third eyelid position and size. STT=19 mm/min bilaterally.
4 and 10 moths; No recurrence of ocular discharge/discomfort. STT=18-20 mm/min.
Annual booster examinations; STT=18-20mm/min, with no recurrence of any ocular disease.
The dog passed away for unknown, reasons at 3 years of age.
Prognosis
Good, with high success rate for surgical correction of the prolapsed gland. Guarded in
relation to the right eye were the lack of a third eyelid could cause corneal surface disease,
due to reduced production and distribution of tears.
Discussion
Prolapse of the third eyelid gland is relatively common, with Bulldogs being one of
predisposed breeds (1). It is thought to result from weakness in the connective tisue
attachment between the base of the gland and the periorbital tissues (2), or also as a direct
consequence of chronic glandular hypertrophy (1). It tends to occur before 2 years of age,
and can be unilateral or bilateral. It is often seen on its own, but may also occur in
combination with nictitans cartilage abnormalities or following cartilage excision (3).
Diagnosis is usually straight-forward, with characteristic appearance of the gland protruding
over the free border of the third eyelid. The prolapse may have an initial increase and later
subnormal tear production. This may again result in abnormalities of the cornea and
subsequently vision if left uncorrected.
In the past, prolapsed tissue would be completely or partially excised. The third eyelid gland
is, however, shown to produce 30%-57% of the ocular tears (2). Removal of the gland has
shown to significant decrease lacrimation (4), and may also influence tear quality and tear
film stability (3). In this case the whole of the right third eyelid was missing, presumably
surgically removed whilst still with the breeder. Complications associated with the lack of
third eyelid was in this case seen by medial lower lid entropion which, presumably due to
lack of physical support by third eyelid tissue, was more marked compared to the left side
entropion. Keratitis associated with the entropion was only present in the right eye. No
further complications were seen in the follow-up period. However, the dog only lived until it
Page 28
was 3 years old, and complications associated with reduced tear quality/quantity and
distribution may have shown at an older age.
Surgical repositioning is now used to reduce risk of development of keratoconjunctivitis sicca
postoperatively. Restoration of normal anatomy is also important for spreading the tear film
and protecting the cornea (5). The Morgan mucosal pocket technique is a frequently and
highly successful method used today (2). Kaswan orbital rim anchoring is another technique
described (6). More recently, a technique of intranictitans tacking, using nonabsorbable
suture to anchor the prolapsed gland to the cartilage of the third eyelid, has also been
described (7).
References
1. A Crispin S.M. Notes on veterinary ophthalmology. Blackwell Publishing.
2005. Pp 76-81.
2. B Morgan R.V., Duddy J.M., McClurg K. Prolapse of the Gland of the Third
Eyelid in Dogs: A retrospective Study of 89 Cases (1980-1990). Journal of the
American Animal Hospital Association. 1993; 29 ,56-60.
3. C Featherstone H. Self Assessment, Small animal ophthalmology. UK vet.
2003; 8 (8), 63-65.
4. G Dugan S.J., Secerin G.A., Hungerford L.L.,Whiteley H.E., Robert S. M. Clinical
and histological evaluation of the prolapsed third eyelid gland in dogs.
Journal of American Veterinary Medicine Association. 1992.15; 201(12),18611867.
5. D Crispin S. Treating the everted membrana nictitans in the dog. In Practice.
1986, 66-67.
6. E Kaswan R.L., Martin C.L. Surgical correction of the third eyelid prolapse in
dogs. Journal of the American Veterinary Medicine Association. 1985; 186,
83.
7. F Plummer C.E., Kllberg M.E., Gelatt K.N., Gelatt J.P., Barrie K.P., Brooks D.E.
Intranictitans tacking for replacement of prolapsed gland of the third eyelid in
dogs. Vet Ophthalmology. 2008;11(4),228-233.
Page 29
Corneal Ulceration In An Alpaca

(Word count 998)
Case history
A 2 year old, female, alpaca (60-70kg) was presented with signs of left ocular discomfort in
association with a sero-mucoid ocular discharge of 6 weeks duration. Improvement had
been seen initially, after 2 applications 48 hours apart with Cloxacillin Benzathine (Orbenin
Ophthalmic Ointment, Pfizer), with subsequent deterioration of the lesion in the 2 weeks
prior to presentation. The alpaca was in close contact with other alpacas, non of which
showed signs of ocular problems.
General clinical and ophthalmic examinations were performed (Appendix 1). The general
clinical examination was unremarkable. The ophthalmic examination of the right showed no
abnormalities (Figure-4). Examination of the left eye showed the following abormalities:
Increased blink rate
Blepharospasm (Figure-1)
Sero-mucoid ocular discharge (Figure-2), Shirmer tear test (STT) >30mm/min (right
eye STT=18mm/min) (Mean values in normal Alpaca is 19mm/min (1))
Mild conjunctival hyperaemia
Linear corneal opacity associated with corneal oedema, neovascularisation,

epithelial ulceration staining positive with fluorescein (Fluorets, Chauvin
Pharmaceuticals) (Figure-3)
Tear in the dorsal portion of the pupillary iridial margins and granula iridica,
resulting in a pigmented strip of iridial tissue traversing the pupil, with anterior
corneal synechia at the area of corneal ulceration (Figure-3)
The following normal, bilateral, ophthalmic findings were noted:
Slow direct and indirect pupillary light reflexes (1)
Intraocular pressure 12 bilaterally mean IOP in alpacas is 16 +/- 4 (2)
Page 30
Large bergmeister papilla (hyaloid remnant) protruding from the optic disks (1)
Concentric cortical lamination, has been described as cataract in Alpaca, but is a

common finding and is seen similarly as a normal finding in the horse (3)
Figure-1. Blepharospasm and ocular discharge
Page 31
Figure-2. Sero-mucoid discharge (fluorescein stain applied to eye ca 1 hour prior

to photograph).
Figure-3. Left eye. Linear corneal opacity; ulceration, oedema and

neovascularisation. Torn granula iridica.
Figure-4. Right eye. No abnormalities detected.

Page 32
Further test:
Corneal scrape for cytology suggestive of bacterial component to the corneal

lesion (Table-1)
Corneo-conjunctival swab for culture and sensitivity no significant growth

(Langford Veterinary Diagnostics - Microbiology)
Corneo-conjunctival swabs, using wire stemmed swabs for Chlamydiophilia psittaci

PCR and Mycoplasma conjunctivae. Specific culture media was supplied by the lab
(Veterinary Laboratories Agency, DEFRA, Langford House) - both tests negative
Differential diagnosis for corneal disease
Ulcer/ Keratitis of unknown cause
Infectious ulcer/keratitis;
o
Mycoplasma conjunctivae
Chlamydiophilia psittaci
Escherichia coli and Staphylococcus aureus (primary or secondary pathogens

(1))
Moraxella (has been isolated in corneal pathology but considered rare(1))
(Parasites e.g. Thelezia californiensis - in conjunctivitis)
Trauma/Laceration
Friction e.g. entropion, lid abnormalities/trauma, foreign body
Tear film abnormality
Exposure
Neurologic disease i.e. tick and facial nerve paralysis
Solar induced inflammation
Self mutilation e.g. following facial eczema
Phenothiazine
Page 33
Dystrophies
Degeneration
Dermoids
Neoplasia
Diagnosis
Corneal ulcer of unknown origin, suspected traumatic in origin. No bacterial growth was
detected on corneo-conjunctival swabs, and indications of bacterial involvement on cytology
could have been secondary and no-specific.
Previous iridiocyslitis was suspected in this case, with evidence of anterior synechiae causing
a tear of the dorsal portion of the pupillary iridial margins and granula iridica, resulting in a
pigmented strip of iridial tissue traversing the pupil. These intra ocular changes may be
associated with the corneal ulcer, however no signof active inflammation was seen and
hence likely to be separate coincidental findings.

Treatment was started after at initial examination, based on suspicion of infectious cause,
including mycoplasma and chlamydophila;
Isolation, with one companion alpaca to reduce stress of isolation, until negative
swab result were obtained
Systemic Oxytetracycline Hydrochloride (Duphacycline 100, Fort Dodge Animal

Health) 4mg/kg by daily intramuscular injections
Topical Chlortetracycline (Aureomycin Ophthalmic Ointment, Fort Dodge Animal

Health) once daily
Meloxicam (Metacam, Boehringer Ingelheim) 0.5mg/kg subcutaneously once daily

for 2 days
Follow-up examinations
1 week: Marked improvement with normal blink rate and reduced blepharospasm
(Figure-5). Reduced corneal oedema and neovascularisation (Figure-6). No corneal
ulceration evident, fluorescein stain negative (Figure-7).
Page 34
2 weeks: Further reduction in oedema and neovascularisation (Figure-8).

3 weeks: Further improvement with faint corneal scarring only as reported by the referring
vet.
Figure-5. 1 week. Reduced blepharospasm and ocular discharge.
Figure-6. Reduced corneal oedema and neovascularisation.
Page 35
Figure-7. Negative fluorescein stain.
Figure-8. Corneal oedema reduced.
Prognosis
Presumably good, with indication of improvement with symptomatic treatment. A clear
prognosis could not be given due to uncertain aetiology. The intraocular changes appeared
inactive at the time of treatment.
Discussion
Limited information specific to eye diseases in Alpacas, but there is an increase in
information on ocular problems of Camelids in general. Corneal disease is the most common
ocular abnormality in Llamas, another of the camelids, with ulcerative keratitis most
frequently seen (1). In one study, 41% of ocular disease was attributed to corneal disease,
and more than half of these were ulcerative keratitis. Most of the ulcers were of unknown
cause, but were assumed likely to be traumatic in origin. The high prevalence of corneal
Page 36
ulcers may be attributable to the prominent size and position of the eyes in camelids, which
predispose the cornea to trauma.
Where a diagnosis of infectious ulceration/keratitis is made, the initial cause may still be
traumatic injury, whereas the infection may be a secondarily occurrence (4). Bacterial
pathogens are often present on the normal camelid eye, hence topical broad-spectrum
antibiotics should be used in all cases of corneal ulceration (1). Swabs were taken in this case
for general culture and sensitivity, as well as Chlamydiophilia and Mycoplasma. Llamas do
not appear to be highly susceptible to direct corneal invasion by microorganisms such as
Moraxella sp (1,4), a main course of infectious bovine keratoconjunctivitis (1). Most bacterial
infections of the cornea occurs in association with other ocular pathogens and previous
corneal abnormalities (5).
Llamas lack meibomian glands on their eyelid margins, and the oily layer of the tear film is
possibly produced by a sebaceous gland on the lacrimal caruncle, as seen in Camels (1,4).
This has been suggested to possibly cause a difference in tear film composition, which again
could contribute to the apparent resistance of Llamas to ocular infectious diseases (4).
The elaborate structure of the iris is a striking feature of the Llama eye. On the dorsal and
ventral margins of the pupil, the posterior pigment epithelium of the iris is proliferated and
folded vertically. This pupillary ruff is analogous to the corpora nigra of horses but is
significantly larger and consists of folded layers rather than globular masses (1). The
unfolded part of the pupillary ruff observed in this case, may support a suspect traumatic
underlying cause to the corneal pathology. Tearing of the granula iridica has been reported
in the literature (1).
Other ocular lesions reported from routine ocular examinations in Llamas include
conjunctivitis e.g. parasitic, conjunctival cysts, corneal scars and oedema, posterior and
anterior synechiae, cataracts, lens subluxation, vitreous opacities, optic disk coloboma,
buphthalmia, and anterior uveitis associated with aspergillosis, gastrointestinal tract disease
and respiratory tract disease (4,6). Ocular malignancies has also been reported (7,8).
Adnexal diseases seen include eyelid hypogenesis, trauma, entropion and nasolacrimal duct
or punctal atresia. Posterior segment disease i.e. panuveitis and chorioretinitis have been
reported secondary to encephalitis associated with a specific strain of equine herpes virus
1carried by zebras. Optic neuritis of unknown aetiology has also been reported. Congenital
posterior segment abnormalities include optic disk colobomas, peripapillary colobomas,
Page 37
vitreous fibrosis and ossification, persistent hyperplastic primary vitreous, retinal dysplasia,
and retinal detachments (4).
Sample site: Corneal scrape

Cell preservation: Good
Cellularity: Moderate
Cytology
Two direct smears examined:
There is a faint eosinophilic proteinacious background within which there are
moderate numbers of squamous epithelial cells. In places these cells are clumped,
basophilic and appear to have a higher N:C ratio and occasional nucleoli. Also noted
are occasional neutrophils, some poorly preserved and occasionally disrupted and
clumped. In one or two areas rafts of finely filamentous bacteria are seen.
Comment
Findings would be suggestive of a bacterial component to this corneal lesion.
Otherwise the corneal cells appear fairly normal with the exception of the more
dysplastic clumps which are most likely cells from deeper within the epithelial layer.
No clear aetiology present however.
Diagnostic Laboratories Langford
Table-1. Corneal cytology
References
1. Gionfriddo J.R. & Friedman. D.S. Ophthalmology of South American Camelids:
llamas, Alpacas, Guanacos and Vicunas. In: Current Veterinary Therapy Food
Animal Practice, Vol4. (ed. Howard J.L.) W.B. Saunders Co., Philadelphia,
1999;644-648.
2. Nuhsbaum M.T., Gionfriddo J.R., Powell C.C., Aubin M.L. Intraocular pressure
in normal llamas (Lama glama) and alpacas (Lama pacos). Veterinary
Ophthalmology 2000;3, 31-34.
3. Matthews A.G. & Barnett K.C. Lens In: Equine Ophthalmology. An Atlas and
Text. Editors: Barnett K.C., Crispin S.M., Lavach J.D., Matthews A.G. Saunders.
Elsevier Ltd. 2nd ed. 2004,165-182.
4. Gionfriddo J.R., Gionfriddo J.P., Khrone S.G. Ocular diseases of Llamas: 194
cases (1980-1993). Journal of American Veterinary Medicine Association.
1997;210:1784-1787.
5. Ledbetter E.C., Scarlett J.M. Isolation of obligate anaerobic bacteria from
ulcerative keratitis in domestic animals. Veterinary Ophthalmology. 2008;
11,2,114-122.
Page 38
6. Gelatt K.N., Otzen G.B., Flaneig J., Schein O.D., Munoz B., West S.K., Duncan
D.D., Nethercott J.R. & Koren H.S. Results of ophthalmic examination of 29
alpacas. Journal of American Veterinary Medicine Association. 1995:8,12041207.
7. Schoeniger S., Donner L.R., Van Alstine W.G. Malignant nonteratoid ocular
medulloepithelioma in a Llama (Llama glama). Journal of Veterinary
Diagnostic Investigations. 2006;18,5,499-503.
8. Fugaro M.N., Kiupel M., Montiani-Ferreira, et all. Retinoblastoma in the eye
of a Llama (Llama glaa). Veterinary Ophthalmology. 2005;4,287-290.
Page 39
Herpetic Keratitis In A Cat

(Word count 997)
Case history
A 9-year-old, female neutered, domestic shorthaired (DSH) cat (4.15kg) was presented with
right ocular discomfort, association with serous ocular discharge. The left eye had been
enucleated one month previously, due to a ruptured globe, after corneal ulceration. The cat
was treated for cat flu as a kitten, with no further clinical signs of respiratory or ocular
problems until recently. The cat was not vaccinated.
General clinical and ophthalmic examinations were performed (Appendix-1).
A general clinical examination was unremarkable.
On ophthalmic examination, the enucleation site had healed satisfactorily, and the right eye
showed the following abnormalities:
Increased blink rate
Blepharospasm
Serous discharge
Conjunctival hyperaemia and chemosis
Reduced corneal reflection
Corneal epithelialerosion/ ulceration and superficial stromal ulceration/deficit

(Figure-1)
Dorsal corneal neovasculariosation (180 degree) centrally from limbus
Corneal oedema (80% involvement)
Peripheral tapetal reflection and direct/indirect ophthalmoscopy appeared normal,

but full intraocular examination was not possible due to surface changes
Page 40
Figure-1. Corneal ulcerations and 2 smaller areas of stromal deficits (1/3 depth)
within the affected area.
Further tests
Corneo-conjunctival swabs (Langford diagnostic centre);
Feline Herpes Virus I (FHV-I) PCR- strong positive, indicating active infection
Chlamydiophilia felis PCR- negative
Bacterial culture and sensitivity- no growth after 48 hours
Pre-operative blood biochemistry and FeLV/FIV test prior to enucleation

unremarkable.
Corneal opacities and ulceration, and conjunctival chemosis;
Infectious keratitis e.g. viral, chlamydial, bacterial, mycotic
Trauma
Foreign body
Corneal sequestration
Chronic abrasion
Eosinophilic keratitis/proliferative keratoconjunctivitis
Corneal dystrophy or degeneration
Acute bullous keratopathy
Page 41
Diagnosis
A diagnosis of feline herpetic epithelial and stromal keratitis was made on clinical
appearance and positive FHV-1 PCR.
Prognosis
Guarded in relation to saving the globe and vision. Poor in regards to a full recovery, with
chronic stromal scarring and impaired vision expected. Intermittent flare-ups of latent FHV-1
infection expected with any form of stress.
Doxycycline (Ronaxan 20, Merial Animal health Ltd), 10mg/kg orally daily, 7 days,
whilst awaiting swab results (chlamydophilia felis possible)
Meloxicam (Metacam, Boehringer Ingelheim Ltd), 10 drops orally once, then 1

drop/kg once daily, 2 weeks
Topical Fucidic acid (Fucithalmic Vet, Leo Laboratories Ltd) twice daily, 7 days, whilst
awaiting swab results
Acyclovir (Zovirax, Glaxo Wellcome) 5-6 times daily 14 days, after FHV-1 results,
whilst awaiting Triflurothymidine order
Triflurothymidine drops 1% (Moorfield eye-hospital) 1 drop every 2 hours for the

first 12 hours, then 1 drop 4-6 times daily 3 weeks
L-lysine, amino-acid, 500mg orally twice daily indefinitely
Clinical development and outcome;

Week 1-(after doxyxycline, metacam, fucidic acid):
Less discomfort and discharge, reduced chemosis and hyperaemia, epithelial ulceration
reduced by 50%, stromal deficits as previous
Week 2+3-(metacam, acyclovir-1week):
No significant change
4 weeks-(Triflurothymidine-1 week):
Page 42
Corneal oedema reduced, epithelial ulcer reduced to 10-20 % of surface, stromal ulcers the
same with no sign of reepithelialisation.
Blepharitis, possibly associated with topical Triflurothymidine, treated with
amoxycillin/clavulonic acid (Synulox, Pfeizer) 12.5mg/kg twice daily, orally, 5 days.
6 weeks-(Triflurothymidine-3 weeks)
Complete reepithelialisation of cornea, including areas of stromal deficits. Neovasularisation
and oedema markedly decreased. Central corneal scarring. Blepharitis resolved.
Figure-2. Reepithelialised stromal deficits, fluorescein negative.

3 months:
No ocular discomfort. Marked central corneal scarring. Vision appeared normal at home,
and the cat had been hunting successfully. Visual testing positive.
3-12 months:
3 episodes of superficial epithelial ulcerations, each treated successfully with
Triflurothymidine. A small superficial stromal sequestrum, formed 6 months after diagnosis
(Figure-3), with no associated ulceration or discomfort. The pigmented lesion was not
present on re-examination 12 months later (Figure 4a&b). Dermatitis of the lids and lid
margins were assumed to be due to chronic ocular discharge and treated successfully with
antibiotics as previously .
Page 43
Figure-3. Sequestrum.
Figure-4a. Chronic keratitis.
Page 44
Figure-4b. Blepharitis.
Discussion
Infection with FHV-1 is common in cats and causes ocular and upper respiratory tract
disease. Primary infection usually causes signs of cat flu with conjunctivitis, blepharitis,
sneezing and nasal discharge. Viral replication may occur in the corneal epithelium, causing
epithelial keratitis, but the replication may also occur without causing any clinical signs (1).
The direct cytopathic effect of the virus can cause corneal epithelial erosion or ulceration
with a characteristic dendritic appearance or geographic corneal ulceration. With
progression, the corneal stroma can become affected. This is thought to be caused by an
immunologic event, rather than a direct effect by the virus (1,2). Corneal tissues are also
affected by qualitative tear film abnormalities seen with FHV-1 (3). Deeper corneal ulcers
may also occur, but is seen less often. Corneal melting and erosions are likely to be due to
concomitant bacterial infections (4). Corneal sequestration may also develop after corneal
insults associated with FHV-1 (1,5,6). Transient active respiratory infections at a young age,
as in this case, may become latent in the trigeminal ganglia. Reactivation of the latent virus
is triggered by many forms of stress including systemic disease, or corticosteroid
administration (6). Minor initiating insults to the eye, such as superficial scratches from
plants or other animals, may also cause repeat ulcerations (4). There were no signs of
underlying disease, reduced immunity, ocular insult, physiological or environmental stress,
or steroid use in this case.
Polymerase chain reaction (PCR) is a sensitive method for detection of FHV-1 DNA (1).
Etiologic diagnosis can, however, be difficult in the chronically affected cats, possibly from
Page 45
DNA levels being too low to be detected (7). The presence of FHV-1 DNA does not, either,
necessarily mean that this is the cause of the corneal disease as the viral DNA is also
detected in corneas of cats not showing ocular disease (1).
In this case, a strong positive FHV-1 PCR indicated active infection, and was assumed to be
the aetiology of the corneal pathology.
There is no simple and effective means of managing chronic disease (6). Unpredictable
response to treatment, realistic expectations of antiviral efficacy and high risk of flare-ups
makes this, most likely, a lifelong ocular disease. The goal of treatment in this case was to
maintain satisfactory vision and ocular comfort rather than expecting full recovery.
Topical antivirals are generally expensive, require frequent application and may cause
secondary irritation (7). Triflurothymidine has shown relatively good efficacy against FHV1(5,7). Suggested treatment time is a minimum of two weeks, or until clinical signs have
been absent more than one week (4). Treatment beyond 3 weeks may cause epithelial cell
toxicity (7). Systemic L-lysine supplementation may alleviate clinical signs by limiting viral
replication (7,8), although some research suggests little evidence of this (9). Topical
antibiotic ointment or artificial tear supplement may provide symptomatic relief by
providing lubrication and surface protection. Obviously these products have no effect on the
underlying viral etiology (7). Other medical treatments are also discussed in the literature
(Table-1). Famciclovir is a newer drug (i.e. since the treatment of the above case) recognized
to improve systemic, ophthalmic, clinicopathologic, virologic and histologic outcomes of
experimentally FHV-1 infected cats (10,11,12). Topical corticosteroids may reduce postherpetic scarring, but should only be used in conjunction with antivirals in chronic cases as
active viral infection would be exacerbated (6). Surgical corrections of deep stromal ulcers
may become necessary in medically refractory cases. Keratectomy may be required in cases
of corneal sequestration. Corneal transplantation (penetrating keratoplasty) has been
suggested in cases of severe stromal keratitis (4).
Page 46
Topical antiviral Triflurothymidine

Cidofovir
Hydroxyphosphonylmethoxypropyl adenine
Penciclovir
Idoxuridine
Bromvinyldeoxyuridine
Vidarabine
Adenine atabinoside
Acyclovir
Systemic antivirals Famciclovir (Famvir) - prodrug of penciclovir

Ganciclovir (used in acute herpes in human)
Acyclovir (side-effect: bone marrow suppression)
Valacyclovir (cannot be used safely in cats)
Other
Oral L-lysine
Oral or topical interferon
Ocular application of intranasal vaccine

Enterococcus faecium SF68 as immune-enhancing
probiotic dietary supplement
Topical povidine-iodine
Antibiotics for secondary infections

Keratectomy
Corneal grafting
Table-1. Other treatments discussed in the literature
(1,5,7,6,10,11,12,13,14,15,16,17).
References
1. A Volopich S., Benetka V., I. Schwendenwein, Mostl K., Sommerfeld-Stur I.,
Nell B. Cytological findings, and feline herpes virus DNA and Chlamydiophilia
felis antigen detection rates in normal cats and cats with conjunctival and
corneal lesions. Veterinary Ophthalmology. 2005;8(1),25-32.
2. B Featherstone H.J., Franklin V.J., Sansom J. Feline corneal sequestrum:
laboratory analysis of ocular samples from 12 cats. Veterinary
Ophthalmology. 2004;7(4),229-238.
Page 47
3. K Lim C.C., Reilley C.M., Thomasy S.M., Kass P.H., Maggs D.J. Effects of feline
herpesvirus type 1 on tear film break-up time, Schirmer tear test results, and
conjunctival goblet cell density in experimentally infected cats. American
Journal of Veterinary Research. 2009. 70; 3, 394-403.
4. F Glaze M.B., Gelatt K.N. Feline Ophthalmology. In: Gelatt KN, ed. Veterinary
5. D Williams D.L., Fitzmaurice T., Lay D., Forster K., Hefford J., Budge C.,
Blackmore K., Robinson J.C., Field H.F. Efficacy of antiviral agents in feline
herpetic keratitis: result of an in vitro study. Current Eye Research. 2004;29(2
3),215-218.
6. G Crispin S.M., notes on veterinary ophthalmology. Blackwell Publishing
2005. Pp198-200.
7. E Cullen C.L., Wadowska D.W., Singh A., Melekhovets Y. Ultrastructural
findings in feline corneal sequestra. Veterinary Ophthalmology. 2005;
8(5),295303.
8. N Stiles J., Townsend W.M., Rogers Q.R., Khrone S.G. Effect of oral
administration of L-lysine on conjunctivitis caused by feline herpesvirus in
cats. American Journal of Veterinary Research. 2002. 63; 1, 99-103.
9. M Rees T.M., Lubinski J.L. Oral supplementation with L-lysine did not prevent
upper respiratory infection in a shelter population of cats. Journal of Feline
Medicine and Surgery. 2008. 10; 5,510-513.
10. I Thomasy S.M., Lim C.C., Reilly C.M.,Kass P.H., Lappin M.R., Maggs D.J.
Evaluation of orally administered famciclovir in cats experimentally infected
with feline herpesvirus type-1. American Journal of Veterinary Reasearch.
2011. 72; 1, 85-95.
11. Q Maggs D.J., Clarke H.E. In vitro efficacy of ganciclovir, cidofovir, penciclovir,
foscarnet, idoxuridine, and acyclovir against feline herpesvirus type-1.
American Journal of Veterinary Research. 2004. 65;4,399-403.
12. R Malik R., Lessels N.S., Meek M., Graham P.G., Vitale C., Norris J.M., Power
H. Treatment of feline herpesvirus-1 associated disease in cats with
famciclovir and related drugs. Journal of Feline Medicine and Surgery. 2009.
11;,1,40-48.
13. H Romanowski E.G., Bartels S.P., Gordon Y.J. Comparative antiviral efficacies
of cidofovir, trifluridine, and acyclovir in the HSV-1 rabbit keratitis model.
Investigative Ophthalmology Vis Science. 1999. 40,2,378-384.
14. J Sandmeyer L.S., Keller C.B., Bienzle D. Effects of cidofovir on cell death and
replication of feline herpesvirus-1 in cultured feline corneal epithelial cells.
American Journal of Veterinary Research. 2005. 66; 2, 217-222.
15. L Lappin M.R., Veir J.K., Satyaraj E., Czarnecki-Maulden G. Pilot study to
evaluate the effect of oral supplementation of Enterococcus faecium SF68 on
Page 48
cats with latent feline herpesvirus 1. Journal of Feline Medicine and Surgery.
2009. 11;8,650-654.
16. Williams D.L. Robinson J.C., Lay E., Field H. Efficacy of topical acyclovir for the
treatment of feline herpetic kerattis: results of a retrospective clinical trial
and data from in vitro investigations. Veterinary Reccord. 2005. 27; 157,9,
254-257.
17. P Fontenelle J.P., Powell C.C., veir J.K., Radecki S.V., Lappin M.R. Effect of
topical ophthalmic application of cidofovir on experimentally induced
primary ocular feline herpesvirus-1 infection in cats. American Journal of
Veterinary Research.2008. 69;2,289-293.
Page 49
Corneal Sequestrum In a Cat

Word count (996)
Case history
A 3 year old, neutered male, Persian (5.15kg) was presented with a 2 months history of left
ocular discomfort, with increasing degree blepharospasm and ocular discharge. The cat was
fully vaccinated and had no history of cat-flu, or previous ocular disease.
General clinical and ophthalmic examinations were performed (Appendix-1). The general
clinical examination was unremarkable. On ophthalmic examination, the left eye showed the
following abnormalities:
Blepharospasm and ocular sero-mucoid discharge
Conjunctival hyperaemia
Corneal oedema/scarring and neovascularisation
Dark brown to black raised central corneal lesion with stromal involvement.
Fluorescein uptake in the area of lesion and 1-2mm peripherally
Ocular discharge was also present in the right eye, but to a lesser degree. Examination of the
right eyeut was otherwise unremarkable. There was no history of trauma, the eyelid to globe
apposition was good with no lid abnormalities or abnormal positioned cilia. Lagophthalmos
was not present and complete blink observe. Corneal sensation was normal and shirmer tear
tests were 14mm/min and 16mm/min right and left respectively. Tear quality/break-up time
appeared normal, although less reliable in the affected eye due to the lesion present.
Feline Herpes PCR, chlamydophila felis PCR and microbial culture were all negative on
Corneo-conjunctival swabs.
Page 50
Figure-1. Bilateral ocular discharge (the reduced opening of the right lids is due
to camera flash, and was fully open otherwise).
Figure-2. Central corneal lesion, with associated neovacsularisation and corneal

oedema, left eye.
Page 51
Figure-3. Right eye, no corneal lesions.
Diagnosis
A diagnosis of Feline corneal sequestrum was made on clinical appearance.
Differential diagnosis for corneal lesion include corneal foreign body, ulceration/keratitis,
trauma and perforation with or without iris prolapse.
Treatment: Surgical Keratectomy combined with conjunctival

pedicle graft.
A standard anaesthetic protocol, and surgical preparation, was used (Appendix-1).
Surgical microscope and microsurgical instruments were used for the procedure.
A lateral canthotomy was performed for increase surgical visibility (routine single layer
closure with figure-of-eight suture at the lid margin, using 6-0 Polyglactin 910 (coated
Vicryl, Ethicon) at the end of the procedure).
The corneal sequestrum was removed surgically by keratectomy, using microsurgical blade
(Beaver No. 64), leaving stromal deficit to approximately 2/3rd depth. A pedicle graft was
taken from the dorsal bulbar conjunctiva. Blunt dissection (using Stevens tenotomy scissors)
was used to undermine an area of the conjunctiva and 2 parallel cuts made to widen slightly
towards the base of the pedicle formed. The pedicle was rotated into position(carefully
handled with fine tissue forceps) to cover the keratectomy site and sutured to the cornea
using a spatulated swaged-on needle 8-0 Polyglactin 910(coated Vicryl, Ethicon). Simple
interrupted sutures were placed at 6 oclock, then 9 and 3 oclock position, and then further
Page 52
sutures between these approximately 1mm apart. The sutures were passed through full
thickness conjunctiva, into the wall of the keratectomy wound, and through the cornea at
about 2/3rd corneal thickness. The bulbar conjunctiva was left open. (Figure 4-8).
Figure-4. Keratectomy (dotted line) to remove the corneal lesion.
Figure-5. Keratectomy site, extending to deep stromal level. Note marked
neovascularisation of cornea in area of excised sequestrum.
Page 53
Figure-6. Conjunctival tissue undermined using blunt dissection. Two parallel

cuts creating the conjunctival pedicle graft (dotted lines).
Figure-7. Graft sutured in place. Suture placed at approximately 2/3rd corneal

thickness.
Page 54
Figure-8. End of surgery.

Postoperative care;
Chloramphenicol 0.5% (Chloramphenicol Eye Drops, Martindale Pharmaceuticals)

TID 7 days
Amoxicillin/Clavulanic acid (Clavucil, Chanelle Animal health) 12.5mg/kg BID 5 days
Meloxicam (Metacam, Boehringer Ingelheim) 0.05mg/kg SID, 10 days
Mydriatic Atropine Sulphate 1% (Minim Atropine, Chauvin Pharmaceuticals) once

post-op
Buster collar
Day 1
Page 55
Day 3
Day 8
Page 56
Day 15, eye comfortable
Day 15. Improved corneal clarity. Graft thick but functional.
Page 57
4 months
Figure-9. Follow up appearance on day 1, 3, 8, 15 and 4months.
Prognosis
Good with surgical correction, although recurrence is possible. Sequestrums are usually
unilateral but could affect the other eye at a later date (1). Long term regular lubrication has
been adviced to maintain improved ocular surface health. Sectioning of the graft would
reduce he corneal opacity over time and was discussed. However, the owner opted to leave
the pedicle in place due to risk of infection and potential associated complications.
Discussion
Corneal sequestrations are degenerative necrotic lesions of the cornea (2) with variable
appearance, ranging from ill-defined darkening stroma to clearly demarcated black plaques
raised above the corneal epithelium (3).
The different appearances may relate to the various causes and stages in the evolution of
the opacity, with epithelial damage allowing pigment deposition in the corneal stroma. The
pigmented material contains melanin particles (4) which may derive from the preocular tear
film (1).
Oedema and neovascularisation, as seen in this case, may be seen as an associated feature
of chronicity (1).
Page 58
The aetiology for the condition is unknown. The lesions are unique to the cat (with the rare
exception in the horse where sequestrums may be seen associated with necrosis and
sloughing of chronic ulceration/deep keratitis (5).
Factors associated with formation of sequestrums include corneal trauma, chronic ulcerative
keratitis, exposure keratopathy, chronic corneal irritation, topical corticosteroid use, primary
corneal dystrophy, altered corneal stromal metabolism and brachycephalic conformation
with lagophthalmos (6). Breed predisposition includes Persians, Birmans, Himalayan,
Siamese and Colourpoints (1).
Herpetic keratitis has also been associated with sequestration, but some research has
indicated that FHV-1 is not nescessarily the inciting factor (Stiles ref 134 gelatt pp1110). Poor
tear quality has also been suggested as a possible predisposing factor, but again, recent
studies have shown no difference in tear film break-up time or conjunctival goblet cell
density in affected and un-affected cats (7).
Treatment depends on the extent and progression of lesions and amount of discomfort
caused. Lesions may slough without complications, using topical tear-replacement,
antibiotics and therapeutic soft contact lenses where required. However, the lesions may
take months to slough, cause discomfort, extend to Descemets membrane and potentially
cause corneal perforation (1).
Keratectomy reduces the time course of the disease and reduces the risk of complications
(1). Depending on the depth of the resulting stromal deficit, the keratectomy may be
combined with a graft. A conjunctival pedicle graft was used in this case, but free pedicle
grafts and porcine small intestinal submucosa grafts may also be used (8).
Corneoconjunctival transposition is another effective way to correct the stromal deficit,
which also creates less scarring (9). Conjunctival grafts, and corneoconjunctival
transpositions, may help prevent recurrence (9,10,11). Penetrating keratoplasty is rarely
necessary (3).
References
1. A Crispin, S M, notes on Veterinary Ophthalmology, Blackwell Science Ltd
(2005) pp200-202.
2. B Cullen C.L., Wadowska D.W., Singh A., Melekhovets Y. Ultrastructural
findings in feline corneal sequestra. Veterinary Ophthalmology. 2005; 8(5);
295303.
Page 59
3. C Matthews A.G. Cornea. In: Equine Ophthalmology. An Atlas and Text.

Editors: Barnett K.C., Crispin S.M., Lavach J.D., Matthews A.G. Saunders.
Elsevier Ltd. 2nd ed. 2004; 107-148.
4. D Stiles J., Townsend W.M. Feline Ophthalmology. In: Gelatt KN, ed.
Veterinary Ophthalmology. Blackwell Publishing. 4th edition. 2007, pp.10951164.
5. E Featherstone H.J., Franklin V.J., Sansom J. Feline corneal sequestrum:
Laboratory analysis of ocular samples from 12 cats. Veterinary
Ophthalmology 2004; 229-238.
6. F Crispin S. The Cornea. In: BSAVA Manual of Small Animal Ophthalmology.
2nd edition. British Small Animal Veterinary Association. 2002, pp.134-154.
7. G Grahn B.H., Sisler S., Storey E. Qualitative tear film and conjunctival goblet
cell assessment of cats with corneal sequestra. Veterinary Ophthalmology.
2005; 8: 167-170.
8. H Featherstone H.J., Sansom J., Heinrich C.L. The use of porcine small
intestinal submucosa in ten cases of feline corneal disease. Veterinary
Ophthalmology. 2001; 4: 147-153.
9. I Andrew S.E., Tou S., Brooks D.E. Corneoconjunctival transposition for the
treatment of feline corneal sequestra: A retrospective study of 17 cases
(1990-1998). Veterinary Ophthalmology. 2001; 4: 107-111.
10. J Blogg J.R, Stanley R.G., Dutton A.G. Use of conjunctival pedicle grafts in the
management of feline keratitis nigrum. J Small Animal Practice. 1989; 30:
678-684.
11. K Morgan R.V. Feline corneal sequestration: A retrospective study of 42 cases
(1987-1991). J American Animal Hospital Association. 1994;30: 24-30.
Page 60
Ocular Melanosis In A Dog

(Word count 998)
Case history
An 11 year old, neutered female, black Labrador Retriever (32kg), was presented with a history of
gradual onset exophthalmos of the right globe over the previous 3 months. The owners did not think
the dog was painful.
General clinical and ophthalmic examination s were performed (Appendix-1). The general clinical
examination was unremarkable. On ophthalmic examination, the right eye showed the following
abnormalities (Figure1-5):
Blepharospasm , mild serous discharge, swelling upper lid
Shying from touch of right hand side of head
Anisocoria with mydriatic right pupil
Menaze response and dazzle reflex abscent
Right eye appear blind on obstacle course (left eye blind-folded)
Buphthalmos
Areas of pigmentation dorsolateral regions of bulbar conjunctiva/sclera
Conjunctival and episcleral congestion
Diffuse total corneal oedema and areas of corneal pigmentation
Increased pigmentation of corneal endothelium at limbus, extending into iridiocorneal

angles and iris
Immature cataract with small iris rest/pigment anterior lens capsule
Vitreal opacities/asteroid hyalosis
Attenuated retinal vasculature and tapetal hyper-reflectivity/retinal atrophy
Optic disc cupping
Page 61
Intra-ocular pressure 29mmHg (Left 15mmHg)
Gonioscopic view limited due to corneal oedema/pigmentation
The right eye showed incipient posterior polar subcapsular cataract changes. There was no increase
in pigmentation of the right eye and gonioscopy appeared normal (Figure-6).
Figure-1. Blepharospasm and peri-ocular swelling R eye.
Figure-2. Buphthalmos, mydriasis and corneal pigmentation.
Page 62
Figure-3. Conjunctival and episcleral congestion.
Figure-4. Scleral thinning and pigmentation.
Page 63
Figure-5. Scleral and corneal pigmentation.
Figure-6. Left eye.

Page 64
Initial treatment and further investigation

Treatment was started for glaucoma whilst awaiting further tests;
Treatment was started with aim to reduce IOP whilst awaiting the owner`s decision regards further
investigation.
Dorzolamide hydrochloride2% (Trusopt, Merck Sharp & Dohme(MSD)) topically TID right eye
Prednisolone acetate 1% (Pred Forte, Allergan) topically TID, added due to concern of
relative low IOP considering other ophthalmic findings, and concurrent uveitis a possibility as
aqeous flare may not have shown due to corneal opacity
Meloxicam (Metacam, Boehringer Ingelheim) 0.1mg/kg PO SID
Latanoprost 0.005% (Xalatan, Pharmacia) topically SID right eye, was added after 24 hours
when IOP remained relatively high R/L=20/7.
After 2 weeks of treatment the IOP had increased further to; R/L 46/4, and the owners agreed to
further investigation.
Routine bloods for biochemistry and haematology, thoracic xrays and abdominal ultrasound, was
carried out to check for concurrent disease or sign of neoplasia/metastasis and found unremarkable.
Ocular ultrasound of the left eye was unremarkable (Figure-7). No retrobulbar lesions were detected
in either eye. The right globe was enlarged with abnormalities as seen in Figure 8&9.
Page 65
Figure-7. Left eye.
Figure-8. Right eye. Iris thickening and irregular thickening ciliary body.
Page 66
Figure-9. Right eye. Hyperechoic vitreous.
Differential diagnosis for pigmentation and glaucoma

Diffuse ocular melanosis, melanocytoma or ocular melanoma with secondary glaucoma were the
main differentials. Primary glaucoma/goniodysgenesis, or other forms of secondary glaucoma e.g.
associated with uveitis, with illusion of increased pigmentation due to darker uveal tissue visible
through thinned scleral tissue was also a possibility. Glaucoma associated with lens luxation was
ruled out on slit-lamp exam and ultrasound.
Further treatment and diagnosis

A routine trans-palpebral enucleation was carried out, with no complications encountered. The
owners reported the dog to be happier after the enucleation, indicating that pain had been
experienced due to the ocular changes.
A diagnosis of melanosis was made on histopathology (Attachment-1&2).
Page 67
Figure 10. Gross pathology, melanosis (Courtesy of John Mould).
Prognosis
The affected eye was blind, presumably painful and non-responsive to medical treatment hence had
no prognosis. The left eye has remained unchanged in the 3 months following initial presentation
(Figure-11a,b,c). Regular ocular examinations have been adviced.
Page 68
Figure-11a. Two months post-enucleation.
Figure-11b&c. No sign of increased pigmentation.
Discussion
Ocular melanosis, previously known as pigmentary glaucoma, is a well-known condition in the Cairn
Terrier first described in USA in 1984 (1). It was described again in the UK in 1991 (2). A report by van
de Sandt suggests that other breeds, such as Boxers and Labrador Retrievers, may be affected as
well. The condition tend to affect middle-aged to older dogs of both sexes (3).
Ocular melanosis is characterized by infiltration of pigment-laden melanocytes and melanophages
predominantly within anterior uvea and anterior sclera/episclera. Cells may also be present in the
Page 69
posterior segment of the globe, optic nerve meninges and optic nerve periphery. In the CairnTerrier,
affected dogs have a dark-coloured thickened iris root, which progress with patches in sclera and
episclera by the ciliary cleft. Pigment particles sediment out coating the posterior surface of
peripheral cornea, the drainage angle and later obscuring the ciliary cleft eventually causing
glaucoma. Bouts of uveitis is also often seen, and is thought to be linked with release of greater
amounts pigment into the aqueous (4). The changes described in the other breeds were similar to
that of the Cairn Terrier (3), as was the changes in the described case.
In Cairn Terrier, the condition is thought to have an autosomal-dominant mode of inheritance (5).
The limited family history in this case, with only one presumed unaffected littermate known to the
family, makes it difficult to comment on possible inheritance.
Ocular melanosis in dogs may affect one or both eyes. The initiation for increase of melanin and
proliferation of melanophages is unknown, and clinical cases appear to occur with no known history
of trauma or ocular disease (3).
The onset of glaucoma and blindness is slow. Medical and surgical treatment tend to fail long term
due to obstruction of any surgical anterior chamber shunts by melanocytes and melanophages
(4,3,6). Prognosis for retention of long term vision is poor (7), with secondary glaucoma causing pain
and blindness (4), and enucleation is a valid treatment option (6).
Enucleation was discussed from the start in this case as the ocular changes were dramatic and
unlikely to respond to medical treatment. However, the owners were reluctant to surgery as they
did not think the eye caused pain. Insidious onset and chronicity may make clinical signs less obvious
to an owner. In this case blepharospasm, ocular discharge and shying from touch of the affected side
indicated pain. These facts together with the possible differential of neoplastic disease lead to
further investigation and enucleation. The IOP of the affected eye was not as high as expected from
the clinical signs when it was first measured. However, it was above the normal range, and high in
comparison to the left eye. The true IOP in the affected eye could also be masked (reduced) by
concurrent uveitis. The increase IOP after start of treatment could be due to reduction in
inflammation, progression of disease, poor owner compliance with treatment or a combination of
these. The owners reported a marked improvement in the dogs demeaena after the enucleation,
indicating presence of ocular discomfort/pain associated with the ocular abnormalities seen in this
case.
Page 70
Macroscopic: The eye measures 25x26x26mm. Externally there is a dense pigmentation of

the peripheral cornea and perilimbal conjunctiva. The anterior sclera has a firm feel all
around and there are extensive scleral pigment patches mostly anteriorly but also significant
areas near the posterior pole.
The dorsal part of the eye is removed for the internal examination. There is thickening of the
uveal in all areas with a solid appearance on cut surface and dense pigmentation. The iris is
2mm thick and the ciliary body 3mm without including the scleral part. Extensive scleral
invasion is visible anteriorly and presumably posteriorlyat deeper levels. Asteroid hyalosis is
present in the vitreous. The retina is detached I suspect only artefactually. The optic disc is
cupped.
Microscopic: Sections are being prepared and will be reported as soon as they are
available. Our normal time from receipt of a specimen to report the histology is 10-14 days
subject to my availability.
Comment: I suspect this is an example of melanosis comparable to that of the cairn terrier.
The Labrador is mentioned as an additional breed prone to the condition but, given how
numerous the breed is, I regard it as really rear in this breed, There is more thickening than
is seen in the cairns but diffuse spread is unusual in melanomas. The differential diagnosis is
melanosis vs melanocytoma vs melanoma. The distinction between melanosis and
melanocytoma(benign pigmentary tumour) may not be sharp even on histology but
melanocytoma does not usually grow diffusely like this. In the cairn terriers both eyes are
always affected though not nescessarily symmetrically and I would even regard that as part
of the diagnosis and so I would be interested to hear of the fellow eye in this case.
This is a very unusual eye and I am very glad to be able to add it our archive.
A digital photograph will be e-mailed to you. Clinical photographs are always appreciated.
If you would like to discuss this case further please contact me on
01568 616616 or johnmould@eyevetclinic.co.uk
Thank you for referring this specimen.
Yours sincerely,
John Mould
Report Date 14 January 2011
John Mould BA BVSc DVOphthal FHEA MRCVS
Eye Veterinary Clinic
Leominster
Herefordshire
HR6 0PH
Attachment-1. Histopathology results (Macroscopic)
Page 71
Macroscopic: The macroscopic features have been reported previously and a digital
photograph can be sent by email.
Microscopic:There is extreme hyperpigmentation and considerable thickening of all ares of
the uvea with extensive invasion of the anterior and posterior sclera. The angles are
occluded; there is retinal atrophy and a deep optic disc cup due to sustained high pressure.
Small areas of necrosis are present. The tumour consists olely of large round heavily
pigmented cells with no smaller proliferating cells.
Diagnosis: Melanosis.
Comment: We are familiar with all aspects of the comparable condition in the cairn terrier
which is relatively common as a referral problem. The Labrador is always mentioned in the
literature as a breed which is susceptible to this problem but I regard it as rare outside the
cairn breed. I have only previously seen very few examples that were not cairns. In the
cairn it is almost a condition of the diagnosis (with me at least) that the problem is bilateral. I
have checked with Dubielzig et al (2010), which is a recent comprehensive ocular pathology
text, and they note that in breeds other than cairns the condition is indeed often unilateral.
The histological appearance would certainly be consistent with melanosis rather than
anything more malignant. The systemic prognosis is therefore good. Clearly there was no
prognosis for managing the severe changes within the eye and the loss of sight was
permanent and the decision to enucleate is proved to be correct.
We have many examples of the cairn melanosis so you will appreciate that this is a valuable
specimen for our archive and is very likely to appear in a lecture or course at some point.
Thank you for giving us access to this specimen.
If you would like to discuss this case further please contact me on
01568 616616 or johnmould@eyevetclinic.co.uk
Thank you for referring this specimen.
Yours sincerely,
John Mould
Report Date 14 January 2011
John Mould BA BVSc DVOphthal FHEA MRCVS
Eye Veterinary Clinic
Leominster
Herefordshire
HR6 0PH
Attachment-2. Further pathology results
References
1. Covitz D., Barthold S., Diters R. Pigmentary glaucoma in the Cairn Terrier.
Transactions of the Fifteenth Annual Scienticif Program of the College of Veterinary
Ophthalmologists. November, Atlanta, Georgia, 1984.
Page 72
2. Perterson-Jones S.M. Abnormal ocular pigment deposition associated with glaucoma

in the Cairn Terrier. Journal of Small Animal Practice. 1991;32, 19-22.
3. Van de Sandt R.R.O.M., Boeve M.H., Stades F.C., Kik M.J.L. Abnormal ocular pigment
deposition and glaucoma in the dog. Veterinary Ophthalmology. 2003; 6,4,273-278.
4. Peterson-Jones S.M., Mentzer A.L., Dubielzig R.R., Render J.A., Steficek B.A., Kiupel
M. Ocular melanosisin the Cairn Terrier: histopathological description of the
condition, and immunohistological and ultrastructural characterization of the
characteristic pigment-laden cells. Veterinary Ophthalmology. 2008; 11, 4, 260-268.
5. Perterson-Jones S.M., Forcier J., Mentzer A.L. Ocular melanosis in the Cairn Terrier:
clinical description and investigation of mode of inheritance. Veterinary
Ophthalmology. 2007;10, Supplement 1, 63-69.
6. Gelatt K.N., Brooks D.E., Kallberg M.E. The cCanine Glaucomas. In Gelatt K.N.
Veterinary Ophthalmology. 4th Edition. Blackwell Publishing. Pp753-811.
7. Crispin, S M, notes on Veterinary Ophthalmology, Blackwell Science Ltd. 2005,
pp.200-202.
Page 73
Lens Opacities In A Horse

(Word count 999)
Case history
An 8 year old Appaloosa mare was presented for assessment of a lens opacity found on routine
examination. The horse showed no signs of visual deficit and it was in general good health. The
horse had no known history of medical treatment, other than routine anthelmintics and vaccination.
The husbandry was excellent, and no environmental factors predisposing to ocular disease was
identified. A small corneal opacity, of no known clinical significance, had also been present prior to
purchase of the horse 2 years previously.
General clinical and ophthalmic examinations were performed (Appendix-1). The general clinical
examination was unremarkable. The following abnormalities were detected on ophthalmic
examination:
Right ocular corneal opacity/leucoma, of the superficial stroma, 3mm diameter, medioventral 5 Oclock position. Fluorescein negative. No sign of associated discomfort (Figure-1).
No ocular surface changes was seen in the left eye (Figure-2).
Bilateral dark lens opacity forming an irregular web like pattern, positioned in a posterior
subcapsular polar position (as seen on parallax same directional movement and slit-lamp
examination), with opacities more marked in the right versus left lens (Figure-1).
Fundus details readily observed around the lens opacity and through parts of the opacities
bilaterally.
Page 74
Figure-1. Right eye. Corneal and lenticular opacities.
Figure-2. Left eye. No corneal opacities. Lens opacities seen on examination is not
evident on the photograph.
Differential diagnosis of opacities of the lens and associated ocular refracting media, classified as
suggested by A.G. Matthews (1):
Developmental cataract;
Extralenticular-no direct involvement of lens
Page 75
Retrolenticular fibroplasia
Mittendorfs dot
Persistent pupillary membranes
Persistent hyperplastic primary vitreous
Pigmentation
Capsulolenticular-involving the lens capsule and subjacent cortex
Anterior capsular cataract
Posterior capsular cataract
Anterior polar cataract
Posterior polar cataract
Lenticular-involving the lens substance
Zonal cataract
Embryonic nuclear cataract
Fetal nuclear cataract
Perinuclear/lamellar cataract
Equatorial cataract
Sutural cataracts
Posterior sutural
Anterior sutural
Axial cataracts
Floriform
Elliptical
Complete cataract
Page 76
Acquired/secondary cataracts associated with;
Intraocular disease
Uveitis - traumatic, infectious, immunogenic Equine recurrent uveitis
Anterior uveitis or iridiocyclitis
Posterior uveitis or chorioretinitis
Panuveitis
Whiplash injury from direct blunt trauma to the globe
Retinal detachment
Glaucoma
Neoplasia e.g. anterior uveal melanomas impinging on lens
Senile cataracts
Systemic disease rare, no specific mechanism identified in horse
Metabolic
Toxic
External sources
UV light
Ionising radiation
Diagnosis
Bilateral posterior polar subcapsular lens opacities were seen on examination. Posterior
capsular involvement could not be ruled out on clinical examination and ocular ultrasound
would be required if a definite diagnosis was required. The cataract was thought to be
developmental as there were no clinical sign of primary disease or external influence to
cause these lens changes. The cataract could be of congenital origin, previously
undiscovered or it could have developed later.
Focal corneal opacity, or leukoma, of unknown origin, possibly a scar from previous trauma.
Page 77
Prognosis
Good, but cautious. The cataract was immature with no obvious effect on vision, and was thought to
be a non-progressive form. However, regular examinations was advised for assessment of signs of
progression and required for a definite prognostic assessment.
Treatment
Not required.
Discussion
Opacities in the ocular refractive media are frequent findings during routine ophthalmic examination
in the horse, with lens opacities present in at least 5-7% of horses with otherwise clinically normal
eyes. The opacities range from small epicapsular remnants of the foetal vasculature to dense and
extensive cataract(2). Cataracts can be unilateral or bilateral, focal or difuse, and may occur as the
only ocular defect or in association with other ocular abnormalities (3,4). Complete cataract is
associated with significant visual disability, whilst focal or incomplete cataracts seldom cause any
apparent visual dysfunction (2).
True cataracts results from loss of optical homogeneity of the lens resulting from derangement of
its highly organized cytosystem and alterations in the refractive index of the cytosol, caused by
several physiochemical processes. Extralenticular opacities, are not true cataracts but are nonprogressive, congenital, retrolental opacities derived from the tunica vasculosa lentis (TVL) and
vascular framework of the iridopupillary membrane. They are likely to contain vascular, pigmentary
and connective tissue elements (1,2) and in some cases other abnormalities suggestive of anterior
segment dysgenesis may also be seen e.g. focal corneal opacity or iris coloboma (1).
No single classification system wholly or satisfactorily encompasses the wide range of cataracts
observed in the horse. One system described by Matthews is based on anatomic location,
appearance, and aetiogenesis see differential diagnosis above.
Lens opacities in the horse are either developmental opacities including congenital cataracts, or
acquired secondary cataracts. Developmetal opacities is the more common, and may be associated
with other congenital ocular abnormalities e.g. microphthalmos, iridial hypoplasia, megalocornea,
ciliary cysts and retinal dysplasia (1). The embryology of the equine lens is assumed to be similar to
that of cattle and dogs (5). Developmental lens opacities arise both in utero and postnatally by
abnormal differentiation and growth of embryonic derivatives, or from disruption of the normal
maturation and lay down of secondary fibers in the foetal and postnatal lens. Congenital cataracts
Page 78
form the largest group of developmental equine lens opacities, and more than one form of opacity
may be present in any one eye (1).
Hereditary, traumatic, nutritional, inflammatory, radiation, metabolic, and toxic causes have all been
proposed, however, the cause is rarely determined (4). Inherited forms of cataract are commonly
described in other domestic animal species and humans (6). In horses heritability has not been
widely studied (1) and few are reported (6). Cataracts suggested as heritable in horses include those
of Morgan horses, although the pattern of inheritance has not been determined. Cataract is also
suggested to be a part of inherited ocular segment dysgenesis in Belgian horses (2,5,6),
Quarterhorses (2) and Rocky Mountain Spotted Horses. In Arabs and Thoroughbreds sporadic
familial occurrence of cataracts have been described (2). In any case of congenital cataracts in which
a specific pattern of inheritance cannot be provided, an implication of environmental factors as the
cause is assumed. The extent and severity of the cataractous changes vary with the stage of
development at which the insult occurs and/or the severity of the insult (5). Irrespective of the
type of cataract, developmental forms tend to progress slowly. However, final analysis of
progression of any particular cataract can only be definitively determined by repeated ophthalmic
examination over a protracted period (1).
Most cataracts have no significant functional effect on vision in the horse, hence treatment is not
often required. In cases of overt vision loss due to cataract, surgical removal of the lens is the
standard management. Ocular ultrasonography and electroretinography is required presurgically to
rule out other ocular pathology. Phacoemulsification and aspiration after anterior capsulorrhexis is
the treatment of choice. The horse must be well handled and likely to be compliant with aggressive
topical medication pre- and postoperatively (2). Intraoperative and postoperative complications,
especially uveitis, can result in a blind horse. However, visual results after cataract surgery appear to
be good, with minimal complications, in both foals and adult horses justifying the procedure in
visually affected individuals (7). Intraocular prosthetic lenses have been associated with post-surgical
complications, but horses seem to cope well with aphakia and visual impairment arising from
uncorrected hypermetropia. This may be due to the relatively large retinal receptor fields in this
species (2). Recent years has also shown imrovements in surgical technique, ocular pharmacology,
viscoeastic devices, phacoemulsification and intraocular lens implantation (8,9).
References
1. Matthews A.G. Lens opacities in the horse: a clinical classification. Veterinary
Ophthalmology 2000;3,65-71.
Page 79
2. Matthews A.G. The lens and cataracts. Veterinary Clinics of Nort. 3rd Editionh
America Equine Practice 2004;20,393-415.
3. Matthews A.G. & Barnett K.C. Lens In: Equine Ophthalmology. An Atlas and Text.
Editors: Barnett K.C., Crispin S.M., Lavach J.D., Matthews A.G. Saunders. Elsevier Ltd.
2nd ed. 2004,165-182.
4. Fifi T.M.,Gemensky-Metzler A.J., Wilkie D.A., Colitz C.M.H., Brast I.D., Klages D.C.
Clinical features and outcomes of phacoemulsification in 39 horses: a retrospective
study (1993-2003). Veterinary Ophthalmology. 2006;9,5,361-368.
5. Beech J., Aguirre G., Gross S. Congenital nuclear cataracts in the Morgan horse.
Nuclear. Journal of the American Veterinary Medicine Association. 1984;184,13631365.
6. Beech J., Irby N. Inherited nuclear cataracts in the Morgan horse. Journal of Heredity.
1985;76,371-372.
7. Dizzy J., Mill champ N.J., Keller C.B. Use of phacofragmentation for cataract removal
in horses: 12 cases (1985-1989). Journal of the American Veterinary Medicine
Association. 1991;198(10),1774-1778.
8. Wilkie D.A., Colitz C.M. Update on veterinary cataract surgery. Current Opinion on
Ophthalmology. 2009. 20;(1),61-68.
9. McMullen R.J., Gilger B.C. Keratometry, biometry and prediction of intraocular lens
power in the equine eye. Veterinary Ophthalmology. 2006. 9;(5),357-360.
Page 80
Presumed Congenital Ocular Defects in a Dog

(Word count 998)
Case history
A four months old, female, ShihTzu (4.85kg) was presented with unilateral increase in reflection of
the right eye, particularly noticeable on photographs, since the purchase of the pup 2 months
previously. The abnormality had not been noted by the breeder. No history was available from the
breeder on ocular abnormalities in the parents or litter mates. The owners had not noted any visual
deficits. The dogs hearing appeared normal.
Clinical examiniation
General clinical and ophthalmic examinations were performed (Appendix-1). The general
examination was unremarkable. The ophthalmic examination showed the following abnormalities;
Anisocoria, right pupil mydriatic and left pupil appeared reduced (Figure-1)
Bilateral dyscoria, more noticeable in left pupil
Correctopia, with left constricted pupil positioned medially (Figure-2)
Multiple small areas of iridial thinning and colobomas
Marked reduction of right pupil constriction, but some movement present
Right eye; posterior polar lens capsule opacity (Figure-3). Left; similar but smaller
Right vitreal linear opacity, stretching caudally from attachment at posterior lens capsule, to
approximately 1/3rd vitreal depth. No vitreal oacity left eye.
Small retinal fold dorsolateral to optic disc right eye (dark line with surrounding halo of
increased tapetal reflectivity) (Figure-4)
1% pilocarpine application did not produce miosis in the right eye
Other notes;
No ocular discomfort, bilateral globes appeared of normal size, persistent pupillary membranes not
present, no cataract beyond the posterior capsular opacities seen, optic discs normal
size/shape/colour, no nystagmus. No ocular or general neurological deficits present.
Page 81
Figure-1. Anisocoria with apparent increased tapetal reflection of the right eye.
Figure-2. Iris hypoplasia with resulting correctopia and dyscoria, left pupil.
Page 82
Figure-3. Posterior lens capsule opacity,unfortunately not as obvious on the photo as it

was on direct ophthalmoscopy and slit-lamp examination (pharmacological mydriasis).
Figure-4. Illustration of direct ophthalmoscopy view of the right fundus. Single small
retinal fold surrounded by small halo of increased reflectivity.
Page 83
Diagnosis
The ocular findings were presumed to be of congenital origin (see discussion below) and included;
Iris hypoplasia with iris colobomas, causing correctopia and dyscoria.
Persistent hyperplastiv tunica vasculosalentis/persistent hyperplastic primary vitreous

(PHTVL/PHPV), seen as bilateral posterior polar capsular cataracts and right vitreal opacity.
Retinal dysplasia.
Differentials:
Iris changes
Acquired iris atrophy e.g. post uveitic/senile changes
Iris melanoma
Synechiae formations
Anisocoria
Glaucoma
Neurogenic
Retinal lesion
Post-inflammatory chorioretinopathy lesions
Prognosis
Good, with no noticeable effect on vision at this stage. Lack of iris sphincter muscle and reduced
papillary constriction effects the amount of light entering the eye and therefore disturb depth of
focus for near vision and reduce optical aberrations (1). Increased light exposure may cause ocular
discomfort, and could theoretically cause retinal damage long term although with UK climate this is
less likely to pose a real threat.
Treatment
Non required. Advice was given to avoid bright sun-light and discussed availability of uv-protection
sunglasses i.e. doggles. Regular ocular examinations was adviced. The owner was planning to have
the bitch neutered, hence the possibility of inheritance was not directly relevant. However, the
owner was advised to inform the breeder of the findings.
Page 84
Discussion
Common ocular problems in Shih Tzu dogs include medial canthal entropion, trichiasis, dermoids,
third eyelid gland prolapse, chronic keratitis/ulceration, progressive retinal atrophy, vitreal syneresis
and retinal detachments (2,3). No hereditary eye diseases, congenital or later onset, have been
registered in this breed for either schedule A or B of the BVA/KC/ISDS UK Eye Scheme (4). The
findings in this case were assumed to be non-inherited malformations. Ocular abnormalities may be
induced in early perinatal life or, more likely, present from birth as true congenital lesions caused by
e.g. intra-uterine infection, irradiation, trauma, drugs or toxins (1).
The iris pigmented and non-pigmented epithelial layers develop from the anterior aspect of the
optic cup (neuroectoderm origin) and the retina from the posterior optic cup. The iris stroma
develop from the anterior segment mesenchymal tissue (neural crest cell origin). By approximately
day 40 of gestation, the 2 epithlial layers develop cilia projecting into the intercellular space. The
smooth muscles of the pupillary sphincter and dilator muscles differentiate from the epithelial
layers. In dogs, development of the anterior chamber continuous in the postnatal period before
eyelid opening. The peripheral iris and cornea are in contact at birth. Pectinate ligaments mature by
3 weeks, and uveal and corneoscleral trabecular meshwork by 8weeks, post-natally (5).
Persistant pupillary membranes is a common example faulty differentiation of the anterior chamber
and results from failure of normal atrophy of the tunica vasculosa lentis anterioris (1), and was not
present in this case. Incomplete iris development in dogs, as seen in this case, range from the rare
occurrence of apparent absence of the whole iris (aniridia), to incomplete development (hypoplasia)
or absence of a full thickness iris portion (coloboma) which are also uncommon (1).
Retinal dysplasia may be inherited as total and mulitfocal (focal and geographic lesions) in many
breeds of dogs. Retinal dysplasia can also be seen as a non-inherited condition in any breed, with
lesions present from birth or induced in early perinatal life as discussed above. The clinical signs of
retinal dysplasia are variable and may alter/remodel over time (6). Small lesions do not usually affect
vision. There is no treatment for retinal dysplasia (1).
PHTVL/PHPV is a complex of lens, tunica vasculosa lentis (TVL) and anterior vitreal anomalies.
Anterior PHTVL/PHPV is the presence of retrolental fibrous connective tissue, persistence of
components of the hyaloid-TVL system, and a variable progressive posterior polar cataract (7,8).
Variable persistence of the hyaloid occurs in association with many types of malformations,
including microphthalmia, microphakia, cataract and retinal dysplasia (9). The globes and lenses did
appear to be of normal size in this dog, but ultrasound would be required for exact measurements.
PHTVL/PHPV may occur secondary to other malformations or as a primary, spontaneous failure of
Page 85
vascular regression. The hyaloid vasculature and tunica vasculosa lentis reach maximal development
by day 45 of gestation in dogs and then begin to regress. Complete regression is usually reached by
14 days postnatally (5).
Cataract is defined as any opacity of the lens and/or the lens capsule (1). In this case the cataract
was caused by the PHTVL/PHPV, involving the lens capsuleonly. The PHTVL/PHP would be equivalent
to grade 2 (retrolental fibrovascular pigmented dots combined with retrolental tissue proliferation
attached to the posterior lens capsule) and grade 3(retrolental fibrovascular plaque combined with
parts of the hyaloid-TVL system) in the left and right eye respectively, compared to that of the six
grades of PHTVL/PHPV described for the inherited form seen in Doberman pinschers.
The posterior polar capsular opacity in this case was not extensive and should cause minimal effect
on the vision. Larger opacity may obscure vision by covering most of the pupil. Phacoemulsification
combined with posterior capsulectomy and insertion of an intra capsular lens is considered as a
viable option for surgical management of cataract associated with PHTVL/PHPV, with long-term
preservation of functional vision expected (7).
Based on the above, the abnormalities in this case are most likely to be caused by abnormal
development (in utero, versus primary failure of regression postnatally) of the optic cup, i.e. iris
hypoplasia and retinal fold/hypoplasia with secondary PHTVL/PHPV.
There was no known history of possible terattogens or illness of the bitch during pregnancy in this
case. A thorough history from the breeder and ocular exams of the parents and littermates would be
required to discuss a possible aetiology further.
References
1. Crispin S.M. Notes on veterinary ophthalmology. Blackwell Publishing. 2005. pp124126.
2. Christmas R.E. Common ocular problems of Shin Tzu dogs.Canadian Veterinary
Journal. 1992. Jun; 33 (6): 390-393.
3. Itoh Y., Maehara S. Yamasaki A., Tsuzuki K., Izumisawa Y. Investigation of fellow eye
of unilateral retinal detachment in Shih-Tzu. Veterinary Ophthalmology. 2010. 13; 5,
289-293.
4. BVA/KC/ISDS Eye Scheme as per 1st January 2011. British Veterinary Association
Website. Canine health scheme.
5. Cook C.S. Ocular Embryology and Congenital Malformations. In: Gelatt K.N.
Veterinary Ophthalmology. 4th Edition. Blackwell Publishing. 2007. Pp3-37.
Page 86
6. McLellan G. The Canine Fundus. In: Peterso-Jones S., Crispin S. BSAVA Manual of
Small Animal Ophthalmology. 2nd Edition. British Small Animal Veterinary
Association. 2002. pp227-246.
7. Gemensky-Metzler A.J., Wilkie D.A. Surgical management and histologic and
immunohistochemical features of a cataract and retrolental plaque secondary to
persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary
vitreous (PHTVL/PHPV) in a Bloodhound puppy. Veterinary Ophthalmology. 2004; 7,
5, 369-375.
8. Stades F.C. Persistent hyperplastic tunica vasculosa lentis and persistent hyperplastic
primary vitreous (PHTVL/PHPV) in 90 closely related Doberman Pinschers: clinical
aspects. Journal of the American Animal Hospital Association. 1980; 16, 739-751.
9. Keller W.F.,Blanchard G.L. Congenital dysplasia in a canine eye: A case report.
Journal of the American Animal Hospital Association. 1972; 8, 29-34.
Page 87
Hypertensive Ocular Disease In A Cat

(word count 997)
Case history
An 18 year old, neutered male, domestic shorthaired cat (2.90 kg) was presented with a 2
week history of reduced vision, polyuria, polydipsia and weight loss. The cat had shown
increased vocalisation over the previous month.
General clinical and ophthalmic examinations were performed (Appendix-1). The following
abnormalities were found on general clinical examination;
Poor condition/thin (Figure-1)
Skin lesion nose (Figure-1)
Disorientated, bumping into obstacles, not tracing falling objects
Increased vocalisation
Small kidneys
Low grade (2/6) systolic murmur, heart rate 240 beats per minute
Strong bilateral femoral pulses
The ophthalmic examination (Table-1) showed the following abnormalities;
Unilateral serous-mucoid discharge right eye and mild lower lid entropion
Bilaterally dilated pupils (Figure-2)
Menace; left negative, right slow
Dazzle reflex; left negative, right positive
Pupillary light responses; direct left and indirect left to right negative, right and right to left
slow and reduced
Left retina; total detachment and anterior displacement (Figure-2)
Right retina; multi-focal haemorrhages, oedema and detachments (Figure-2)
Page 88
Figure-1. Poor condition, skin lesion nose
Figure-2. Left total retinal detachment. Right retinal oedema, haemorrhages and focal
detachments
Further investigation
Blood biochemistry and haematology, in house uraemia (Table-2)
Urine analysis, in house Multistix (Bayer) hyposthenuria, proteinuria (Table-2)
Total serum thyroxine concentration (Axiom Veterinary Laboratories within normal range
(Table)
Page 89
Blood pressure (BP) measurements (Doppler flow)- repeated measurements 210-220 mm

Hg
Ocular ultrasonography (Veterinary specialist, M.Castello) multiple focal detachments right

retina (Figure-3), total retinal detachment left eye (Figure-4)
Further investigation (full cardiac evaluation, virology, serology, abdominal ultrasonography

and chest radiographs) was not performed due to clinical findings achieved, as well as cost
to the owner in this old cat.
Page 90
Figure-3. Focal retinal detachments, right eye
Page 91
Figure-4. Total retinal detachment, left eye
Diagnosis
Hypertensive retinopathy was diagnosed on general and ocular examinations and blood pressure
consistently over 160mmHg. Chronic renal failure was diagnosed on clinical examination, blood and
urine sample. The normal creatinine levels may be a reflection of poor muscle mass seen in this case
(1).
Either condition may have preceded the other, or the two conditions may have developed
independently. Hypertension, causing retinal lesions, may also be primary idiopathic or secondary to
other diseases such as;
Endocrine abnormalities e.g. hyperthyroidism, diabetes mellitus, hyperaldosteronism
Cardiac abnormalities
Hyperkinetic heart syndrome e.g. anaemia, hyperviscosity, polycythemia, fever,

arteriovenous fistula
Page 92
Intracranial disease e.g. neoplasia
Hypercalcaemia e.g. hyperparathyroidism, paraneoplastic syndrome
Other causes of retinal haemorrhage and detachments include:
Coagulopathy associated with e.g. platelet and clotting abnormalities

(liverdx/rodenticides/autoimmune disease)
Inflammatory or neoplastic vasculitis
Uveitis associated with e.g. Feline Leukaemia Virus (FeLV), Feline Immunodeficiency virus
(FIV), Feline Infectious Peritonitis (FIP), toxoplasmosis, Cryptococcosis, Blastomycosis,
Histoplasmosis, Coccidiomycosis
Trauma
Diabetic retinopathy
Ethylene glycole toxicosis
Prognosis
Good for improved control of hypertension. Poor for CRF, which is likely to progress despite
treatment. Poor and guarded for return of vision in left and right eye respectively.
Amlodipine (Istin, Pfizer) 0.625 mg/cat orally once daily
Low phosphorus Low Protein diet
Benazepril (Fortekor, Novartis Animal health) 1.0mg/kg, added after 1 week
Progress:
1 week BP=180mmHg. No murmur audible. Some resorption of haemorrhages/exudates with
improved visual responses (also noted at home). Left retina unchanged. Benazepril started due to
persistent hypertension.
2 weeks- BP=160mmHg. No further retinal changes. Visual responses unchanged. Despite
improvement in vision, the owner did not feel previous quality of life was regained and opted for
euthanasia.
Page 93
Discussion
Hypertensive retinopathy is commonly seen in the older cat, over 10 years of age, and possibly more
often in females and neutered cats (1). Acute or progressive blindness may be the primary
complaint, with hyphaema, uveitis and secondary glaucoma also commonly seen (1,2). Persistent
hypertension may cause damage to other organs such as the brain, heart and kidneys (3).
Hypertension may be diagnosed by measuring indirect blood pressure monitoring devices e.g.
oscillometric or ultrasonic device (3). Repeat readings in a calm environment is important for
accuracy, as the cat can have significantly elevated blood pressure if stressed, and reliable results
can be difficult to obtain (2). Persistent systolic blood pressure of 170 mmHg or above should be
categorised as hypertensive (3). If end-organ damage, such as hypertensive retinopathy, is
documented along with a single elevated blood pressure reading, the diagnosis can be made more
readily (4).
Ocular lesions have been reported in 77% of cats with systemic hypertension (3). Consistently
elevated arterial blood pressure leads to sustained vasoconstriction of retinal arterioles.
Compromise of endothelium and vascular smooth muscle leads to leakage of plasma and red blood
cells into surrounding retinal tissue. Retinal haemorrhage, oedema, and the intra-retinal fluid
accumulation is most likely to occur from retinal vascular disease, while retinal detachment is
thought to be associated primarily with choroidal vascular disease (4). In retinal detachment the
neuroretina is usually separated from the underlying retinal pigment epithelium, with
subsequentretinal degeneration and loss of function. Denuded tapetal fundus will appear hyper
reflective. Focal detachment may not cause clinically detectable vision loss, whilst a total retinal
detachment is blinding (1,5).
Hypertension may be a primary idiopathic problem, but is often diagnosed concurrently with
systemic diseases such as chronic renal failure (CRF), hyperthyroidism, diabetes mellitus and chronic
anaemia (6). The most commonly associated diseases of feline hypertension is CRF (6,3,2,4).
Determining if renal dysfunction precedes, follows, or develop independently of hypertension may
however be difficult (6,2). In the more recent years, hyperaldosteronism is also beeing recognised as
an underlying cause, with hypokalaemia and systemic hypertension hallmarks of the disease.
Diagosis may be made on serum aldosterone levels and ultrasound of affected adrenal glands (7).
Hypertensive retinopathy is usually a slow, insidious, process and vision may be spared if the
process is identified and controlled before severe ocular disease can develop (1).
Page 94
Treatment of hypertensive retinopathy is aimed at controlling any known underlying disease and
treating the systemic hypertension (2). The calcium-channel blocker, amlodepine besylate, has been
shown to be effective and safe in lowering blood pressure in cats (6,3). Recommended dosing is
0.625-1.25 mg/cat daily, with the aim to keep systemic arterial blood pressure below 165 mmHg.
Further antihypertensive drugs may be added if the blood pressure remains high despite highest
dose of amlodepine used i.e. Angiotensine converting enzymes (ACE) inhibitors, -blockers or
thiazide diuretics (3). The ACE inhibitor benazepril is also used in treatment of feline CRF, indicated
in cats with known proteinuria and/or hypertension (8).
Retinal lesions may partly resolve with treatment. Haemorrhage and serous exudate may resorb,
improving vision, but structurally damaged vessels and retinal tissues are unlikely to become
functional again (4).
Early recognition of systemic hypertension is important to a cats general health as well as preventing
retionpathy and permanent blindness (4). In this case, the cats general condition and demaena
determined the outcome to euthanase despite improvement in BP and vision.
Biochemistry
Result
Reference range
Total protein
72.00
g/l
55-80
Albumin
32.00
g/l
20-30
Urea
19.20
mmol/l
2.9-11
Creatinine
168.00
umol/l
87-160
Alkaline phosphatase
149.00
u/l
0-82
Alanine aminotransferase
95.00
u/l
0-80
Glucose
3.80
mmol/l
2.8-7.2
Total bilirubin
2.50
umol/l
0-12
Calcium
2.80
mmol/l
2-3
Phosphate
1.75
mmol/l
0.55-2.71
Amylase
1362.00
u/l
500-1500
Cholesterole
6.3
mmol/l
2-6.5
Globulin
40.00
g/l
28-51
Sodium
152.40
mmol/l
138-155
Potassium
4.70
mmol/l
3.9-6.4
Chloride
122
mmol/l
112-129
Haematology
Page 95
Red blood cells
8.01
x10.9/l
5-9.9
Mean corpuscular volume
46.2
fl
43-55
Mean corpuscular
haemoglobin
0.81
g/dl
0.86-1.17
Mean corpuscular
haemoglobin concentration
17.60
g/dl
18.5-22.2
Mean platelet volume
9.20
fl
8-13
Haematocrit
0.37
0.26-0.48
Haemoglobin
6.50
mmol/l
5.6-9.6
Platelets
348
x10.9/l
200-800
White blood cells
14.00
x10.9/l
6.6-18
Lymphocytes
6.10
x10.9/l
1.5-7
Granulocytes
14.90
x10.9/l
1.7-14
Lymphocytes %
38.10
25-33
Granulocytes %
61.90
0-0
Other tests
Urine specific gravity
refractometer reading
1.024
Urine multistix
Protein +30
pH 6.5
Other readings normal
Total thyroxine Axiom

Veterinary Laboratories
25.7
nmol/l
10-50
Table-2. Laboratory results (in house)
References
1. Polzin D.J., Osborne C.A., Bartges J.W., James K.M., Churchill J.A. The urinary system.
Chronic renal failure. In: Textbook Veterinary internal medicine 4th. edition. Editor
Ettinger S.J. 1953,1734-1760
2. Dukes J. Hypertension: A review of the mechanisms, manifestations and
management. Journal of Small Animal Practice. 1992;33,119-129.
3. Elliott J., Barber P.J., Syme H.M., Rawlings J.M., Markwell P.J. Feline hypertension:
clinical findings and response to antihypertensive treatment in 30 cases. Journal of
Small Animal Practice. 2001;42,122-129.
4. Stile J., Polzin D.J., Bistner S.I. The Prevalence of Retinopathy in Cats with Systemic
Hypertension and Chronic Renal Failure or Hyperthyroidism. Journal of the American
Animal Hospital Association. 1994;30,564-572.
5. Glaze M.B., Gelatt K.N. Feline Ophthalmology. In: Gelatt KN, ed. Veterinary
Page 96
6. Maggie F., DeFrancesco T.C., Atkins C.E., Pizzirani S., Gilger B.C., Davidson M.G.
Ocular lesions associated with systemic hypertension in cats: 69 cases (1985-1998).
Journal of the American Veterinary Medicine Association. 2000;217:695-702.
7. Feline Primary hyperaldosteronism. Veterinary Clinics of North America Small Animal
Practice. 2010. 40;2,353-359.
8. Sturgess K. Renal disease. In: Notes on feline internal medicine. Blackwell 2003,147164.
Page 97
Appendix 1
Examination Protocol
All patients were examined using the same standard routine. Any abnormal findings are recorded in
the relevant case-reports. Further tests and procedures were used as appropriate, as stated for each
individual case.
Equipment available for ophthalmic examination, diagnostic procedures

and treatment of patients
Examination room capable of being darkened
Focal illumination Finoff focal transilluminator
Handheld ophthalmoscope (Vista 20, Keeler UK)
Slit lamp bio microscope (SL-15, Kowa)
Condensing lens for indirect ophthalmoscopy (Volk Pan Retinal Lens 2.2, Keeler
UK)
Binocular indirect ophthalmoscopy (Keeler Wireless)
Applanation tonometer Tono-Pen XL (Medtronic, Solan) and Schitz
Goniolens, Koeppe 18mm (Ocular Instruments)
Cytological Diff Quik stain
Schirmer tear test papers - sterile tear flow test strip (Sno strips, Chauvin
Pharmaceuticals)
Ophthalmic stains;
-
Fluorescein sodium BP 1mg sterile ophthalmic strip (Fluorets, Chauvin

Pharmaceuticals) and Fluorescein sodium BP 1.0% (Minims Fluorescein Sodium,
Chauvin Pharmaceuticals)
Rose Bengal 1% (Minims Rose Bengal, Chauvin Pharmaceuticals)
Sterile water/saline for flushing ocular surfaces
Topical local anaesthetic agent Proxymetacaine Hydrochloride 0.5% (Minims

Proxymetacaine, Chauvin Pharmaceuticals)
Page 98
Mydriatic Tropicamide BP 1% (Minims Tropicamide, Chauvin Pharmaceuticals)
Topical ocular vasoconstrictor and mydriatic agent - Phenylephrine Hydrochloride BP

10% (Minims Phenylephrine, Chauvin Pharmaceuticals)
Topical miotic agent Pilocarpine Nitrate BP 1% (Minims Pilocarpine Nitrate,

Chauvin Pharmaceuticals)
Sterile swabs & culture media
Sterilised scraper for cytology sampling - scalpel blade
Microscope slides
Callipers/ruler
Nasolacrimal probes/cannulae intravenous catheters
Sterile syringes and needles
Microsurgical ophthalmic kit (Veterinary Instrumentation)
Soft contact lenses (Bandage lens, Veterinary Specialist products)
Ultrasonography 7.5MHz probe (also access to in-house specialist referral)
Radiography (Ultrapower 100+, Vetxrays)
Blood pressure machine CAT Doppler Blood Pressure Kit, Thames Medical
Computed tomography (CT) recently installed 2010 (LightSpeed) images

interpreted by specialist service
Patient requiring further specialised procedures including electroretinography (ERG), scan and
magnetic resonance imaging (MRI) would be referred.
Initial examination
Patient observation in normal light condition on entering consult room and whilst taking a
case history. History including breed, age, sex, duration of ocular problem, speed of onset
and progression, circumstances around onset e.g. trauma or contact with other animals,
changes in ocular appearance, vision, ocular discomfort, and general health.
Obstacle course created in the consult-room in cases of visual problems - bright and dimmed
light. Blindfolding used to assess each eye in turn where required.
Page 99
Patient observation, hands-off - sign of ocular discomfort, discharge and corneal reflex,
blink-rate, blepharospasm and photophobia. Adnexal, orbital and ocular conformation and
symmetry assessed.
Full physical examination, usually after the initial assessment as above, including
examination for signs of inflammation, swelling, symmetry, discharges and discomfort. Areas
examined included; eyes, nose, ears, head, mouth and teeth - including opening of the
mouth, skin, body and extremities - including musculoskeletal system if required.
Submandibular, pre-scapular and popliteal lymph nodes palpated. Auscultation of the chest
carried out for chest, lung and heart abnormalities. Femoral pulses, mucous membrane
colour and capillary refill times check for circulatory or other vascular abnormalities.
Abdominal palpation to assess the presence of free fluid, masses and pain. Rectal
thermometer to assess body temperature. A more complete neurological examination
would be carried where neurological deficits were suspected.
Further ophthalmic examination - Bright light

Reflexes and vision was further assessed;
Ability to follow falling cotton wool balls
Visual placing reaction in cats and small dogs
Palpebral reflex:
Trigeminal nerve i.e. cranial nerve V - sensory
-
medial canthus (ophthalmic branch)
lateral canthus (maxillary branch)
Facial nerve i.e. cranial nerve VII blink i.e. motor
Menace response:
Optic nerve i.e. cranial nerve II, with care not to create air current - sensory
Facial nerve (VII) blink
Corneal sensation/reflex:
Afferent pathway of the Trigeminal nerve (V)
Efferent pathway of the Facial nerve (VII )
Vestibulo-ocular reflexes maintenance of ocular stability during head movements
Page 100
More detailed examination of the eyes i.e. examination and palpation of the head and extraocular regions for areas of swellling and pain, palpation of orbital rim and ligament(or
complete bony orbital rim in the horse and alpaca). Note made of adequacy and rate of
blink, lid-corneal apposition, direction of upper eyelid lashes, presence and position of any
abnormal cilia, position and size of lacrimal punctae (and nasal ostium in horse and alpaca),
prescence and position of the third eyelid. The corneal light reflex was assessed, followed by
examination of the bulbar conjunctiva, episclera and sclera, the limbus, cornea, anterior
chamber, pupil, iris and lens.
Scirmer tear test before further examination
Further ophthalmic examination - Dark/dimmed light
Distant direct ophthalmoscopy assessing pupil shape and symmetry and symmetry of gaze.
Identifying any opacities of the lens and the ocular media, including differentiation of lens
opacities.
Retinal and optic nerve function (subcortical pathways i.e. remain intact in presence of visual
cortex lesion) were further assessed; Dazzle reflex for optic nerve (II) i.e. retinal stimulation,
and facial nerve (VII) i.e. blink. Pupillary light reflexes, direct and consensual for optic nerve
(II) and oculomotor (III) nerve functions.
More detailed exam, with a focal light source (slit lamp biomicroscopy) of the adnexa and
globe as above i.e. colour, thickness, blood vessels and pigmentation of the bulbar
conjunctiva, episclera and sclera. Limbus definition, pigmentation and vasculature. Corneal
reflection and clarity, presence and position of any opacities including any blood vessels.
Appearance of the grey zone in the horse and alpaca and the drainage angle in cats, horse
and alpaca. Anterior chamber depth and transparency noting colour and position of any
opacities. Iris position, colour and stability. Pupil size, position and margin appearance.
Colour, size and shape of granula iridica in the horse and alpaca. Lens checked for position
and stability.
Tonometry to ensure the intraocular pressure is normal before the application of a mydriatic
agent for examination of the posterior ocular segment.
Slit lamp examination of the posterior chamber after mydriasis achieved; lens checked for
position, size and opacities. Position, size and nature of any opacities in the anterior vitreous
noted.
Page 101
Fundus examination by indirect ophthalmoscopy; optic nerve appearance (i.e. size, colour
and degree of myelination, vasculature), immediate peripapillary area, retinal and choroidal
vasculature, tapetal and non-tapetal fundus.
Close direct ophthalmoscopy to focus in for more examination of the optic nerve, retinal and
choroidal vasculature, tapetal and non-tapetal fundus.
Gonioscopy in dog for examination of the drainage angle width and pectinate ligament
appearance where required.
Ancillary ophthalmic tests
Schirmer tear test assessing tear production, especially important in cases of recurrent
corneal/conjunctival inflammation and/or mucoid/muco-purulent discharge.
Fluorescein stain- where ocular surface disease was suspected. Excess dye flush away with
sterile saline. Rose Bengal stain only used with suspect herpetic keratitis
Topical anaesthesia assessing painful eyes, allowing swabbing for cytology and other
superficial corneal/conjunctival procedures.
Tonometry - assessing intra-ocular pressure.
Mydriasis pupil dilation for visualisation of peripheral fundus/retina.
Microbiology corneoconjunctival, culture and sensitivity where infection is suspected,

specific media for certain bacterial or viral infections as indicated in case-reports.
Cytology corneoconjunctival, for in-house or laboratory evaluation for bacteria,

inflammatory cells, neoplastic cells, viral/mycoplasmal/chlamydial inclusion bodies, fungal
hyphae, yeast bodies.
Phenylephrine 10% - only used to assess Horners syndrome. May also be used to blanch
conjunctival vessels to differentiate between conjunctival and scleral/episcleral congestion
and to reduce haemorrhage after surgical procedure e.g. sectioning pedicle grafts.
Nasolacrimal flush examination of patency and treatments e.g. dacryocystitis in rabbits.
Radiography for investigation including primary disease and for metastatic spread in
neoplastic conditions.
Page 102
Ultrasonography ocular, cardiac and abdominal. Referral specialist service available inhouse or use of practice ultrasound machine.
Blood analysis in-house laboratory:

-
Routine pre-operative biochemical screen includes: Total protein, Albumin, Alkaline

phosphatase, Alanine aminotransferase, Urea, Creatinine, Glucose, Haematocrit.
Standard comprehensive biochemistry profiles includes: Total Protein, Albumin, Alanine

aminotransferase, Alkaline Phosphatase, Gamma GT, Total Bilirubin, Urea, Creatinine,
Glucose, Calcium, Amylase, Lipase, Cholesterole, Phosphate, Sodium, Potassium,
Chloride.
Standard comprehensive haematology profile includes: RBC, HCT, MPV, HGB, MCHC,
MCV, MCH, PLT, WBC, LYMPH, LYMPH %, GRAN, GRAN %
Further bloods to outside laboratory as specified in each case-report
Urine analysis specific gravity by refractometry, semi quantitative biochemical analysis

with chemical reagent strips (Multistix and Keto-Diastix, Bayer)
Blood pressure Doppler Flow
Sedation procedures
No sedation used in any cases discussed
General anaesthetic procedures

Standard protocol for cats and dogs followed unless otherwise stated:
Premedication, subcutaneous injection acepromazine (ACP, Novartis Animal Health UK)

0.03ml/kg-0.06mg/kg and buprenorphine (Vetergesic, Alstoe Animal Healh) 0.009 mg/kg.
Meloxicam (Metacam, Boehringer Ingelheim) were given unless contraindicated. Antibiotics
were administered pre-operatively when indicated.
Induction, intravenous injection - Propofol (Rapinovet, Schering-plough Animal Health), cat

6mg/kg, dog 4mg/kg
Maintenance Isoflurane (Isoflo, Abbot Laboratories) and oxygen.
Page 103
Surgical preparation
Minimal clipping was used to avoid clipper-induced rashes. Carbomer 980, polyacrylic acid,
(Viscotears, Novartis Ophthalmics) was applied to ocular surfaces prior to clipping to minimise hairfragments in the ocular area. The surgical area was cleaned with Povidone-iodine 7.5% surgical
scrub, in a non-ionic surfactant basis (Betadine, Seton Healthcare) 0.2-0.5% solution, followed by
flushing of ocular surfaces with 0.9% sterile saline (Aquapharm, Animal Care).
Sterile surgical drapes used on op-site. Routine surgical scrubbing and sterile gown, gloves, hat and
mask used by the surgeon.
Postoperative care
A buster collar was fitted where interference of the wound could be a problem. Meloxicam
(Metacam, Boehringer Ingelheim) were given, at reccomended doses, unless contraindicated.
Antibiotics were continued systemically or as a topical preparation when indicated. Routine postoperative examinations were carried out at 3 and 10 days, or as required in each specific case.
Page 104
Appendix 2
Modified Hotz-Celsus technique for the correction of medial lower
eyelid entropion.
Routine general anaesthetic procedure and surgical preparation was carried out. A skin-muscle
resection, large enough to correct the entropion, was carried out after pre-sedative assessment of
the entropion.
A finger was placed within the conjunctival sac to tense the eyelid. An incision was made, using a 15gauge Bard-Parker blade, approximately 2mm from the lower eyelid, parallel to the affected part of
the lid. Two further incisions were made away from the eye to meet to form of a triangle. The
triangular piece of tissue was excised with Stevens tenotomy scissors. The defect was closed with
simple interrupted sutures using 6/0 Polyglactin 910 (Coated Vicryl, Ethicon), with the suture knots
placed away from the eye. The sutures were left to dissolve.
Figure-1. Incisions at the lower medial canthus (dotted lines) formed a triangle which
was excised. Wound closure with single layer simple interrupted sutures
Page 105

Sistema Circulatório

Enviado por

Dados do documento

Título original

Direitos autorais

Formatos disponíveis

Compartilhar este documento

Compartilhar ou incorporar documento

Opções de compartilhamento

Você considera este documento útil?

Este conteúdo é inapropriado?

Direitos autorais:

Formatos disponíveis

Sistema Circulatório

Enviado por

Direitos autorais:

Formatos disponíveis

CASEBOOK

FOR THE CERTIFICATE IN

Meibomian Adenoma In A Dog

Conjunctival hyperaemia associated with the lesion (Figure-3).

Figure 1. Swelling of the upper right eyelid.

Figure 2. Small pigmented mass at the lid margin.

Figure 3. Palpebral extension of mass. Conjunctival hyperaemia.

Papilloma (squamous/fibro benign epithelial neoplasm)

Less common eyelid neoplasms include histiocytoma, keratocanthoma, mastocytoma/mast cell

Treatment and outcome

Figure 5. Sliding lateral canthoplasty.

Meloxicam(Metacam, Boehringer Ingelheim) 0.1mg/kg once daily for 7 days

Figure 6, 3 days post-operatively

Figure 7, 3 days post-operatively.

Figure 8. A comfortable eye 21 months after initial surgery

Lipogranulomatous Conjunctivitis In A Cat

Mucoid discharge at medial canthus (Figure-2)

Hyperaemic lid margins (Figure-2)

Hyperaemia and mild chemosis of the palpebral conjunctiva (Figure-3)

Multiple smooth, non-ulcerated, nodular, white-pink lesions, 0.5-1mm in diameter,

Figure-1. Dermatitis of bilateral pinnae and ocular blepharospasm.

Figure-2. Hyperaemic non-pigmented lids and mucoid ocular discharge.

Figure-3. Nodular lesions of the upper lower palpebral conjunctiva.

Conjunctival biopsy for histopathology a small sample including nodular lesions

Neoplasia e.g. Squamous cell carcinoma, Lymphosarcoma

Infectious conjunctivitis e.g. Chlamydiophilia felis, Feline herpes virus-1, Feline,

Foreign body/dust reaction

Treatment and outcome

Amoxicillin trihydrate/clavulanic acid (Synulox Palatable Tablets, Pfizer) 50mg twice

Surgical procedure for conjunctival excision

Figure-4. Conjunctival excision.

Amoxicillin trihydrate/clavulanic acid (Synulox Palatable Tablets, Pfizer) 50mg twice

Buster collar fitted

Figure-5. Comfortable eye 4 weeks post-surgery.

Figure-6. Histopathology - A focally extensive area of the conjunctival

Table-1. Histopathology - Conjunctival biopsy.

Table-2. Histopathology conjunctival excision.

Cherry Eye in a Bulldog

Figure-2a. Fleshy mass and thick mucoid ocular discharge.

Differential diagnosis of third eylid prominence also include:

Bent, everted, third eyelid cartilage

Hyperplasia/hypertrophy of glandular tissue

Anatomical protrusion of the third eyelid

Enophthalmos e.g. ocular pain/debilitating disease/horners syndrome

Exophthalmos, retrobulbar space occupying lesion e.g. neoplasia, inflammation,

Foreign body reaction

Orbital fat prolapse

Morgan mucosal pocket technique

Figure-3. Morgan mucosal pocket technique.

Figure-4. Gland sutured in place.

Figure-5. Third eyelid gland prolapse corrected. Immediate post-operative

Meloxicam (Metacam, Boehringer Ingelheim) 0.1 mg/kg daily by mouth, 5 days

Fucidic acid 1% (Fucithalmic Vet) topically twice daily, 7 days

Corneal Ulceration In An Alpaca

Increased blink rate

Mild conjunctival hyperaemia

Linear corneal opacity associated with corneal oedema, neovascularisation,

The following normal, bilateral, ophthalmic findings were noted:

Slow direct and indirect pupillary light reflexes (1)

Intraocular pressure 12 bilaterally mean IOP in alpacas is 16 +/- 4 (2)

Concentric cortical lamination, has been described as cataract in Alpaca, but is a

Figure-1. Blepharospasm and ocular discharge

Figure-2. Sero-mucoid discharge (fluorescein stain applied to eye ca 1 hour prior