4 The orbit consists of the bones that surround the globe, the orbital fat and fascial planes, the extraocular muscles, and the afferent and efferent nerves that supply the orbital contents or simply pass through the orbit to serve the nose or other fascial structures. The orbit of the dog is a not infrequent site for congenital, traumatic, inflammatory and neoplastic diseases. Variations in orbital conformation influence the types of disorders that affect dogs. Breeds with shallow orbits have very prominent globes that are subject to trauma and exposure (brachycephalic ocular syndrome, see Appendix B), while breeds with very deep orbits and enophthalmia have greater protection. Age is another consideration for etiology of disease. Young dogs tend to get into harm’s way and various forms of trauma; older dogs, in general, represent the majority of patients with orbital neoplasia. Orbital disease may affect the orbital tissues within the extraocular muscle cone, the orbital tissues surrounding the extraocular muscles, and the periorbita (periosteum) and bones that delineate the orbit. Microphthalmia is an eye that is abnormally small and may contain normal but reduced intraocular tissues (nanophthalmia), or more commonly true microphthalmia in which additional ocular abnormalities occur, especially cataracts and retinal dysplasia. The condition is the most common orbital anomaly in the dog and is observed most often in the Beagle, Akita, Chow Chow, Cavalier King Charles Spaniel, and Irish Wolfhound breeds. The condition can usually be detected after the eyelids open (10–14 days postnatal) and is unilateral or bilateral. The palpebral fissure is smaller than normal, and the nictitating membrane protrudes to a variable extent. The cornea is smaller than normal. The pupillary light reflexes can be present or absent. Cataracts may be present, as in the Miniature Schnauzer. Retinal detachments/dysplasia can be present in the Bedlington Terrier, Yorkshire Terrier, Labrador Retriever, and other breeds. In the merle‐colored breeds (merle ocular dysgenesis), such as the Australian Shepherd, Rough Collie, Shetland Sheepdog, and Dachshund, microphthalmia, iridal defects and heterochromia, equatorial staphylomas, cataracts, retinal dysplasia and retinal detachments frequently occur in the homozygous merle dogs with excessive white coats (Figure 4.1, see also Figure 10.2 and 18.1). Figure 4.1 (A) Bilateral but not symmetrical microphthalmia in a homozygous blue merle Australian Shepherd puppy. (B) Close up of microphthalmia with multiple ocular defects including heterochromia, corectopia (off center pupil), and basal iridal coloboma (atypical equatorial coloboma). (C) Australian Shepherd litter of puppies with 3 normal eyed blue merles and 3 excessively white blue merles with colobomatous microphthalmia (merle ocular dysgenesis). (D) Bilateral microphthalmia in a mixed breed puppy. Severe microphthalmia usually causes vision loss, but mild or moderate microphthalmia may still permit reasonable functional vision. Progression of cataracts or retinal abnormalities can eventually impair vision. There is no treatment, and the possibility of inheritance is high in selected breeds of dogs. Orbital cellulitis is common in dogs, and tends to occur in younger animals (<5 years). Acute disease is usually diffuse without specific pockets of exudate (Figure 4.2). Occasionally, orbital cellulitis becomes subacute to chronic and inflammatory exudate will accumulate, and is termed, orbital abscessation, which is more resistant to antibiosis. Figure 4.2 (A) Acute orbital cellulitis in a Basset Hound of three days duration. (B) Resolution of the condition several days later after therapy with high levels of systemic antibiotics, and topical antibiotics and 1% atropine. (C) German Pointer with unilateral retrobulbar abscess. (D) Oral view on a dog revealing swelling and hyperemia of the palatal tissue posterior to the last maxillary molar. This is an access point for sample collection and drainage of a retrobulbar abscess. The history is usually an acute onset of eyelid and orbital swelling, pain upon opening and complete closing of the mouth, difficulty with mastication, and general malaise. Common clinical signs include unilateral orbital swelling, exophthalmia, strabismus (if the infection is more isolated or focal within the orbit), protrusion and hyperemia of the nictitating membrane, conjunctival chemosis and hyperemia and mucopurulent discharge. Corneal edema, miosis, and aqueous flare occur with severe disease. Palpation of the orbit is usually painful and attempts to fully open the mouth generate pain and sometimes aggression. An elevated leukocyte count (20,000–30,000) with neutrophilia (80–90%) and pyrexia are usually present. Treatment requires systemic broad spectrum antibiotics and, if a discrete pocket of exudate is present, surgical establishment of drainage (usually behind the last upper molar tooth). Fine needle aspiration of the inflamed orbital tissue (ultrasound guidance is helpful) for cytology and microbial culture and susceptibility testing is recommended. Topical treatment includes broad spectrum antibiotics and mydriatics, if corneal disease and uveitis are present. If an impaired blink and exposure keratitis occur, a temporary complete tarsorrhaphy is recommended. Prognosis is generally good provided the infection responds rapidly to the systemic antibiotics. Enophthalmia, impaired ocular mobility (due to fibrosis), and optic nerve atrophy are infrequent sequelae. The main differential diagnoses for acquired orbital disease include orbital neoplasia (usually slow onset; biopsy), eosinophilic/masticatory myositis and extraocular polymyositis (both conditions usually bilateral; muscle biopsy), zygomatic sialoadenitis and cysts, as well as sinus and upper tooth root infections. Zygomatic salivary inflammations, cysts or mucoceles, and neoplasms affect the orbit because the gland is located in the ventroanterior orbit. With mucoceles, slow onset exophthalmia and protrusion of the nictitating membrane are the typical presenting signs (Figure 4.3). A fluctuating swelling can occur in the dorsolateral, ventromedial or ventral conjunctiva, or in the mouth, and attempts to open and examine the mouth do not cause discomfort. Diagnosis is confirmed with ultrasonography and aspiration of the contents of the mucocele. Recommended treatment is the surgical excision of the mucocele and the zygomatic gland. Figure 4.3 (A) Zygomatic salivary mucocele in large dog. The condition had progressed over several weeks. (B) Zygomatic salivary mucocele in a small breed dog. Note the swelling ventral to the globe. The eye was mildly exophthalmic and resistant to retropulsion. Zygomatic adenitis and neoplasia appear less frequently. Both adenomas and adencarcinomas produce clinical signs similar to the mucoceles, but can be differentiated with ultrasonography. Surgical excision is recommended but borders of the mass are frequently difficult to identify during surgery. Exenteration with removal of all orbital tissues probably offers the best prognosis. Masticatory or eosinophilic myositis appears as an acute disease that progresses to chronicity with inflamed muscles undergoing atrophy and fibrosis. Affected muscles typically include the temporalis, masseter, and pterygoid muscles. The disease appears to be immune‐mediated and targets these specific muscles.
Canine Orbit
Congenital Orbital Anomalies
Acute and Chronic Orbital Cellulitis
Zygomatic Salivary Inflammations, Cysts & Mucoceles
Masticatory or Eosinophilic Myositis
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