optho clinical Flashcards
what sort of patients get optic neuritis?
young white women
patient presents with:
- Pain with eye movement
- Unilateral decrease in vision developing over 1-2 weeks
- Relative afferent pupillary defect (RAPD)
- Optic disc may be swollen
optic neuritis
what patterns of visual field defects can you see in optic neuritis
o May be altitudinal
o May be central scotoma
o May be cecocentral pattern (central scotoma that has expanded to include the blind spot)
retrobulbar neuritis
describe optic neuritis that occurs in the portion of the optic nerve posterior to the globe
o Optic neuritis with a normal appearing optic disc
o Associated with multiple sclerosis
o Vision ranges from okay (> 20/40) to terrible (< 20/200)
patients with optic neuritis should have a brain MRI to assess for?
multiple sclerosis
-would see enhancement of optic nerve and white matter lesions
Treatment of patients with optic neuritis who have…
1) brain evidence of MS
2) no brain evidence of MS
1) IV corticosteroids +/- IFNb
2) no treatment, will resolve on it’s own
* do not treat with oral corticosteroids (will make optic neuritis worse)
papilledema
o Elevation of the optic nerve is more marked than in retrobulbar neuritis and is bilateral
o Due to increased intracranial pressure
o Normal visual acuity
o Normal pupillary response
o Intact visual field, with the exception of an enlarged blind spot in each eye
who gets non-arteritic ischemic optic neuropathy?
- Typical age of onset is 50s-60s
- Risk factors include hypertension, atherosclerosis, diabetes, hyperlipidemia, smoking and sleep apnea
- Predisposing factors include reduced cup-to-disc ratio, optic nerve drusen and increased intraocular pressure
what is the mechanism of vision loss in non-arteritic ischemic optic neuropathy?
• Results from occlusion of the posterior ciliary arteries (in the lamina cribrosa area, behind the optic nerve head)
clinical presentation of non-arteritic ischemic optic neuropathy
- Sudden, painless, unilateral loss of vision (often occurs upon awakening)
- Swollen optic nerve with disc edema occurs within 24 hours after the onset of visual symptoms
- It is NOT NAION if the optic nerve isn’t swollen
- The contralateral eye will have a small, crowded disc
- Visual defects tend to be altitudinal, with inferior defects being worse than superior defects
- NO prodrome
clinical course and managment of non-arteritic ischemic optic neuropathy
clinical course:
• The loss of vision stays stable and generally does not progress
• Some visual recovery may occur
management: assess and treat underlying d/o, smoking cessation
Who gets temporal arteritis (arteritic ischemic optic neuropathy)?
• Exclusively in persons over 55 years of age (incidence increases with age)
what is the mechanism of disease in temporal arteritis (arteritic ischemic optic neuropathy)?
• Related to autoimmune response to internal elastic lamina of medium size arteries, caused by ulcerated atherosclerotic plaques
what is the clinical presentation of temporal arteritis (arteritic ischemic optic neuropathy)?
- May have sudden, severe, initially unilateral loss of vision which can quickly become bilateral
- Headache or pain over the temporal arteries
- Jaw claudication – facial muscle pain with chewing (most sensitive and specific finding)
- Weight loss, fever of unknown origin, anemia
- Polymyalgia rheumatica
what lab values would you expect in temporal arteritis?
what do you need for a definitive diagnosis?
- High ESR (always order Westergren ESR method)
- High C-reactive protein
- Thrombocytopenia
Temporal arterial biopsy (>2cm sample)
• Ordered within 2 weeks of presentation
• But do NOT wait for the results before initiating therapy
• If a biopsy is negative, repeat the biopsy in the contralateral temporal artery
what is the clinical course and treatment of temporal arteritis?
clinical course:
• Visual loss tends to be permanent
• If diagnosis is missed at early presentation in a single eye, it can often lead to bilateral blindness within hours to days
treatment:
• Immediate, high dose corticosteroids (IV methylprednisone, followed by oral prednisone)
• Do NOT wait for biopsy results; treat empirically and immediately if there is clinical suspicion!!!
• Steroids are given long term and tapered very slowly, under the management of a rheumatologist
what is the most common cause of unilateral or bilateral proptosis in adults?
thyroid related orbitopathy
what is the mechanism of disease in thyroid orbitopathy?
o Autoimmune disease where antibodies are formed against components in the orbit, especially (but not only) the extraocular muscles
• Tendons are spared
• Antibody deposition results in secondary edema
• In addition, cellular inflammatory response causes additional edema and eventual fibrosis
what do you need for the diagnosis of thyroid orbitopathy?
• Eyelid retraction + 1 of the following: • Thyroid dysfunction • Exophthalmos • Optic nerve dysfunction • Extraocular motility involvement OR • Thyroid dysfunction + 1 of the following: • Exophthalmos • Optic nerve dysfunction • Extraocular movement involvement
treatment of thyroid orbitopathy
o 1st-line systemic treatment for INFLAMMATORY PHASE is oral corticosteroids
• Considered a short-term, temporizing measure for patients in the inflammatory phase of thyroid-related orbitopathy
• Corticosteroids have little effect on the exophthalmos or on the lid retraction
o 2nd-line systemic treatment for INFLAMMATORY PHASE is low dose radiotherapy
• Radiotherapy is given to the retro-orbital region
o In cases of severe involvement of the optic nerve, intravenous pulse therapy with methyprednisone has been shown to help (short-term)
o For severe optic neuropathy with visual loss and proptosis, surgery is preferred
• Orbital decompression
• Strabismus surgery
• Eyelid surgery
o Local treatment of thyroid-related orbitopathy includes supportive measures to prevent corneal exposure, such as the following:
• Topical lubricants
• Moisture chambers
• Tarsorrhaphy
o Diplopia can be helped with prisms and occlusion
o Urge smoking cessation! (smoking makes thyroid-related orbitopathy worse)
what is the mechanism of disease of idiopathic inflammatory orbital pseudotumor
diffuse inflammation involving any structure of the eye (including tendons! vs thyroid orbitopathy)
frequent cause of proptosis in adults
orbital psuedotumor
clinical presentation of orbital pseudotumor
o Usually sudden
o Usually accompanied by severe pain
o In adults, it is typically unilateral
o In children, it can be bilateral and associated with systemic symptoms (e.g. fever malaise), mimicking bacterial orbital cellulitis
o In some cases, “orbital apex syndrome” can be present and vision can be decreased because of compression
o Although infrequent, it can affect the paranasal sinuses
o There is a rare sclerosing variant can lead to blindness and necessitate orbital exenteration
clinical course and treatment of orbital pseudotumor
clinical course:
• Clinical Course
o Recurrences are very common
o Long-term sequelae can include any of the following: Diplopia, Exophthalmos, Visual loss
Treatment:
o Oral prednisone, with slow tapering over several weeks
• The response to corticosteroids is extremely dramatic, with the patient often feeling better after a single dose!
o If pseudotumor continues to recur, low-dose radiation should be considered
what tests can you do to confirm the diagnosis of myasthenia gravis?
o Edrophonium injection
• Provides a quick response in positive patients
o Applying an ice pack over a ptotic eyelid will provide temporary resolution of the ptosis is myasthenia gravis is the causative etiology
o Note: acetylcholine receptor antibodies are negative in up to 50% of patients who only have ocular myasthenia gravis
o If acetylcholine receptor antibody test is negative and suspicion, a single fiber EMG can be performed
o If diagnosis is confirmed, a chest CT should be performed, to check for a thymoma
what is the treatment for myasthenia gravis?
o Pyridostigmine (acetylcholinesterase
key features of conjunctivitis
moderate discharge
no pain
no decreased vision
normal pupil
key features of keratitis
=inflammation of cornea \+/- discharge \+ pain \+decreased vision nl pupil
key features of iritis
=inflammation b/t lens and cornea - discharge \+ pain \+ dec. vision smaller pupil
key features of glaucoma
(acute angle closure) - discharge \++pain \++ dec vision dilated and fixed pupil
Pt presents with red eyes. There is watery discharge, tender palpable preauricular node. The patient recently recovered from a URI
viral conjunctivitis (highly contagious, spread hand to eye) -tx: cool compresses and drops
Pt presents with red eyes. There is bilateral itching of eyes. There is a stringy mucous discharge. He has a hx of asthma
allergic conjunctivitis
tx: cool compresses, topical or systemic antihistamines, NSAIDS, mast cell stabilizers
patient presents with red eyes and purulent discharge of the eyes.
bacterial conjunctivitis
tx: quinolones for broad spectrum coverage including psuedomonas, (cipro, ofloxacin, levofloxacin, moxifloxacin)
patient presents with a red eye, that is painful and sensitive to light. He wears contacts. You also notice a white spot on the cornea (corneal epithelial defect).
bacterial ulcer
1) mild-moderate (peripheral): topical fluoroquinolones
2) moderate-severe (central): topical fortified antibiotics (tobramycin/gentamycin + cefazolin/vancomycin)
A patient presents with red eye accompanied by moderate pain. You do a topical fluorescein stain and notice a tree branching area of staining
HSV keratitis
- aggravated by topical steroids (don’t give!)
- tx with topical or oral antivirals
- tends to recur, may result in permanent scarring
Iritis
signs/sx: circumcorneal injection, photophobia secondary to blunt trauma, keratitis
-assoc/ w/ systemic diseases (sarcoidosis, CT conditions) or idiopathic
Topical anesthetics assoc/ w/
severe corneal infections/ulcerations
never perscribe!
topical steroids in eye assoc w/
complications including glaucoma, cataracts, enhancing HSV infection
chlamydia conjunctivitis
neonates=systemic disease
sexually active adults
tx: systemic erythromycin, tetracycline, azithromycin
blepharitis
inflammation of eyelid margin, assoc w/ dry eyes
-tx: warm compress, eyelid scrub, antibiotic gel/ointment, systemic tetracylclines
opthalmia neonatorum (neonatal conjunctivitis) DDX
- chemical conjunctivitis (silver nitrate prophylaxis)
- chlamydia
- gonococcus
- staph, strep, pseudomonas, HSV
prophylaxis is erythromycin ointment
contact lens complications
- giant papillary conjunctivitis
- tight contact lens syndrome
- toxic/allergic rxn to chemicals in contact lens solution
- bacterial corneal ulcers (esp. pseudomonas)
- acanthamoeba keratitis
Red eye danger symptoms
- dec. vision
- pain
- photophobia
Red eye danger signs
- corneal fluorescein staining
- corneal edema
- circumcorneal injection
- abnormal pupil size or reaction (abnormal eye pressure)
urgent red eye conditions
- corneal infection
- iritis
- acute angle closure glaucoma
- orbital cellulitis
- trauma: hypema (blood in anterior chamber) or laceration
one way to differentiate optic neuritis vs papilledema
papilledema has bilateral swelling of optic disc vs optic neuritis is unilateral
which drug increases the risk of recurrent optic neuritis
oral prednisone
patients with optic neuritis and brain MRI findings should be treated with
IV methylprednisone
older patient with hypertension, diabetes, and atherosclerosis develops monocular, sudden, painless visual loss. There is evidence of disc edema. Dx?
non-arteritic ischemic optic neuropathy
no effective treatment
-some visual function can be recovered
patient (age>55) presents with sudden, severe, unilateral vision loss and jaw claudication
arteritic ischemic optic neuropathy
tx is immediate, high dose corticosteroids (don’t delay b/c can lead to bilateral vision loss quickly)
-visual loss tends to be permanent
treatment of myasthenia gravis
pyridostigmine
what is the leading cause of vision loss in diabetics?
macular edema
sx: blurred or distorted vision and poor night vision
describe diabetic retinopathy
microvascular disease; early histo findings include capillary damage characterized by thickening of basment membrane and pericyte dropout mediated by VEGF
what would you see in mild non-proliferative diabetic retinopathy? What about severe?
mild: o Microaneurysms o Dot and blot hemorrhages o Hard exudates o Cotton wool spots (small retinal infarctions) o Macular edema
moderate: o Increased hemorrhages o Dilated and beaded veins o Macular ischemia o Intraretinal microvascular abnormalities
what happens in proliferative diabetic retinopathy?
o Capillary nonperfusion leads to neovascularization
o Fragile new vessels tend to bleed
o Fibrous tissue grows along new vessels→touches vitreous body→vitreous hemorrhages→Floaters, traction retinal detachment (lead to blindness)
risk factors for presence of diabetic retinopathy?
o Duration of disease o Age of onset o Glycemic control o BP control o Serum lipid levels
medical management of diabetic retinopathy
o Excellent glycemic control (HbA1c<130/85
surgical treatment of diabetic retinopathy
o Laser treatment—panretinal photocoagulation
o Intravitreal injection of triamcinolone (can cause cataracts and glaucoma so reserved for patients with worst vision and unresponsive to other therapy)
o Vitrectomy surgery: remove vitreous and fibrovascular tissue; indicated in non-clearing vitreous hemorrhage and traction retinal detachment
