Ординатура / Офтальмология / Английские материалы / Small Animal Ophthalmology Secrets_Riis_2002
.pdf
230 |
Acquired Diseases of the Fundus |
Figure 6. Multifocal intraretinal hemorrhage in a dog with thrombocytopenia.
14. What if, instead of a hyporeflective lesion, a darker lesion that looks like melanin or some other pigment is seen? What can cause this?
Hyporeflective lesions, which generally have a grayish appearance, are distinguished from pigmented lesions, which have a dark brown to black color. There are several mechanisms by which melanin or other types of pigment may become deposited in the tissues of the fundus. Most commonly, this is seen with focal or multifocal retinal and choroidal degeneration or atrophy. This results from damage to the tapetum or proliferation of pigment by the retinal pigment epithelium (RPE) following inflammation or vascular insult. Typically, these lesions would be chronic and "inactive," with no current inflammation. For example, a pigmented center is often seen in hyperreflective lesions from these mechanisms. Also, pigment clumps are often seen in depigmented, inactive lesions in the nontapetal fundus.
Although very rare, melanomas arising from the choroid can cause pigmented, raised lesions in the fundus. These would progress slowly over time and are generally considered benign in dogs.
Remember that patchy clumps of pigment in the tapetal fundus can be a normal finding, caused by focal areas where the tapetum did not develop. Therefore, look for other lesions such as the appearance of hyperreflectivity or depigmentation before considering the pigment abnormal.
Rarely, other types of pigment besides melanin may be deposited in the retina. For example, systemic vitamin E deficiency in dogs may cause an accumulation of lipofuscin, a golden-brown pigment, in the RPE.
15.What is a retinal detachment?
Retinal detachment is actually a separation of two layers of the retina: the sensory retina and
the RPE, rather than a separation of the retina from the underlying choroid. Fluid accumulates in the potential space between these two layers of the retina, referred to as the subretinal space.
16.What causes a retina to detach?
1.Exudative detachment is caused by edema or cells effusing into the subretinal space. This is generally caused by inflammation in the choroid (or a chorioretinitis) or a profound vascular insult to the retinal or choroidal vessels (e.g., severe systemic hypertension).
Acquired Diseases of the Fundus |
231 |
2.Rhegmatogenoos detachment results from a tear in the retina, usually peripherally, that allows liquefied vitreous to leak through the tear and into the subretinal space. This tear often is created by pathologic changes in the vitreous. Vitreal changes can occur with aging, from cataracts and other lens diseases, and following intraocular surgery.
3.Tractional retinal detachment results from blood or fibrin clots (or rarely from anomalous vessels) in the vitreous that are attached to the retinal surface. As the clot retracts, it pulls the retina, creating a detachment. Often, the traction also creates a tear that causes a rhegmatogenous detachment. Tractional detachments are uncommon in veterinary patients.
17.How does retinal detachment appear on ophthalmoscopic exam?
Because fluid collects in the subretinal space and in front of the tapetum (or the pigmented
RPE for the nontapetum), retinal detachments often appear as large areas of hyporeflectivity in the tapetal fundus or as whitish, indistinct areas in the nontapetal fundus (Fig. 7). Hemorrhage in the retina or even in the vitreous also can be seen, and occasionally this hemorrhage will migrate anteriorly into the anterior chamber, producing hyphema. Because the retina is displaced forward into the vitreous, the surface is out of focus to the ophthalmoscopic lens and observer and appears fuzzy and indistinct. If the retina if detached forward to a great extent, the retinal blood vessels may be seen clearly and in focus without the use of an ophthalmoscope, simply by looking through the pupil with a focal light source.
Figure 7. Total, bullous retinal detachment in a cat with systemic hypertension.
18.Is there any treatment for a retinal detachment? Can the eye regain vision?
The specific treatment and prognosis for retinal detachment depend largely on the mecha-
nism (exudative versus rhegmatogenous) and duration of the detachment. Exudative detachments are managed by treating the specific disease process (i.e., antimicrobial agents if infectious inflammation; anti-inflammatory agents if traumatic or immune-mediated inflammation; antihypertensive agents if systemic hypertension is the cause). Rhegmatogenous detachments must be treated surgically by sealing the tear, generally with laser or cryoprobe and various other adjuvant surgical techniques. The eye has an effective mechanism to pump the subretinal fluid out, so if the underlying problem is corrected, retinal reattachment and recovery of some vision are possible. However, because the retina becomes ischemic, retinal detachment of > I week duration is unlikely to become functional again. Unfortunately, most retinal detachments in animals are not recognized in a timely fashion, and the visual prognosis is relatively poor (see Chapter 42).
BIBLIOGRAPHY
I. Barnett KC: A Colour Atlas of Veterinary Ophthalmology. London, Wolfe Publishing, 1990.
2.Barnett KC, Crispin SM: Feline Ophthalmology: An Atlas and Text. Philadelphia, W.B. Saunders, 1998.
3.Ketrlng K, Glaze MB: Atlas of Breed-Related Canine Ocular Disorders. Trenton, NJ, Veterinary Learning Systems, 1998.
4.Rubin LF: Atlas of Veterinary Ophthalmoscopy. Philadelphia, Lea & Febiger, 1974.
38. INHERITED EYE ANOMALIES OF AUSTRALIAN SHEPHERDS, COLLIES, AND SHETLAND SHEEPDOGS
Ronald C. Riis, D.V.M., M.S.
1. At what age should collies, Shetland sheepdogs, and Australian shepherds be examined for eye anomalies?
The eye size and cooperation of the puppy have a lot to do with a successful evaluation of the fundus, regardless of the expertise of the examiner. Ideally, puppies that are 7-8 weeks old should be examined, but 6-9 weeks of age should be a sufficient window of time to accommodate the variables.
2.Are the anomalies progressive?
No, generally, not, but there are exceptions.
3.Which are not progressive?
•Colobomas of the iris, ciliary body, and retina (Australian shepherd)
•Colobomas of the optic disc (small to medium)
•Choroidal hypoplasia
•Scleral ectasia
4.Which anomalies are progressive?
Large colobomas may predispose to retinal detachment. Small or incomplete retinal detachment may enlarge to generalized or bullous detachments.
5.Which anomalies cause vision problems?
Large colobomas have related visual impairment, but complete retinal detachment causes
blindness.
6.What does the breeder term "go normal" mean?
When puppies are examined at the recommended age and a finding of small or trace choroidal
hypoplasia is found, those characteristics may change with maturity, especially in triand sablecolored dogs. The maturing migrating pigment of the retinal pigment epithelium disguises the underlying choroid, and the hypoplasia appears to resolve. Although the choroidal hypoplasia remains, breeders say the eyes "go normal."
7.What is the importance of a "go normal" evaluation?
Evaluations done in the 6-9-week window allow minimally affected animals to be classified
correctly as phenotypically affected.
8.What breeding recommendations produce the best eye evaluations?
Obviously, the mating between two genotypically normal-eyed dogs is ideal. However,
breed standards dictate other qualities that allow for minor anomalies in order to express other physical desirable traits.
9. What is allowable in eye anomalies for a breedable trait?
In order to breed away from undesirable traits, use a mate with extreme minimal traits (i.e., breeding a dog with minor choroidal hypoplasia with a normal-eyed dog).
232
Inherited Eye Anomalies |
233 |
10. Does this breeding guarantee good eye examinations?
That depends on the breeder's interpretation of "good." Usually, any eye found with a trace, small, or medium amount of choroidal hypoplasia is acceptable or "good." However, even dogs bred with this degree of choroidal hypoplasia may produce offspring with colobomas and retinal detachments if a dog considered "normal" is not genotypically normal.
11.When is breeding not recommended?
Dogs affected with colobomas and retinal detachments should not be bred. Poorly pigmented
dogs, such as whites and merles, that are bred together produce offspring with multiple sensory deficits and ocular anomalies.
12.What is a scleral crescent?
A white elliptical characteristic adjacent to the optic disc. This is a patch of sclera without
overlying choroid (i.e., a focal choroidal hypoplastic area).
13.What is a staphyloma?
In association with these breeds, it is a protrusion of sclera posteriorly, lined with uveal tis-
sue. It is also called scleral ectasia.
14.Is an eye with choroidal hypoplasia blind in the area affected?
No, the overlying retina is normal. Even though the vasculature of the choroid is deficient in
these areas, the retina has its own vascular sources.
15.Is retinal dysplasia (folds) a manifestation of choroidal hypoplasia, coloboma, and retinal detachment?
No, retinal dysplasia may be seen along with the other conditions or by itself. It is not thought to be inherited as a manifestation related to the others (see Chapter 40).
16.Is optic nerve hypoplasia a manifestation of choroidal hypoplasia, coloboma, and retinal detachment?
No, optic nerve hypoplasia is thought to be on a separate gene. It, too, can be seen with other anomalies, but rarely.
17.Is microphthalmos a manifestation of coloboma, choroidal hypoplasia, and retinal detachment?
No, microphthalmos is on a separate gene. Although the breed standard for collies and shelties states an almond eye is desirable, a globe that is asymmetrically smaller than the opposite eye
or bilaterally small globes with protruding nictitans are undesirable.
18. What other ocular abnormalities are seen in these breeds?
Corneal dystrophies, persistent pupillary membranes, retinal degenerations, lid deficits, granulomatous proliferations, and cataracts.
19. Is the incidence of coloboma, choroidal hypoplasia, and retinal detachment decreasing? Somewhat. Over the last 30 years, more animals have been examined and certified as free from anomalies, but the percentage of affected collies with choroidal hypoplasia remains high.
Other anomalies are relatively low, mainly through the efforts of conscientious breeding.
234 Inherited Eye Anomalies
Incidence of Optic Disc/Nerve Coloboma, Choroidal Hypoplasia,
and Retinal Detachment, 1991-1999
|
AUSTRALIAN SHEPHERD |
COLLIE |
SHETLAND SHEEPDOG |
|
|
|
|
Optic disc/nerve coloboma |
0.27% |
8.75% |
0.79% |
Choroidal hypoplasia |
0.22% |
66.7% |
0.39% |
Retinal detachment |
0.13% |
1.88% |
0.05% |
|
|
|
|
Data from Canine Eye Registration Foundation, West Indianapolis, IN.
20.If a retinal detachment is diagnosed, is there anything that can be done?
Possibly. A partial detachment in an eye with pigment can be treated with laser surgery. Some
success at arresting the detachment and even reattaching the flat detachments has been achieved. A subalbinotic or albinotic fundus absorbs the laser energy poorly, and success is less likely. Therefore, cryosurgery may be the treatment of choice.
21.If a nonvisual eye is diagnosed in a puppy, is it necessary to surgically enucleate or eviscerate the globe?
Surgical intervention is necessary only if the globe has other complications causing discomfort to the dog. Generally, an inherited blind eye is well-tolerated by the dog for the duration of its life. Visually, the dog compensates with one eye. Ironically, the expression of severe or extreme colobomas and retinal detachments are rarely bilaterally symmetrical.
22.What other breeds of dogs have excessively white hair coats and inherited ocular and otic defects?
By breeding two merle-coat color patterns together, litters of puppies have been produced with variable degrees of ocular anomalies, microphthalmia, and hearing deficits. These breeds include border collies, dachshunds, fox hounds, Great Danes, and Norwegian dunkerhounds.
23.Because breeding merle-coated animals results in undesired traits, can the fundic examination identify subtly merled dogs such as the sable merle?
Yes, the retinal characteristics can distinguish solid-coat dogs from merle-coat dogs. The solid-coat dogs will have a normal tapetum and fundic pigment, whereas merles will be subalbinotic or albinotic. In the fundus of a merle, there is partial or complete absence of pigment in the uveal tract, so that choroidal vessels can be seen as well as the retinal vasculature. Choroidal vessels are broader, paler red, and parallel, inspiring the name "tigroid fundus" to the describe the striped effect. Thinner retinal vessels run over or on top of the choroidal vessels. The tapetum is faint or absent. Grossly, there is a very red reflex from the merle fundus; this also occurs in other albinotic or subalbinotic animals such as the Siberian husky, Samoyed, white cat, Siamese cat, Appaloosa horse, and albino or partial albino cattle.
24.Should the merle eye anomaly be considered different from the collie eye anomaly?
Yes. The eye anomaly of the homozygous merle has been confused with the collie eye anomaly because the two conditions are similar in some respects. Both are inherited, have variable severity of fundic lesions, and may result in blindness. Both anomalies have been documented in the Australian shepherd, border collie, collie, and Shetland sheepdog. In these breeds, the differential diagnosis is based on a few dissimilarities.
25.What are these dissimilarities?
In nearly all cases, homozygous merles are products of merle-to-merle breeding, and the coat
colors are whiter than their littermates. Collie eye anomaly can be found in all coat colors.
The homozygous merle condition is inherited as an autosomal recessive trait linked to the incompletely dominant coat color-merle. The mechanism of linkage involves a transposable
Inherited Eye Anomalies |
235 |
genetic element. Collie eye anomaly has been reported to be inherited through several genes, one or more of which may be dominant. No linkage of collie eye anomaly to other traits has been identified.
Microphthalmia is not associated with collie eye anomaly, although collies frequently appear symmetrically and mildly microphthalmic. Microphthalmia in collies is inherited independently of collie eye anomaly. Severe or asymmetric microphthalmia is a prominent feature of the homozygous merle anomaly.
The lesions of collie eye anomaly involve the sclera, choroid, retina, retinal vessels, and optic disc only. No uveal or lens changes are associated with collie eye anomaly. In the homozygous merle, the lens and iris are frequently involved.
Funduscopically, focal choroid hypoplasia is common in collie eye anomaly. The hypoplastic area has a characteristic location temporal to the optic disc. Choroid hypoplasia in the homozygote merle is multifocal or diffuse.
Colobomas in collie eye anomaly occur most commonly in the optic disc and occasionally in the peripapillary area as scleral ectasia. Colobomas in the homozygous merle are most frequently equatorial (i.e., iris and ciliary body). Ocular examinations of merle puppies should always include a predilation as well as postdilation evaluation of the iris.
26.Has the incidence of merle eye anomaly decreased?
Yes, dramatically over the last 30 years. Occasional inadvertent breeding results in affected
puppies, but the word is being spread that merle eye anomaly can be eliminated only by not breeding merle to merle.
Figure I. Collie puppy fundus showing white sclera with anomalous choroidal vessels (i.e., choroidal hypoplasia).
Figure 2. A normal blue merle fundus. This eye was albinotic and displayed the choroidal vascular patterns.
236 |
Inherited Eye Anomalies |
Figure 3. An albinotic fundus with choroidal hypoplasia and slight optic disc depression.
Figure 4. Choroidal hypoplasia, small coloboma at 6 o'clock within the optic disc, and a scleral crescent around the disc from 3 o'clock to 9 o'clock.
Figure 5. An albinotic fundus with choroidal hypoplasia.
Inherited Eye Anomalies |
237 |
Figure 6. Varying degrees of choroidal hypoplasia and optic disc coloboma involving most of the disc area
Figure 7. Large choroidal hypoplasia and a small optic disc coloboma at 3 o'clock.
Figure 8. Very large optic disc coloboma
(*) and associated retinal elevation (X).
238 |
Inherited Eye Anomalies |
Figure 9. Optic disc coloboma, choroidal hypoplasia, and scleral ectasia in an Australian shepherd dog.
Figure 10. A collie with a focal retinal detachment adjacent to the optic disc at the 10 o'clock to 12 o'clock position (*).
Inherited Eye Anomalies |
239 |
Figure II. A Shetland sheepdog with unilateral scleral crescent and faint choroidal hypoplasia.
COLLIE EYE ANOMALY
Figure 12. Artist's interpretation of the collie eye anomaly showing anatomic abnormalities as they relate to the normal ocular layers.