Orbital Disease

Chapter 256


Orbital Disease



Orbital disease in dogs and cats can be caused by a variety of pathologic processes. Accurate assessment of the patient is essential for the selection of appropriate diagnostic studies and therapy. Orbital disease generally can be divided into those processes that lead to exophthalmos (protrusion of a normal-sized globe from the orbit) due to space-occupying disease, enophthalmos (recession of the globe within the orbit) due to decreased orbital contents, or strabismus (deviation of the globe within the orbit) (Box 256-1). The diagnostic challenge lies in the fact that clinical signs of orbital disease are evident only indirectly and involve changes in a wide variety of orbital tissues and surrounding structures.



Box 256-1   Orbital Diseases Causing Exophthalmos, Enophthalmos, and Strabismus
























































Exophthalmos Enophthalmos Strabismus
Abscess (bacterial, fungal) Relative enophthalmos (dolichocephalic breeds) Neoplasia
Cellulitis Phthisis bulbi Proptosis
Neoplasia Microphthalmia Relative strabismus (brachycephalic breeds)
Zygomatic mucocele Pain Masticatory myositis
Varix or vascular anomaly Horner’s syndrome Zygomatic mucocele
Hemorrhage secondary to trauma Chronic inflammation Lacrimal cyst
Coagulopathy Atrophy of orbital tissues Hydrocephalus
Masticatory myositis Starvation or dehydration Orbital fracture
Extraocular polymyositis Orbital fracture  
Relative exophthalmos (brachycephalic breeds)    
Proptosis    
Craniomandibular osteopathy    



Orbital Anatomy


Dogs and cats have an incomplete bony orbit. The orbit consists of the frontal, lacrimal, zygomatic, sphenoid, maxillary, and palatine bones. The lateral orbital wall is completed by a collagenous orbital ligament that attaches the frontal process of the zygomatic bone to the zygomatic process of the frontal bone. The masseter muscle completes the orbit posterolaterally, whereas the zygomatic salivary gland and medial pterygoid muscle fill the floor of the orbit. Most of the extraocular muscles arise from the posterior and medial aspect of the orbit to form a cone as they attach to the anterior aspect of the globe. The lacrimal gland is located dorsolaterally beneath the frontal bone in the lacrimal fossa. The frontal sinus is located dorsal to the orbit, and the maxillary sinus is rostral and ventral to the orbit. The ventral floor of the orbit is directly adjacent to the oral cavity as well as the roots of the upper premolar and molar teeth. The orbital cavity also contains the second, third, and fourth cranial nerves; the ophthalmic branch of the fifth cranial nerve; the sixth cranial nerve; numerous arteries and veins; and smooth muscle, and is surrounded by periorbital tissue. The orbit is most shallow and directed more laterally in brachycephalic breeds and is most deep and directed more medially in dolichocephalic breeds, with the orbit in mesaticephalic breeds lying somewhere in between.



Clinical Signs of Orbital Disease


Pathologic processes affecting the orbit involve one or more of three anatomic compartments: (1) within the extraocular muscle cone, (2) outside the cone but inside the periorbital tissue, and (3) inside the orbit but outside the periorbital tissue. Orbital disorders are characterized by clinical signs that alter the function, appearance, or position of the globe, eyelids, or ocular adnexal structures.


The orbit is a confined space with little capacity for its contents to expand. Primary and secondary clinical signs of orbital disease are the hallmark of orbital disorders. Primary clinical signs include exophthalmos, enophthalmos, and strabismus. Secondary clinical signs include chemosis, swelling of the eyelids and periorbital tissue, elevation of the third eyelid, pain upon opening the mouth, lagophthalmos (incomplete eyelid closure), exposure keratitis, visual impairment, abnormal pupillary light reflexes, scleral indentation, mild to moderate increase in intraocular pressure (only with extreme exophthalmos), and facial asymmetry.


One of the challenges in the diagnosis of orbital disease is the accurate interpretation of clinical signs. It is crucial for the clinician to differentiate buphthalmos (enlargement of the globe) from exophthalmos. Exophthalmos is a clinical sign of orbital disease, whereas buphthalmos is secondary to chronic glaucoma. Measuring the horizontal corneal diameter (from limbus to limbus) may be useful in differentiating buphthalmos from exophthalmos. The horizontal corneal diameters of the two globes should differ by 1 mm or less. Ultrasonography also can be used to measure the axial globe length. When assessing axial globe length, the operator should ensure that the ultrasound probe is positioned in the center of the globe so that the image is captured through the thickest section of the lens.



Diagnostic Approach


A thorough history taking and physical examination are prerequisites for the diagnostic workup of orbital disease. When orbital disease is suspected, initial examination should include palpation of the eye and periocular structures, retropulsion of the globe, and careful examination of the oral cavity. The sizes of the palpebral fissures should be compared, the orbit should be palpated, the position of the eyelids and third eyelid should be observed, the location and mobility of the globe within the orbit should be assessed, and the presence of any ocular discharge should be noted. The globe generally can be retropulsed if there are no space-occupying lesions in the orbit. Retropulsion of the globe is performed through closed eyelids by placing an index finger on the upper eyelid of each eye and gently pressing or pushing the globe caudally within the orbit. Brachycephalic breeds may have quite shallow orbits, and the amplitude of retropulsion may be decreased even in normal orbits.


Digital pressure should never be used to assess intraocular pressure. Exophthalmic globes feel “hard” because of the resistance to retropulsion secondary to a space-occupying lesion within the orbit. When an exophthalmic globe is diagnosed incorrectly as glaucomatous because the globe feels hard, an incorrect differential diagnostic list and therapeutic plan will be formulated. In general, exophthalmic globes have normal intraocular pressure until the globe is quite exophthalmic, which causes the globe to be pressed against the eyelid margin. In these cases, the globe generally is not buphthalmic and does not have other clinical signs consistent with chronic glaucoma, including diffuse corneal edema, a dilated and unresponsive pupil, lens subluxation, retinal atrophy, and optic nerve cupping.


Once orbital disease is suspected, the most important clinical diagnostic test is to check for the presence or absence of resistance to opening the mouth. Pain upon opening or attempting to open the mouth as the coronoid process of the mandible impinges on the orbital tissues is indicative of retrobulbar inflammation. This test should be executed slowly, carefully, and gently because patients with orbital inflammation can have significant pain. A thorough oral examination should be performed. Sedation or general anesthesia may be necessary. Lack of pain upon opening the mouth more often is consistent with orbital neoplasia. Orbital neoplasia generally causes less orbital inflammation for a similar degree of exophthalmos. Some orbital neoplastic diseases may produce significant orbital inflammation, and some cases of orbital inflammation may not cause pain when the mouth is opened; however, evidence of pain on opening the mouth is more common in orbital inflammatory disease. Inappetence may be reported by the owner in association with oral pain.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Orbital Disease

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