Ophthalmo and neurosurg1 Flashcards
Visual acuity testing distance
20 ft (6m)
20/40 acuity means:
20/ smallest line pt can read
Or
What pt can see at 20, a nl person can see at denominator
Testing hierarchy for low vision
Snellen acuity
Counting fingers
Hand motion
Light perception with projection
Light perception
No light perception
When does a child gain normal visual aquity
2-4 yr
Definition of legal blindness
Best corrected visual acuity that is 20/200 or less
Minimum visual requirement to operate a non-commercial automobile
20/50, with both eyes open and examined together.
120° Continuous horizontal visual field.
15° continuous visual field above and below fixation.
Visual acuity testing in newborn
Cannot be tested conventionally
VA testinf in 3mo-3 yr
Can only access visual function, not acuity
Test each eye for fixation symmetry using an interesting object
Normal function= central, steady, maintained
VA testing from 3yr until alphabet known
Pictures or letter cards/charts
Tumbling E chart
Colour vision testing
Ishihara pseudoisochromatic plates
Indications for color vision testing
Testing for optic nerve function:
Optic neuritis
Chloroquine use
Thyroid ophthalmopathy
Visual field testing
Confrontation
Automated testing
Amsler grid (tests for central/paracentral scotoma in pts with AMD)
PERRLA
Pupil Equal
Round
Reactive to Light
Accommodation
Shallow anterior chamber
Light shown tangentially from temporal side
If > 2/3 of nasal side of iris in shadow= shallow chamber
Gold standard method for assessing anterior chamber depth
Gonioscopy
Stain for de-epithelialized cornea
Fluorescein dye
Stain for Devitalized corneal epithelium
Rose Bengal dye
Normal IOP
9-21 mmHg
Has diurnal variation
Gold-std for measurement of IOP
GAT, using slit lamp
Contraindications to pupillary dilation
Shallow anterior chamber
Iris-supported anterior chamber lens implant
Potential neurologic abnormality requiring pupil evaluation
Caution with cardiovascular disease
Nerve to superior oblique muscle
CN IV
If myopia started after the age 25 think of
DM
Cataract
Complications of myopia
Retinal tear/detachment
Macular hole
Open angle glaucoma
Accommodative esotropia may develop in
Hyperopia
Complications of hyperopia
Angle-closure glaucoma
Age of presbyopia
> 40 yr
Decreased accommodative ability of lens due to decreased deformability
Exophthalmus
Protrusion > 18 mm
Inv for exophthalmos
CT/MRI head/orbit
U/S orbit
TFT
Most common cause of exophthalmos in adults
Grave’s
Most common cause of exophthalmus in children
Orbital cellulitis
Inv for enophthalmus
CT/MRI
The systemic manifestations of infection in preceptal cellulitis
Fever: may be present
WBC: moderate elevation
ESR: Normal or elevated
Tx of preseptal cellulitis
Systemic ABx (HI, S. Aureus, Strep)
Amoxicillin-clavulanate
If severe: Treat as orbital cellulitis
If child < 1 yr: Treat as orbital cellulitis
Mx of orbital cellulitis
Admit
B/C x2
Orbital CT
IV AB (ceftriaxone, vanco) x 1wk
Surgical drainage of abcsess
Close F/U
Meds causing dry eye
Anticholinergics
Antihistamines
BB
Diuretics
Which nerve palsy causes dry eyes?
CN VII
Vitamin deficiency causing goblet cell dysgenesis
Vit A
Inv for dry eye
Rose Bengal/Fluorecein staining (punctate staining of cornea)
Schimmer test
Tx of dry eye
Preservative-free artificial tears
Ointment at bedtime
Short course of mild topical CS
Omega3 fatty acids orally
Eyelid hygiene
Ophthalmic cyclosporin for moderate cases
Surgical
Treat underlying
Inv for epiphora
Fluorescein dye
Jone’s dye test to detect lacrimal drainage obstruction
Dacryocystitis organism
S. Aureus
S.pneumoniae
Pseudomonas
Tx of dacryocystitis
Warm compress
Nasal decongestant
Systemic and topical AB
If chronic:
Obtain culture by aspiration
After resolution of infection:
Dacryocystorhinostomy
Dacryoadenitis organisms
S. Aureus
Mumps
EBV
VZV
N. Gonorrhea
Tx of dacryoadenitis
Warm compress
NSAIDs
Systemic AB if bacterial
If chronic: treat underlying
Most common type of ptosis
Aponeurotic ( disinsertion/dehiscence of levator aponeurosis)
Meds causing ptosis
Pregabalin
Opioids
Heroin
Tx of ptosis
Surgery
Underlying causes of trichiasis
Entropion
Involutional age change
Chronic inflammatory lid disease
Trauma
Burns
Tx of trichiasis
Topical lubricants
Eyelash epilation
Electrolysis
Cryotherapy
Causes of entropion
Aging
Cicatricial (trauma, surgery, burn, zoster)
Orbicularis oculi muscle spasm
Congenital
Tx of enteropion
Lubricant
Evert lid with tape
Surgery
Causes of ectropion
Aging Paralysis of CN VII Cicatricial Mechanical Congenital
Tx of ectropion
Lubricant
Eyelid taping overnight
Surgery
Stye (hordeolum) micro-organism
S. Aureus
Stye Tx
Warm compresses
Lid care
Gentle massage
Resolves within 2 wk
+/- incision and drainage
Chalazion site of disease
Meibomian (chronic granulomatous inflammation)
Tx of chalazion
Warm compress
If no improvement after 1 mo:
Incision and curettage
If chronic recurrent lesion: Bx
Toothpaste sign
Blepharitis:
Discharge with pressure on lids
Etiology of anterior blepharitis
Staph: (ulcer, dry scales)
Seborrheic: no ulcer, greasy scale
Etiology of posterior belpharitis
Meibomian glands dysfunction
Complications of blepharitis
Recurrent hordeola
Conjunctivitis
Keratitis
Corneal ulceration/neovascularization
Tx of blepharitis
Warm compress
Lid massage
Lid washing
Topical/systemic AB
+/- short course of topical steroids if severe
Omega 3
Pinguecula
Hyaline and elastin deposit
No involvement of cornea
Associations: sun and wind exposure,
Aging
Tx of piguecula
Lubricating drops
Surgery for cosmesis
Pterygium
Fibrovascular
Encroachment on cornea
Can induce: astigmatism, decreased vision
Tx
Lubricants for irritative symptoms
Excision for:
Chronic inflammation
Treat to visual axis
Cosmesis
One-third recur
When to suspect globe rupture in subconjunctival hemorrhage?
360° hemorrhage and Hx of trauma
Tx if subconjunctival hemorrhage
Resolves spontaneously in 2-3 wk
Inv for subconjunctival hemorrhage
Not needed if negative Hx
Medical/hematologic w/u if recurrent
Tx of allergic conjunctivitis
Avoidance
Cool compresses
Non-preserved artificial tears
Oral/topical antihistamines
Topical mast-cell stabilizers:
Cromolyn
Ketotifen
Olopatadine
Topical CS
Onset of atopic conjunctivitis
Late adolescence, early adulthood
Perennial
Papillae in atopic conjunctivitis
Tarsal papillary hypertrophy
Tx of atopic conjunctivitis
CNI oint
Topical CS
Conjunctivitis in contact lens wearers
Giant papillary conjunctivitis
Superior palpebral conjunctiva
Tx of giant papillary conjunctivitis
Clean, change or discontinue use of contact lens
Topical CS
Vernal conjunctivitis timing
Seasonal (warm weather)
Papilla of vernal conjunctivitis
Large papillae on superior palpebral conjunctiva
Conjunctivitis with corneal ulcer and keratitis
Vernal
Time course of vernal conjunctivitis
In children
Lasts for 5-10 y
Tx of vernal conjunctivitis
Non-preserved artificial tears
Topical CS
Topical cyclosporine
Main virus causing conjunctivitis
Adenovirus
How long is viral conjunctivitis contagious?
Up to 12 days
Tx of viral conjunctivitis
Cool compress
Topical lubricant
Proper hygiene to prevent transmission
Self-limiting
Organisms causing bacterial conjunctivitis
S. Aureus
S. Pneumoniae
H. Influenza
M. Catarrhalis
If neonate or sexually active:
N. Gonorrhoeae
Bacterial conjunctivitis which invades cornea
Gonorrhea
The most common cause of conjunctivitis in neonates
C. Trachomatis
Causing inclusion conjunctivitis
Tx of bacterial conjunctivitis
Topical broad spectrum ABs
Systemic AB of indicated (neonates, children)
Self-limited
Course of 10-14 d w/o treatment. 1-3 d with treatment
Follicles usually seen in
Viral and chlamydial conjunctivitis
Infective conjunctivitis with papilla
Bacterial
Conjunctivitis with LAP
Viral
Chlamydial
LAP: pre-auricular , submandibular
Onset of gono/chlamy conjunctivitis
Neonatal gono:
First 5 d
Neonatal chlamy:
3-14 d
Adults if sexually active
Chlamydia disease in the eye
Trachoma
Inclusion conjunctivitis
Leading infectious cause of blindness in the world
Trachoma caused by chlamydia
Tx of trachoma
Oral azithromycin
Topical tetracycline
Inclusion conjunctivitis
Chronic
Chlamydia
Follicles
Tx of inclusion conjunctivitis
Oral:
Azithro
Tetra
Doxy
The most common cause of conjunctivitis in newborns
Inclusion conjunctivitis caused by Chlamydia
Episcleritis
F>M
Mostly idiopathic
1/3 bilateral
Pain and discomfort
Associations of episcleritis
Collagen vascular disease
Infections (VZV, HSV, syphilis)
IBD
Rosacea
Atopy
Interpalpebral red eye
Episcleritis
Tx of episcleritis
Self-limited (recurrent in 2/3)
Topical CS
Oral NSAID
Differentiation of episcleritis vs scleritis
Phenylephrine blanches redness in episcleritis
Scleritis assiciations
Collagen vascular: SLE, RA, GPC, AS
TB, Sarcoidosis, Syphilis
Gout, thyrotoxicosis
Staph, pneumococcus, pseudomonas, HSV
Chemical/physical agents
Idiopathic
The best indicator of scleritis progression
Pain
Quality of pain: deep, boring
Scleritis symptoms
Pain
Photophobia
Decreased vision
Red eye
Topical erythromycin for prevention of ophthalmia neonatorum
Questionable efficacy
Effective means for preventing ophthalmia neonatorum
Screening all pregnant women for gonorrhea and chlamydia infection, Tx and F/U of those infected
Testing mothers who were not screened, during delivery
Infants of mothers with untreated gonococcal infection at delivery:
Receive ceftriaxone
Infants of mothers with untreated chlamydial infection at delivery:
Close F/U for signs of infection
Scleromalacia perforans
Strong association with RA
Asymptomatic
Anterior necrotizing scleritis
No inflammation
May cause scleral thinning
Types of scleritis
Anterior:
Pain radiating to face
Scleral thinning
Necrotizing
Posterior:
Rapidly progressive blindness
Exudative RD
more common in women and elderly
Tx of scleritis
Systemic NSAID
Systemic steroid
Systemic immunomodulators
Treat underlying (indicator of poor control)
Tx of corneal foreign body
Remove with sterile needle under local anesthetic and magnification
Topical AB (pseudomonas coverage if abrasion from organic material)
Topical NSAID (risk of corneal melt with prolonged use)
Cycloplegic (relieves photophobia)
Patch
Tx of corneal abrasion
Topical AB (pseudomonas coverage if abrasion from organic material)
Topical NSAID (risk of corneal melt with prolonged use)
Cycloplegic (relieves photophobia)
Patch
DDx of recurrent corneal abrasions
Previous traumatic corneal abrasion
Corneal dystrophy
Idiopathic
Tx of recurrent corneal abrasion
Same as corneal abrasion
Topical hypertonic saline oint at bedtime for 6-12 mo
Topical lubrication
Bandage contact lens
Anterior stromal puncture
Phototherapeutic keratotomy
Etiology ofcorneal ulcer
Infection (bacterial > viral)
Exposure, abrasion, foreign body, contact lens
Conjunctivitis, blepharitis, keratitis
Vit A deficiency
Tx of corneal ulcer
Urgent referral
Culture
Topical AB/ h
Inv for corneal ulcer
Seidle test (fluorescein under cobalt blue filter)
Corneal hyposthesia in
Viral keratitis
HSV epithelial keratitis form
Dendritic lesion
Terminal end bulbs
Stain with fluorescein
Also:
Other forms of infectious epithelial keratitis
Stromal keratitis
Endotheliitis
Complications of HSV keratitis
Scarring
Chronic interstitial keratitis
Secondary iritis
Secondary glaucoma
Tx of HSV keratitis
Topical trifluridine
Or
Systemic acyclovir
Debridement of dendrite
NO STEROIDS INITIALLY (unless by ophthalmologist and with caution)
Herpes Zoster ophthalmicus P/E
Pseudodendrite
Superficial punctate keratitis
Corneal hyposthesia
Herpes Zoster ophthalmicus complications
Keratitus Ulceration Perforation Scarring Secondary iritis Secondary glaucoma Cataract Muscle palsy (CNS involvement) Severe PNH
Tx of Herpes Zoster ophthalmicus
Immediate oral antivirals
If immune-mediated keratitis/iritis: topical CS/cycloplegics
Erythromycin oint if conjunctival involvement
Associations of keratoconus
Down
Atopy
Vigorous eye rubbing
Contact lens
Broken cornea kayers in keratoconus
Bowman
Descemet
Tx of keratoconus
Correction with spectacles
Or
Rigid gas-permeable contact lens
Corneal collagen cross-linking Tx (halts progression)
Intrastromal corneal ring segments (can flatten the cone)
Penetrating keratoplasty
Deep anterior lamellar keratoplasty
Reasons for decreased vision in keratoconus
Stromal edema
Scarring
Irregular astigmatism
(Bilateral)
Arcus senilis
Hazy white ring
<2 mm wide
Clearly separated from limbus
Bilateral
Benign
Corneal degeneration due to lipid deposition
No visual Sx
Significance of arcus senilis
<40 yr associated with hypercholestrolemia
Kayser-Fleischer ring
Brown-yellow-green
Peripheral cornea
Starts inferiorly
Deposits of copper in descmet’s membrane
Wilson
Tx: underlying
Munson’s sign
Detects keratoconus
Bulging of lower eyelid when pt looks downward
Associations of iritis/iridocyclitis
Usually idiopathic
CTD:
HLA-B27: reactive arthritis, AS, PsA, IBD
Non-HLA-B27: Juvenile idiopathic arthritis
Infectious:
Syphilis, lyme, toxo, TB, HSV, herpes zoster
Others:
Sarcoidosis, trauma, post-ocular surgery, large abrasion
Iritis effect on IOP
Decreases IOP
Exception:
If severe, HSV, VZV, can cause inflammatory glaucoma (trabeculitis)
Tx of iritis/iridocyclitis
Mydriatics
Steroids
Systemic analgesia
Indication of W/U in iritis/iridocyclitis
If recurrent
The major site of inflammation in intermediate uveitis
Vitreous
Causes of intermediate uveitis
Mostly idiopathic
Sarcoidosis
Lyme
MS
Snowballs, snowbank
Snowballs: vitrous aggregates of inflammatory cells
Snowbank: gray-white fibrovascular plaque at the pars plana
Both are signs of intermediate uveitis
Tx of intermediate uveitis
Steroids
Immunosuppressive agents
Vitrectomy
Cryotherapy/ laser photocoagulation to the snowbank
Posterior uveitis causes
Syphilis TB HSV CMV Histoplasmosis Candidiasis Toxoplasmosis Toxocara
Immunesuppression predisposes to above infections
Behcet
Malignancies
Pain and uveiitis
Anterior:
Ocular pain
Globe tenderness
Brow ache
Intermediate: -
Posterior: -
Uveitis with visual field loss
Posterior uveitis
Tx of posterior uveitis
CS
Most common cause of reversible blindness all over the world
Cataract
The most common cause of cataract
Age related
Underlying etiologies for cataract
DM Wilson Galactosemia Homocystinuria Hypocalcemia Traumatic Intraocular inflammation Steroids Phenothiazines Radiation High myopia
Congenital cataracts presentation
Altered red reflex
Leukocoria
Second sight phenomenon is seen in
Cataract
Patient is more myopic than previously noted
Patient may read without previously needed reading glasses
Cortical cataract seen in:
Aging
DM
Cause of nuclear sclerosis cataract
Age-related
Posterior subcapsular cataract causes
Steroids
Intraocular inflammation
DM
Trauma
Radiation
Aging
Tx of cataract
Surgical:
Phacoemulsification
Indications for cataract surgery
If vision loss leads to functional impairment
To aid management of other ocular diseases
Congenital cataract
Traumatic cataract
Complications of cataract surgery
RD
Endophthalmitis
Dislocated IOL
macular edema
Glaucoma
Posterior capsular opacification
Etiology of lens dislocation
Marfan
Homocystinuria
EDS
lens coloboma
Syphilis
Traumatic
Complications of dislocated lens
Cataract
Glaucoma
Uveitis
Tx of dislocated lens
Surgical replacement
Etiology of posterior vitrous detachment
Syneresis due to age
Complications of posterior vitreous detachment
Retinal tear
Retinal detachment
Bleeding
Treatment of posterior vitreous detachment
R/O retinal tear/detachment
No specific treatment
Vitreous hemorrhage etiologies
Proliferative diabetic retinopathy
Retinal tear/detachment
Posterior vitreous detachment
Retinal vein occlusion
Trauma
Tx of vitreous hemorrhage
R/O RD by U/S B-scan
If non-urgent:
Expectant Mx. Blood resorbs in 3-6 mo
Surgical:
Vitrectomy
RD repair
Retinal endolaser to possible bleeding sites
Vitreous/retinal hemorrhage in child
R/O child abuse
Etiology of endophthalmitis
Most common: post operative
Penetrating injury
Endogenous spread
Intravitreal injection
Bacterial > fungal
Tx of endophthalmitis/vitritis
Ocular emergency
If LP vision or worst:
Admit
Immediate vitrectomy
Intravitreal AB
If HM or better:
Vitreous tap fir culture
Intravitreal AB
Topical fortified AB
Tetanus Px if post-traumatic
Fundoscopy of central/branch retinal artery occlusion
Cherry-red spot
Retinal pallor
Cotton wool spots
Cholesterol emboli at arteriole biforcations
Tx of CRAO
Emergency
Restore blood flow within 2 h:
Massage the globe (10s compress, 10s release x5’)
Decrease IOP: Topical BB IV acetazolamide IV mannitol Anterior chamber paracentesis
Nd:YAG laser embolectomy
Intra-arterial or intravenous thrombolysis
When does irreversible retinal damage happen in complete RCAO
> 90 min
Central/brand retinal vein occlusion etiologies
Arteriosclerotic vascular disease HTN DM Glaucoma Hyperviscosity Drugs (OCP, diuretics)
Fundoscopy of CRVO
Blood and thunder
Diffuse retinal hemorrhage
Cotton wool
Venous engorgement
Swollen optic disc
Macular edema
Complications of CRVO
Neovascularization
Secondary glaucoma
Vitreous hemorrhage
Macular edema
Tx of CRVO
Treatment available for complications:
Photocoagulation
Anti-VEGF
CS injection
Ranibizumab
Curtain of blackness
Retinal detachment
IOP in retinal detachment
Decreases
Tx of retinal detachment
Emergency
Rhegmatogenous:
Scleral buckle
Pneumatic retinopexy
Vitregtomy+ gas injection
Tractional:
Vitrectomy
+/- membrane removal/ scleral buckling/ intraocular gas or silicon oil
Exudative:
Tx of underlying
Px of RD
If symptomatic tears (flashes, floaters):
Seal off with laser/cryotherapy
Retinotis pigmentosa
Mostly:AR
Rod > cone photoreceptor degeneration and retinal atrophy
Sx of retinitis pigmentosa
Night blindness
Tunnel vision
Decreased central vision
Glare (posterior subcapsular cataract)
Fundoscopy of retinitis pigmentosa
Bone-spicule pigment clumping in mid-periphery of retina
Pale disc
Narrowed arteriols
Investigations for retinitis pigmentosa
Electroretinography
Electrooculography
Tx of retinitis pigmentosa
No Tx
Vit A and Vi E
Cataract extraction
Most common cause of irreversible blindness in west
AMD
Types of AMD
Non-exudative (dry):
Slow progression
Drusen
Geographic RPE atrophy
Can progress to wet form
Exudative (wet):
Choroidal neovascularization.
Can result in detachment of RPE and retina.
Hemorrhage/lipid deposition into sub-retinal space.
Elevated subretinal mass (disciform scarring, severe central vision loss).
RFs for AMD
Female
Age
FHx
Smoking
Caucasian
Blue irides
Sx of AMD
Progressive central vision loss
Metamorphosis
Inv for AMG
Amsler grid
Fluorescein angiography
OCT imaging
Tx of AMD
Dry:
Monitor Low vision aids Anti-oxidants Green leafy vegetables Sunglasses/visors
Wet AMD:
Intravitreal anti-VEGF
Laser photocoagulation (for neovascularization)
PDT with verteporfin
No Tx for disciform scarring
Substance increasing the risk of lung cancer and its substitute
Carotenoid
Substitute: lutein + zeaxanthin
Normal cup/disc ration
0.4 or less
Which cup/disc is suspicious of glaucoma?
C:D > 0.6
C:D difference between eyes > 0.2
Cup approaches disc margin
Most common form of glaucoma
Primary open angle glaucoma
minor RFs for Primary open angle glaucoma
Myopia
HTN
DM
Hyperthyroidism
Chronic topical CS
Previous ocular trauma
Anemia/hemodynamic crisis
Eye surveillance in ophthalmic CS users
If > 4wk
Yearly exam
Earliest sign of Primary open angle glaucoma
Optic disc changes
Increased C:D ratio
C:D asymmetry between eyes > 0.2
Eye exam in Primary open angle glaucoma
Increased C:D ratio
Thinning, notching of neuroretinal rim
Flame-shaped disk hemorrhage
360° peripapillary atrophy
Nerve fiber layer defect
Large vessels nasally displaced
Visual field loss: Paracentral defect Arcuate scotoma Nasal step Central vision (late)
Major RFs for Primary open angle glaucoma
IOP > 21
Age
African ethnicity
Familial
Thin central cornea
Tx of Primary open angle glaucoma
Increase aqueous outflow:
Topical cholinergics
Topical PG analogues
Topical a-adrenergics
Decreased aqueous production:
Topical BB
Topical/oral carbonic anhydrase inhibitor
Topical a-adrenergics
Laser trabeculoplasty
Cyclophtocoagulation
Trabeculotomy
Minimally invasive glaucoma surgery
Follow up of primary open angle glaucoma
Serial optic nerve head examination
Serial IOP measurement
Serial visual field testing
The only modifiable risk factor that has been proven to prevent progression of glaucoma
Elevated IOP
Normal tension glaucoma
Normal IOP
Primary open-angle glaucoma
Women > 60
Associations: Migraine Peripheral vasospasm Systemic nocturnal hypotension Sleep apnea
Tx: underlying
Secondary open angle glaucoma
Steroid
Trauma
Pigmentary dispersion syndrome
Pseudoexfoliation syndrome
Causing meshwork obstruction
RFs for primary angle-closure glaucoma
Hyperopia Age > 70 F FHx Asian and inuit Mature cataract Shallow anterior chamber Pupil dilation (stress, darkness, anticholinergics)
Cornea and pupil in open angle vs angle-closure glaucoma
Open: nl
Angle-closure:
Corneal edema
Fixed, mid-dilated pupils
Tx of primary angle-closure glaucoma
Emergency
Miotic drops (pilocarpine)
Multiple topical IOP lowering agents (BB, AA, Choli)
Hyperosmotic agents (oral glycerine, IV mannitol)
Secondary angle-closure glaucoma
Uveitis
Neovascularization (proliferative diabetic retinopathy, CRVO)
Test for loss of sympathetic innervation
4-10% cocaine
Will cause dilation of normal pupil (prevents re-uptake of NE)
No dilation if loss of sympathetic fibers
Eye receptors
a1:
Mydriasis
B2:
Ciliary muscle relaxation
Increased aqueous humour production
M3:
Miosis
Accommodation (ciliary contraction)
Differentiating pre- vs post-ganglionic sympathetic lesions
0.125 % epinephrine:
If dilated : postganglionic (increased receptors)
Normal pupil: no dilation
Pre- vs post-ganglionic parasympathetic lesion differentiation
0.125% pilocarpine
If constriction: pupil constricts
Normal pupil: no constriction
Idiopathic/physiologic anisocoria
20% of population
Round
Regular
<1 mm difference
Reactive to light/accommodation
Responds to miotic/mydriatics
Post eye surgery
Argyll-Robertson pupil
Abn miotic pupils (<3mm)
Poor light response, better accommodation
Irregular
Usually bilateral
Site of lesion in Argyll-Robertson pupil
Midbrain
Horner’s syndrome
Unilateral
Abn miotic + Ptosis + anhydrosis + pseudoenophthalmus
Round
Brisk light and accommodation response
Anisocoria in Horner
Worse in the dark
Site of lesion in Horner
Sympathetic system
Adie’s tonic pupil
Abn mydriatic pupil (impaired constriction)
Irregular
F>M
Poor light response
Better accommodation
Hypersensitivity to dilute pilocarpine
Anisocoria in Adie’s tonic pupil
Worse in light
Site of lesion in Adie
Ciliary ganglion
Pupil in CN III palsy
Mydriatic
Fixed in acute phase at 7-9 mm
Round
Constricts with pilocarpine
Anisocoria in CN III palsy
Worse in light
If no pupil response to mydriatic/miotics
Problem at iris sphincter level
If Horner pupil dilated with hydroxyamphetamine,
Central or preganglionic lesion
Etiologies of Argyll-Robertson pupils
Syphilis
DM
MS
Encephalitis
Chronic alcoholism
CNS degenerative diseases
Marcus Gunn pupil
RAPD
Lesion in visual afferent pathway anterior to optic chiasm
Does not occur with media opacity
Pupil reacts poorly to light/ better to accommodation
Most common intra-ocular malignancy in adults
Mets
Breast, lung
Most common primary intra-ocular malignancy in adults
Melanoma
Most common intra-ocular malignancy in children
Neuroblastoma mets
DDx of RAPD
Large RD BRAO CRAO CRVO Advanced glaucoma Optic nerve compression Optic neuritis (most common)
CATARACT NEVER PRODUCES RAPD
HIV retinopathy
Most common retinopathy in HIV
Cotton wool
Intraretinal hemorrhage
CMV retinitis
CD4 < 50
Necrotizing Hemorrhage Vasculitus Brushfire Pizza pie
Progression to other eye in 4-6 wk
Tx of CMV retinitis
Gancyclovir
Foscarnet
(IV, intravitreal)
Necrotizing retinitis of HIV
HSV VZV Toxo Disseminated choroiditis Pneumocystis carinii Mycobacterium avium intracellulare Candida
Candidal endophthalmitis
Fluffy
White-yellow
Superficial retinal infiltrate.
May eventually result in vitritis
Tx: systemic amphoB, oral fluconazole
Toxoplasmosis retinitis
Focal
Gray-yellow-white
Chorioretinal
Surrounding vasculitis
Vitreous infiltration
Visual impairment more with congenital form
Tx of toxo retinitis
Pyrimethamine
Sulfonamide
Folinic acid
Clindamycin
+/- steroid
Most common cause of blindness in young people in north America
DM
Loss of vision in DM due to:
Progessive microangiopathy:
Macular edema
Progressive retinopathy:
Neovascularization, retinal detachment, vitreous hemorrhage
Rubeosis iridis:
Neovascularization of iris, glaucoma
Non-proliferative diabetic retinopathy findings
Microaneurysms
Dot and blot hemorrhage
Hard exudate (lipid deposits)
Macular edema
Advanced non-proliferative diabetic retinopathy
Microaneurysms
Dot and blot hemorrhage
Hard exudate (lipid deposits)
Macular edema
Plus:
Venous beading in at least 2 of 4 quadrants
IRMA (intraretinal microvascular anomalies) in at least 1 quadrant. Dilated leaky vessels
Cotton wool spots
Proliferative diabetic retinopathy
Neovascularization of iris, disc, retina
=>
Neovascular glaucoma
Vitreous hemorrhage
Retinal detachment
Screening for diabetic retinopathy in DM 1
5 yr after Dx, annually
All pts >12 y, annually
All pts entering puberty, annually
Screening for diabetic retinopathy in DM 2
Start examination at time of Dx, annually
Screening for diabetic retinopathy in Pregnancy
Gestational diabetes:
No need for screening
DM1/2:
Ocular exam in T1 and close F/U throughout
Effect of pregnancy on diabetic retinopathy
Can exacerbate
Tx of diabetic retinopathy
Tight control of blood sugar
BP control
If clinically significant macular edema:
Focal laser
Intravitreal CS
Intravitreal anti-VEGF
If proliferative DR:
Pan-retinal laser photocoagulation
If non-clearing vitreous hemorrhage:
vitrectomy
If tractional retinal detachment in PDR:
Vitrectomy
Lens changes in DM
Earlier senile cataract
Hyperglycemic cataract due to sorbitol accumulation
Sudden refractive changes by changes in blood glucose level
DM and extraacular muscle palsy
CN III infarct
CN IV and VI
Course:
Usually recover within few month
Optic nerve and DM
Optic neuropathy due to infarction of optic disc/nerve
Most common manifestation of HTN in the eye
Retinopathy
Acute HTN retinopathy
Retinal arteriolar spasm
Superficial retinal hemorrhage
Cotton wool
Optic disc edema
Chronic HTN retinopathy
AV nicking
Flame/blot retinal hemorrhages
Microaneurisms
Cotton wool
Effect of medical therapy on DR
Reduction in DR rate by:
Intensive glycemic control
Intensive combination treatment of dyslipidemia
(But not HTN)
MS optic neuritis treatment
IV steroid, taper to oral form
DO NOT TREAT WITH ORAL CS IN ISOLATION, this increases likelihood of eventual MS
Most common source of Amaurosis Fugax
Ipsilateral carotid
Amaurosis Fugax sign/symptoms
< 5-10 min
Hollenhorst plaques
Effect of thyroid gland treatment in Grave’s on ophthalmopathy
None!
Pathophysiology of Grave’s ophthalmopathy
Sympathetic overdrive
Inflammatory infiltrate of orbital tissue
Course of Grave’s ophthalmopathy
Initially: inflammatory
Followed by: quiescent cicatricial phase
Tx of Grave’s ophthalmopathy
Tx of hyperparathyroidism
Corneal exposure:
Hydration
Diplopia/ proptosis/ compressive optic neuropathy:
CS (acute phase)
Orbital bony decompression
RT of orbit
Strabismus/ eyelid problem:
Surgery once inflammation subsides
Most common eye manifestation of collagen vascular diseases
Keratoconjunctivitis sicca
Negative Bx for GCA, next step?
Bx the other side
Mutton fat keratitic precipitates
Sarcoidosis
Sarcoidosis eye Sx
Granulomatous uveitis
Optic neuropathy
Oculomotor abnormalities
Visual field loss
Strabismus in children < 4mo
Sometimes resolves
Esp if:
Intermittent deviation
Variable
Measures < 40 prism diopters
Incomitant (paralytic strabismus)
Most often acquired
Neural, muscular, structural causes
Diplopia: common
Amblyopia: uncommon
Concomitant strabismus (nonparalytic)
Gradual or shortly after birth
Infancy
No restriction in ROM of eye
Monocular, alternating, intermittent
Diplopia: uncommon
Risk of amblyopia (unless alternating or intermittent)
Accommodative esotropia seen in
Hyperopes (constantly accommodating)
Reversible with correction of refractive error
Average age of onset of accommodative esotropia
2.5 yr
Non accommodative esotropia
50% of childhood strabismus
Mostly idiopathic
Maybe due to monocular visual impairment or divergence insufficiency
The most common cause of amblyopia
Strabismus (esp esotropia)
Detection of amblyopia
Holler test:
Young child upset if good eye is covered
Quantitative visual acuity by age 3-4 yr, using picture charts, matching game
Amblyopia Tx less successful if not treated by age:
8-10yr
A trial should be given no matter what age
Prognosis of amblyopia
Good if treated < 4yr
Mx of amblyopia
Strabismus:
Restore ocular alignment + patching until 8 yr
Anisometropia:
Glasses
Patching if visual acuity difference persist after 4-8 wk
Deprivation amblyopia:
Treat underlying
Patching
In anisotropia, amblyopia happens in which eye?
The more hyperopic eye
Indications for safety glasses or poly carbonate lenses in amblyopia
If visual equity in worse eye < 20/50
Mx of leukocoria
Urgent referral
DDx of leukocoria
Cataract Retinoblastoma Retinal coloboma ROP persistent hyperplastic primary vitreous Persistent fetal vasculature Toxocariasis RD
Most common primary intraocular malignancy in children
Retinoblastoma
Retinoblastoma
1/3 bilateral
Malignant
Leukocoria/strabismus
Mx of retinoblastoma
Screening of siblings/offspring
U/S or CT: calcified mass
RT
Chemo
Laser
Cryopexy
Enucleation
RFs for retinopathy of prematurity
Non-black race
Low GA
Birth weight < 1500g
High O2 exposure after birth
Tx of ROP
If fibrovascular tissue:
Laser: standard treatment
Cryo
Anti-VEGF (off-lable)
If retinal detachment:
Watch carefully
Vitrectomy
Scleral buckle
Prognosis of ROP
High rate of myopia
Nasolacrimal defect presentation
At 1-2 mo of age
Sx of nasolacrimal system defects
Epiphora Crusting Discharge Recurrent conjunctivitis Mucopurulent discharge with pressure
Tx of nasolacrimal obstruction
Massage over lacrimal sac
Spontaneous resolution within 9-12 mo
If no resolution, referral for duct probing
Dx of ophthalmia neonatorum
Stains, cultures
Epiphora in infant
R/O congenital glaucoma
Nasolacrimal obstruction
First thing to check when ocular trauma
Visual acuity
Referral of eye trauma if:
Decreased VA Shallow anterior chamber Hyphema Abnormal pupil Ocular misalignment Retinal damage
Mx of penetrating eye trauma
Initial Mx: refer immediately
ABC
Don’t press on eye globe
Don’t check IOP if possibility of glob rupture
Check VA/ EOM
Rigid eye shield
Keep head 30-45° elevated
NPO
Tetanus status
IV AB (depending on trauma mechanism):
Mostly gram positives
If foreign body: bacillus
If organic matter: fungal
Usually: AG+ Cefazolin
R/O foreign body
CT orbit
Post traumatic infectious endophthalmitis
Increased risk if delayed repair (>24h)
If intra-ocular foreign body:
Early vitrectomy and foreign body removal (within 24h)
Extreme pain+ hypopyon + vitritis
Obtain samples
AB (IV, intravitreous)
Shaken baby syndrome
No external signs
Respiratory arrest
Seizures
Coms
Extensive retinal/intravitreal hemorrhage
Inv for blow-out fx
Plane film (Water’s, lateral)
CT: AP, coronal
Tx of blow-out fx
Refrain from coughing, blowing nose
+/- Systemic AB
Surgery if:
Fx > 50% orbital floor
Diplopia not improving
Enophthalmus > 2mm
Indicative of poor prognosis in eye chemical burn
Opaque cornea
Alkali burn
Tx of chemical burn
Immediate irrigation with water or buffered solution
ED:
Irrigate with IV drip and eyelid retracted until pH physiologic
Swab upper/lower fornices
DO NOT ATTEMPT TO NEUTRALIZE
Cycloplegic drops
Topical AB and patching
Topical CS (<2wk if persistent epithelial defect)
Drops for red itchy eyes
Anti-histamines:
Sodium cromoglycate
Decongestants:
Nephazoline
Phenylephrine
(Rebound vasodilation with overuse)
Abulia in damage to
Frontal lobe
Disinhibition in damage to
Frontal lobe
Apathy
in damage to
Executive function impairment in damage to
Frontal
Defect in orientation and judgment in damage to
Frontal
Primitive reflex re-emergence in damage to
Frontal
Upgoing babinski in damage to
Contralateral frontal
Pronator drift in damage to
Contralateral frontal
Lesion in frontal eye fieldcauses
Gaze towards destructive lesion
Gaze away from seizure focus
Lesion in occipital lobe
Contralateral homonymous hemianopsia
Dressing apraxia in damage to
Parietal, either side
Cortical sensory loss in lesion of
Parietal, either side
Lower homonymous hemianopsia in lesion of
Parietal, either side
Damage to dominant parietal lobe
In attention or extinction of non-dominant side
Aphasia
Gertsmann syndrome
Non-dominant parietal lesion
Hemispatial neglect
Apraxias
Agnosias
Antegrade amnesia in damage to
Hippocampus (temporal lobe)
Upper homonymous hemianopia
Temporal lobe
Hemiballismus in damage to
Subthalamic nucleus
Parinaud syndrome
Supranuclear upward gaze palsy
Damage to pineal gland/ dorsal midbrain
Decerebrate/decorticate posture in damage to
Decorticate: above red nucleus
Decerebrate: below red nucleus
Damage to cerebellar vermis
Truncal ataxia
Dysarthria
Damage to cerebellar hemisphere
Intention tremor
Ipsilateral limb ataxia
Fall towards side of lesion
Compensatory reserve of ICP Volume
Young: 60-80
Elderly: 100-140
Cerebral perfusion pressure
MAP-ICP
Almost constant cerebral blood flow in CPP 60-150
Circumstances under which cerebral autoregulation mechanism is not able to keep constant CBF
High ICP (Cerebral perfusion pressure < 40) MAP > 150 MAP < 50 Increased CO2 O2< 50 Brain injury
Normal ICP
Adults: 10-15 mmHg
Children: 3-7 mmHg
Infant: 1.5-6 mmHg
> 20: moderate elevation
40: severe elevation
Gold std for ICP measurement
Intraventicular cath
MAP target in TBI
> 80
Sx of acutely elevated Icp
H/A N/V Lethargy Significant decline in GCS Subtle optic disc changes Visual changes uncommon CN VI palsy Sunset eyes, esp in children with obstructive hydrocephalus Often herniation syndromes occure Focal deficits present
Sx of chronic ICP elevation
H/A N/V Irritability Inattentiveness LOC: Nl or modestly decreased Obvious papilledema Optic atrophy/blindness/enlarged blond spot Full EOM Herniation if acute on chronic FND can be present
Inv fir suspected ICP rise
CT/MRI
+/- ICP monitoring
Mx of elevated ICP
Head elevation: 30°
Fever Mx
Prevent hypotension
Ventilate to pCO2: 35-40
pO2: >60 mmHg
20% IV mannitol
Maintain sBP > 90
Dexa (if tumor, abscess)
Sedation
Paralysis
Barbiturate induced coma
Drain CSF
Decompressive craniectomy
Goals in ICP rise Tx
Tx when ICP > 20
Goal: ICP < 20
MAP > 90
CPP>65
Goals in trauma:
MAP > 80 in traumatic brain injury
MAP 85-90 in spinal cord injury
Effect of barbiturate coma Tx on ICP rise outcome
Decreased mortality
No effect on neurologic outcome
Associations of pseudotumor cerebri
Dural sinus thrombosis
Obesity
Hypervitaminosis A
Reproductive age
Mense irregularity
Addison/Cushing
IDA
Polycythemia vera
Steroid withdrawal
Tetracycline
Amiodarone
Lithium
Nalidixic acid
OCP
Neurologic deficit in pseudotumor cerebri
CN VI palsy
Visual Sx in pseudotumor cerebri
VA deficit
Field deficit
Papilledema
Optic atrophy
Blindness
Course of pseudotumor cerebri
Self limited
Inv for pseudotumor cerebri
MRI (+/- contrast):
Slit-like ventricles
Distended perioptic sub-arachnoid space
LP:
Opening pressure > 20
Normal CSF
Ophthalmologic exam:
VA/Field defect
Papilledema
Tx of pseudotumor cerebri
Wt loss
Fluid/salt restriction
Acetazolamide :(decreased CSF production)
Thiazide/furosemide
If failure:
Serial LP
Shunt
Optic nerve sheath decompression
F/U + repeat imaging + ophthalmo F/U
Most common cause of non-communicating hydrocephalus
Post-infectious CSF absorption block
Magnetic gait seen in
Normal pressure hydrocephalus
Triad of Hakim
Ataxia(magnetic gait)
Incontinence
Dementia
NPH
Inv for hydrocephalus
CT/MRI
U/S through anterior fontanelle in infants
ICP monitoring
Tx of hydrocephalus
External ventricular drain
Intermittent LP
Surgery for underlying
Shunt infection organisms
S. Epidermidis
S. Aureus
P. Acnes
Gram-negative becilli
Inv for suspected shunt infection
Shunt tap
B/C
CBC
Headache which is relieved by lying down in pts with shunt:
Over shunting
Overshunting investigations
CT: slit ventricles, subdural hematoma
DDx for ring enhancing lesion on CT with contrast
Mets
Abscess
Glioblastoma
Infarct
Contusion
Toxo
Lymphoma
Demyelination
Resolving hematoma
Radiation necrosis
Inv for brain cancer
CT MRI stereotactic Bx (tissue, molecular markers) Mets w/u Tumor markers
Tx of brain tumors
If slow growing/benign:
Conservative (serial Hx, PE, imaging)
CS (reduce ICP, cytotoxic edema)
Pharmacologic treatment for pituitary adenoma
Surgical excision
Shunt
RT
Chemo
New onset communicating hydrocephalus in cancer pts
Suspicion of leptomeningeal carcinomatosis
Most common brain tumor in <15yr
Supratentorial:
Astrocytoma
Infratentorial:
Meduloblastoma
Most common brain tumor > 15 yr
Supratentorial:
Adtrocytoma (GBM)
Mets (most common overally)
Infratentorial:
Mets
Brain mets
Most common intracranial tumor in adults
Often at:
Gray-white matter junction
Temporal-parietal-occipital lobe junction
Inv for mets
Find source: CXR CT abdomen/chest U/S abd Mammo Nuclear scan/PET
CT+ contrast for brain
+/- MRI
Tx of brain mets
Phenytoin/levotiracetam
Dexa + ranitidine
Chemo RT (if discrete, deep seated, inoperable): Stereotactic RT if < 3 lesions WBRT if multiple lesions Post-operative adjuvant RT
Surgical:
If single/solitary
Most common cancers metastasizing to brain
Lung > breast
Astrocytoma
Cerebral hemispheres»_space; other sites
CT: hypodense
MRI T1: hypointense
MRI T2: hyperintense
Low grade:
Calcification
No enhancement
High grade:
Enhancement
Central necrosis
Tx of astrocytoma
Low grade diffuse:
Surgery (better outcome)
RT (prolongs survival)
Chemo (for progression)
High grade (anaplastic, GBM) Goal: prolong quality survival Surgery \+RT \+Temozolomide
Multiple gliomas:
WBRT +/- chemo
Meningioma
Arises from arachnoid membrane
Calcified
Hyperostosis of adjacent bone
Bx: psammoma bodies
F> M
Increase in size with pregnancy (progesterone receptor)
Middle age
Association with NF2
Inv for meningioma
CT with contrast: Homogeneous, dense enhancement Dural tail Well circumscribed Usually solitary
MRI with contrast
Angiography (arterial supply, venous involvement)
Tx of meningioma
Conservative if:
Asymptomatic and non-progressive
Surgery(1st std therapy)
If symptomatic or documented growth
Endovascular embolization:
If highly vascularized, to facilitate surgery
Radiation:
If <3cm, partially occluding superior sagittal sinus
Vestibular Schwannoma
Slow-growing
If bilateral: NF2
Middle age
<2cm: hearing loss, disequilibrium, tinnitus
Compression on CN VIII, CN VII, CN V (>2cm)
> 4cm: cerebellar signs, BS signs, hydrocephalus…
Inv for acoustic neuroma
MRI with contrast
2nd choice: CT contrast
Audiogram
Brainstem auditory evoked potentials
Caloric test
Tx of acoustic neuroma
Expectant:
If small, hearing preserved, high perioperative risk, elderly
RT
Surgery if: >3cm BS compression Edema Hydrocephalus
Testing family members for NF2 mutation
CN palsies in pituitary adenoma
CN III
CN IV
CN V1, V2
CN VI
Order of function impairment in pituitary adenoma
GH LH FSH TSH ACTH PRL
Pituitary apopexy
Sudden expansion of mass due to hemorrhage or necrosis
Abrupt: H/A Visual disturbance Ophthalmoplegia Reduced mental status Panhypopituitarism DI
Inv for pituitary adenoma
Formal visual fields
CN testin
Endocrine tests:
PRL level, TSH, 8 AM cortisol, fasting glucose, FSH/LH, IGF-1
Lytes, urine lytesand osmolality
MRI +/- contrast
Tx of pituitary adenoma
Apoplexy:
Rapid CS
Surgical decompression
Prolactinoma:
Dopamine agonist
Cushing:
Cyproheptadine (serotonin antagonist)
Ketoconazole
Acromegaly:
Octreotide +/- bromocriptine
Endocrine replacement
Surgcal
Nerves in cavernous sinus
CN II, III, IV, V2, VI