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711.e2 Optic Neuritis

Optic Neuritis Client Education
Sheet
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○ Feline: viral (feline infectious peritonitis
BASIC INFORMATION
[FIP]), systemic mycoses, protozoal (T. • Cortical (central) blindness (normal pupillary
light reflexes; normal fundic exam; possible
Definition gondii) additional neurologic abnormalities)
Inflammation of one or both optic nerves leads • Neoplastic: lymphoma, orbital neoplasia • Papilledema: edema of the optic nerve head
to vision loss. This acquired condition may • Traumatic: leading to orbital cellulitis or (no blindness) secondary to increased intra-
be primary or secondary to systemic central abscess cranial pressure
nervous system (CNS) disease. The optic nerve • Nutritional: vitamin A deficiency (rare) • Pseudopapilledema: excessive myelin of the
is surrounded by meninges and communicates • Secondary to orbital inflammation, menin- optic nerve head; variation of normal (no
with the subarachnoid space. gitis, scleritis, retinitis, posterior uveitis blindness)
Synonym DIAGNOSIS Initial Database
Papillitis (inflammation of the optic disk) • Complete ophthalmic exam (p. 1137)
Diagnostic Overview ○ Menace response and dazzle reflex (absent
Epidemiology The diagnosis is suspected with loss of vision, in affected eyes)
SPECIES, AGE, SEX fixed and dilated pupil(s), and abnormal ○ Pupillary light reflexes (PLRs): if bilateral
Dogs and cats; more commonly seen in middle- appearance of the optic disk(s). A complete optic neuritis, pupils typically are fixed
aged dogs physical and neurologic exam is para- and dilated, producing negative direct and
mount. Because the mainstay of treatment consensual PLRs; if unilateral, direct PLR
Clinical Presentation is rapid immunosuppression, any evidence absent in affected eye and consensual PLR
DISEASE FORMS/SUBTYPES of systemic disease has great importance absent in contralateral eye.
• Intraocular: inflammation of the optic disk; for diagnostics and treatment. A normal ○ Assessment of IOP; rule out acute primary
detected with ophthalmic exam electroretinogram (ERG) further supports the glaucoma (IOP > 30 mm Hg).
• Orbital: inflammation of the retrobulbar/ diagnosis of optic neuritis. Evidence of sterile ○ Examine posterior segment of eye (i.e.,
orbital portion of the optic nerve; not inflammation in cerebrospinal fluid (CSF) fundus) using direct and/or indirect
detectable with ophthalmic exam is consistent but not required. To confirm ophthalmoscopy after pupillary dilation
• Intracranial: inflammation of the portion of orbital/intracranial optic neuritis, advanced with topical tropicamide 1% if needed.
the optic nerve after its exit from the orbit imaging such as MRI is required. Because • Neurologic exam (p. 1136)
at the optic foramen and to the level of the treatment (corticosteroids) may alter the
optic chiasm; not detectable with ophthalmic results of advanced diagnostic tests, prompt Advanced or Confirmatory Testing
exam but may be associated with neurologic referral to a veterinary ophthalmologist or • ERG to assess retinal function: normal in
deficits neurologist should be considered for optic optic neuritis
neuritis suspects. • CBC and serum chemistry panel may show
HISTORY, CHIEF COMPLAINT evidence if systemic disease.
Sudden blindness of one (rare) or both Differential Diagnosis • Thoracic radiographs may show evidence of
(common) eyes Unilateral: systemic mycoses or metastatic neoplasia.
• Acute primary glaucoma (elevated intraocular • MRI or CT (p. 1132)
PHYSICAL EXAM FINDINGS pressure [IOP] > 30 mm Hg) and signs of ○ Advanced imaging can help detect inflam-
• Blindness if bilateral glaucoma matory and neoplastic processes along the
• Absent unilateral or bilateral menace Bilateral: optic nerve and optic chiasm. MRI is more
response(s), pupillary light and dazzle reflexes • Sudden acquired retinal degeneration sensitive than CT for optic nerve lesions.
• Fixed and dilated pupil (unilateral or syndrome (SARDS) in dogs: normal • CSF analysis (pp. 1080 and 1323): may be
bilateral) fundic (e.g., posterior segment) exam abnormal, depending on the cause of optic
• Swollen, edematous, and hyperemic optic early with flat-lined ERG revealing no neuritis
disk if intraocular portion of optic nerve retinal function versus ERG waveforms • Histopathologic evaluation of tissue (±
(i.e., optic disk) is affected with possible confirming retinal function in acute optic immunohistochemical staining) may confirm
peripapillary retinal edema, granulomas, neuritis cause (e.g., canine distemper virus) but is
and/or hemorrhages • Immune-mediated retinitis in dogs: uncom- usually only performed as part of necropsy.
• Normal-appearing optic disk if the inflam- mon to rare; normal fundic exam possible
mation is limited to the orbital and/or early on; low retinal function on ERG; vision TREATMENT
intracranial portions of the optic nerve may return with oral prednisone 1 mg/kg PO
• Small, pale optic disk (i.e., optic disk atrophy) q 24h in combination with oral doxycycline Treatment Overview
in advanced cases 5 mg/kg PO q 24h Prompt antiinflammatory therapy is warranted
• Depending on the cause (see Etiology and • Enrofloxacin toxicosis in cats: optic disk for this condition, but prognosis for return of
Pathophysiology below), systemic abnormali- atrophy and retinal degeneration noted on vision remains poor. Usually, treatment needs
ties may be present. fundic exam versus usually normal-appearing to be initiated within 24 hours for return of
retina with optic neuritis vision.
Etiology and Pathophysiology • Neoplasm at the optic chiasm (advanced
• Idiopathic imaging such as MRI to differentiate from Acute and Chronic Treatment
• Immune-mediated: granulomatous menin- bilateral orbital/intracranial optic neuritis) • Treat the underlying cause if determined.
goencephalitis (GME) • Ivermectin toxicosis in dogs: retinal edema • Idiopathic or traumatic (e.g., noninfectious)
• Infectious may be apparent in the nontapetum on cause: prednisone 1-2 mg/kg PO q 12h for
○ Canine: viral (canine distemper; tick-borne fundic exam; low retinal function on ERG; 7-14 days; then 0.5-1 mg/kg PO q 12h for
encephalitis), systemic mycoses, protozoal may respond to intravenous lipid infusion 7-14 days; then gradual decrease to reach a
(Toxoplasma gondii; Neospora caninum) therapy (pp. 566 and 1127). maintenance dosage
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