Download Ophthalmology Review 2014

Maryam Abtahi
Paul Yan
Trauma
And red eye
In a patient with alkali chemical
burn to the eye, what is your
first action,
Irrigate eye with normal saline
Next steps:
Check PH of the conjunctival fornix
Check vision
Check pupils for afferent pupillary defect
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Chemical burn :
Acid , coagulate proteins and inhibit further
corneal penetration
Alkali, worse prognosis
Never try to neutralize
Very severe alkali burn or if not get
irrigated early
If a ruptured globe is suspected,
the first action to take is to:
Shield the eye
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R/o intraocular foreign body with orbital CT
scan, specially in metal on metal hammering
NPO
IV antibiotic
Tetanus status
Need to be referred,
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Decreased vision
Shallow anterior chamber
Hyphema
Abnormal pupil
Ocular misalignment
Retinal damage
The best study to evaluate a patient with
intraocular foreign body is
CT scan of the orbits
Management includes surgical repair only
in
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Fracture of more than 50% of the floor,
Diplopia not improving,
Enophthalmos more than
2 mm
Blow out fracture, white eye
 In children , might cause muscle entrapment
and ischemia,
 Risk of bradycardia .
 One of the ophthalmology emergency,
Corneal abrasion in
contact lens wearer
Never patch the eye
AB
Refer to an ophthalmologist
The risk of ulceration is significantly higher
than in not –contact Lens wearer, specially
pseudomona infection
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Never prescribe topical anesthetics,
No topical steroid
In case of linear abrasions
examine under the lid
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Conjunctival injection with discharge,
Should be treated with a topical antibiotic
if discharge is purulent,( bacterial )
Should be treated with parenteral
antibiotic if gonococcal.(fig.)
Prominent itching symptoms is in allergic
conjunctivitis
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Papillae
Allergic conjunctivitis
Bacterial conjunctivitis
Follicles
Viral conjunctivitis
Chlamydial conjunctivitis
Remember:
Gonococcal conjunctivitis should be treated
with parenteral antibiotic.
Why?
Risk of corneal perforation
Characteristic of acute angel closure glaucoma
High IOP
Sever eye pain
Decreased vision
A fixed and dilated pupil
Primary angle closure glaucoma, risk factors
Hyperopia
Age>70
Female
Family history
Asian, Inuit people
Mature cataract
Shallow anterior chamber
Pupil dilation
What is your next plan:
 Refer to ophthalmologist for laser iridotomy
What would be the next plan
 Laser iridotomy
 Aqueous suppression with BACH
 Miotics to reverse the pupillary block
Distinguishes orbital cellulites from preseptal
cellulitis is,
Limited ocular motility
Decreased vision
RAPD
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Sinusitis can cause orbital cellulitis
Trauma , skin abrasoin, any skin lesion can
cause preseptal.
Evaluation and management of orbital cellulitis
includes
Patient admission
Intravenous AB
Ophthalmologic consultation
Orbital CT scan
Blood culture
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Request stat ophthalmology and ENT
consultations to rule out a life–threatening
fungal infection (mucoromycosis)
Diabetic patient with ketoacidosi,
Frozen globe, + RAPD
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F > 60 y/o
Abrupt monocular loss of vision, pain over
temporal artery , jaw claudication, diplopia,
PMR, constitutional
scalp tenderness, temporal artery beading
Diagnosis : temporal artery biopsy
Treatment high dose steroid, start
immediately , before the biopsy
Immediately ESR, CRP,
A low or normal sedimentation rate does not
exclude the diagnoses
The most common cranial nerve paralysis that
occur involves the third cranial nerve.
13. Possible causes for sudden Visual loss
include
Temporal arteritis
Retinal detachment
Non-arteritic optic neuropathy
CRAO
CRVO
What mechanism of action do cycloplegic
use to relieve pain?
Paralysis of ciliary spasm
Sudden unilateral vision loss and cherry red spot
in the macula,
Management
Digital massage of the globe to dislodge an
embolus
Topical beta blockers
AC paracenthesis by an
ophthalmologist
Re-breathing CO2
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Cause
Emboli from carotid artery
Emboli heart( arrhythmia, valvular,
endocarditis)
Thrombosis
Temporal arteritis
It is the result of a tear in an iris vessel.
It can be associated with other ocular injuries.
It should be referred to ophthalmologist.
There is risk of re-bleeding in 2-5 days after
trauma
In management , no aspirin , no valsalva
Risk of re-bleed highest on days 2-5 , resulting in
 Increased IOP, corneal staining, iris necrosis,
Herpes zoster involving the ophthalmic
division of cranial nerve V is more likely to
have ocular involvements if the tip of the
nose is involved
Hutchinson sign
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Management
Oral antiviral
In cases of conjunctival involvement erythromycin
Refer to ophthalmologist
Steroid should be prescribed by ophthalmologist, if
needed.
Redness
Pain
Photophobia
Decreased vision
With fluorescein and cobalt blue,
dendritic ulcer
Referral to an ophthalmologist
Treatment by ophthalmologist
 Antiviral topical or oral
 Steroid not at the beginning and with
caution, due to risk of geographic ulcer
Lid laceration repair should include
Assessment of possible canalicular injury
Foreign body removal
Tetanus prophylaxis
Lid laceration repair should include
a)
b)
c)
d)
Assessment of possible canalicular
injury
Foreign body removal
Tetanus prophylaxis
All of the above
Asymptomatic
Can be associated with HTN, or
vasculopathy , or anticoagulant
therapy, specially in recurrent one
Resolve spontaneously in 2-3 weeks
Ne need for stopping NSAID or Systemic
anticoagulant for resolution.
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Prolonged use of topical ophthalmic
anesthetics can cause
Corneal damage
Worsening of corneal fungal ulcers
Worsening of bacterial keratatis
Worsening of herpetic dendritic keratitis
Cataracts
Open-angle glaucoma
Presents with acute, tender
swelling of the lid
Management includes
warm compresses and lid hygiene for 2
Weeks
Chronic case after 2-3 month might requires
incision and drainage
Still a chalazion
Neonatal Chlamydial conjunctivitis
Occurs usually after 21 days of age, between 23 weeks
Requires two weeks of systemic erythromycin
for effective treatment
If not treated can cause pneumonitis, arthritis,
and other systemic infection
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Toxic conjunctivitis occurs in day one
secondary to instillation of silver nitrate or
erythromycin ointment that used as
conjunctivitis prophylaxis , no treatment
needed
Gonococcal day 5-7 , is the most serious one
Chlamydial , need systemic treatment
Herpes simplex after 2-3 weeks
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It is a benign growth of
conjunctiva over the cornea
Sun exposure
More common on the nasal side of the
conjunctiva
In an early stage into maybe managed with
use of artificial tears and topical
vasoconstrictors
In advanced stages needs surgery
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Usually complain of mild pain.
Are less likely to have a systemic connective
tissue disease, comparing to scleritis.
Have engorged superficial vessels overlying the
sclera below the conjunctiva.
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To differentiate, Place a drop of
Phenyephrine 2.5% , re-examine after 10-15
min , episceleral vessel should blanch.
Scleritis, causses vision loss , sever pain ,
wakes patient up at night tiem, causes
thining(blue hue) and necrosis of sclera
POAG
PACG
Common 95%
 Chronic
 Painless
 Moderate IOP
 Normal cornea , pupil
 No symptom
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Rare 5%
Acute onset
Painful red eye
Extremely IOP
Haze cornea, middilated
pupil , N/V, halo around
light
Risk factor for open-angel glaucoma include
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African racial heritage
Age greater than 60 years
Positive family history for glaucoma
Corneal thickness
Secondary a glaucoma can be is caused by
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Uveitis
Chronic steroid use
Trauma
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Remember
IOP is a risk factor for open angle glaucoma ,
its not part of its definition
An optic nerve with glaucomatous damage
may have all of the following except
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A disc hemorrhage
Mild pallor of the neuroretinal rim
Displacement of the retinal vessels to the
margin of the disc
Thinning of the neuroretinal rim
•beta-adrenergic agonist
•alpha-2 adrenergic antagonists
•cholinergic agonists
•carbonic anhydrase agonists
Topical beta blockers
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Beta blockers can worsen congestive heart
failure, Myasthenia Gravis,
Betaxolol is relatively selective beta 1
blockers
Topical beta blockers decrease the
production of the aqueous humor
Can masked symptoms of hypoglycemia
Latanoprost (xalatan) side effects
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Conjunctival hyperemia
Increased iris pigmentation
Lengthening of the eyelashes
Macular edema
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Central retinal vein occlusion
Blood and thunder fundus
Second most common
retinopathy after DM,
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Risk factor
HTN, DM, glaucoma,
arteriosclerotic vascular disease,
hyperviscosity, (PV, OCP, sickle
cell, lymphoma, leukemia,
Treatment of underlying disease
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3 forms
 Rhegmatogeneous (most common)
caused by tear or hole,
Treatment with scleral buckle, or
pneumatic retinopexy,…
Tractional
In diabetic retinopathy, CRVO, sickle cell, ROP,
trauma,
Treatment surgery
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Exudative
posterior uveitis, central serous retinopathy tumor
Treatment of the underlying disease
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Supratemporal retina , most common site for
horseshoe tears
Caused by PVD posterior vitreous
detachment or trauma,
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Normal aging of vitreous liquefaction
Floater , flashes
Complication:
Tear, RD, more in high myopia
Refer to ophthalmologist, dilated exam , F/U
No specific treatment
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Leading cause of blindness, cause
metamorphosia,
Risk factors
F, age, family hx, smoking, Caucasian, blue
eye
Dry (nonexudative): medical. Monitor,
antioxidants
Wet (exudative): laser, PDT, intravitreous
injection of anti-VEGF
In diabetic retinopathy vision loss
may be caused by
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macular edema
macular ischemia
vitreous hemorrhage
Signs of nonproliferative diabetic
retinopathy
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Microaneurysm
Dot and blot hemorrhages
Hard exudates
Intraretinal hemorrhages
Cotton wool spot
Patient with type 2 diabetes should be
evaluated by an ophthalmologist, at the time
of diagnoses.
Type 1 diabetes should be evaluated five years
after diagnoses but not before puberty
Proliferative diabetic retinopathy, optic disc neovascularization
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Dx? Triad?
APO
Arteriolar narrowing
Perivascular bonyspicule
Optic disc pallor
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Remember that
3th nerve palsy : Exotropia and
hypotropia , ptosis,
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6th: Esotropia,
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Remember that need imaging
if in young pt or associated with
neurological signs,
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 4th :hypertropia and head tilt
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Reduction of best corrected visual acuity due
to cortical suppression of sensory input,
Or more than 2 lines difference in acuity
between two eyes.
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Etiologies
Strabismus , Refractive, Deprivation
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Treatment
Occlusion of the good eye
Ptosis
Miosis
Anhydrosis
Heterochromia
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DDx
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DDx
Retinoblastoma
Cataract
Retinal
coloboma
ROP
Toxocariasis
Retinal
detachment
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Kawasaki disease
No to steroid
Yes Aspirin
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conjunctivits
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Conjunctivitis
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Oral mucosal rash
The most common site for metastasis to the
eye is the
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Choroid
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Metastasis , most common intraocular
malignancy in adult
Breast in F, lung in M ,
Neuroblastoma in children
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Malignant melanoma , most common
primary intraocular tumor in adult
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BCC of lid most common lid malignany
The most common ocular manifestation is
bilateral optic disc edema, papilledeam
 The most common visual symptoms are
transient visual obscurations.
 Idiopathic intracranial hypertension can be
associated with
 vitamin A or D toxicity
 tetracycline ,
 steroid withdrawal.
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Other symptoms
Nausea/Vomiting/Headache
Pulsatile tinnitus
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Normal neuro-imaging
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High ICP , in LP, lumbar puncture
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Sjogren syndrome
Is associated with dry eye and antibodies such
as anti -SS-A antibodies,
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Not always accompanied by headache
Visual symptoms vary from scintillations to
total bilateral loss of vision, which is
usually temporary.
Optic disc swelling in the malignant hypertension
 Indicates that the patient is at increased risk for
developing heart failure and hypertensive
encephalopathy.
Retinopathy the most common ocular
manifestation of HTN.
Key features of chronic HTN: AV nicking, blot
hemorrhages, cotton wool spots, microaneurysm
Thyroid eye disease
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Might occurs even when the patient has
normal serum thyroid hormone level.
Can result in severe visual loss from optic
nerve compression or corneal damage.
NO SPECS
 No sign
 Only sign lid retraction, lag
 Soft tissue swelling periorbital edema
 Proptosis
 Extra-ocular muscle weakness (diplopia)
 Corneal exposure
 Sight loss
Cotton-wool Patches in AIDS patients
a)
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Indicate obstruction of the precapillary arterioles with infarction of
the superficial retina
DDx of CWS
Diabetic retinopathy
HTN retinopathy
HIV
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Young female
Blurred vision , decreased color vision, 2º to
optic neuritis, eye pain specially in ocular
movement
Diplopia 2º to internuclear ophthalmoplegia
RAPD, ptosis, uveitis, optic atrophy,
nystagmus, optic neuritis
In optic neuritis, treatment with oral steroid
will increase the risk of MS
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Toronto notes