Ординатура / Офтальмология / Английские материалы / Small Animal Ophthalmology Secrets_Riis_2002
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Iris and Ciliary Cysts |
Figure 6. Multiple cysts deflated by Nd:YAG laser in a dog. Note the holes made by the laser as well as the deflated position. The remnants of the cyst will remain in this undesirable site permanently.
12.Are uveal cysts associated with any other ocular abnormality?
Uveal cysts often have been diagnosed in conjunction with pigmentary uveitis in golden re-
trievers. A pathologic study of 18 glaucomatous eyes from golden retrievers revealed iridociliary cysts in 13.
BIBLIOGRAPHY
I. Deehr AJ, Dubielzig RR: Glaucoma in golden retrievers. Trans Am Coli Vet OphthalmoI28:105, 1997.
2.Genetics Committee of the American College of Veterinary Ophthalmologists: Ocular Disorders Presumed to be Inherited in Purebred Dogs, 2nd ed. Little Falls, NJ, ACVO, 1996.
3.Sapienza JS, Simo-Dornenech FJ, Prades-Sapienza A: Golden retriever uveitis: 75 cases (1994-1999). Vet OphthalmoI3:24l-246,2000.
48. ORBITAL INFLAMMATIONS
AND NEOPLASMS
David T. Ramsey, DVM.
1.What are the primary clinical signs of orbital disease?
Clinical signs of orbital disease are divided arbitrarily into primary and secondary categories.
Primary signs are referable only to the globe-orbit relationship and denote three-dimensional changes in position, placement, or alignment of the globe within the orbit. There are four primary signs of orbital disease. Exophthalmos and enophthalmos are terms applied to anterior and posterior displacement of the globe along the orbital axis. Strabismus is the term applied to involuntary deviation of the globe from the normal optical axis. Shift is the term used to describe displacement of globe position in the horizontal (lateral, medial) or vertical (dorsal, ventral) meridian or a combination thereof (oblique). Oblique shifts in position are designated as a combination of the two directions in which the globe is displaced (e.g., dorsolateral oblique displacement).
2.What are the secondary clinical signs of orbital disease?
Secondary signs of orbital disease occur as a result of exophthalmos, enophthalmos, strabis-
mus, or shift. Secondary signs include changes in anatomy or function of the globe, eyelids, orbital structures, or surrounding tissues. These include alterations in vision, globe, ocular movements, eyelid and nictitating membrane position, pupillomotor function, sensation (pain or numbness), globe indentation, vascular engorgement (conjunctiva, episclera, fundus), corneal or conjunctival exposure, and pain during (or limitation of) mandibular excursion.
3.How do you localize the mass effect within the orbit to a specific location?
Lesion localization within the orbit may be broadly divided into three orbital compartments:
intraconal (within the endorbital muscle cone), extraconal (outside the endorbital muscle cone but within the soft tissue confines of the orbit) and extraendorbital (beneath the periosteum). When an orbital mass effect is present, the direction of globe displacement is generally opposite the location of the mass or directly away from the mass lesion and along the path of least tissue resistance. The table below summarizes the direction of globe displacement and localization of the mass.
DIRECTION OF GLOBE DISPLACEMENT |
LOCAnON OF ORBITAL MASS |
|
|
Lateral displacement |
Medial mass effect |
Medial displacement |
Lateral mass effect |
Dorsal displacement |
Ventral mass effect |
Ventral displacement |
Dorsal mass effect |
Dorsolateral displacement |
Ventromedial mass effect |
Dorsomedial displacement |
Ventrolateral mass effect |
Ventrolateral displacement |
Dorsomedial mass effect |
Ventromedial displacement |
Dorsolateral mass effect |
Axial anterior displacement |
Posterior mass effect |
|
|
Intraconal mass lesions cause axial exophthalmos, minimal or absence of protrusion of the nictitating membrane, and minimal strabismus (unless extensive in volume). Extraconal and extraendorbital mass lesions are characterized by exophthalmos, protrusion of the nictitating membrane, shift in globe position, and strabismus.
4.How are exophthalmos and buphthalmos differentiated?
Buphthalmos is absolute enlargement of the globe secondary to glaucoma. Both buphthal-
mos and exophthalmos result in a widened palpebral fissure. In most instances, buphthalmos will
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not occur as the only clinical sign of glaucoma. When buphthalmos is evident, funduscopic examination may show cupping and atrophy of the optic papilla and peripapillary or diffuse retinal degeneration. Exophthalmos attributable to orbital mass effect may have moderately increased intraocular pressure, but exophthalmos does not occur in glaucoma. Horizontal corneal diameter may be measured and compared between eyes to differentiate buphthalmos from exophthalmos.
5.What are the major considerations when the eye recesses or ''sinks'' into the orbit?
Axial posterior displacement of the globe is termed enophthalmos. Enophthalmos does not
occur from a mass effect. Enophthalmos occurs most frequently as an active retraction response to ocular pain. It also may occur with sympathetic denervation to the eye (Horner's syndrome) or when there is loss of orbital mass (soft tissue, bone) in a disease process. Disease processes causing loss of orbital mass include severe dehydration, weight loss, cachexia, orbital neoplasia, severe chronic myopathy (masticatory myopathy), neuropathy (trigeminal), constrictive myopathy (tetanus), or restrictive myopathy (trauma, extraocular polymyositis) of the extraocular muscles (Fig. 1).
Figure 1. Enophthalmos of the right eye with prominent elevation of the nictitating membrane secondary to loss of orbital mass.
6.Does protrusion of the third eyelid signify an orbital mass effect?
The base of the nictitating membrane (third eyelid) lies within the orbit. It has passive move-
ment in the dog but can actively be protruded in the cat. Protrusion of the third eyelid may occur with exophthalmos (orbital mass effect displacing the base of third eyelid) or enophthalmos (globe volume and extraocular muscle contraction displacing the base of the third eyelid). Protrusion of the third eyelid does not invariably signify orbital mass effect as the cause. Sympathetic innervation to the third eyelid is primarily responsible for keeping the third eyelid retracted. Loss of sympathetic innervation to the eye (Homer's syndrome) results in protrusion of the third eyelid. Globe retraction also may occur in response to ocular pain (voluntary contraction of extraocular muscles) or tetanus (involuntary contraction of extraocular muscles).
7.Does the rate of onset of clinical signs correlate with the type of orbital disease?
As a general rule, a history of rapid onset of clinical signs is most likely attributable to an in-
flammatory orbital disease process. The opposite correlative is that slowly progressive signs of orbital disease are most consistent with orbital neoplasia or cystic orbital disease. However, some neoplastic orbital diseases (lymphoma, mast cell sarcoma) have an associated inflammatory component that can result in rapid onset of clinical signs and pain. Other neoplasms may have rapid periods of growth or volume expansion and enlarge in mass rapidly, thereby exceeding their blood supply and nutritional requirements, and result in necrosis of the neoplasm. When this occurs, an inflammatory component is also common and may result in a rapid progression of clinical signs, and pain may become more conspicuous suddenly.
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8. How do you differentiate neoplastic, inflammatory, and cystic classifications of orbital disease?
Orbital neoplasia generally affects older animals (mean age for dogs, 8 years; mean age for cats 8.9 years), resulting in slowly progressive clinical signs over a period of weeks to months, and usually does not cause pain until the neoplasm is of considerable size. Orbital inflammation can affect cats and dogs at any age but most often affects younger animals. Inflammatory orbital disease usually has a history of sudden onset of clinical signs, pain when opening the mouth, and chemosis, and the animal may be febrile. Cystic orbital disease may have a slow or rapid onset of clinical signs, and pain is usually absent or minimal. When history and clinical signs direct your index of suspicion toward a specific classification of orbital disease, diagnostic tests are indicated to confirm or deny your tentative diagnosis and to identify the specific type of inflammatory, neoplastic, or cystic orbital disease (see Chapters 3 and 4) (Figs. 2-5).
Figure 2. Exophthalmos with dorsolateral displacement indicative of a ventromedial mass that turned out to be an adenocarcinoma.
Figure 3. Exophthalmos with lateral displacement indicative of a medial mass that turned out to be a hemangiosarcoma.
9.What is an orbital abscess?
An orbital abscess is a localized septic or nonseptic inflammatory response composed of pu-
rulent exudate (primarily dead white blood cells and products of inflammation). Orbital abscess occurs most frequently secondary to periodontal or endodontic disease in the dog and cat. It may also occur from hematogenous, transscleral, or transmucosal (conjunctiva, nasal, oral, sinus) in-
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Orbital Inflammations and Neoplasms |
Figure 4. Exophthalmos with dorsolateral displacement secondary to orbital sarcoma.
Figure 5. Exophthalmos with axial anterior displacement secondary to a posterior orbital intraconal meningioma.
jury or disease resulting in inoculation of the orbital space with infectious organisms. When an orbital abscess is suspected, orbital ultrasound should be done. When an orbital ultrasound clearly shows an orbital abscess, surgery is indicated. However, the cause of orbital abscess should be pursued. The oral cavity should be examined under general anesthesia. The caudal maxillary teeth should be evaluated using a periodontal probe and dental explorer, and radiographs of the caudal maxillary teeth should be made. The conjunctival fornices and oral cavity should be examined closely for abnormalities (Figs. 6 and 7).
Figure 6. Orbital abscess causing significant swelling. Note the asymmetry.
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Figure 7. Orbital abscess (same case as Figure 6) shown from a lateral view. Fistulization of the abscess through the ventral conjunctival fornix is sometimes a natural route.
10.How do you treat an orbital abscess?
Surgical drainage must be established. When concurrent dental disease is evident by direct ex-
amination or radiographically with orbital abscess, transalveolar drainage of the abscess is indicated. Extraction of the offending tooth to establish transalveolar drainage and treatment with orally administered broad-spectrum antibiotics are indicated after extraction. When dental disease is not evident as the cause of the abscess, transmucosal surgical drainage may be done using ultrasound to select the most appropriate surgical approach. A small incision is made in the oral mucosa candomedial to the maxillary second molar tooth. A sterile blunt instrument is then introduced into the incision, forced gently through the medial pterygoid muscle using a short finger stop so that damage to the globe does not occur. Purulent exudate should be collected for cytology and culture. The surgical wound should be allowed to drain on its own or with a drain positioned into the orbital space.
11.How do you differentiate an orbital abscess from orbital cellulitis?
Making a distinction between orbital abscess and cellulitis based on clinical signs and phys-
ical examination is virtually impossible. Ultrasound of the orbit should be done to differentiate orbital cellulitis from abscess. Diffuse orbital cellulitis produces a generalized loss of definition of the orbital tissues, resulting in the optic nerve and extraocular muscles being difficult to visualize when compared with the opposite eye. Cellulitis also may produce focal mass lesions that may be mistaken for a neoplasm. Abscesses are variable in appearance, but most are recognized as a hypoechoic area within a well-defined hyperechoic wall. The abscess wall may not be seen with ultrasound in all cases. When an orbital abscess is not evident ultrasonographically, broadspectrum oral antibiotic and nonsteroidal anti-inflammatory drugs should be administered and the animal monitored closely for improvement of clinical signs. Frequent orbital ultrasound is recommended to determine if cellulitis is resolving, unchanged, or transformed into an abscess cavity. If unchanged or transformed to an abscess, or if clinical signs deteriorate, surgical intervention is indicated (see abscess) (Figs. 8 and 9).
12.What causes masticatory myositis?
Masticatory myositis is immune-mediated inflammation and swelling of the muscles of mas-
tication (temporalis, medial pterygoid, and masseter) that has been reported in dogs. Cellular and humoral mediated destruction of type 11M myofibers (common to masticatory muscles) is thought to cause masticatory myositis. Because these muscles define the medial, ventral, and lateral borders of the orbit, inflammation imposes upon and compresses orbital structures, resulting in anterior displacement of orbital contents (exophthalmos and/or protrusion of the third eyelid) (Fig. 10).
13. How is masticatory myositis diagnosed?
Dogs with masticatory myositis may have either the acute or chronic form of the disease. Acute myositis is typified clinically by pain on opening the mouth, difficulty eating, swelling of the mas-
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Figure 8. Orbital cellulitis from a dorsal view. Much pain is elicited upon opening the mouth, which stems from impingement of the coronoid process of the mandible on inflamed orbital soft tissue.
Figure 9. Orbital cellulitis (same case as Figure 8) from a frontal view. Retropulsion of the globe is usually restrictive.
Figure 10. Myositis causing exophthalmos and strabismus with lateral shift.
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ticatory muscles, unilateral or bilateral exophthalmos, protrusion of the third eyelids, and conjunctival hyperemia and chemosis. Infrequently, vision may be compromised. Atrophy and loss of masticatory muscle mass, enophthalmos, protrusion of the third eyelid, pain or reluctance to open the jaw, and trismus typify the chronic form, Mean age of affected dog is 3 years; male and female dogs are affected equally. Definitive diagnosis is based on histologic evaluation of frozen muscle biopsies sent to specialized neuromuscular laboratories. Serum from affected dogs may also be submitted to these laboratories to determine if circulating antitype lIM antibodies are present.
14.What is extraocular polymyositis?
Extraocular polymyositis is a rare, immune-mediated inflammatory myopathy that is limited
to the extraocular muscles in dogs. Young, female golden retrievers are affected most frequently (median age of 8 months). An antecedent "stressor" (ovariohysterectomy, estrus, castration, boarding at a kennel) occurred within 14 days of the onset of clinical signs in 43% of affected dogs. The mononuclear cell infiltrate of extraocular muscles is composed primarily of CD3+ T lymphocytes and macrophages directed against fine extraocular myofibers. Affected dogs have axial exophthalmos, retraction of the upper eyelid, and absence of third eyelid protrusion, and dogs are not in pain. This disease responds to a prolonged course of topical and oral corticosteroids (Fig. 11).
Figure II. Extraocular polymyositis with the classic "bug eyes." Although this condition is usually seen in golden retrievers, it is also seen in other breeds such as this young rottweiler.
15.Are masticatory myositis and extraocular polymyositis the same disease?
Extraocular muscles do not contain type IIM myofibers. Type lIM myofibers are found only
in specific muscles innervated by the mandibular branch of the trigeminal nerve. Although both diseases have similar inflammatory cell infiltrate within affected muscles, cellular and humoral immunity is directed at distinctly different muscle antigens. Age, breed, and gender predilections also exist and are different for both diseases. Therefore, these two diseases are distinctly different immunologically and clinically.
16.How is zygomatic mucocele differentiated from zygomatic sialoadenitis?
The floor of the orbit, in most animals, is formed by the zygomatic salivary gland. A zygo-
matic mucocele is a collection of saliva outside the salivary ductal system. Zygomatic sialoadenitis is inflammation of the zygomatic salivary gland. Zygomatic mucocele and zygomatic sialoadenitis mayor may not have signs of ocular involvement, depending on severity of disease. Mucocele may protrude beneath the lower conjunctival fornix and appear as pale blue-gray when transilluminated. It also may appear as a fluctuant swelling beneath the lower eyelid or as a protrusion beneath the oral mucosa caudal to the maxillary molar teeth. Mucocele is usually nonpainful or minimally painful; however, clinical signs of pain similar to sialoadenitis may be pre-
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sent if mucocele has associated inflammation. Fine-needle aspiration of a mucocele will produce a thick, tenacious, clear or rust-colored mucoid substance. Animals with zygomatic sialoadenitis exhibit signs of pain when the mouth is opened and mayor may not have swelling along the side of the face ventral to the palpebral fissure. Affected animals frequently have thick, tenacious, mucoid saliva emanating from the zygomatic salivary papillae. Orbital ultrasound is useful to differentiate mucocele (hypoechoic or anechoic cavity) from sialoadenitis (diffuse hyperechogenecity) (Fig. 12).
Figure 12. Zygomatic mucocele that was stubbornly recurrent after repeated surgeries.
17. How should zygomatic mucocele and sialoadenitis be treated?
Although surgical removal of zygomatic mucocele by orbitotomy is recommended in standard surgical textbooks, treatment with a broad-spectrum antibiotic resolves zygomatic mucocele in many instances. Culture and susceptibility testing of material collected from mucocele (aspirate) and sialoadenitis (collected from zygomatic papillae) should be done. When clinical signs do not improve within several days of medical treatment, surgical intervention may be necessary for the resolution of mucocele. Zygomatic sialoadenitis also should be treated with a broadspectrum antibiotic or the antibiotics specified by culture and sensitivity. When exophthalmos is present, the cornea and conjunctiva should be treated topically with an ophthalmic ointment to prevent exposure and desiccation.
BIBLIOGRAPHY
1.Gilmour MA, Morgan RV, Moore FM: Masticatory myopathy in the dog: A retrospective study of 18 cases. J Am Anim Hosp Assoc 28:300-306, 1992.
2.Hendrix DVH, Gelatt KN: Diagnosis, treatment, and outcome of orbital neoplasia in dogs: A retrospective study of 44 cases. J Small Anim Pract 41:105-108,2000.
3.Ramsey DT: Exophthalmos. In Bonagura JD (ed): Kirk's Current Veterinary Therapy, 13th ed. Small Animal Practice. Philadelphia, W.B. Saunders, 2000, pp 1086-1089.
4.Ramsey DT, Manfra Marretta S, Hamor RE, et al: Ophthalmic manifestations and complications of dental disease in dogs and cats. J Am Anim Hosp Assoc 32:215-224,1996.
5.Ramsey DT, Fox DB: Surgery of the orbit. Vet Clin North Am Small Anim Pract 27:1215-1264,1997.
49. THE ULTIMATE OCULAR HISTOPATHOLOGY
Ronald C. Riis, D.V.M., M.S., and Mary Lou Norman, B.S., H.T. (ASCP)
1. From a pathologist's standpoint, is an eye an unfortunate mixture of tissue?
Yes, because the sclera is a dense fibrous tissue through which fixatives permeate slowly. Uveal retinal tissues have high metabolic characteristics which deteriorate rapidly and must be fixed quickly. If these important factors are not addressed, then histopathology of the eye is a study of postmortem artifacts.
2. What is the first secret of meaningful results?
First and foremost, the eye must be removed rapidly after death, at necropsy, or rapidly at surgery. Trim off extraocular adnexa, fat, muscle, and promptly immerse in a fixative.
3.Is there anything special about enucleation techniques?
Although the enucleation must be done quickly, it must be done carefully to minimize the
production of artefacts. It is particularly easy to produce an artifactual retinal detachment. Although this can be determined histologically from an antemortem lesion, it is better to view and analyze the photoreceptors intact and not around artifacts.
4.What is the best fixative for a globe?
Zenker's fixative (containing mercury) is the best considering the tissues being evaluated.
The fixative requires adding glacial acetic acid just before use, and this can be seen as inconvenient. Bouin's fixative has been used with good results and compliance from necropsy. Davidson's fixative is also among those that penetrate rapidly into the eye for excellent results.
5.What should be the fixative to globe ratio?
This is a very important point. The volume of fixative should be 20 times the volume of the
tissue being fixed.
6.Once the globe is rapidly removed, trimmed, and immersed in fixative, what is required next?
The globe will float in Zenker's glacial acetic acid and Bouin's fixatives only until the fixative penetrates equally into the globe chambers. Once the globe sinks to the bottom, it is fixed. However, it is not recommended to leave it in the fixative for more than 24 hours. The globe should be washed in running tap water and stored in 70% alcohol. If Bouin' s is used, the picric acid will color the alcohol yellow. Changes of alcohol are recommended until the alcohol remains clear.
7.Can the globe be kept in fixative until processed?
This is not ideal because prolonged exposure to Zenker's or Bouin's fixatives causes the lens
to become rock hard, adding another artifactual challenge to the sections. The exception to this is 10% neutral buffered formalin.
8.What about cutting a bole in the globe to allow fixatives to enter or injecting fixative into the globe?
Both the procedures are unnecessary if Bouin' s or Zenker's fixatives are used. It is actually harmful to do either one of these because it adds an iatrogenic lesion that may be noted.
9.What fixative can be used if Zenker's or Bonin's are not available?
Ten percent neutral buffered formalin is better than no fixative. Formalin is good for the cornea and lens, but terrible for the retina. If formalin is all that is available, it can be injected into
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