Transcript basic 2015 Ophthalmology Dr Maryam Abtahi

Ophthalmology
Back to Basic
Maryam Abtahi
March, 2015
Part one
Red Eye and Emergencies
Chemical burn
In chemical burn, what is your
first action:
Irrigate the eye with, water,
normal saline,…
Next steps:
Check PH of the conjunctival fornix
Check vision, pupil, continue the exam
…..
Chemical burn
 Acid , coagulate proteins and inhibit further corneal
penetration
 Alkali, worse prognosis
 Opaque cornea has poor prognosis
 Never try to neutralize
 Rx:
Topical cycloplegic
Topical antibiotics
Topical steroid
Ruptured globe
If a ruptured globe is suspected, the first
action to take is to:
First ABC, R/O head trauma
Don’t press on the eye ball
Don’t check the IOP
Check Vision
Shield the eye
NPO
Tetanus
IV antibiotics
Ruptured globe
 R/o intraocular foreign body with orbital CT scan,
specially in metal on metal hammering
Blunt Trauma
Need to be referred,
 Decreased vision
 Shallow anterior chamber
 Hyphema
 Abnormal pupil
 Ocular misalignment
 Retinal damage
Intraocular foreign body
The best study to evaluate a patient with intraocular
foreign body is
CT scan of the orbits
Orbital Floor Fracture
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Medical management :
 no nose blowing
 Systemic antibiotic only if sinusitis
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Surgical repair :
 Fracture of more than 50% of the floor,
 Diplopia not improving,
 Enophthalmos more than
2 mm
Blow-Out Fracture
Blow out fracture, white eye
 In children , might cause muscle entrapment and ischemia,
 Risk of bradycardia .
 One of the ophthalmology emergency,
Hyphema
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,
Corneal Abrasion
Corneal abrasion in contact lens wearer
Never patch the eye
Topical antibiotic
Refer to an ophthalmologist
The risk of ulceration is significantly higher than in not
–contact Lens wearer, specially pseudomonas
infection
Corneal abrasion
 Never prescribe topical anesthetics,
 No topical steroid
 In case of linear abrasions
examine under the lid
Corneal ulcer
 Local necrosis of the cornea due to infection (white vs.
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clear in abrasion)
Lesion extend to the stroma, associated with thinning,
Urgent referral to ophthalmologist
Culture
Topical antibiotic every hour
Herpes simplex
HSV type 1 90%,
Redness
Pain
Photophobia
Decreased vision
With fluorescein and cobalt blue,
dendritic ulcer
Referral to an ophthalmologist

Antiviral topical or oral
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Steroid risk of geographic ulcer
Herpes zoster ophthalmicus
Herpes zoster involving the ophthalmic division of cranial
nerve V (V1) is more likely to have ocular involvements if
the tip of the nose is involved, Hutchinson sign
Complications :
Keratitis, corneal perforation, scar
Iritsis, secondary glaucoma, cataract,
Cranial nerve palsy
….
Herpes Zoster
Ophthalmicus
Management
 Oral antiviral
 In cases of conjunctival involvement erythromycin
 Refer to ophthalmologist
 Steroid should be prescribed by ophthalmologist, if needed.
Cornea Tips
 Keratoconus
 Bilateral thinning and
bulging of the cornea
 Kayser-Fleischer ring
 Wilson disease
 Associated with down’s
syndrome, atopy, CL
use?(Toronto notes)

irregular astigmatism ,
scar, stromal edema
 Rx: spectacle, CL, cross
linking, penetrating
keratoplasty,
 Arcus senile
 Hypercholesterolemia if
under 40 yrs.
Conjunctivitis
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
Lymphatic drainage of temporal conj to preauricular
area, nasal conjunctiva to submandibular nodes.
Conjunctivitis
 Papillae
 Allergic conjunctivitis
 Bacterial conjunctivitis
 Follicles
 Viral conjunctivitis
 Chlamydial conjunctivitis
Pterygium
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It is a benign growth of fibro-vascular
triangular tissue over the cornea
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Sun exposure
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More common on the nasal side of the conjunctiva

In an early stage into maybe managed with use of artificial tears and
topical vasoconstrictors

Excision in chronic inflammation, cosmesis, threat to visual axis,

5% recurrence rate if with conjunctival autograft.
Subconjunctival
hemorrhage
Asymptomatic
Can be associated with HTN, or vasculopathy , or
anticoagulant therapy, specially in
recurrent one
Resolve spontaneously in 2-3 weeks
No need for stopping NSAID or Systemic
anticoagulant for resolution.
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Episcleritis
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Usually complain of mild pain.
Are less likely, 1/3, to have a systemic connective tissue
disease, comparing to scleritis.
Have engorged superficial vessels overlying the sclera below
the conjunctiva.
1/3 bilateral
3:1, F:M
Scleritis vs. episcleritis
 To differentiate, Place a drop of Phenylephrine 2.5% , re-
examine after 10-15 min , epi-scleral vessel should blanch.
 Scleritis , severe pain
 Collagen vascular disease,
 Granulomatous disease
 Infections
 Metabolic, gout,
 Chemical
 Idiopathic
Cellulitis
Pre-septal : trauma, skin infection
Orbital : secondary to sinus infection, facial, tooth, or
trauma
Differentiating signs , in orbital cellulitis:
Proptosis
Limited ocular motility
Decreased vision
RAPD
Marked Conjuctival chemosis
Pain on eye movement
Marked leukocytosis,
Cellulitis
Treatment of pre-septal cellulitis
 Warm compress
 Systemic antibiotic
 If severe or under 1 year old treat as orbital
Cellulitis
Evaluation and management of orbital cellulitis includes
Patient admission
Blood culture 2
Intravenous AB
Ophthalmologic consultation
Chalazion
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 need incision and
drainage
Chalazion
Still a chalazion
Mucoromycosis
 Request stat ophthalmology and ENT consultations to rule
out a life–threatening fungal infection (mucoromycosis)
 Diabetic patient with ketoacidosi,
 Frozen globe, + RAPD
Acute angel closure
glaucoma
Characteristic of acute angel closure glaucoma
Sever eye pain, N&V,
Decreased vision
High IOP
Shallow angle
A fixed and dilated pupil
Corneal edema
Acute angel closure
glaucoma
Primary angle closure glaucoma, risk factors
Hyperopia
Age>70
Female
Family history
Asian, Inuit people
Mature cataract
Shallow anterior chamber
Pupil dilation
Acute angel closure
glaucoma
What is your next plan:
 Refer to ophthalmologist for laser iridotomy
What would be the next plan
 Laser iridotomy
 Aqueous suppression with BACH
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Beta-blocker. adrenergic., cholinergic, hyperosmolar
 Miotics to reverse the pupillary block
Temporal Arteritis or Giant
Cell Arteritis
 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
Temporal Arteritis
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.
Sudden Vision Loss
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
CRAO
Sudden unilateral vision loss and cherry red spot in the macula,
Cause
 Emboli from carotid artery , heart( arrhythmia, valvular,
endocarditis)
 Thrombosis
 Temporal arteritis
Management, within 2 hour
Digital massage of the globe to dislodge an embolus
Topical beta blockers
AC paracenthesis by an
ophthalmologist
Lid laceration repair should include
a)
b)
c)
d)
Assessment of possible canalicular injury
Foreign body removal
Tetanus prophylaxis
All of the above
Prolonged use of topical ophthalmic anesthetics can
cause
Corneal damage
Topical steroid side
effects
Worsening of corneal fungal ulcers
Worsening of bacterial keratatis
Worsening of herpetic dendritic keratitis
Cataracts
Open-angle glaucoma
Ophthalmia Neonatarum
 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
Conjunctivitis
Neonatal Chlamydial conjunctivitis
Occurs usually after 21 days of age, between 2-3 weeks
Requires two weeks of systemic erythromycin for
effective treatment
If not treated can cause pneumonitis, arthritis, and other
systemic infection
Uveitis
Anterior,
pain photophobia blurred
ciliary flush, miotic pupil, KP,
Etiologies :HLA B27 , idiopathic , infection like lyme,
syphilis, TB, herpes, sarcoid, trauma,
Rx: steroid, cycloplegic
Intermediate,
foater , blurred vision
Causes: sarcoidosis, lyme, MS
Posterior ,
blurred vision, floaters,
Etiologies: infections, inflammations, autoimmune,
malignancies,
Glaucoma
Glaucoma
POAG
PACG
 Common 95%
 Rare 5%
 Chronic
 Acute onset
 Painless
 Painful red eye
 Moderate
IOP
 Normal cornea , pupil
 No symptom
 Extremely IOP
 Haze cornea, middilated
pupil , N/V, halo around
light
Glaucoma
Risk factor for open-angel glaucoma include
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Elevated intraocular pressure
African racial heritage
Age
Positive family history for glaucoma
Corneal thickness
Secondary glaucoma caused by
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Uveitis
Chronic steroid use
Trauma
Remember
 IOP is a risk factor for open angle glaucoma , its not
part of its definition
An optic nerve with glaucomatous damage
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Increased C:D ratio
Significant C:D asymmetry
Flamed shape disc hemorrhage
360 prepapillary atrophy
Nasal displacement large vessels
Thinning and notching of the neuroretinal rim
Beta blockers
Decrease production
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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
Prostaglandin analogue
Latanoprost (xalatan) side effects,
 Increased outflow
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Conjunctival hyperemia
Increased iris pigmentation
Lengthening of the eyelashes
Macular edema
Retinal disease
CRVO
 Central retinal vein occlusion
 Blood and thunder fundus
 Second most common vascular
retinopathy after DM,
 Risk factor
 HTN, DM, glaucoma, arteriosclerotic
vascular disease, hyperviscosity, (PV,
OCP, sickle cell, lymphoma, leukemia,
 Treatment of underlying disease and
complications
 Macular edema, neovascularization of
retina and iris, vitreous hemorrhage
RD , Retinal Detachment
 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
 Exudative
posterior uveitis, central serous retinopathy tumor
Treatment of the underlying disease
Retinal tear
 Supratemporal retina , most common site for horseshoe
tears
 Caused by PVD posterior vitreous detachment or trauma,
Posterior vitreous
detachment
 Normal aging of vitreous liquefaction
 Sign and symptom
 Floater , flashes
 Weiss ring : glial tissue around the optic disc
 Complication:
 Tear, RD, more in high myopia
 Refer to ophthalmologist, dilated exam , F/U
 No specific treatment
Age-related macular
degeneration
 Leading cause of blindness, cause metamorphosia,
 Risk factors
F, age, family hx, smoking, Caucasian, blue eye
 Drusen in dry (hyaline material)
 Dry (nonexudative) 90%: medical. Monitor,
antioxidants
 Wet (exudative) 10%: laser, PDT, intravitreous
injection of anti-VEGF
Diabetic retinopathy
In diabetic retinopathy, most common cause of
vision loss in young people, may be caused by
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macular edema ,
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Most common cause of vision loss in BDR
macular ischemia
vitreous hemorrhage
BDR: background DR, non-prolifrative
Non-proliferative
Diabetic Retinopathy
Signs of nonproliferative diabetic retinopathy
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Microaneurysm
Dot and blot hemorrhages
Hard exudates
Intraretinal hemorrhages
Cotton wool spot
Screening
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
Proliferative diabetic retinopathy, optic disc neovascularization
Retinitis pigmentosa
 Dx? Triad?
 APO
 Arteriolar narrowing
 Perivascular bony-spicule
 Optic disc pallor
Crania nerves palsy
 Remember that
 3th nerve palsy : Exotropia and hypotropia , ptosis,
 6th: Esotropia,
 Remember that need imaging
 if in young pt or associated with neurological
signs,
th
4
 4th :hypertropia and head tilt
nerve palsy
Amblyopia
 Reduction of best corrected visual acuity due to
cortical suppression of sensory input,
 Or more than 2 lines difference in acuity between two
eyes.
 Etiologies
 Strabismus , Refractive, Deprivation
 Treatment
 Occlusion or atropine cycloplegic of the good eye
?
Horner syndrome
Ptosis
Miosis
Anhydrosis
Heterochromia
?
 DDx
Leukocoria
 DDx
 Retinoblastoma
 Cataract
 Retinal coloboma
 ROP
 Toxocariasis
 Retinal detachment
?
?
Kawasaki
 Kawasaki disease
No to steroid
Yes Aspirin
?
 conjunctivits
?
 Conjunctivitis
 Oral mucosal rash
Measles
Manifestation of
systemic diseases
Ocular malignancies
The most common site for metastasis to the eye is the
 Choroid
Ocular malignancies
 Metastasis , most common intraocular malignancy in adult
 Breast in F, lung in M ,
 Neuroblastoma in children
 Malignant melanoma , most common primary intraocular
tumor in adult
 BCC of lid most common lid malignany
Intracranial hypertension
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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.
Intracranial hypertension
 Other symptoms
 Nausea/Vomiting/Headache
 Pulsatile tinnitus
 Normal neuro-imaging
 High ICP , in LP, lumbar puncture
Connective tissue
disorders
Sjogren syndrome
Is associated with dry eye and antibodies such as anti SS-A antibodies,
Migraine
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Not always accompanied by headache
Visual symptoms vary from scintillations to total
bilateral loss of vision, which is usually temporary.
Hypertension
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
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.
Thyroid eye disease
NO SPECS
 No sign
 Only sign lid retraction, lag
 Soft tissue swelling periorbital edema
 Proptosis
 Extra-ocular muscle weakness (diplopia)
 Corneal exposure
 Sight loss
HIV, AIDS
Cotton-wool Patches in AIDS patients
a)
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Indicate obstruction of the pre-capillary
arterioles with infarction of the superficial
retina
DDx of CWS
Diabetic retinopathy
HTN retinopathy
HIV
MS and Optic neuritis
 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
Thank you!
[email protected]
Toronto notes