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The cat with an abnormal third eyelid
66. The cat with an abnormal third eyelid Michael E. Bernays
KEY SIGNS ● ● ● ● ●
Abnormal prominence of third eyelid. Focal or generalized swelling of third eyelid. Erythemia, chemosis. Eyelid lacerations. Ocular discharge.
MECHANISM? ●
Abnormalities of third eyelid appearance usually result from abnormalities in eyelid innervation, especially of the autonomic sympathetic nerves, or inflammation or neoplasia involving the conjunctiva of the third eyelid.
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Third eyelid cartilage. Conjunctiva covering the third eyelid. Gland of the third eyelid.
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The most common cause of altered third eyelid appearance is autonomic nervous system disease especially sympathetic neuropathy. Neoplasia and inflammatory disease is occasionally seen.
WHERE?
WHAT?
QUICK REFERENCE SUMMARY
Diseases causing an abnormal third eyelid WHERE? THIRD EYELID METABOLIC ●
Third eyelid prominence related to severe weight loss* (p 1137)
Occurs secondary to loss of orbital fat and enophthalmos (caudal globe retraction).
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66 – THE CAT WITH AN ABNORMAL THIRD EYELID
NEOPLASTIC ●
Squamous cell carcinoma*** (p 1134)
Proliferative pink mass growing from the third eyelid with verrucous or ulcerated surface. ●
Other neoplastic disease of the third eyelid (adenoma, adenocarcinoma, mast cell tumor, lymphoma, hemangioma)* (p 1138)
Tumors result in generalized swelling, a localized mass lesion, or erosion on the third eyelid. Hemangioma may form a discrete mass on the third eyelid, usually red to purple in color, which may hemorrhage.
PHYSICAL ●
Prolapsed gland of the third eyelid (p 1340)
Pink to red mass protruding from behind the leading edge of the third eyelid (rare). ●
Everted nictitans cartilage (p 1331)
Folded edge of third eyelid margin, without fleshy mass suggestive of gland prolapse (rare). ●
Third eyelid prominence related to ocular pain* (p @)
Occurs secondary to enophthalmos (globe retraction) due to the pain.
INFECTIOUS ●
Infectious disease involving the conjunctiva of third eyelid (feline herpesvirus1**, Chlamydophila felis** Mycoplasma*) (p 1337)
Signs include acute onset of hyperemia and chemosis of conjunctival surfaces and serous or mucopurulent ocular discharge, often together with concurrent upper respiratory tract signs. Chlamydial and mycoplasmal conjunctivitis may involve one or both eyes initially, and herpesvirus causes bilateral involvement. ●
Tetanus (p 1339)
Bilateral third eyelid prominence in association with contraction of facial muscles, and increased tone in muscles of mastication (“lockjaw”). Rare in cats.
IMMUNE ●
Eosinophilic keratoconjunctivitis** (p 1335)
Pink to whitish plaque-like thickening of the third eyelid, sometimes associated with similar lesions on the cornea.
IDIOPATHIC ●
Third eyelid dysautonomia (“Haws”)*** (p 1338)
Acute onset of bilateral third eyelid prominence, which is non-painful, and resolves over days to weeks without treatment. ●
Feline dysautonomia (p 1338)
Third eyelid prominence, in association with any of a range of other systemic signs, e.g. keratoconjunctivitis sicca, dilated non-responsive pupils, anisocoria, dry nose and/or mouth, bradycardia, constipation megaesophagus and urinary or fecal incontinence. Onset of signs is over 48 h, and is associated with depression and anorexia. continued
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continued
TRAUMA ●
Trauma to the third eyelid* (p 1330)
Asymmetric notch-like defects in the third eyelid margin due to claw injury from fighting with other cat(s). ●
Sympathetic neuropathy of the third eyelid (Horner’s syndrome)** (p 1335)
Prominent third eyelid, usually unilateral, in association with any combination of enophthalmos, upper lid ptosis or miosis, in association with or without other localizing signs such as ipsilateral forelimb lameness, cervical lesions (e.g. abscess, cellulitis) or middle ear disease.
INTRODUCTION MECHANISM? The most common cause of change in third eyelid appearance is an abnormality in innervation, especially involving the autonomic sympathetic nerves. The abnormal third eyelid is most often noticed because it is prominent. Prominence or protrusion of the third eyelid is a passive phenomenon in most animal species. Protrusion is usually facilitated by active contraction of muscle in adjacent orbital structures, and occurs because either: ● The globe is retracted caudally into the orbit by the action of the rectus and retractor bulbi muscles (the normal position of the globe tends to push the third eyelid into its retracted position at the medial aspect of the globe) or ● Sympathetically innervated smooth muscle at the base of the third eyelid (arising from deep in the orbit around facial coverings of the medial and ventral rectus muscles) is not contracting, causing a failure of retraction of the third eyelid. In the cat, the third eyelid may become actively protruded, independent of globe movement, by the action of skeletal muscle fibers, which are extensions of the levator palpebrae superioris and the lateral rectus muscles, innervated by the oculomotor (CN III) and abducens (CN VI), respectively. Because the third eyelid is covered by conjunctiva on both its posterior and anterior surface, any disease which affects the conjunctiva (see The Cat With Ocular Discharge or Changed Conjunctival Appearance,
page 1212) can also involve the surface of the third eyelid. Such conjunctival diseases are either: ● Inflammatory disease due to: – Infectious agents such as FHV1, Chlamydophila felis, Mycoplasma. – Non-infectious, allergic or other immune-mediated etiologies, e.g. eosinophilic keratoconjunctivitis or follicular conjunctivitis. ● Neoplastic disease, especially squamous cell carcinoma.
WHERE? Disease anywhere along the sympathetic neural pathways (i.e. thalamus, cervical spinal cord long tracts, T1–T3 spinal nerves, ascending pre-ganglionic fibers, cranial cervical ganglion, sympathetic postganglionic fibers in middle ear or orbit), and the smooth muscle fibers innervated by them, may cause protrusion of the third eyelid. Conjunctival surface diseases cause abnormal appearance of the third eyelid. Cartilage of the third eyelid may fold causing an everted appearance.
WHAT? The most common cause of altered third eyelid appearance is autonomic nervous system disease especially primary third eyelid dysautonomia (“haws”). Horner’s syndrome is associated with other clinical signs such as enophthalmos, miosis and upper lid ptosis. Primary third eyelid dysautonomia is associated with prominence of the third eyelid with lack of other signs of sympathetic denervation.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Inflammatory disease is occasionally seen, and can be of infectious or non-infectious, immune-mediated or allergic etiology. Neoplasia involving the conjunctiva of the third eyelid occurs infrequently.
DISEASES CAUSING ABNORMAL THIRD EYELID APPEARANCE INFECTIOUS DISEASE INVOLVING CONJUNCTIVA OF THE THIRD EYELID*** (FELINE HERPESVIRUS-1**, CHLAMYDOPHILA FELIS** AND MYCOPLASMA* INFECTION) Classical signs ●
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Inflammation and chemosis (swelling) specifically involving the conjunctiva of the third eyelid. Discharge varies from serous or mucoid to mucopurulent.
See main references on feline herpesvirus, chlamydial and mycoplasmal infection on pages 1212, 1218 for details (The Cat With Ocular Discharge or Changed Conjunctival Appearance).
Although herpesvirus, Chlamydophila felis and Mycoplasma infection may be difficult to distinguish clinically in some cats, in other cats signs may be suggestive of the causative agent. ● Herpesvirsus typically causes bilateral serous conjunctivitis in conjunction with other upper respiratory signs (sneezing, nasal discharge). Discharge rapidly becomes mucopurulent and the cat is depressed, anorexic and febrile. In some cats, dendritic ulcerative keratitis may occur initially. Non-ulcerative stromal keratitis and/or corneal sequestration may occur several weeks to a few months after the initial infection, which may have been unnoticed. Symblepharon may be seen as a sequel in young cats. ● Chlamydial conjunctivitis typically appears as severe hyperemia and chemosis of conjunctival surfaces. It is associated with mucopurulent discharge, usually starting in one eye and later progressing to involve the contralateral eye. ● Mycoplasmal conjunctivitis appears as unilateral or bilateral conjunctivitis, associated with epiphora, papillary hypertrophy of conjunctiva, conjunctival follicles, chemosis, and occasionally thick white pseudomambrane.
Diagnosis Clinical signs Typically there is inflammation and chemosis (swelling) specifically involving the conjunctiva of the third eyelid. Usually the associated bulbar and palpebral conjunctivae are also affected.
A tentative diagnosis is often made on the signs of inflammation, chemosis and discharge associated with upper respiratory tract signs.
There may be signs of upper respiratory tract disease in the early stages, although all these organisms may also cause conjunctivitis unassociated with typical upper respiratory tract signs. Conjunctivitis alone may occur in cats with previous exposure that have developed immunity, or it may represent recrudescence of signs in carrier cats.
A definitive diagnosis requires identification of the organism on conjunctival cytologic preparations stained with Wright–Giemsa, e.g. ● Membrane-bound basophilic intracytoplasmic inclusions indicate chlamydial infection. ● Small basophilic-staining pleomorphic organisms closely associated with the cell membrane surface indicate mycoplasmal infection.
Discharge varies from serous or mucoid to mucopurulent. The type of discharge seen is dependent on the stage of the infection, for example, FHV-1 herpesvirus infections usually cause a serous discharge in the early stages, which progresses to a mucopurulent discharge secondary to bacterial infection.
Specific tests are available for the diagnosis of infectious disease especially in the early stages, e.g. ● Herpesvirus: immunofluorescent antibody (IFA), virus isolation (VI) and polymerase chain reaction (PCR). ● Chlamydophila felis: IFA and PCR.
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Differential diagnosis
Differential diagnosis
Infectious conjunctivitis is usually distinctive and differentiation between the infectious agents needs to be made. The chronic forms of infection may appear similar to eosinophilic keratoconjunctivitis, which can be differentiated based on cytological examination of deep scrapings or on histopathology.
Horner’s syndrome results in acute onset of unilateral prominence of the third eyelid whereas Haws is bilateral. Horner’s syndrome is associated with other signs such as ptosis and a miotic pupil.
Treatment See The Cat With Ocular Discharge or Changed Conjunctival Appearance (page 1207) for more details. Herpesvirus: topical trifluorothymidine, Idoxuridine, Vidarabine, topical or oral Acyclovir, topical or oral alpha interferon, oral lysine. Chlamydophila felis: topical tetracycline, oral doxycycline, oral azithromycin.
Treatment No treatment is necessary. All cases will resolve with time.
SQUAMOUS CELL CARCINOMA*** Classical signs ● ●
Verrucous, raised mass usually arising from non-pigmented conjunctival surface. Erosion and mucopurulent discharge.
Mycoplasma: topical tetracycline or chloramphenicol.
Clinical signs THIRD EYELID DYSAUTONOMIA (“HAWS”)*** Classical signs ● ●
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Bilateral non-painful third eyelid prominence. Usually acute onset, and often resolves rapidly without treatment within days to weeks. Unassociated with other signs of sympathetic denervation.
Clinical signs Bilateral, non-painful third eyelid prominence, usually acute in onset and resolves rapidly within days to weeks. Not associated with other signs of sympathetic denervation such as ptosis and a miotic pupil. Sometimes seen in association with acute gastrointestinal signs, e.g. diarrhea. One report in the literature found an association with torovirus infection.
Diagnosis Diagnosis is usually based solely on the clinical signs.
Pink, proliferative mass with a cauliflower-like (verrucous) or ulcerated surface usually arising from the non-pigmented conjunctival surface of the third eyelid. Typically the lesion is associated with erosion, loss of normal tissue architecture and mucopurulent discharge.
Diagnosis Initial diagnosis is based on the appearance of the lesion. Cytology and/or histopathology are required for a definitive diagnosis. Typical cytological appearance includes large clumps of eosinophilic keratinized epithelial cells, and sometimes loss of normal architecture is visible in the form of whorls or keratin “pearls”.
Differential diagnosis Eosinophilic keratitis is an uncommon proliferative disease of the third eyelid. It may also be associated with corneal disease and cytology is characteristically in the form of eosinophilic infiltrates. Other neoplastic disease. Hemangiomas are not as common, have a smoother surface, and appear as a darker red to purple-colored mass.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Treatment
Differential diagnosis
Surgical excision with good margins is required to ensure complete removal. The lesions can sometimes invade deep into the extra-ocular tissues by the time the lesion is recognized.
Squamous cell carcinoma usually causes more disfigurement of the third eyelid due to proliferation and ulceration.
Cryosurgery using liquid nitrogen or nitrous oxide with double freeze thaws and slow controlled thawing can be effective for small tumors less than 0.5 cm diameter. Maximal destruction of tumor cells occurs when temperatures of between −20˚C to −40˚C are achieved at the center of the tumor. b-irradiation with strontium 90 can be effective if available.
EOSINOPHILIC KERATOCONJUNCTIVITIS** Classical signs ● ●
Pink to whitish plaque-like thickening of the third eyelid. ± Similar lesions on the cornea.
Clinical signs Appears as pink to whitish plaque-like thickening of the third eyelid. Similar lesions may appear on the cornea in some cats. The pathogenesis is unknown, but is postulated to involve insect bite hypersensitivity or herpesvirus infection in some cats. Generally there is not a strong association with the presence of other feline eosinophilic disease.
Other neoplasms such as hemangioma have a characteristic appearance. Chronic Mycoplasma and Chlamydophila felis infection may appear similar in some cats, but can be differentiated on cytological examination of Wright– Giemsa-stained slides, immunofluorescent antibody and PCR.
Treatment Oral corticosteroids: Prednisolone 5 mg orally q 12–24 h, with dose reducing as effect is achieved. Oral progestagens at a low dose (e.g. megestrol acetate 5 mg twice weekly) should be used only in cases refractory to oral prednisolone. Beware of possible side effects such as insulin resistance, diabetes and obesity. Topical corticosteroids are usually contraindicated because of an underlying association with ocular herpesvirus infection. These drugs may potentiate the herpesvirus infection by local immunosuppression. Treat the underlying cause if identified, e.g. treat the ocular herpesvirus infection.
SYMPATHETIC NEUROPATHY OF THE THIRD EYELID (HORNER’S SYNDROME)** Classical signs
Diagnosis
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Tentative diagnosis is based on the presence of typical lesions on the third eyelid and cornea.
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Cytological examination of deep scrapings of the lesion or histopathology of a biopsy specimen demonstrate an infiltrate of plasma cells and lymphocytes with variable numbers of eosinophils. Eosinophils may not always be the most numerous cell type. Tests for herpesvirus infection, e.g. in situ PCR and (see The Cat With Ocular Discharge or Changed Conjunctival Appearance, page 1213, for more details).
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Usually unilateral. Non-painful prominence of the third eyelid. Miosis of the ipsilateral pupil. Upper lid ptosis. Enophthalmos.
Pathogenesis Protrusion of the third eyelid occurs where there is disruption of the sympathetic neural pathways innervating the smooth muscle of the third eyelid (Horner’s syndrome). Disruption may occur anywhere along the pathway including in the thalamus, cervical spinal cord
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long tracts, T1–T3 spinal nerves or nerve roots, ascending pre-ganglionic fibers, cranial cervical ganglion and sympathetic post-ganglionic fibers in middle ear or orbit. Less commonly protrusion is the result of dysfunction of the smooth muscle fibers innervated by the sympathetic nerve. More common causes in the cat include: ● Middle ear disease especially nasopharyngeal polyps. Nasopharyngeal polyps arise in the middle ear and emerge into the external ear canal or nasopharynx. Typically they occur in young cats (< 5 years), but any age can be affected. ● Disruption of ascending sympathetic pathways in the neck due to injury or inflammation associated with fight wounds. ● Injury to nerve roots of T1–T3 associated with forelimb trauma, usually from motor vehicle accidents. ● Anterior thoracic cavity disease, e.g. mediastinal lymphoma. Rarely, is third eyelid protrusion the result of nerve damage within the brain or spinal cord, or smooth muscle disease.
Clinical signs Usually there is a unilateral, non-painful prominence of the third eyelid, together with other signs of sympathetic denervation, i.e. miosis, upper lid ptosis (“drooping”), enophthalmos. Other signs may be present in some cases, which may enable further localization of the lesion, e.g. ● An abscess or cellulitis of cervical soft tissue structures suggests disruption of ascending preganglionic fibers. ● Signs of middle or inner ear disease such as a head tilt or circling. Nasopharyngeal polyp may be seen as a fibrous mass emerging into the external ear canal, or cause noisy breathing, dyspnea with or without nasal discharge, sneezing or coughing and gagging. ● Ipsilateral forelimb lameness may occur from damage to nerve roots or nerves innervating the leg. Radial nerve paresis or paralysis may occur concurrently with avulsion of T1–T3 nerve roots if C8 or T1 nerve roots are injured. If the musculocutaneous nerve roots (C5–7) are also injured, the
elbow cannot be flexed or the paw picked up, resulting in excoriation of the dorsum of the paw. Muscle atrophy is apparent within 5–7 days of injury to the motor nerve roots. Damage to C7–T1 may also result in loss of the ipsilateral cutaneous trunci (panniculus) reflex.
Diagnosis Any cat with an apparently non-painful, non-inflamed prominent third eyelid, which also has miosis, upper lid ptosis and enophthalmos should be suspected as having Horner’s syndrome. Pharmacological testing with sympathomimetics is controversial, and the indirect-acting sympathomimetic hydroxyamfetamine is no longer available in some countries. Reliable diagnostic protocols are not available, however a rapid (within 5–8 minutes) reversal of signs following the administration of one drop of 10% phenylephrine is suggestive of post-ganglionic denervation hypersensitivity, indicating that the lesion is somewhere rostral to the cranial cervical ganglion. Anatomically this corresponds to localization of the lesion in the middle ear or orbital structures rostral to the middle ear. The response should always be compared with that in the contralateral normal eye. Lesion localization will not be possible in many cases, and many cases seem to be idiopathic.
Differential diagnosis Third eyelid dysautonomia (Haw’s) is always bilateral, and is not associated with other signs of sympathetic denervation. Horner’s syndrome is almost always unilateral.
Treatment Where possible, treatment should be directed at the associated problems which may be causing interruption of sympathetic pathways. The disfigurement created by Horner’s syndrome can be reversed by frequent (at least 2–3 times daily) application of one drop of 10% phenylephrine in the affected eye. This treatment only alters the appearance of the eye and does nothing else for the cat’s well-being,
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
except that vision might be improved where the third eyelid prominence and enophthalmos is extreme, causing most of the globe to be covered by nictitans.
Clinical signs
Prognosis
It is associated with ipsilateral signs of ocular pain, for example, enophthalmos, blepharospasm, corneal disease, pupil miosis or anterior uveitis.
Depending on the cause many cases may resolve over time as denervated smooth muscle re-innervates, provided that oculosympathetic fibers are not totally destroyed.
TRAUMA TO THE THIRD EYELID MARGIN* Classical signs ● ●
Notch-like or linear tears arising from the third eyelid margin. Usually unilateral, with the contralateral eye unaffected.
The third eyelid is prominent because of retraction of the globe, associated with ocular pain.
Diagnosis Diagnosis is based on signs of ocular pain together with prominence of a normal-appearing third eyelid.
Differential diagnosis Horner’s syndrome and Haws are usually nonpainful. Horner’s syndrome, tetanus and feline dysautonomia each have their own specific associated clinical signs, which are more suggestive of that particular condition.
Clinical signs Trauma to the third eyelid may result in notch-like or linear tears starting at the margin of the third eyelid. These occur most commonly from cat fights. Third eyelid trauma may be associated with other ocular signs, when seen in the acute stages, e.g. conjunctival chemosis and ocular discharge (see The Cat With Ocular Discharge or Changed Conjunctival Appearance, page 1211).
Treatment Treat the cause of the ocular pain as indicated.
THIRD EYELID PROMINENCE RELATED TO SEVERE WEIGHT LOSS* Classical signs ●
Diagnosis Diagnosis is based on the clinical signs, and the history of unilateral third eyelid notch or tear occurring after a possible fight with another cat.
THIRD EYELID PROMINENCE RELATED TO OCULAR PAIN* Classical signs ● ●
Third eyelid prominence. Associated with other ipsilateral signs of ocular pain, e.g. enophthalmos, blepharospasm, corneal disease, pupil miosis.
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Signs of generalized muscle wasting associated with chronic disease. Thin face with signs of muscle wastage around the lateral aspects of the orbit. Bilaterally symmetrical third eyelid prominence without miosis or upper lid ptosis.
Clinical signs Typically these cats have a bilaterally symmetrical third eyelid prominence due to marked enophthalmos, and there are no other signs normally associated with other causes of third eyelid prominence such as miosis or upper lid ptosis. Generalized whole-body muscle wasting is present in association with signs of other organ system disease,
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e.g. chronic renal failure, inflammatory bowel disease or hyperthyroidism.
the cornea is impaired because of an uneven eyelid margin.
Third eyelid prominence occurs secondary to loss of orbital fat and enophthalmos.
Diagnosis
Diagnosis
Diagnosis is initially based on the appearance of the lesion, which varies according to the type of tumor.
Diagnosis is based on the generalized body muscle and fat loss, in association with the pronounced enophthalmos and third eyelid prominence.
Definitive diagnosis is by cytological and histological examination.
FELINE DYSAUTONOMIA OTHER NEOPLASTIC DISEASE OF THE THIRD EYELID* (ADENOMA, ADENOCARCINOMA, MAST CELL TUMOR, LYMPHOMA, HEMANGIOMA)
Classical signs ● ●
Classical signs ● ●
Mass or erosive lesion involving the third eyelid. Ocular discharge.
Clinical signs Tumors of the third eyelid appear as a mass or erosive lesion involving the third eyelid. Appearance depends on the type of tumor, which includes lymphoma, hemangioma, mast cell tumor, adenoma and adenocarcinoma. ● Hemangiomas are rare, are usually dark red to purple in color, and are fragile with a tendency to hemorrhage. ● Lymphoma will usually cause more generalized swelling of the third eyelid and the peri-orbital tissues, and may be associated with other systemic signs of multricentric lymphoma. ● Mast cell tumors can form either well- or poorly circumscribed areas of swelling in the eyelid. They appear as rapidly growing nodular tumor, often with poorly defined borders, and variable surface ulceration. ● Adenomas or carcinomas are seen as a nodular or diffuse mass causing localized thickening of the eyelid. The tumor may have an ulcerated surface. The neoplastic mass may cause increased ocular discharge because of third eyelid dysfunction. The normal distribution of the precorneal tear film across
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Unilateral or bilateral third eyelid prominence. Acute onset of anorexia and depression. Other signs of autonomic dysfunction such as keratoconjunctivitis sicca, mydriasis, anisocoria, dry nose or mouth, bradycardia, constipation, megaesophagus, urinary or fecal incontinence.
See main references on page 792 for details (The Constipated or Straining Cat).
Clinical signs Third eyelid prominence, in association with any of a range of other systemic signs suggestive of autonomic dysfunction including keratoconjunctivitis sicca, dilated non-responsive pupils, anisocoria, dry nose and/or mouth, bradycardia, constipation, megaesophagus and urinary or fecal incontinence. Typically, the onset of signs is acute over 48 h and associated with depression and anorexia.
Diagnosis Diagnosis is based on signs of generalized autonomic dysfunction. Condition is rare or at least uncommon, and most frequent in UK. Definitive diagnosis is based on the demonstration of characteristic ultrastructural lesions within cell bodies in autonomic ganglia at post mortem.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Differential diagnosis Abnormality of the third eyelid without the presence of other signs of autonomic dysfunction would suggest localized sympathetic dysfunction such as Horner’s or Haws syndrome.
Treatment No definitive treatment is available. Prognosis is generally guarded to poor, however supportive treatment is reported to be variably effective.
sue environment to support toxin production, and the number of organisms present. Tetanus is rare in cats, because they are more resistant to the toxin than humans and horses. This innate resistance is related to the inability of the toxin to penetrate and bind to nervous tissue, and likely accounts for the frequency of localized signs in cats. Tetanus has occurred after routine surgery (such as ovariohysterectomy), fetal death during pregnancy, and trauma. Tetanus may occur in young cats associated with a gum wound secondary to losing a deciduous tooth.
TETANUS Classical signs ● ● ●
Bilateral third eyelid prominence. Contraction of facial muscles, increased tone in muscles of mastication (“lockjaw”). Stiffness of one or more limbs which worsens with stimulation.
Pathogenesis Signs of tetanus result from the toxin produced by Clostridium tetani, a spore-forming, Gram-positive rod. C. tetani is found in the soil, and also occurs as part of the normal gastrointestinal tract flora of some animals. Spores of the Clostridium tetani bacillus enter the body commonly via surface wounds. The toxin, tetanospasmin, is produced during cell growth, sporulation and lysis, if there is a suitable anaerobic environment for the bacteria. The toxin migrates along nerve axons from a local wound, to sites of action in the central nervous system, where it initially binds to presynaptic inhibitory motor nerve endings. The effect of the toxin is to block the release of inhibitory neurotransmitters (glycine and gamma-amino butyric acid) across the synaptic cleft. This results in uninhibited muscle contraction. The incubation period for signs to develop varies from 3–21 days after an injury, depending on the proximity of the injury to the CNS, the ability of the local tis-
Clinical signs Signs of tetanus may be localized or generalized, or may begin with localized signs and progressively involve more muscle groups over a week or more, and become generalized. Generalization is more likely if there is inadequate wound management, or inadequate antibiotic therapy. Diagnosis may be difficult in the early stages of the disease when characteristic signs of generalized tetanus are absent. Classical signs of generalized tetanus include bilateral third eyelid prominence in association with contraction of the facial muscles giving the appearance of a “sardonic smile”, and increased tone in the muscles of mastication (“lockjaw”). The cat may have a “startled” appearance. Focal tetanus results in stiffness of the muscles in closest proximity to the wound, and is often evident as stiffness of one or two limbs. In many cats, a neglected wound with necrotic tissue is found, suggesting a site for toxin production. Tetanus may be associated with infection of the female reproductive tract, and may produce local signs in the pelvic limbs. The history of a penetrating or neglected wound, and the presence of persistent involuntary muscle rigidity in a mentally alert cat is highly suggestive of tetanus.
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If there is generalized muscle stiffness, the cat may have an increased temperature associated with the muscle contraction.
Diagnosis Diagnosis is based on the characteristic clinical signs. EMG testing of affected muscles is strongly suggestive of tetanus if it demonstrates persistent spontaneous motor unit potentials.
Differential diagnosis Any condition which causes bilateral third eyelid prominence such as haws or dysautonomia should be considered. However, facial muscle or limb rigidity is not seen with these conditions. Mild hypocalcemia in late pregnancy or following whelping could be confused with tetanus, especially as the reproductive tract may be a site of infection and toxin production. Rapid response to intravenous calcium in pregnancy-associated hypocalcemia will rule out tetanus. Meningoencephalitis or encephalopathy including thiamine deficiency may occasionally have tetanic spasms worsened with touch or sound. In these animals mentation is usually depressed and other neurological signs are evident.
Treatment Treatment involves appropriate antibiotic therapy, wound care, supportive treatment, and use of tetanus antitoxin. It is important to debride necrotic tissue, so the tissue environment is less attractive for persistence of the organism and toxin production. Antibiotics with anaerobic activity especially metronidazole (10 mg/kg, q 8 h), and those belonging to the penicillin group, e.g. amoxicillin or amoxycillin/clavulanate are indicated to prevent further proliferation of bacteria in the wound. ● Metronidazole has been shown to be superior to penicillin G and tetracycline. It is bactericidal against most anaerobes and achieves effective therapeutic concentrations even in anaerobic tissues.
Tetanus antitoxin binds to circulating toxin, and cannot dislodge toxin within peripheral nerves. Its main purpose is to neutralize circulating toxin outside the nervous system. If the signs are localized and non-progressive, administering tetanus antitoxin systemically is not likely to be beneficial, and is associated with a risk of anaphylaxis. ● The dose of antitoxin is usually about 1000 U/kg IV administered slowly over 5–10 minutes, with some (1000 U) injected locally in the wound. As most tetanus antiserums are generally prepared in equines, consideration should be given to the pre-emptive use of corticosteroids and antihistamine to prevent possible anaphylaxis. Give a test dose (0.1–0.2 ml) intradermally or subcutaneously 15–20 minutes before IV administration and check for a wheal. Muscle relaxants such as diazepam can be used to control the muscle rigidity and make the cat more comfortable. Efficacy of the drug varies between individual cats. Alternatively, small doses of acepromazine (1.25–2.5 mg/cat PO q 6 hours as required), chlorpromazine (IV) or phenobarbital may be effective in reducing muscle stiffness. Other supportive treatment should be given as indicated, e.g. alimentation, intravenous fluids. Keep the cat in a quiet, dark area to reduce the muscle spasms, which are stimulated by touch or sound Difficulty urinating or defecating may occur, and needs to be managed.
Prognosis The prognosis is generally good with appropriate treatment, and full resolution of signs usually occurs within 2–3 months. Prognosis is poorer if signs develop very rapidly.
PROLAPSED GLAND OF THE THIRD EYELID Classical signs ● ● ●
Pink to red mass protruding from behind the third eyelid. Variable inflammation and discharge. Rare and only reported in Burmese cats.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Clinical signs
Clinical signs
Pink to reddish mass with a smooth conjunctival surface protrudes from behind the leading edge of the third eyelid margin.
Everted third eyelid margin occurs because of folding of the cartilage of the third eyelid. This condition should be distinguished from a prolapsed gland of the nictitans.
Prolapse may be accompanied by variable degrees of inflammation and discharge, ranging from mucoid to mucopurulent. Rare in cats compared with dogs, and reported only in Burmese cats.
Diagnosis Diagnosis is based on the appearance of the mass. Differential diagnosis would be a tumor or a folded (everted or inverted) third eyelid cartilage, also rarely reported, and only in Burmese cats.
Rare in cats. Reported only in Burmese cats.
Diagnosis Diagnosis is based on the appearance of the third eyelid margin. Usually there is no sign of a fleshy mass protruding from behind the third eyelid.
Treatment Resection of the folded section of cartilage will enable straightening of the third eyelid.
EVERTED NICTITANS CARTILAGE Classical signs ● ●
Folded everted third eyelid margin. Rare and only reported in Burmese cats.
RECOMMENDED READING Glaze MB, Gelatt KN. Feline ophthalmology. In: Scagliotti R (ed) Comparative Neuro-ophthalmology. In: Gelatt KN (series ed) Veterinary Ophthalmology, 3rd edn. Baltimore, Maryland, Lippincott, Williams & Wilkins, 1999, pp. 1004–1010, 1366–1370. Ketring KL, Glaze MB. Atlas of Feline Ophthalmology. Trenton, New Jersey, Veterinary Learning Systems, 1994, pp. 69–76. Sharp NJH, Nash AS, Griffiths IR. Feline dysautonomia (the Key-Gaskell syndrome): a clinical and pathologic study of forty cases. J Small Anim Pract 1984; 25: 599–615.
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KEY SIGNS ● ● ● ● ●
Abnormal prominence of third eyelid. Focal or generalized swelling of third eyelid. Erythemia, chemosis. Eyelid lacerations. Ocular discharge.
MECHANISM? ●
Abnormalities of third eyelid appearance usually result from abnormalities in eyelid innervation, especially of the autonomic sympathetic nerves, or inflammation or neoplasia involving the conjunctiva of the third eyelid.
●
Third eyelid cartilage. Conjunctiva covering the third eyelid. Gland of the third eyelid.
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The most common cause of altered third eyelid appearance is autonomic nervous system disease especially sympathetic neuropathy. Neoplasia and inflammatory disease is occasionally seen.
WHERE?
WHAT?
QUICK REFERENCE SUMMARY
Diseases causing an abnormal third eyelid WHERE? THIRD EYELID METABOLIC ●
Third eyelid prominence related to severe weight loss* (p 1137)
Occurs secondary to loss of orbital fat and enophthalmos (caudal globe retraction).
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NEOPLASTIC ●
Squamous cell carcinoma*** (p 1134)
Proliferative pink mass growing from the third eyelid with verrucous or ulcerated surface. ●
Other neoplastic disease of the third eyelid (adenoma, adenocarcinoma, mast cell tumor, lymphoma, hemangioma)* (p 1138)
Tumors result in generalized swelling, a localized mass lesion, or erosion on the third eyelid. Hemangioma may form a discrete mass on the third eyelid, usually red to purple in color, which may hemorrhage.
PHYSICAL ●
Prolapsed gland of the third eyelid (p 1340)
Pink to red mass protruding from behind the leading edge of the third eyelid (rare). ●
Everted nictitans cartilage (p 1331)
Folded edge of third eyelid margin, without fleshy mass suggestive of gland prolapse (rare). ●
Third eyelid prominence related to ocular pain* (p @)
Occurs secondary to enophthalmos (globe retraction) due to the pain.
INFECTIOUS ●
Infectious disease involving the conjunctiva of third eyelid (feline herpesvirus1**, Chlamydophila felis** Mycoplasma*) (p 1337)
Signs include acute onset of hyperemia and chemosis of conjunctival surfaces and serous or mucopurulent ocular discharge, often together with concurrent upper respiratory tract signs. Chlamydial and mycoplasmal conjunctivitis may involve one or both eyes initially, and herpesvirus causes bilateral involvement. ●
Tetanus (p 1339)
Bilateral third eyelid prominence in association with contraction of facial muscles, and increased tone in muscles of mastication (“lockjaw”). Rare in cats.
IMMUNE ●
Eosinophilic keratoconjunctivitis** (p 1335)
Pink to whitish plaque-like thickening of the third eyelid, sometimes associated with similar lesions on the cornea.
IDIOPATHIC ●
Third eyelid dysautonomia (“Haws”)*** (p 1338)
Acute onset of bilateral third eyelid prominence, which is non-painful, and resolves over days to weeks without treatment. ●
Feline dysautonomia (p 1338)
Third eyelid prominence, in association with any of a range of other systemic signs, e.g. keratoconjunctivitis sicca, dilated non-responsive pupils, anisocoria, dry nose and/or mouth, bradycardia, constipation megaesophagus and urinary or fecal incontinence. Onset of signs is over 48 h, and is associated with depression and anorexia. continued
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continued
TRAUMA ●
Trauma to the third eyelid* (p 1330)
Asymmetric notch-like defects in the third eyelid margin due to claw injury from fighting with other cat(s). ●
Sympathetic neuropathy of the third eyelid (Horner’s syndrome)** (p 1335)
Prominent third eyelid, usually unilateral, in association with any combination of enophthalmos, upper lid ptosis or miosis, in association with or without other localizing signs such as ipsilateral forelimb lameness, cervical lesions (e.g. abscess, cellulitis) or middle ear disease.
INTRODUCTION MECHANISM? The most common cause of change in third eyelid appearance is an abnormality in innervation, especially involving the autonomic sympathetic nerves. The abnormal third eyelid is most often noticed because it is prominent. Prominence or protrusion of the third eyelid is a passive phenomenon in most animal species. Protrusion is usually facilitated by active contraction of muscle in adjacent orbital structures, and occurs because either: ● The globe is retracted caudally into the orbit by the action of the rectus and retractor bulbi muscles (the normal position of the globe tends to push the third eyelid into its retracted position at the medial aspect of the globe) or ● Sympathetically innervated smooth muscle at the base of the third eyelid (arising from deep in the orbit around facial coverings of the medial and ventral rectus muscles) is not contracting, causing a failure of retraction of the third eyelid. In the cat, the third eyelid may become actively protruded, independent of globe movement, by the action of skeletal muscle fibers, which are extensions of the levator palpebrae superioris and the lateral rectus muscles, innervated by the oculomotor (CN III) and abducens (CN VI), respectively. Because the third eyelid is covered by conjunctiva on both its posterior and anterior surface, any disease which affects the conjunctiva (see The Cat With Ocular Discharge or Changed Conjunctival Appearance,
page 1212) can also involve the surface of the third eyelid. Such conjunctival diseases are either: ● Inflammatory disease due to: – Infectious agents such as FHV1, Chlamydophila felis, Mycoplasma. – Non-infectious, allergic or other immune-mediated etiologies, e.g. eosinophilic keratoconjunctivitis or follicular conjunctivitis. ● Neoplastic disease, especially squamous cell carcinoma.
WHERE? Disease anywhere along the sympathetic neural pathways (i.e. thalamus, cervical spinal cord long tracts, T1–T3 spinal nerves, ascending pre-ganglionic fibers, cranial cervical ganglion, sympathetic postganglionic fibers in middle ear or orbit), and the smooth muscle fibers innervated by them, may cause protrusion of the third eyelid. Conjunctival surface diseases cause abnormal appearance of the third eyelid. Cartilage of the third eyelid may fold causing an everted appearance.
WHAT? The most common cause of altered third eyelid appearance is autonomic nervous system disease especially primary third eyelid dysautonomia (“haws”). Horner’s syndrome is associated with other clinical signs such as enophthalmos, miosis and upper lid ptosis. Primary third eyelid dysautonomia is associated with prominence of the third eyelid with lack of other signs of sympathetic denervation.
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Inflammatory disease is occasionally seen, and can be of infectious or non-infectious, immune-mediated or allergic etiology. Neoplasia involving the conjunctiva of the third eyelid occurs infrequently.
DISEASES CAUSING ABNORMAL THIRD EYELID APPEARANCE INFECTIOUS DISEASE INVOLVING CONJUNCTIVA OF THE THIRD EYELID*** (FELINE HERPESVIRUS-1**, CHLAMYDOPHILA FELIS** AND MYCOPLASMA* INFECTION) Classical signs ●
●
Inflammation and chemosis (swelling) specifically involving the conjunctiva of the third eyelid. Discharge varies from serous or mucoid to mucopurulent.
See main references on feline herpesvirus, chlamydial and mycoplasmal infection on pages 1212, 1218 for details (The Cat With Ocular Discharge or Changed Conjunctival Appearance).
Although herpesvirus, Chlamydophila felis and Mycoplasma infection may be difficult to distinguish clinically in some cats, in other cats signs may be suggestive of the causative agent. ● Herpesvirsus typically causes bilateral serous conjunctivitis in conjunction with other upper respiratory signs (sneezing, nasal discharge). Discharge rapidly becomes mucopurulent and the cat is depressed, anorexic and febrile. In some cats, dendritic ulcerative keratitis may occur initially. Non-ulcerative stromal keratitis and/or corneal sequestration may occur several weeks to a few months after the initial infection, which may have been unnoticed. Symblepharon may be seen as a sequel in young cats. ● Chlamydial conjunctivitis typically appears as severe hyperemia and chemosis of conjunctival surfaces. It is associated with mucopurulent discharge, usually starting in one eye and later progressing to involve the contralateral eye. ● Mycoplasmal conjunctivitis appears as unilateral or bilateral conjunctivitis, associated with epiphora, papillary hypertrophy of conjunctiva, conjunctival follicles, chemosis, and occasionally thick white pseudomambrane.
Diagnosis Clinical signs Typically there is inflammation and chemosis (swelling) specifically involving the conjunctiva of the third eyelid. Usually the associated bulbar and palpebral conjunctivae are also affected.
A tentative diagnosis is often made on the signs of inflammation, chemosis and discharge associated with upper respiratory tract signs.
There may be signs of upper respiratory tract disease in the early stages, although all these organisms may also cause conjunctivitis unassociated with typical upper respiratory tract signs. Conjunctivitis alone may occur in cats with previous exposure that have developed immunity, or it may represent recrudescence of signs in carrier cats.
A definitive diagnosis requires identification of the organism on conjunctival cytologic preparations stained with Wright–Giemsa, e.g. ● Membrane-bound basophilic intracytoplasmic inclusions indicate chlamydial infection. ● Small basophilic-staining pleomorphic organisms closely associated with the cell membrane surface indicate mycoplasmal infection.
Discharge varies from serous or mucoid to mucopurulent. The type of discharge seen is dependent on the stage of the infection, for example, FHV-1 herpesvirus infections usually cause a serous discharge in the early stages, which progresses to a mucopurulent discharge secondary to bacterial infection.
Specific tests are available for the diagnosis of infectious disease especially in the early stages, e.g. ● Herpesvirus: immunofluorescent antibody (IFA), virus isolation (VI) and polymerase chain reaction (PCR). ● Chlamydophila felis: IFA and PCR.
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Differential diagnosis
Differential diagnosis
Infectious conjunctivitis is usually distinctive and differentiation between the infectious agents needs to be made. The chronic forms of infection may appear similar to eosinophilic keratoconjunctivitis, which can be differentiated based on cytological examination of deep scrapings or on histopathology.
Horner’s syndrome results in acute onset of unilateral prominence of the third eyelid whereas Haws is bilateral. Horner’s syndrome is associated with other signs such as ptosis and a miotic pupil.
Treatment See The Cat With Ocular Discharge or Changed Conjunctival Appearance (page 1207) for more details. Herpesvirus: topical trifluorothymidine, Idoxuridine, Vidarabine, topical or oral Acyclovir, topical or oral alpha interferon, oral lysine. Chlamydophila felis: topical tetracycline, oral doxycycline, oral azithromycin.
Treatment No treatment is necessary. All cases will resolve with time.
SQUAMOUS CELL CARCINOMA*** Classical signs ● ●
Verrucous, raised mass usually arising from non-pigmented conjunctival surface. Erosion and mucopurulent discharge.
Mycoplasma: topical tetracycline or chloramphenicol.
Clinical signs THIRD EYELID DYSAUTONOMIA (“HAWS”)*** Classical signs ● ●
●
Bilateral non-painful third eyelid prominence. Usually acute onset, and often resolves rapidly without treatment within days to weeks. Unassociated with other signs of sympathetic denervation.
Clinical signs Bilateral, non-painful third eyelid prominence, usually acute in onset and resolves rapidly within days to weeks. Not associated with other signs of sympathetic denervation such as ptosis and a miotic pupil. Sometimes seen in association with acute gastrointestinal signs, e.g. diarrhea. One report in the literature found an association with torovirus infection.
Diagnosis Diagnosis is usually based solely on the clinical signs.
Pink, proliferative mass with a cauliflower-like (verrucous) or ulcerated surface usually arising from the non-pigmented conjunctival surface of the third eyelid. Typically the lesion is associated with erosion, loss of normal tissue architecture and mucopurulent discharge.
Diagnosis Initial diagnosis is based on the appearance of the lesion. Cytology and/or histopathology are required for a definitive diagnosis. Typical cytological appearance includes large clumps of eosinophilic keratinized epithelial cells, and sometimes loss of normal architecture is visible in the form of whorls or keratin “pearls”.
Differential diagnosis Eosinophilic keratitis is an uncommon proliferative disease of the third eyelid. It may also be associated with corneal disease and cytology is characteristically in the form of eosinophilic infiltrates. Other neoplastic disease. Hemangiomas are not as common, have a smoother surface, and appear as a darker red to purple-colored mass.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Treatment
Differential diagnosis
Surgical excision with good margins is required to ensure complete removal. The lesions can sometimes invade deep into the extra-ocular tissues by the time the lesion is recognized.
Squamous cell carcinoma usually causes more disfigurement of the third eyelid due to proliferation and ulceration.
Cryosurgery using liquid nitrogen or nitrous oxide with double freeze thaws and slow controlled thawing can be effective for small tumors less than 0.5 cm diameter. Maximal destruction of tumor cells occurs when temperatures of between −20˚C to −40˚C are achieved at the center of the tumor. b-irradiation with strontium 90 can be effective if available.
EOSINOPHILIC KERATOCONJUNCTIVITIS** Classical signs ● ●
Pink to whitish plaque-like thickening of the third eyelid. ± Similar lesions on the cornea.
Clinical signs Appears as pink to whitish plaque-like thickening of the third eyelid. Similar lesions may appear on the cornea in some cats. The pathogenesis is unknown, but is postulated to involve insect bite hypersensitivity or herpesvirus infection in some cats. Generally there is not a strong association with the presence of other feline eosinophilic disease.
Other neoplasms such as hemangioma have a characteristic appearance. Chronic Mycoplasma and Chlamydophila felis infection may appear similar in some cats, but can be differentiated on cytological examination of Wright– Giemsa-stained slides, immunofluorescent antibody and PCR.
Treatment Oral corticosteroids: Prednisolone 5 mg orally q 12–24 h, with dose reducing as effect is achieved. Oral progestagens at a low dose (e.g. megestrol acetate 5 mg twice weekly) should be used only in cases refractory to oral prednisolone. Beware of possible side effects such as insulin resistance, diabetes and obesity. Topical corticosteroids are usually contraindicated because of an underlying association with ocular herpesvirus infection. These drugs may potentiate the herpesvirus infection by local immunosuppression. Treat the underlying cause if identified, e.g. treat the ocular herpesvirus infection.
SYMPATHETIC NEUROPATHY OF THE THIRD EYELID (HORNER’S SYNDROME)** Classical signs
Diagnosis
●
Tentative diagnosis is based on the presence of typical lesions on the third eyelid and cornea.
●
Cytological examination of deep scrapings of the lesion or histopathology of a biopsy specimen demonstrate an infiltrate of plasma cells and lymphocytes with variable numbers of eosinophils. Eosinophils may not always be the most numerous cell type. Tests for herpesvirus infection, e.g. in situ PCR and (see The Cat With Ocular Discharge or Changed Conjunctival Appearance, page 1213, for more details).
● ● ●
Usually unilateral. Non-painful prominence of the third eyelid. Miosis of the ipsilateral pupil. Upper lid ptosis. Enophthalmos.
Pathogenesis Protrusion of the third eyelid occurs where there is disruption of the sympathetic neural pathways innervating the smooth muscle of the third eyelid (Horner’s syndrome). Disruption may occur anywhere along the pathway including in the thalamus, cervical spinal cord
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long tracts, T1–T3 spinal nerves or nerve roots, ascending pre-ganglionic fibers, cranial cervical ganglion and sympathetic post-ganglionic fibers in middle ear or orbit. Less commonly protrusion is the result of dysfunction of the smooth muscle fibers innervated by the sympathetic nerve. More common causes in the cat include: ● Middle ear disease especially nasopharyngeal polyps. Nasopharyngeal polyps arise in the middle ear and emerge into the external ear canal or nasopharynx. Typically they occur in young cats (< 5 years), but any age can be affected. ● Disruption of ascending sympathetic pathways in the neck due to injury or inflammation associated with fight wounds. ● Injury to nerve roots of T1–T3 associated with forelimb trauma, usually from motor vehicle accidents. ● Anterior thoracic cavity disease, e.g. mediastinal lymphoma. Rarely, is third eyelid protrusion the result of nerve damage within the brain or spinal cord, or smooth muscle disease.
Clinical signs Usually there is a unilateral, non-painful prominence of the third eyelid, together with other signs of sympathetic denervation, i.e. miosis, upper lid ptosis (“drooping”), enophthalmos. Other signs may be present in some cases, which may enable further localization of the lesion, e.g. ● An abscess or cellulitis of cervical soft tissue structures suggests disruption of ascending preganglionic fibers. ● Signs of middle or inner ear disease such as a head tilt or circling. Nasopharyngeal polyp may be seen as a fibrous mass emerging into the external ear canal, or cause noisy breathing, dyspnea with or without nasal discharge, sneezing or coughing and gagging. ● Ipsilateral forelimb lameness may occur from damage to nerve roots or nerves innervating the leg. Radial nerve paresis or paralysis may occur concurrently with avulsion of T1–T3 nerve roots if C8 or T1 nerve roots are injured. If the musculocutaneous nerve roots (C5–7) are also injured, the
elbow cannot be flexed or the paw picked up, resulting in excoriation of the dorsum of the paw. Muscle atrophy is apparent within 5–7 days of injury to the motor nerve roots. Damage to C7–T1 may also result in loss of the ipsilateral cutaneous trunci (panniculus) reflex.
Diagnosis Any cat with an apparently non-painful, non-inflamed prominent third eyelid, which also has miosis, upper lid ptosis and enophthalmos should be suspected as having Horner’s syndrome. Pharmacological testing with sympathomimetics is controversial, and the indirect-acting sympathomimetic hydroxyamfetamine is no longer available in some countries. Reliable diagnostic protocols are not available, however a rapid (within 5–8 minutes) reversal of signs following the administration of one drop of 10% phenylephrine is suggestive of post-ganglionic denervation hypersensitivity, indicating that the lesion is somewhere rostral to the cranial cervical ganglion. Anatomically this corresponds to localization of the lesion in the middle ear or orbital structures rostral to the middle ear. The response should always be compared with that in the contralateral normal eye. Lesion localization will not be possible in many cases, and many cases seem to be idiopathic.
Differential diagnosis Third eyelid dysautonomia (Haw’s) is always bilateral, and is not associated with other signs of sympathetic denervation. Horner’s syndrome is almost always unilateral.
Treatment Where possible, treatment should be directed at the associated problems which may be causing interruption of sympathetic pathways. The disfigurement created by Horner’s syndrome can be reversed by frequent (at least 2–3 times daily) application of one drop of 10% phenylephrine in the affected eye. This treatment only alters the appearance of the eye and does nothing else for the cat’s well-being,
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
except that vision might be improved where the third eyelid prominence and enophthalmos is extreme, causing most of the globe to be covered by nictitans.
Clinical signs
Prognosis
It is associated with ipsilateral signs of ocular pain, for example, enophthalmos, blepharospasm, corneal disease, pupil miosis or anterior uveitis.
Depending on the cause many cases may resolve over time as denervated smooth muscle re-innervates, provided that oculosympathetic fibers are not totally destroyed.
TRAUMA TO THE THIRD EYELID MARGIN* Classical signs ● ●
Notch-like or linear tears arising from the third eyelid margin. Usually unilateral, with the contralateral eye unaffected.
The third eyelid is prominent because of retraction of the globe, associated with ocular pain.
Diagnosis Diagnosis is based on signs of ocular pain together with prominence of a normal-appearing third eyelid.
Differential diagnosis Horner’s syndrome and Haws are usually nonpainful. Horner’s syndrome, tetanus and feline dysautonomia each have their own specific associated clinical signs, which are more suggestive of that particular condition.
Clinical signs Trauma to the third eyelid may result in notch-like or linear tears starting at the margin of the third eyelid. These occur most commonly from cat fights. Third eyelid trauma may be associated with other ocular signs, when seen in the acute stages, e.g. conjunctival chemosis and ocular discharge (see The Cat With Ocular Discharge or Changed Conjunctival Appearance, page 1211).
Treatment Treat the cause of the ocular pain as indicated.
THIRD EYELID PROMINENCE RELATED TO SEVERE WEIGHT LOSS* Classical signs ●
Diagnosis Diagnosis is based on the clinical signs, and the history of unilateral third eyelid notch or tear occurring after a possible fight with another cat.
THIRD EYELID PROMINENCE RELATED TO OCULAR PAIN* Classical signs ● ●
Third eyelid prominence. Associated with other ipsilateral signs of ocular pain, e.g. enophthalmos, blepharospasm, corneal disease, pupil miosis.
● ●
Signs of generalized muscle wasting associated with chronic disease. Thin face with signs of muscle wastage around the lateral aspects of the orbit. Bilaterally symmetrical third eyelid prominence without miosis or upper lid ptosis.
Clinical signs Typically these cats have a bilaterally symmetrical third eyelid prominence due to marked enophthalmos, and there are no other signs normally associated with other causes of third eyelid prominence such as miosis or upper lid ptosis. Generalized whole-body muscle wasting is present in association with signs of other organ system disease,
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e.g. chronic renal failure, inflammatory bowel disease or hyperthyroidism.
the cornea is impaired because of an uneven eyelid margin.
Third eyelid prominence occurs secondary to loss of orbital fat and enophthalmos.
Diagnosis
Diagnosis
Diagnosis is initially based on the appearance of the lesion, which varies according to the type of tumor.
Diagnosis is based on the generalized body muscle and fat loss, in association with the pronounced enophthalmos and third eyelid prominence.
Definitive diagnosis is by cytological and histological examination.
FELINE DYSAUTONOMIA OTHER NEOPLASTIC DISEASE OF THE THIRD EYELID* (ADENOMA, ADENOCARCINOMA, MAST CELL TUMOR, LYMPHOMA, HEMANGIOMA)
Classical signs ● ●
Classical signs ● ●
Mass or erosive lesion involving the third eyelid. Ocular discharge.
Clinical signs Tumors of the third eyelid appear as a mass or erosive lesion involving the third eyelid. Appearance depends on the type of tumor, which includes lymphoma, hemangioma, mast cell tumor, adenoma and adenocarcinoma. ● Hemangiomas are rare, are usually dark red to purple in color, and are fragile with a tendency to hemorrhage. ● Lymphoma will usually cause more generalized swelling of the third eyelid and the peri-orbital tissues, and may be associated with other systemic signs of multricentric lymphoma. ● Mast cell tumors can form either well- or poorly circumscribed areas of swelling in the eyelid. They appear as rapidly growing nodular tumor, often with poorly defined borders, and variable surface ulceration. ● Adenomas or carcinomas are seen as a nodular or diffuse mass causing localized thickening of the eyelid. The tumor may have an ulcerated surface. The neoplastic mass may cause increased ocular discharge because of third eyelid dysfunction. The normal distribution of the precorneal tear film across
●
Unilateral or bilateral third eyelid prominence. Acute onset of anorexia and depression. Other signs of autonomic dysfunction such as keratoconjunctivitis sicca, mydriasis, anisocoria, dry nose or mouth, bradycardia, constipation, megaesophagus, urinary or fecal incontinence.
See main references on page 792 for details (The Constipated or Straining Cat).
Clinical signs Third eyelid prominence, in association with any of a range of other systemic signs suggestive of autonomic dysfunction including keratoconjunctivitis sicca, dilated non-responsive pupils, anisocoria, dry nose and/or mouth, bradycardia, constipation, megaesophagus and urinary or fecal incontinence. Typically, the onset of signs is acute over 48 h and associated with depression and anorexia.
Diagnosis Diagnosis is based on signs of generalized autonomic dysfunction. Condition is rare or at least uncommon, and most frequent in UK. Definitive diagnosis is based on the demonstration of characteristic ultrastructural lesions within cell bodies in autonomic ganglia at post mortem.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Differential diagnosis Abnormality of the third eyelid without the presence of other signs of autonomic dysfunction would suggest localized sympathetic dysfunction such as Horner’s or Haws syndrome.
Treatment No definitive treatment is available. Prognosis is generally guarded to poor, however supportive treatment is reported to be variably effective.
sue environment to support toxin production, and the number of organisms present. Tetanus is rare in cats, because they are more resistant to the toxin than humans and horses. This innate resistance is related to the inability of the toxin to penetrate and bind to nervous tissue, and likely accounts for the frequency of localized signs in cats. Tetanus has occurred after routine surgery (such as ovariohysterectomy), fetal death during pregnancy, and trauma. Tetanus may occur in young cats associated with a gum wound secondary to losing a deciduous tooth.
TETANUS Classical signs ● ● ●
Bilateral third eyelid prominence. Contraction of facial muscles, increased tone in muscles of mastication (“lockjaw”). Stiffness of one or more limbs which worsens with stimulation.
Pathogenesis Signs of tetanus result from the toxin produced by Clostridium tetani, a spore-forming, Gram-positive rod. C. tetani is found in the soil, and also occurs as part of the normal gastrointestinal tract flora of some animals. Spores of the Clostridium tetani bacillus enter the body commonly via surface wounds. The toxin, tetanospasmin, is produced during cell growth, sporulation and lysis, if there is a suitable anaerobic environment for the bacteria. The toxin migrates along nerve axons from a local wound, to sites of action in the central nervous system, where it initially binds to presynaptic inhibitory motor nerve endings. The effect of the toxin is to block the release of inhibitory neurotransmitters (glycine and gamma-amino butyric acid) across the synaptic cleft. This results in uninhibited muscle contraction. The incubation period for signs to develop varies from 3–21 days after an injury, depending on the proximity of the injury to the CNS, the ability of the local tis-
Clinical signs Signs of tetanus may be localized or generalized, or may begin with localized signs and progressively involve more muscle groups over a week or more, and become generalized. Generalization is more likely if there is inadequate wound management, or inadequate antibiotic therapy. Diagnosis may be difficult in the early stages of the disease when characteristic signs of generalized tetanus are absent. Classical signs of generalized tetanus include bilateral third eyelid prominence in association with contraction of the facial muscles giving the appearance of a “sardonic smile”, and increased tone in the muscles of mastication (“lockjaw”). The cat may have a “startled” appearance. Focal tetanus results in stiffness of the muscles in closest proximity to the wound, and is often evident as stiffness of one or two limbs. In many cats, a neglected wound with necrotic tissue is found, suggesting a site for toxin production. Tetanus may be associated with infection of the female reproductive tract, and may produce local signs in the pelvic limbs. The history of a penetrating or neglected wound, and the presence of persistent involuntary muscle rigidity in a mentally alert cat is highly suggestive of tetanus.
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If there is generalized muscle stiffness, the cat may have an increased temperature associated with the muscle contraction.
Diagnosis Diagnosis is based on the characteristic clinical signs. EMG testing of affected muscles is strongly suggestive of tetanus if it demonstrates persistent spontaneous motor unit potentials.
Differential diagnosis Any condition which causes bilateral third eyelid prominence such as haws or dysautonomia should be considered. However, facial muscle or limb rigidity is not seen with these conditions. Mild hypocalcemia in late pregnancy or following whelping could be confused with tetanus, especially as the reproductive tract may be a site of infection and toxin production. Rapid response to intravenous calcium in pregnancy-associated hypocalcemia will rule out tetanus. Meningoencephalitis or encephalopathy including thiamine deficiency may occasionally have tetanic spasms worsened with touch or sound. In these animals mentation is usually depressed and other neurological signs are evident.
Treatment Treatment involves appropriate antibiotic therapy, wound care, supportive treatment, and use of tetanus antitoxin. It is important to debride necrotic tissue, so the tissue environment is less attractive for persistence of the organism and toxin production. Antibiotics with anaerobic activity especially metronidazole (10 mg/kg, q 8 h), and those belonging to the penicillin group, e.g. amoxicillin or amoxycillin/clavulanate are indicated to prevent further proliferation of bacteria in the wound. ● Metronidazole has been shown to be superior to penicillin G and tetracycline. It is bactericidal against most anaerobes and achieves effective therapeutic concentrations even in anaerobic tissues.
Tetanus antitoxin binds to circulating toxin, and cannot dislodge toxin within peripheral nerves. Its main purpose is to neutralize circulating toxin outside the nervous system. If the signs are localized and non-progressive, administering tetanus antitoxin systemically is not likely to be beneficial, and is associated with a risk of anaphylaxis. ● The dose of antitoxin is usually about 1000 U/kg IV administered slowly over 5–10 minutes, with some (1000 U) injected locally in the wound. As most tetanus antiserums are generally prepared in equines, consideration should be given to the pre-emptive use of corticosteroids and antihistamine to prevent possible anaphylaxis. Give a test dose (0.1–0.2 ml) intradermally or subcutaneously 15–20 minutes before IV administration and check for a wheal. Muscle relaxants such as diazepam can be used to control the muscle rigidity and make the cat more comfortable. Efficacy of the drug varies between individual cats. Alternatively, small doses of acepromazine (1.25–2.5 mg/cat PO q 6 hours as required), chlorpromazine (IV) or phenobarbital may be effective in reducing muscle stiffness. Other supportive treatment should be given as indicated, e.g. alimentation, intravenous fluids. Keep the cat in a quiet, dark area to reduce the muscle spasms, which are stimulated by touch or sound Difficulty urinating or defecating may occur, and needs to be managed.
Prognosis The prognosis is generally good with appropriate treatment, and full resolution of signs usually occurs within 2–3 months. Prognosis is poorer if signs develop very rapidly.
PROLAPSED GLAND OF THE THIRD EYELID Classical signs ● ● ●
Pink to red mass protruding from behind the third eyelid. Variable inflammation and discharge. Rare and only reported in Burmese cats.
66 – THE CAT WITH AN ABNORMAL THIRD EYELID
Clinical signs
Clinical signs
Pink to reddish mass with a smooth conjunctival surface protrudes from behind the leading edge of the third eyelid margin.
Everted third eyelid margin occurs because of folding of the cartilage of the third eyelid. This condition should be distinguished from a prolapsed gland of the nictitans.
Prolapse may be accompanied by variable degrees of inflammation and discharge, ranging from mucoid to mucopurulent. Rare in cats compared with dogs, and reported only in Burmese cats.
Diagnosis Diagnosis is based on the appearance of the mass. Differential diagnosis would be a tumor or a folded (everted or inverted) third eyelid cartilage, also rarely reported, and only in Burmese cats.
Rare in cats. Reported only in Burmese cats.
Diagnosis Diagnosis is based on the appearance of the third eyelid margin. Usually there is no sign of a fleshy mass protruding from behind the third eyelid.
Treatment Resection of the folded section of cartilage will enable straightening of the third eyelid.
EVERTED NICTITANS CARTILAGE Classical signs ● ●
Folded everted third eyelid margin. Rare and only reported in Burmese cats.
RECOMMENDED READING Glaze MB, Gelatt KN. Feline ophthalmology. In: Scagliotti R (ed) Comparative Neuro-ophthalmology. In: Gelatt KN (series ed) Veterinary Ophthalmology, 3rd edn. Baltimore, Maryland, Lippincott, Williams & Wilkins, 1999, pp. 1004–1010, 1366–1370. Ketring KL, Glaze MB. Atlas of Feline Ophthalmology. Trenton, New Jersey, Veterinary Learning Systems, 1994, pp. 69–76. Sharp NJH, Nash AS, Griffiths IR. Feline dysautonomia (the Key-Gaskell syndrome): a clinical and pathologic study of forty cases. J Small Anim Pract 1984; 25: 599–615.
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