Docstoc

OCULAR EMERGENCIES

Document Sample
OCULAR EMERGENCIES Powered By Docstoc
					                                 OCULAR EMERGENCIES

EYE EXAMINATION
History
        Past ocular trauma, surgery, eye related problems
Preexisting visual impairment, glassess, contacts
Onset and description of current problems
Work exposure (grinding, welding, etc), eye treatment
General medical health
Eye questions .........
changes in vision, flashers, floaters, black spots
redness
discharge
foreign body sensation
photophobia
Physical Examination
General Inspection
Trauma
Anatomy
Basilar skull #
Orbital #
Face
Globe disruption: limited exam
                Visual Acuity and Visual Fields
MUST always be measured and documented (legal issues)
Use glasses or pin hole
Snell chart - count fingers - hand motion - light perception
Can use near card in trauma room
Document clearly
PINHOLE: corrects refractive error
Vision corrects with pinhole: not worried
Vision doesn’t correct: retinal problem, vitreous problem, korneal, lens
Pupils
PERLA
Afferent pupilary defect (optic nerve abnormality)
Poorly reactive could be due to previous eye surgery or trauma, miotics (pilocarpine), or
mydriatics (atropine), or cyclopentolate
EOM
Paralysis can be seen in many lesions including diabetes, intracranial aneurysm/tumors,
intraorbital masses, myasenia gravis, demyelinating diseases, intracranial inflammatory lesions,
sphenoid sinusitis, trauma
Lids/Ocular Adnexa
Evaluate the position, contour, and color of the lids and periocular areas. Check for swelling,
discharge.
Anterior Segment
Includes cornea, conjunctiva, anterior chamber, iris, lens
Evaluated with slit lamp
Examine anterior chamber for wbc (inflam), rbc.s (hyphema), or increased protein in aqueous
fluid (flare = “fog”phenomenon)
Blue light used to look for corneal or conjunctival epithelial defects after putting in flouroscein
dye.
Intraocular Pressure
Measure when concerned about gluacoma (hyphema or iritis) or low pressure (ruptured globe)
Use tonopen, tonometer,dodmann applanation
Normal IOP ranges from 10 - 21
Anesthetize the cornea b/f measurement
Fundus
Optic nerve, retina, retinal vessels
Contraindication for dilation: iris-supported intraocular lens, untreated narrow angle glaucoma
Dilation: Mydiacyl 1%, Phenylephrine 2.5%
Orbit
Orbital symmetry, proptosis
Palpate orbital rim
Think about orbital floor or wall fractures in blunt trauma
Examine occular motility for entrapment
Xrays: AP and Water’s view
CT
Proptosis ddx: orbital hemorrhage, emphysema, edema, tumors

Differential diagnosis of unilateral Proptosis
Retroorbital hematoma
Retroorbital abscess
Retroorbital tumor
C/I TO DILATING A PUPIL
Hx of Glaucoma
Iris of Bombay
Ocular Trauma
Retrorbital emphysema
Edema
Differential diagnosis of bilateral Proptosis
Hyperthyroidism
Lymphoma
Metastasis
Lacrimal gland inflammation
Leukemias: kids
Metastatic neuroblastomas: kids
Differential diagnosis of a RED EYE
Conjunctivitis, conjunctival FB
Keratitis, corneal ulcer, corneal fb, UV keratitis
Episcleritis
Scleritis
Uveitis
Acute angle closure glaucoma

OCULAR TRAUMA

ORBIT AND LID CONTUSION
Echymosis, swelling of orbits and surrounding tissues
Most important thing is to look for other injuries
Examine under eyelids, obtain visual acuity
Ice, elevation, NSAIDs or tylenol; See MD for increase in symptoms

ORBITAL WALL FRACTURES
Blunt force, acute rise in intraorbitral pressure, prolapse of orbital soft tissues (usually into the
maxillary sinus because the orbital floor is the weakest orbital wall)
Orbital floor fracture/Blow out fracture
Entrapment of the inferior rectus, inferior oblique, orbital fat and connective tissue -------------->
enopthalmos, ptosis, diplopia, limitation of upward gaze
MAY have infraorbital nerve sensory loss if associated inferior orbital rim #
Subcutaneous orbital emphysema may be palpable
LOOK for associated globe injury: 10 - 25%
Tear-drop sign: bulge extending from the orbital floor into the maxillary sinus on Xray, and A/F
level in maxillary sinus are indirect signs of orbital floor fractures
Surgical repair: only for persistent diplopia or cosmetic concerns and is not usually performed
until 7 - 10 days to allow swelling to subside
Avoid blowing nose and valsalva to minimize orbital emphysema
Maxillary sinusitis: antibiotics, ice packs, decongestants
F/U with plastics
Antibiotic prophylaxis only if concurrent sinusitis
Medial orbital wall
                Fractures through the ethmoid bone and enters the ethmoid sinus
                Orbital emphysema (because of ethmoid air sinuses) and epistaxis
                Diplopia from medial rectus impingement can occur
                Orbital emphysema should prompt search for associated injury
                Orbital emphysema can be significant (rarely): compression of optic nerve and
acute visual loss; usually resolves on own, abx coverage not indicated unless fracture involves
infected sinus
RETRO-ORBITAL HEMATOMA
HEmorrhage in the potential space behind or around the eye
Significant hemorrhage leads to rise in intraorbital pressure that is transmitted to globe and optic
nerve ; central retinal artery occlusion possible (“compartment syndrome”)
SIGNS
                Proptosis
                Decreased visual acuity
                Afferent pupillary defect
                Increased IOP
                Decreased extraocular movement
Orbital CT will demonstrate the hematoma
Immediate opthamology consult warranted
Decrease intraocular pressure with carbonic anhydrase inhibitor, beta-blocker topically, iv
mannitol
Lateral canthotomy is definitive tx and should be done in ED if indicated
Prep the lateral canthus site
Inject lidocaine + epinephrine
Mosquito clamp to lateral canthus
Horizontal 1cm incision with cutting scissors
Release the lateral canthal (palpebral) ligament

CHEMICAL BURNS TO CORNEA/CONJUNCTIVA
True ocular emergency
Alkalis: drain cleaners, detergents, solvents, lime ------> liquefaction necrosis that penetrates and
dissolves tissues until the alkaline agent is removed
Acids: coagulation necrossis, less severe because precipitation of tissue proteins limits injury
General rule: alkaline with pH < 12 and acid with pH > 2 are thought not to cause significant
injury BUT concentration and time of contact are important factors also
Immediate, copious irrigation should be started at scene and continued for at least 30 min before
any attempt at transport (do NOT interrupt irrigation to transport)
Severity: degree of corneal clouding and scleral whitening
Long-term complications: perforation, scarring, glaucoma, neovascularization of the cornea,
adhesions of the lids to the globe (symblepharon), cataracts, retinal damage
ED
Topical anesthetic
Manual lid retraction to r/o retained chemical particles (remove with swab)
Insert a Morgen lens and irrigate 2L NS
After irrigation, wait test pH, wait 15 min and retest if OK
Irrigate until the tear film pH is neutral 7.40
Examination after irrigation: topical aneshtetic, look carefully for retained material especially in
fornicies, check IOP (esp important in alkali burns)
Update tetanus
Discuss with opthamology to arrange f/u and ask what they want to treat with
Cycloplegic (avoid phenylephrine)
Topical antibiotics
Pain management
Artificial tears q2hr


MISC SOLVENTS/IRRITANTS
Treat all exposures as acids/alkalis: assume the worst and irrigate like hell
Detergents: conjunctival irritation, may cause anterior chamber inflammation: tx as corneal
abrasion
Aerosol exposures: irrigate, check pH, topical antibiotics, pain control, consider intraocular
foreign body with propellants
Management of ocular superglue exposures:
               Immediate irrigation if possible
               Artificial tears qid
               Patch both eyes
               Arrange optho f/u
               Superglue will dissolve with time; if eyelids inverted may need surgical
intervention; consult opthamology regardless

THERMAL BURNS
More common to affect eyelids than globe because of reflex blinking and Bell’s phenomenon
Superficial eyelid burns: irrigation, topical antibiotic ointment
2nd or 3rd degree eyelid burns: opthamology consult
Hot liquid splashes and ashes to cornea: superficial corneal injury and treat as corneal abrasion
Molten metals and other hot objects may result in globe perforation
Polysporin bid to eyelid burns



RADIATION BURNS (ULTRAVIOLET KERATITIS, SOLAR KERATITIS)
Ultraviolet light: sun lamps, tanning booths, high-altitude env, welder’s arc
Ultraviolet light is directly toxic to the cornea
Latency of 6 - 12 hrs before symptoms
Symptoms
                Ocular pain
                FB sensation
                Tearing
                Photophobia
Signs
Blephorospasm
Decreased visual acuity
Conjunctival infection
Diffuse punctate keratitis (often with a discrete lower border defining the cornea protected by the
inferior lid)
Management
Tx: short acting cycloplegic, topical antibiotic ointment, eye patching for comfort, oral narcotics,
opthamology f/u in 24hrs

NEVER prescribe topical anesthetic drops ------> retards healing and can lead to corneal ulcer
formation




CORNEAL ABRASIONS
Pathophysiology
Cornea has abundant nerve supply thus very sensitive
Cornea heals quickly thus improvement expected rapidly
Small abraisons heal in 24hrs
Moderate in 48hrs
Large in 72hrs
Symptoms
               Ocular pain
               FB sensation
               Photophobia
               Blurry vision
Signs
Decreased visual acuity
Blepharospasm
Conjunctival injection
Epithelial defect with fluerescein staining
Must LOOK for FB
Management
               Topical anesthetics to aid exam and decrease pain
               No routine patching (can use if very large and it seems to help)
               No routine abx (consider if very large)
               Oral analgesics: ibuprofen, few percocet
               Topical NSAIDS: Acular 0.5% one gtt qid X 3/7 (expensive $45) or voltaren
               Cycloplegics: two drops of 5% homoatropine in ED, could give prescription after
but the duration of this is 10-48hrs thus well on the way to healing.
               Avoid contact lenses
               Update tetanus
               Small: no follow up unless problems
               Large: f/u in 24-48hrs in ED or optho
               Indications for opthamologic consultation
Very large corneal abraison
Center of visual access
Failure to improve in 24-48hrs
De-epithelialization = when patient blinks they remove the new corneal surface thus preventing
or delaying healing; use ++ artificial tears and refer to optho
Evidence re Patching
Kaiser P. Opthamology 1995. 102: 1936-1942.
Mydriatric, abx ointment, then randomized to patch
Days to heal: 2.3 no patch vs 2.6 patch (significant)
Pain scale: 1.8 no patch vs 2.53 patch (signficant)
Subgroup of large abraisons > 10 mm: “trend” towards faster healing with patching
                Campanile et al. J of Emerg Med 1997. 15 (6): 769-774.
                                        % healed at 24hrs: 97% no patch, 84% with patch




Evidence re Antibiotic prophylaxis
King J. Can Fam Phys 39: 2349-2352. 1993.
Corneal abraisons, FB, minor burns, UV keratitis
Prospective observational study
F/u at 1-3 days (90%)
0.7 % had a corneal or conjunctival infection
Evidence re topical NSAIDS
Szucs. Annals 2000. 35(2)
Voltaren 0.1% vs placebo drops
Pain scale decreased 3.1 points vs 1.0 with placebo
                Kaiser. Opthamology 1997. 104(8)
Ketorolac vs placebo
Decreased pain at 24hrs
Decreased photophobia, FB sensation
No delay in healing
Earlier return to work (½ day)

CORNEAL FOREIGN BODIES
Symptoms
               FB sensation
               Ocular pain
               Tearing
               +/- blurry vision
Signs
Blepharospasm
FB on cornea
Conjunctival
+/- decreased acuity
Underlying corneal abraison
Removal
Cotton tip
Irrigation
Needle: 25 guage
Commercial eye spud
CONSIDER intraocular FOREIGN BODIES
                High-speed drills, saws, grinders, pounding objects, explosions
                Dye streaming, extruded ocular contents, pupillary defect,
                Orbital Xray if radiopaque, orbital CT other option
Corneal Rust Rings
Occurs with oxidization after contact with a metal corneal FB
Must remove metallic rust particles
Rust stain: attempt early removal or recheck in 24-48hrs as it may “migrate” to the surface as the
cornea reepithelizes
Removal: needle, burr
Manage after as a corneal abraison
Referral for very large or deep rust rings or problems removing




CONJUNCTIVAL FOREIGN BODY
Attempt removal before local anesthetic then patient will be able to tell you it is gone!
Make sure you ever both eyelids and do a double eversion!
Persistent FB sensation and you can’t find anything
Wait 24 hrs
Optho referral if doesn’t improve (you can rarely have things hidden way up where you can’t
see)
Unique complicaiton of perilimbal foreign body
Can trigger a pterygium = conjunctiva grows onto the corneal surface


INTRAOCULAR FOREIGN BODIES
Small intraorbital and intraocular FB can occur with any perforating injury
Difficult to diagnose
SUSPECT with grinding, sanding, drilling, hammering, explosions
Investigate based on HISTORY alone; physical may be normal
Xray, U/S, CT for diagnosis
Xray: metal, or glass
U/S: wood
CT: everything
Orbital CT probably the most useful
MRI contraindicated if metallic FB suspected
Siderous Oxidation: late complication of iron containing FB that can lead to visual loss
Chalcosis: sterile inflammatory reaction to copper containing compounds that may require
removal of offending agent
History
                Grinding, sanding, drilling, hammering, explosion
                Felt a “twinge” in my eye but it doesn’t hurt now (compared to corneal or
conjunctival FB which cause ongoing pain)
Signs
May be none
Distorted pupil
Extruding intraocular contents
Streaming of dye on the cornea
Localized collection of blood over the sclera
Management as per globe penetration
Opthamology consult
NPO
Eye shield
Antibiotics
Removal: depends on what it is; organic FB are removed b/c of risk of infection; inorganic
(metal, glass, plastic) may be left b/c removal may cause more damage




SUBCONJUNCTIVAL HEMORRHAGE
Rupture of small subconjunctival blood vessel as a result of trauma or valsalva maneuver
Can occur spontaneously without apparent cause
Should be asymptomatic: pain, diminished visual acuity, photophobia suggest other problem
Flat, bright red, smooth, limited to the bulbar conjunctiva, sharply demarcated at the limbus
MUST distinguish from bloody chemosis (edema of conjunctiva) which is indicative of more
serious globe pathology
MUST consider globe rupture with large, circumferential, elevated subconjunctival hemm
Bilateral or recurrent subconjunctival hemorrhages may require work up for bleeding diathesis
Treatment: cold compress X 24hrs, resolution in 2 - 3 weeks

TRAUMATIC HYPHEMA
Disruption of blood vessel in iris or ciliary body
Blood layers if pt sitting and forms a meniscus with the aqueous humor
Size ranges from microscopic hyphema to “eightball”
Symptoms
               Ocular pain
               Photophobia
               Blurry vision
Signs
Decreased visual acuity
Anterior chamber microscopic red cells
Anterior chamber hyphema
Elevated IOP
NO afferent pupilllary defect unless eight ball
Complications
                Elevated intraocular pressure
                Corneal staining
                Rebleeding
                Synechiae
Management
R/O other ocular injuries
List five discharge instructions:
Tylenol for pain
Avoid aspirin, ibuprofen, antiplatelets
Limited activity
Avoid reading
Avoid valsalva
Discuss with optho to arrange followup (they can decide what to treat with if anything): miotics,
mydriatics, cycloplegics, steroids, antifibrinolytics (aminocaproic acid)
Increased intraocular pressure: discuss with optho; topical beta blocker; add topical alpha agonist
or topical carbonic anhydrase inhibitor if needed; oral acetaxolamide or IV mannitol may be used
Surgical intervention with raised IOP that isn’t responsive to medical mx
Case reports of anterior chamber thrombolysis




Rebleeding
                Major complication, usually 2 - 5 days when the initial clot retracts and loosens
                There is NO DIFFERENCE in rebleeding rates with inpatient vs outpatient Rx
                List five predictors of rebleeding
                                (i) poor initial visual acuity (20/200)
                                (ii) large initial hyphyema (covering > 1/3 of anterior chamber)
                                (iii) late presentation (presents > 1 day after injury)
                                (iv) elevated IOP at initial exam
Hemoglobinopathies
Sickle cell anemia, thalasemia, etc
Increased risk for complications
RBC in anterior chamber is acidic and hypoxic leading to decreased aqueous humor outflow and
rapid rise in IOP
Tx: topical beta blockers: leave other antiglaucoma Rx to opthamology (methazolamide may be
used instead of acetazolamide)

TRAUMATIC IRIDOCYCLITIS
Contusion and inflammation of the iris and ciliary body resulting in ciliary spasm
Hx: deep eye pain, photophobia, excessive tearing
O/E: perilimbal conjunctival injection (ciliary flush), cells and flare in the anterior chamber,
small poorly dilated pupil
Treatment
Long acting cycloplegics to paralyze the iris and ciliary body (homatropine methylbromide 5%
1 gtt qid X 7 days)
Prednisolone acetate 1% may be given to reduce inflammation if there is no improvement in 5 -
7 days but should be avoided in patients with a corneal epithelial defect (leave to opthamology)
Resolution in 1 week

MISC ANT CHAMBER/IRIS NONPENETRATING TRAUMA
Traumatic mydriasis and miosis
Blunt injury may result in either pupillary dilation or constriction
May persist for days
Must r/o cranial nerve palsy before ascribing to local contusion
Permanent mydriasis may result from small radial tears in the pupillary sphincter muscle; pupil
margin may be irregular or scalloped, no specific tx
Iridodialysis
Tearing of the iris root from the ciliary body leading to the formation of a “secondary accessory
pupil”
Often the cause of a hyphema
No specific tx
Large tears may need surgery, f/u with optho
Anterior Chamber angle recession
Blunt injury to ciliary body may cause posterior displacement of the iris increasing the anterior
chamber and damaging the trabecular meshwork that drains the aqueous humor
Can cause acute glaucoma



CATARACT
Lens capsule disruption, dehydrated stroma of lens absorbs fluid, swells, and becomes cloudy
Acute glaucoma may develop from blockage of the aqueous humor flow through the pupil
necessitating surgery
Cataract formation may occur over weeks to months

LENS SUBLUXATION AND DISLOCATION
Complete disruption of lens zonule fibers may result in complete ant or posterior dislocation
Incomplete disruption of lens zonlule fibers results in subluxation
MINOR trauma: Marfans’s, homocystinuria, tertiary syphilus, other predisposing conditions
Hx: monocular diplopia or visual distortion with subluxation and marked visual blurring with
dislocation
O/E: decreased visual acuity, edge of subluxed lens can be seen when pupil is dilated,
iridodonesis is the trembling or shimmering of the iris after rapid eye movements and is a helpful
sign of lens dislocation
Tx: observation to surgical removal depends on location of dislocated lens and associated eye
injury as per immediate opthamology consult
GLOBE RUPTURE
Sudden elevation in IOP from blunt trauma may cause scleral rupture
Two most common locations are where the sclera is thinnest: (i) insertions of intraocular
muscles or (ii) limbus where sclera is thinnest
Diagnosis may not be obvious when intraocular contents are seen
Symptoms
                Hx of ocular trauma
                Ocular pain
                Blurry vision
Signs
Extruding ocular contents: brown/black jelly
Decreased visual acuity
Streaming dye on the cornea
Distorted pupil = teardrop pupil
Severe bloody chemosis
Severe subconjunctival hemorrhage at scleral rupture sits
Decreased I.O.P:
Hx: eye pain, decreased vision: Tonometry is CONTRAINDICATED if suspecting ruptured
globe
Management
                Avoid any maneuver that increased IOP: analgesia, antiemetics
Avoid further examination or manipulation of the eye
Eye shield to prevent accidental pressure on eye: Fox eye shield or tap a cup over eye (NO gauze
over eye b/c it will draw out fluid)
NPO
Tetanus
Do NOT measure IOP
IV broad spectrum antibiotics
Avoid succinylcholine (ya right!)
                Consult opthamology: CT, U/S, indirect opthalmoscopy may play a role in occult
globe ruptures

Succinylcholine, IOP, and globe rupture or penetrating eye injury
Globe rupture/penetration listed as contraindication to succinylcholine
Succinylcholine increases IOP 1 - 4 min after administration, lasts 7 min
Many agents have been tried to prevent incr IOP: nondepolarizing paralytics, diazepam,
gallamine, tubocurarine
Libonati 1985: 100 patients with penetrating eye injury pretreated with nondepolarizing agent
then given succinylcholine -----> NO adverse events
NOTE: succinylcholine increaes IOP by 3 - 8 mmHg, blinking increases by 10 - 15 mmHg,
coughing/bucking/resisting will increase IOP MORE than succinylcholiine, airway management
more important
Could use nondepolarizer instead for paralysis but will be paralyzed for 30+ minutes

MISCELLANEOUS OCULAR INJURIES
Vitreous hemorrhage: floaters, decreased acuity, manage like a hyphema and refer to optho
Retinal tears and detachments: flashers and floaters, decreased acuity, f/u with optho
Retinal hemorrhages
                Preretinal (subhyaloid), superficial retinal, or deep (subretinal) spaces
Preretinal hemorrhage: boat shaped
Superficial retinal hemorrhage: flame shaped
Deep retinal hemorrhage: rounded and grape-purple colorvement
Commotio Retinae
Decreaed visual acuity or asymptomatic
Cloudy whitening of the involved retina that will subside in weeks
No specific treatment
F/U to ensure that retinal tear or detachment hasn’t occurred
Optic nerve injuires: avulsion, transection, contusion, compression of optic nerve
                Suspect with orbital fractures
                Decreased visual acuity, A.P.D.
                Orbital CT, r/o retrorbital hematoma
                Optho consult




EYELID LACERATIONS
LOOK for globe rupture and intraocular foreign bodies
Simple = ED repair
Horizontal or oblique
Partial thickness
6-0 or 7-0 nylon
Removal in 3 - 5 days
Complex = Opthamology or plastics
Vertical
Full thickness
Involving the tarsal plate (correction must be perfect)
Involving the lid margins
Involving the canalicular system (medial to puncta of lower eyelid)
Involving the levator or canthal tendons
Lacerations with tissue loss
Through the orbital septum: orbital fat will protrude through septal lacerations into the wound;
eyelids have no subcutaneous fat thus the appearance of fat in a lid laceration confirms the
diagnosis; HIGH incidence of globe penetration and intraorbital foreign bodies

CONJUNCTIVAL LACERATIONS
LOOK for intraocular FB or scleral perforations (common)
Slit lamp examination to help distinguish superficial versus deep lacerations
Small, superficial lacerations: no suturing, heal quickly, topical antibiotics
Large (>1cm) or deep: may require repair, consult opthamology

CORNEAL AND SCLERAL LACERATIONS
Corneal lacerations
Signs of full thickness corneal lacerations include loss of anterior chamber depth, teardrop-
shaped pupil caused by iris prolapse through the corneal laceration, blood in the anterior
chamber
Small lacerations can be difficult to dx: slit - lamp examination may reveal aqueous humor
leaking from the corneal wound and is seen as streaming fluorescent dye surrounded by an
orange pool of solution
Full-thickness corneal lacerations are managed as traumatic globe rupture: avoid eye
manipulation, eye shield, NPO, iv antibiotics, antiemetics, optho consult
Superficial partial - thickness corneal lacerations: cycloplegic, topical abx, pressure patch if not
gaping; to OR for closure if gaping
Scleral lacerations
Presentation and managment as per blunt globe rupture




COMPLICATIONS OF OCULAR TRAUMA
Post - Traumatic corneal ulcers
Any defect in the corneal epithelium may become infected
Ulcers are surounded by a cloudy white or gray cornea
Reactive sterile hypopyon may present in the anterior chamber
Mx: opthamology consult, cycloplegics, topical abx, often admission (corneal perforation is a
complication)
Endophthalmitis
Infection of deep structures of eye (anterior, posterior, vitreous chambers)
Hx: pain and decreased acuity
O/E: decreased acuity, chemois, hyperemia of conjunctiva, infected chambers (hazy or opaque)
Complication of blunt globe rupture, penetrating trauma, FB, ocular surgery
Staph, strep, bacillus are common bugs
Topical, intravitreal, systemic antibiotics are all used
Sympathetic Ophthalmia
Inflammation that occurs in the uninjured eye weeks to months after the initial insult thought to
be an autoimmune response to the normally sequestered uvual tissues of the injured eye
becoming exposed with the injury
Hx: pain, photophobia, decreased acuity
Tx: steroids, other immunosuppressants, optho consult, enucleation of blind eye can help




CONJUNCTIVITIS

INTRODUCTION
Conjunctivitis = Inflammation of the bulbar and palpebral conjunctiva
Keratoconjunctivitis = Inflammation of cornea and conjunctiva
Bacterial, viral, allergic, toxic, mechanical

BACTERIAL
Common bugs: Pnneumococcus, Hflu, Staph, Moraxella, Gonoccocus
Uncommon bugs: Pseudomonas, Klebsiella
Neonates: think of chlamydia and gonorrhea
Symptoms: irritation, FB sensation, lid swelling, drainage, eye crusting in morning
NO photophobia or visual loss
Cultures: only if Rx failure, severe infection, suspected gonorrhea, or neonatal
Complications: corneal ulcer, keratitis, corneal perforation
Treatment
Warm compresses qid
F/U in 5/7 if not improving (viral may last longer but bacterial usu doesn’t)
Topical antibiotics: fucopthalmic, polysporin ointment, or gentamycin 5-7d
Avoid neomycin opthalmic solutions because of high incidence of hypersensitivity
NO eyepatching
NO corticosteroids
If using topical antibiotics
Ointments likely better b/c it stays longer; use polysporin bid
Drops: use q2hr while awake, occlude lacrimal system after administration
Neisseria gonorrhoeae
Uncommon but important b/c of complications
Direct contact from urethritis or pelvic infections
Symptoms more severe; copious purulent drainage is a clue
Gram stain may reveal diagnosis; cultures more sensitive (SEND cultures)
Management more aggressive
Mild: outpatient mx with ceftriaxone 1gm im, topical erythromycin ointment, saline irrigation,
azithromycin 1gm po X 1 to cover concomitant chlamydia
Moderate, Severe, any corneal involvement: admission, iv abx, saline irrigations, topical
antibiotics
Adults: cetriaxone iv, PCN 100,000 U/ml one gtt q2hr
Neonatal:
Manifests w/i 2 - 4 days after birth
Look for sepsis (?LP, BC)
Should do eye cultures
Ddx: gonorrhea, chlamydia, HSV keratitis, dacrocytitis
Tx: Pencillin 20,000 IU/ml ong gtt q1hr X 12hr
Ceftriaxone 125 mg im X 1
Saline washes
Add covererage for chlamydia


Chlamydia trachomatis
              Neonatal
              Manifests w/i 5 - 13 days after birth
              Topical erythromycin ointment, oral erythromycin X 14 days
Chemical conjunctivitis from ointment administration immediately after birst occurs w/i 1 - 2
days



VIRAL CONJUNCTIVITIS
Bugs: adenovirus, coxsackie, entorviruses
Hx: pink eye, drainage, more redness, more itching/irritation, periauricular lymphadenopathy,
viral symptoms (rhinitis, cough, myalgias)
Often starts in one eye then spreads to the other
Management
                Artificial tears
                Cool compresses qid
                Can use topical antihistamine for itching (patanol)
Epidemic KeratoConjunctivitis (EKC)
Adenovirus
Combined keratitis and conjunctivitis
VERY CONTAGTIOUS
Contagious for 10 - 12 days
Average duration is 2 weeks but may last 4 weeks
Often associated with a mild punctate keratitis by day 5-8 (80%); usually central; may be
replaced by central subepithelial infiltrates which don’t stain with fluroscence
Characteristics
Outbreaks of “pink-eye”
Follicles on conjunctiva
Thin pseudomembrane
                Management
Cool compresses +/- antihistamines
Wash hands thoroughly
Examiner should wear gloves
Slit lamp needs to be disinfected
Avoid contact with family, throw out kleenex
Stay home, out of day care for 2 weeks




ALLERGIC CONJUNCTIVITIS
Drugs, cosmetics, environmental
Itching is generally more pronounced : MUST be pruritic
Stringy white discharge, itching, seasonal
Symptoms tend to be bilateral (can be unilateral)
May have chemosis (conjunctival edema) and/or blepharitis
Vernal conjunctivitis
               Less common but more severe
             Young males, hereditary, fhx of atopy
             Similar to allergic conjunctivitis but more itching
             The upper tarsal plate is “cobblestoned” from giant raised papilae which are
pathognomonic for the disease (lower lid less common)
             Drainage is copious, thick, and ropy
             The cornea often has punctate lesions or can be ulcerated
             Tx: tears, cool compresses, cromolyn solution, aspirin, d/w optho
Management
             Artificial tears: dilutes the allergen
             Saline eye drops help in 1/3
             Cool compresses qid
             Patanol 0.1% one gtt bid X 7 days (topical antihistamine and mast cell stabilizer)
             Oral antihistamines may help

TOXIC/CHEMICAL/ALLERGIC
Toxic/chemical: exposures to irritants
EYE DROP RELATED
Common scenario: presents after being put on eye drops 5-7 days and things are getting worse
instead of better; often multiple MD visits
Many eye drops can irritate the eye and there can also be allergic reactions
May have associated blepharitis
R/O iritis etc
Mx: stop all drops, cool compresses qid, f/u with optho likely warranted if going on that long
 BACTERIAL                         VIRAL                            ALLERGIC
 Copious purulent discharge      Less discharge volume and        White, stringy discharge
 Eye matted shut in am           purulence
 No hx                           No hx                            Hx of seasonal env allergies
 Uni or bilateral                Bilateral > unilateral           Almost always bilateral
 Not generally pruritic          Prutitic                         Very pruritic
 No viral symptoms               Cough, rhinitis, fever, sore     May have rhinitis
                                 throat
Bacterial vs viral
Studies that look at eye cultures show we aren’t very good at predicting who has bacterial vs
viral conjunctivitis
Abx necessary: Studies with culture proven bacterial infections were randomized to abx vs
placebo and both resolved in ave 5 days (abx was slightly faster)
UVEITIS/IRITIS
Uveitis = inflammation of the iris (MC), ciliary bd, and choroid
Iritis = inflammation of the iris (Acute, chronic, or recurrent)
Associations/Etiologies
Connective tissue disorders: RA, sjogrens, sarcoidosis, Behcet’s
Ankylosing spondylitis
Reiter’s syndrome
Infections: TB, toxoplasmosis, toxocariasis, lyme dz, syphillus, leprosy
IBD
Idiopathic
Trauma
Lymphoma
Kawasaki’s
Symptoms
               Ocular pain/irritation
               Photophobia
               Blurred vision
Signs
Decreased VA
Anterior chamber white cells: looks like floating dust particles
Anterior chamber flare (protein): looks like headlights in fog
Keratitic precipitates (spots on “ back” of cornea)
Hypophyon
Perilimbal conjunctival injection: ciliary vessel hyperemia
Posterior synechiae (remnant of prior iritis: pieces of iris stuck to the lens, can also occur with
hyphemas)
Management
Oral analgesics
Arrange optho f/u
Discuss interim tx: steroids, cycloplegics

EPISCLERITIS
Inflammation of the tissue between the conjunctiva and sclera
Common, benign, etiology unknown, often young adults
FB sensation, irriation, photophobia, MILD pain
Minimal tenderness
Normal visual acuity
Nodular localized pink/red conjunctiva and episclera
Tx: artificial tears, optho prn

SCLERITIS
Vision threatening inflammation of the sclera
Associated with CTD: young female with R.A. is the MC scenario
Severe pain, wakes patient at night, “my eyes are killing me”
Pain with EOM, DECREASED visual acuity, severe eye tenderness
VERY red eye with prominent vessels that do NOT move when the overlying conjunctiva is
moved with a cotton tip (clue to scleral inflammation)
Associated uveitis and keratitis common
Tx: consult optho, steroids, immunosuppressants
DISEASES OF THE CORNEA

PTERYGIUM/PINGUECULUM
Pterygium
               Wedge shaped area of conjunctival fibrovascular tissue that extends onto the
cornea
               Pink, triangular, medial side is most common
               Benign proliferation of fibrovascular tissue
               May periodically become inflammed
               Refer to optho on a non-urgent basis (occasionally need excision)
Pinguecula
              White, yellow, or brown flat to slightly raised tissue on the conjunctiva
immediately next to but not on the cornea
              Looks like “heaped up” conjunctiva
              Near limbus on medial side is most common
              Amorphous conjunctival tissue adjacent to the limbus
              Periodically becomes inflammed
              Tx: protection from wind, dust, sunlight, and use artificial tears, topical NSAID if
inflammed

SUPERFICIAL PUNCTATE KERATITIS
Superficial, punctate, multiple pinpoint corneal epithelial defects
Nonspecific finding that is seen in many conditions
Most common precipitant conditions are ultraviolet burns, conjunctivitis, topical eye drug
toxicity (drugs with preservatives including artificial tears, gentamycin, neomycin), contact
lenses, dry eye, exposure keratopathy, blepharitis, mild chemical injury, minor trauma, viral
infections
May present with pain, photophobia, redness, FB sensation
Should consider HSV keratitis
Minor Keratitis in non-contact wearer
Treat associated condition
Artificial tears (no preservatives)
Topical antibiotics and/or cycloplegics
Minor Keratitis Contact lens wearers
                 Stop wearing contacts
                 Ciprofloxacin opthalmic: 2 gtt q 15 min X 6hr, q30 min X 18hr WA, q1hr X
24hrs, q4hr X day 3 on




CORNEAL ULCERS AND INFILTRATES FROM INFECTION
Corneal infiltrates: focal white opacities without an epithelial defects
Corneal ulcers: overlying corneal epithelial defect that stains with fluorescein in addition to the
corneal infiltrate
Contacts: pseudomonas and Acanthamoeba (swimming with contacts!) are common
Usually starts as a minor corneal abraison which leads to bacterial entry
Hx: pain, redness, irritation, photophobia, decreased acuity
PE: decreased VA, conjunctival hyperemia, chemosis, epithelial corneal defect with dye uptake
You can see anterior chamber cells, flare, hypopyon
Tend to be central (further away from blood supply from limbus!)
Corneal abraison vs ulcer
MCC is bacterial, but fungal and HSV also occur
Contact wearers: pseudomonas
Managment:
                Discuss with optho
                D/C contact use
                Ciprofloxacin opthalmic

HERPES SIMPLEX INFECTIONS
Primary or reactivation
Findings
                 Punctate keratitis (early, first episode)
                 Corneal dendritic ulcers: single or multiple (later, recurrent episodes);
TERMINAL bulbs are pathognomonic for HSV ulcers
                 Conjunctivitis
                 Iritis
                 Blepharitis: vesicles on eyelids
History
Pain, irritation
FB sensation
Blurry vision
Exam
Decreased visual acuity
Conjuncitivits, keratitis, ulcer, uveitis, blepharitis
Decreased acuity
Tx
                 Topical antiviral agents (trifluidine 1% q2hr X 2-3 weeks), topical prophylactic
antibiotics and cycloplegics
                 Acyclovir po if isolated eyelid vesicles
                 NO topical steroids (contraindicated)
                 Optho consult
                 Neonatal: admit for iv acyclovir (usually associated encephalitis)
CONTACT LENS COMPLICATIONS
List five complications of contact lens use
                Corneal abrasions
                Corneal neovascularization
                Keratitis
                Corneal ulcers (pseudomonas)
                Hypersensitivity reactions to solution (conjuncitivis, keratitis)
                Contact lens deposits
Corneal ulcers due to pseudomonas a problem with contacts: corneal destruction in 24 hrs
possible
No s/s of infection: d/c contact lens use and f/u with opthamology
Corneal infection suspected: optho consultation




HERPES ZOSTER
Activation of virus along opthalmic division of trigeminal nerve leads to keratoconjunctivitis
V1 Involvement: zoster at tip of nose (Huchinson’s sign) is predictor of eye involvement in 75%
due to involvement of nasociliary nerve (compared to 25% ocular involvement if V1 distribution
does not involve tip of nose)
Opthamology consult: various treatments with antivirals, steroids depending on location and
severity
Findings (many!)
               Punctate keratitis and pseudodendrites are the most common
               Pseudododentrites are formed from deposition of mucus, usually peripheral, and
lack the rounded terminal bulbs at the end of the branches
               Corneal aneshtesia common
               Uveitis is 2nd most common finding
               Mild conjunctitivitis also common



STEROIDS + INFECTIVE KERATITIS = Scarring and possible permanent visual loss
PERIORBITAL CELLULITIS (Preseptal)
Anterior to orbital septum                  Swelling around the eyelid
Bugs: staph, strep, Hflu (kids)             Red, warm around the eye
Strep is MCC                                History
Common in kids                                     - NO pain with eye mvmt
Abraisons, FB, sinusitis, and dental               - Minimal pain
infections are common causes
Physical                                          - Normal E.O.M.
        - Periorbital cellulitic changes          - No proptosis
        - Normal V.A.                             - No eye pain with EOM
Clinical dx
Mx
Cefuroxime iv
F/U with HPTP
Admit if sick
PO after 2/7




                                            ORBITAL CELLULITIS




POSTERIOR to orbital septum                       - Significant resting eye pain
Staph, strep, Hflu, anaerobes                     - Pain with ROM
History
Physical                                          - Decreaed E.O.M.
        - Proptosis                               - Pain with E.O.M.
        - Decreased V.A.
Needs a CT orbits (look for gas, abscess)
Mx
Admit
IV abx: clinda/gent
Consult opthamology (may need I&D)




DISORDERS OF LIDS AND
OCULAR SOFT TISSUES
HORDEOLUM (STYE)/CHALAZION
Stye = External Hordolum
Localized abscess of the meibomian glands in the eleylid near the root of the eyelash
Essentially an eyelash abscess
Presents with pain, swelling, redness, discharge
Usually staph
Difficult to distinguish from a chalazion
Managment
Warm compresses X 15 min, q2hr
Many will decompress spontaneously
Polysporin to conjunctival sac qid (decreases bacterial load to the area)
Resolves in 7 days
Oral abx if associated facial cellulitis
Localized, nodular, inflammatory processes of the eyelids
Surgery for chronic, failure of conservative rx
Chalazion
                Chronic inflammation of meibomian glands and obstruction by fat an fibrious
tissue that may result from a stye but is usually just obstruction of the gland
                Secretions are extruded into the tissue causing a local reaction
                Similar presentation
                Same management
                PEARL: older patient, recurrent/resistant: could be an eyelid tumore, refer

DACRYOCYSTITIS
Acute infection of the lacrimal sac from nasolacrimal duct obstruction
Staph aureus is the MC organism, strep, Hflu
Pain, tenderness, swelling, erythema over the lacrimal sac
Pressure over the sac may express purulent material from the puncta
Management
               Warm compresses q few hors
               Keflex or clavulin po
               Cefuroxime iv if severe/sick/immunocompromised (staph, strep, hflu)
               Refer if chronic or recurrent

BLEPHARITIS
Toxic, allergic, infection related
Thick, mattered, red eyelid margins with pronounced blood vessles
Burning, itching, tearing, FB sensation, morning crusting of eyelids
Tx: rubbing the eyelid margins with a mild shampoo using a cotton-tipped applicator or cloth
bid, warm compresses, artificial tears, topical antibiotic ointment if severe



GLAUCOMA

PRINICPLES OF DISEASE
Aqueous humor is produced by ciliary processes
Aqueous humor provides structural support to the anterior chamber, delivers oxygen and
nutrients to the avascular lens and cornea and removes waste products
Aqueous humor passes from the posterior chamber to the anterior chamber through the pupil
Aqueous humor is transported into the trabecular meshwork located at the anterior chamber
angle formed by the junction of the root of the iris and the peripheral cornea; the trabecular
meshwork functions as a one-way valve and filter for the aqueous humor to drain into the canal
of Schlemm which then drains into the episcleral veins
Intraocular pressure (IOP): function of aqueous humor production/removal; N = 10 - 20 mmHg
Glaucoma = optic neuropathy caused by increased IOP, irreversible damage can occur
Classification
Primary: NO associated ocular or nonocular event
Secondary: associated ocular or nonocular event
Closed angle: anterior chamber angle is narrowed reducing the outflow of aqueous humor
Open angle: normal anterior chamber angle

PRIMARY OPEN-ANGLE GLAUCOMA
Most common form of glaucoma; a leading cause of blindness
Increased resistance to aqueous humor outflow through the trabecular network
Insidious onset, slowly progressive, chronic, bilateral, painless
Advanced disease occurs before symptoms
Hx: visual field loss that moves from periphery to central
O/E: optic cup to nerve ratio > 0.6, vertically oval/deep/pale optic cup, nasal displacement
vessels
Tx: topical Beta - blockers, selective alpha2 agonists, carbonic anhydrase inhibitors,
prostaglandin agonists, miotics, sympathomimetics -----------> argon laser trabeculoplasty --------
---> guarded filtration surgery
Topical medications CAN produce systemic side-effects:
Beta-blockers have produced asthma, heart block, CHF, hypoglycemai
Adrenergics have produced hypertension, arrythmias
Carbonic anhydrase inhibitors: renal stones, hypokalemia
Acetylcholinesterase inhibitors: prolonged apnea after succinylcholine

SECONDARY OPEN-ANGLE GLAUCOMA
Lens induced, inflammatory, exfoliative, pigmentary, steroid induced, traumatic, angle recession,
ocular tumors
Tx directed at underlying etiology and same meds as primary open-angel glaucoma

SECONDARY ANGLE CLOSURE GLAUCOMA
Pupillary block: may develop from swollen or dislocated lens, or posterior synechia (adhesions
b/w the iris and lens)
No pupillary block: secondary angle closure without pupillary block can be caused by intraocular
tumors, CRVO, or postoperatively



PRIMARY ANGLE CLOSURE GLAUCOMA
Anatomic variation: occurs in patients who have anatomically small and shallow anterior
chambers; results in iris being nearly in contact with the lens resulting in resistance to aqueous
humor flow from the posterior to anterior chamber (pupillary block)
Pathophysiology
                MAIN problem is the iris is “stuck to” the lens
                Iris bulges forward obliterating the angle between the cornea and iris obstructing
the trabecular meshwork, decreasing outflow and leading to rapid rise in IOP
                Explains why the primary treatment is laster iridectomy (they aren’t lasering the
trabecular network)
Precipitants = pupillary dilation
Walk into dimly lit room
Emotional upset
Medications: anticholinergics, sympathomimetics
Flat or plateau iris
Less common mechanism
Flat or plateau iris leads to a narrow angle recess
Dilatation of the pupil causes the iris to fold and bunch over the angle blocking aqueous humor
outflow
Symptoms
EVERY HEADACHE NEEDS THEIR EYES CHECKED: H/A + DILATED PUPIL HAS
BEEN GLAUCOMA
Eye pain
Headache
Blurry vision
N/V
Occassionally abdominal pain
Halo around lights
Signs
Perilimbal conjunctival injection
Conreal edema (steamy corneal appearance): fluid is forced into the cornea when IOP is > 50-60
range
Mid to dilated pupil
Sluggish reaction to light (or fixed)
Decreased visual acuity
Increased IOP (> 20, usually will be at least 40 and more like 70 range)
General Management
All require opthamology consult as definitive tx is surgical (peripheral iridectomy)
Mild visual acuity loss and IOP < 50 ---------> topical medical management
Significant visual loss (hand mvmts) and IOP > 50 ---------> topical and iv Rx
Pharmacologic Approach
Goals: decreased IOP by (i) miosis (ii) decreased aqueous humor production (iii) osmotic fluid
shifts (iv) prevention of valsalva effects
Timolol 0.5%: decreases aqueous humor production and decreases IOP in 30 min; also causes
miosis
Pilocarpine 1-2%: 1 ggt q 15 min X 2; cholinergic :. pupil constriction
Apraclonidine 1%: A2 agonist
Prednisolone 1%: q15 min X 4
Acetazolamide 250 - 500 mg iv: decreases aqueous humor production
Mannitol 1-2 mg/kg iv over 45 min: osmotic shift of fluid to decrease IOP
Sedatives and Antiemetics: prevent agitation, N/V (valsalva -----> incr. IOP)

 T                            TIMOLOL 0.5 % gtt to other side
                              Decreases acqueos humour production and constricts pupil.
 A                            ACETAZOLAMIDE 250 - 500 mg iv or po
                              Decreased acqeous humor production.
 P                            PILOCARPINE 2% one gtt q 15 min X 2, one gtt to other side
                              Repeat if pupil does not constrict.
                              Causes pupillary constriction.
 A                            ANALGESIA: morphine
                              ANTIEMETICS: maxeran.
 M                            MANNITOL 0.5 -1.0 gm/kg iv
                              Osmotic shift to decrease IOP.
                              Give early if pressures very high (>70) or if pressures don’t
                              respond to above within 30 min.




PEARLS
Space drops one minute apart
Consult optho for mannitol recommendation, go ahead with the rest
Treat first, phone later
Check I.O.P. q 30 min: pressures should drop within 30 minutes
ANISOCORIA

INTRODUCTION
Head trauma or decreased LOC warrants immediate investigation/intervention
Normal LOC is less concerning (head trauma, asymmetric pupils but normal LOC does not have
significant intracranial pathology)
Which pupil is abnormal? Pupil that has sluggish constriction is likely abnormal
Anisocoria greater in the dark suggests the abnormal pupil is the smaller one
Anisocoria greater in the light suggests the abnormal pupil is the larger one
Anisocoria with normal afferent visual system: innervational or structural defect
Structural defects usually detectable with slit lamp examination
Normal slit-lamp exam, both react well to light ------> see whether anisocoria increases in light
or darkness
Anisocoria increases in light: adie tonic pupil, pharmacologic blockade, third-nerve palsy
Anisocoria increases in dark: benign anisocoria, Horner’s

ADIE TONIC PUPIL
Blurred near vision but normal distant vision
Poor accomodation with a very slow constriction to near testing
Pupil will redilate slowly when the vision is agoin mad distant
Slit-lamp: sector palsies of the iris
Young women, associated symmetrically reduced DTRs
Diagnosis confirmed by weak cholinergic agent (pilocarpine 0.1%) causes intense pupillary
constriction as a result of cholinergic supersensitivity in the affected pupil c/p to normal one
Referral to optho on non-emergent basis for cholinergic therapy

PHARMACOLOGIC MYDRIASIS
Deliberate or inadvertant administration of sympathetics or parasympatholytic agents
Sympathomimetics: phenylephrine or cocaine for nasal use may get into eye
Paraympatholytics: atropine, scopolamine; transdermal scopolamine patches can cause
anisocoria
Pilocarpine 1.0% test: cholinergic agent that should constrict the pupil; will rapidly constrict the
pupil if dilation is secondary to 3rd nerve palsy; will NOT constrict the pupil if due to
anticholinergics

THIRD NERVE PALSY
Anisocoria, increases in light, no evidence of Adie tonic pupil or pharmacologic reason
Almost always have other signs of 3rd nerve palsy: ptosis, EOM dysfunction
Hx: diplopia
O/E: pupil will be down and out (loss of sup rectus, medial rectus)
MUST r/o aneurysm or other intracranial pathology
HORNER’S SYNDROME
MIOSIS + PTOSIS + ANHYDROSIS
Interruption of sympathetic innervation
Dilation lag is classical finding: pupil requires up to 15 seconds to fully dilate
Anisocoria will be greater at 3 - 5 seconds of darkness than 15 seconds although the anisocoria
will still be more pronounced than in light
Topical opthalmologic cocaine 10%: horner’s pupil will dilate less than the normal pupil
inreaction to cocaine
Horner’s etiology: CVA, CNS tumor, lung ca, thyroid maass, herpes zoster, OM, pancoast
tumors, headache syndrome, carotid dissection, congenital horner’s (birth trauma)
Hydroxyamphetamine 1% administered 24hrs after the cocaine test can be used to determine the
level of sympathetic interruption and dictate the work up
New onset Horner’s should have thorough work up

PHYSIOLOGIC ANISOCORIA
20% of population has 0.4mm difference
Transient, persistent, alternating pupils
Increases in darkness, but NO lag seen as with Horner’s
SUDDEN ATRAUMATIC VISUAL LOSS

INTRODUCTION
Usually monocular, duration seconds to days, vision generally 20/200 or worse
Aggressive investigation to determine etiology
Opthamomology or neurology consultation
Acute visual loss may not be an acute process: sudden discovery of visual field loss
Acute visual loss may not be related to eye
Differential dx of sudden, atraumatic, painless, unilateral vision loss
Spontaneous lens dislocation
Vitreous hemorrhage
Retinal detachment
Central Retinal Artery Occlusion: embolism/TIA, vasculitis, sickle cell, migraine
Central or Branch Retinal Vein Occlusion
Ischemic Optic neuritis: TIA, migraine (should have pain), vasculitis, sickle cell
Inflammatory optic neuritis (usually painful)
Conversion disorder
CHIASM OR BEHIND WOULD BE BILATERAL
Malingering
Differential dx of sudden unilateral PAINFUL blindness
Acute angle closure glaucoma
Inflammatory optic neuritis
Differential dx of bilateral visual loss
Bilateral ischemic optic neuritis
Bilateral inflamatory optic neuritis
Optic chiasmal lesion: tumor, craniopharyngioma, meningioma (bitemporal hemianopsia)
Optic radiation: infarct, bleed, tumor, abscess, trauma (homonomous hemianopsia or
quadrantaopia)
Optic cortex: infarct, bleed, tumor, abscess, trauma (homonomous hemianopsia)
Conversion
Malingering
Differential dx of complete bilateral visual loss
Conversion
Malingering
Any of the above but bilateral (unusual)
Large chiasmal event
Papilledema
POSTERIOR VITREOUS DETACHMENT
Very common > 60 yo
Vitreous gel pulls away from the retina with aging which can lead to symptoms similar to retinal
breaks, vitreous hemorrhage, and retinal detachment
No specific treatment is indicated unless accompanied by a retinal break, vitreous hemorrhage,
or retinal detachment
Should have prompt evaluation by opthamologist to r/o associated retinal pathology




VITREOUS HEMORRHAGE
Definition = bleeding into the preretinal space or int the vitreous cavity
Etiology
                Retinal tears and detachment are the MCC
                Diabetic retinopathy
                Trauma
                Intraocular tumors
                Retinal microaneurysms
                Vitreous detachment
                Sickle cell dz
                Macular degeneration of the retina
History
Floaters = Cobwebs in vision = Snakes/spiders in vision
Flashers if associated retinal tear
Blurry vision
Signs
Decreased red reflex (may be absent or black)
Reddish haze of vitreous
Worms
Decreased visual acuity
Retinal detachment might be seen
Afferent pupillary deficit might be seen (retinal detachment)
Long-standing preretinal hemorrhages can become a whit mass that may look like
tumor/infection
Managment
                Consult optho
                Bed rest, elevation of head, no anticoagulants or antiplatelet agents
                Definitive tx targeted at underlying cause
                Vascular retinopathy: laser photocoaguation or cryotherapy
                Retinal tears or detachments: repaired
                U/S to determine if retinal detachment is present and may determine the cause
                Vitrectomy in certain cases
RETINAL BREAKS AND DETACHMENT
Retinal layers: inner neuronal retina, outer pigment epithelial layer
Layers can be separated by fluid
Retinal break is a tear in the retinal membranes and may or may not lead to retinal detachments
Retinal detachments occur by three mechanisms: exudative, tractional, rhegmatogenous
Rhegmatogenous
Tear/hole in neuronal layer (vitreous fluid leaks b/w and separate the two layers)
Generally >45yo, more common in men, associated with degenerative myopia
Trauma may be associated with rhegmatogenous detachment by causing tears in the retina or
disinsertion of the retina from its attachment at ora serrata anteriorly
Traumatic retinal detachments can occur at any age; increased risk with myopia
Exudative
Result of fluid or blood leakage from vessels within the retina
Hypertension, toxemia of pregnancy, CRVO, glomerulonephritis, papilledema, vasculitis,
choroidal tumor
Traction
Consequence of fibrous band formation in the vitreous and band contraction
Fibrous bands result from the organization of inflammatory exudates or blood from prior
vitreous hemorrhage
History
Flashers: traction and stimulation of retina
Blurry vision (described as filmy, cloudy, curtainlike appearance)
Floaters if associated vitreous hemorhage
Absence of pain
Signs
Decreased visual acuity (can be minimally changed)
Visual loss is commonly
Visual field loss relates to location and size
Afferent pupillary defect only if detachment is large
Detachment visualized via opthalmoscopy: retina will appear out of focus; bullous detachment
with retinal folds are seen with large detachments
Indirect opthalmoscopy is needed to r/o detachment b/c direct fundoscopy cannot visualize the
anterior portions of the retina
Management
Difficult to see, refer based on history
Macula involved is more urgent
Some forms require urgent surgical repair
Acute retinal breaks are surgically repaired w/i 24hrs
All other acute rhegmatogenous and tractional retinal detachments can be repaired w/i a few days
Exudative detachment: tx underlying cause, laser photocoagulation
Suspected retinal break or detachment requires emergent optho consult




BRANCH (BRVO) and CENTRAL RETINAL VEIN OCCLUSION (CRVO)
Painless loss of vision due to CRVO causing edema, hemorrhage, vascular leakage
Wide spectrum of appearances and depends on degree of venous obstruction
Minimal loss of vision to near total loss of vision
Associations: CVD, HTN, DM, OCP, > 50yo, vascultits
History = blurry vision
Nonischemic findings
               Minimal fundus changes
               NO afferent pupillary defect
               Visual loss minor (2/3 of pts having 20/40 or better)
               Retinal hemorrhages
Ischemic findings:
               Marked abnormal fundus = blood and thunder
               Blurry disc margin
               Dilated, tortous veins
               Cotton wool spots
               Retinal edema
               Marked decreased visual acuity
               Often an afferent pupillary defect
Branch retinal vein occlusion
Distal to an AV crossing and hemorrhages occur distal to the site of occlusion
Symptoms depend on location; often asymptomatic if macula spared
Retinal edeam, superficial hemorrhage, dilated vein
Mx: nothing or photocoagulation depending on location/severity
Neovascular glaucoma is major complication of ischemic CRVO
Emergent optho consult
Treatment: complex, decreasing IOP, steroids, cyclocryotherapy, photocoagulation

CENTRAL RETINAL ARTERY OCCULSION (CRAO)
Painless acute visual loss due to occlusion of central retinal artery
Painless sudden loss, r/o lens dislocation, vitreous hemorrage, retinal detachment
Occlusion causes an ischemic stroke of the retina
50 - 70 yo, 50% have carotid atherosclerosis
RF: HTN, CV dz, DM, collagen vascular dz, vasculitis, valve disease, sickle cell dz, increased
intraocular pressure (glaucoma, retrobubar hemorrhage, endocrine exopthalmos)
100 minutes until complete visual LOSS
Hx: sudden visual loss over seconds
O/E: markedly reduced visual acuity, prominent afferent pupillary defect
Edematous retina with pale gray-white appearance and the fovea appears as a cherry-red spot
Management
               Digital Global Massage: begin immediately, apply direct digital pressure through
closed eyelid for 15 seconds then sudden release
Breath in a bag: Increased PC02 to retinal artery to cause vasodilation: rebreathing into a bag for
10 min each hour
Consult optho stat: ? LYTICS, anterior chamber paracentesis, mannitol etc
Reduce IOP; timolol 0.5% topically, acetazolamide 500mg iv or po will lower IOP and retinal
blood flow increases

NEUROOPHTHALMOLOGIC VISUAL LOSS
Visual loss not explained by physical examination
Decreased vision and decreased visual acuity VS
Visual loss but have normal visual acuity (careful visual field testing important)




PRECHIASMAL VISUAL LOSS
Decreased visual acuity or visual field loss in the eye on the affected side
May be unilateral or bilateral
Affected side will have afferent pupillary defect unless the process is bilateral (may be a relative
afferent defect)
Visual field defects do not respect the vertical meridean and is often localized to the center of the
visual field
Etiology: optic neuritis, ischemic optic neuritis, compressive optic neuritis, toxic and metabolic
optic neuritis
Optic Neuritis
Acute monocular loss of vision caused by demyelination of the optic nerve
Age usually 15 - 40
Hx: visual loss over hours to days, ocular pain with eye mvmt
O/E: acuity can be minimal loss to near blindness; afferent pupillary defect always present,
central scotoma is MC visual field defect
Fundoscopy: normal or swollen disc
Nhx: visual acuity reaches its poorest w/i 1 week, then slow improvement over the next few
weeks; 30% will develop MS in next 5years
Methylprednisolone IV X 3/7 versus po prednisone vs no steroids: controversial, may speed
recovery but NO effect on long-term vision or rates of MS
Ischemic Optic Neuropathy (ION)
                MCC of optic neuropathy and is one of the MCC of visual loss past middle age
Temporal arteritis
giant cell arteritis
weight loss, malaise, jaw pain, headache, scalp tenderness, PMR, low grade fever, severe
painless visual loss
extremely rare < 50yo
visual loss can be sudden, severe and bilateral
study: unilateral 50%, sequential 35%, bilateral 15%
occassionally preceded by amaurosis fugax
large afferent pupillary defect, visual field defect may respect the horizontal meridian
optic disc is pale and swollen
ESR: men (age/2) vs women (age+10/2)
temporal artery biopsy for definitive dx
start steriods ASAP; ie, before biopsy, ESR
methylprednisolone iv > prednisone po (less visual loss)




                Non-arteritic Ischemic Optic Neuropathy
much more common than temporal arteritis
lack classic symptoms of temporal arteritis and have normal ESR
vasopaths: DM, smoking, HTN, cholesterol, etc
temporary, followed by headache ------> migraine with vasoconstrictive phase leading to
amarosis fugax
painless visual loss, afferent pupillary defects, disc swelling, visual field defects that respect the
horizontal meridian
visual loss more severe than temporal arteritis
improvement in 1/3
steroids controversial: tx with steroids while waiting bx if there is any chance that it may be
temporal arteritis
Compressive Optic Neuropathy
Tumor, aneurysm, sphenoid sinusitis or mucocele, blunt trauma, thryoid disorders
Often involves chiasm
Visual loss that continues to progress over 7 days
Tends to involve other cranial nerves (helps distinguish b/w optic neuritis)
Head CT or MR to r/o compressive lesion (consider if presentation is atypical for optic neuritis
or ischemic optic neuropathy)
Toxic and Metabolic Optic Neuropathy
                Bilateral, symmetric, can be severe, visual field defects are central
Toxins: methanol, ethylene glycol, barbiturates, chloramphenicol, emetine, ethambutol,
isoniazid, heavy metals
Metabolic: thiamine deficiency, pernicous anemia
Treatment based on cause


CHIASMAL VISUAL LOSS
Chiasmal compression by pituitary tumors, craniopharyngioma, or meningoma
Gradual and progressive visual loss
Classic defect is bitemporal hemianopsia BUT optic nerve compression often also occurs and
leads to combinecd central and temporal visual field loss
Any time the visual field defect respects the vertical meridian from a neuroophthalmic loss, the
lesion is out of the globe and must be chiasmal or postchiasmal

POSTCHIASMAL
MCC are infarction, hemorrhage, tumor, AV malformation, migraines
Optic tract ------------> visual cortex (occipital cortex)
Classic defect is homonomous hemianopsia
Cortical blindness: caused by bilateral occipital infarctions, often mistaken for functional
blindness b/c NORMAL fundoscopy and NORMAL pupillary reflexes
Anton’s syndrome: bilateral blindness, normal pupillary reflexes, bilateral occipital lesions, and
DENIAL of blindness




FUNCTIONAL VISUAL LOSS
Conversion reactions (hysteria) and Malingering
Conversion reaction: pt unaware of absence of medical problem and is not motivated by
secondary gain; flat affect under circumstances of visual loss (should be freaked out!)
Malingerer: aware of absence of pathology, motivated by secondary gain; usually dramatically
emotional
Clues: NORMAL fundoscopy, NO afferent pupillary defect, NORMAL pupillary reflexes
Tests to TRICK
Hesitant to try to oppose index fingers of each hand
Write name in disorderly fashion (blind can usually write w/o problems)
Mirror in front of face, ask patient to look straight ahead, tilt mirror slightly back and forth -------
> MOST will follow their reflection in the mirror as it changes position proving feigned visual
loss




MACULAR DISORDERS
Many disorders affecting macula can cause acute visual loss
Key to dx: loss of central vision with preservation of peripheral vision
C/o central visual disotrostion and anatomic changes
Vascular, infections, trauma, inflammatory, toxic, radiation, hereditory, idiopathic
Infection/Inflammation
Bacterial, viral, protozoans can cause maculopathy
Inflammaotry debris from exudate may fill the vitreous leading to a cloudy appearance
Severe pain, redeness, periocular edema common
Lesion will appear white if the retina and choroid are obliterated
Emergent optho consult
Age - related macular degeneration
Most common reason for visual loss
>65yo; usually gradual onset but can be rapid
Drusen: small sharply defined yellow-white masses
Some develop a choroidal (preretinal) neovascular membrane which appears as a grayish-green
membrane beneath the retina --------> can lead to hemorraghe, transudation, scar fromation, or
exudative detatchment of the retina
Large hemorhage form the neovascular membrane can cause severe visual loss and may break
through the retina into the vitreous causing peripheral loss
Laser photocoagulation is the tx for choroidal neovascular membrane and should be done as soon
as possible




MISCELLANEOUS OPTHAMOLOGY

PAPILLEDEMA
Changes in optic disc from increased intracranial pressure
Etiology: blood, tumor, pus, CSF (pseudotumor cerebri)
Swelling of optic disc and blurring of disc margins, hyperemia, and loss of physiologic cuppin
Flame-shaped hemorrhages and yellow exudates appear near the disc margins as the edema
progreses
May be asymptomatic; symptoms variable and depend on etiology
Visual acuity NOT affected until papilledema longstanding
Brief obscurations of vision, enlargement of blind spot, inferior nasal field loss are common
Bilateral process but may be asymmetric
Mimics of pepilledema: CRVO, papillitis, hypertensive retinopathy, ischemic optic neuropathy,
optic disc vasculitis, diabetic papilliits with retinopathy
Required CT head

NYSTAGMUS
Clinically significant nystagmus is an oscillation of the eyes that occurs w/i 30 degrees of the
midline
Pendular nystagmus is of equal velocity in both directions
Jerk nystagmus has velocity greater in one direction
Pathologic movement is the SLOW movement; cortex is the compensatory FAST movement
Monocular or binocular
Conjugate (both eyes moving in same direction) or disconjugate (eyes moving in opposite
directions)
Primary gase position or gaze positi8on
Congenital nystagmus
Birth or neonatal period
Horizontal, conjugate, bilateral, symmetric and peduncular
May become jerky on lateral gaze but remains horizontal despite upward or downward gaze
Damped by convergence, increased with fixation, accentuated by covering one eye, and
abolished with sleep
No neurologic complaints
Acquired nystagmus
Toxic, retinal, labyrinth, vestibular nuclei, BS lesion, CB lesion




DISORDERS OF OCULAR MOVEMENT
Diplopia caused by certain eye movements: monocular or binocular?
Monocular: less concerning, usually refractive errors, dislocated lens, iridodialysis, feigned
disease
Binocular: disappears with either eye covered
Mechanical: hematoma, orbital floor fracture, abscess
Muscular: hypothryoid, muscle fibrosis
NMJ: myasthenia gravis (PD3)
CN palsies: III, IV, VI
BS (CN nuclei): multiple sclerosis, CVA, etc
Third Nerve Palsy
Fourth Nerve Palsy
Easily missed
Superior oblique paresis (LR6SO4)
Diplopia made worse by downgase, gaze away from paretic side
Head tilt to the opposite shoulder to compensate for the vertical extorsion and will have
weakness in downward gaze
Trauma, vasculare, aneurysm, tumor, myasenia gravis
Sixth Nerve Palsy
Esotopia that is worsened by lateral gaze and will often turn their heads laterally toward the
paretic side to compensate
Aneurysm, vascular disease (DM, HTN, AS), trauma, tumor, MS, meningitis, thyroid eye
disease, any cause of increased intracranial pressure (false localizing sign)

OPHTHALMIC MEDICATIONS
Drops increase concentration in eye, reduces unwanted side-effects, rapid absorption, brief
effect, minimal interference with visual media but are rapidly cleared by tears
Multiple eye drops: should wait 10 minutes b/w drops
Digital pressure to medial canthus prevents drainage vial nasolacrimal duct
Remember that systemic absorption can cause side-effects (BB and asthma)
Topical anesthetics: aid examination, never prescribe
Antibiotics and antivirals: guided by suspected organism
Corticosteroids: commonly used by opthamologists, minimal role in ED; post - traumatic
iridocyclitis is probably only situation for ED used
NSAIDs: topical use good for a variety of inflammatory conditions
Artificial tears
Cycloplegics
Block muscarinic receptors of ciliary muscle; always cause mydriasis
Relief of pain from ciliary spasm related to corneal abrasions, ocular truama, and iridocyclitis
Mydriatics dilate the pupil but not all mydriatics are cycloplegics
Mydriateics contraindicated in hx of glaucoma, increased IOP, shallow anterior chamber,
suspected globe rupture, lens inplant present
Atropine: long duration of action (weeks) and best avoided in ED




RED EYE
Conjunctivitis (inflammation of conjunctiva): bacterial, viral, allergic, toxic
Bacterial, viral, allergic, toxic
Episcleritis (inflammation of tissue b/w the conjunctiva and sclera)
                Vascular dilation or edema, nodular (CVD, gout, RA, zoster)
Scleritis (inflammation of sclera)

Keratitis (inflammation of cornea)
                Bacterial, viral, fungal
                Zoster
Iritis (inflammation of iris)/Uveitis (inflammation of uveal tract - iris, ciliary body, choroid)
Sarcoid, ankylosis spondylitis, TB, reiter’s, toxoplasmosis, toxocariasis, jeuvenile RA, lyme dz,
IBD
Acute angle closure glaucoma
NEUROPTHAMOLOGY
1. VISION
(a) visual acuity
        = resolving power, spatial limit of visual discrimination, ability to make out detail
        - requires accurately focussing lens, fovea, pathway to occipital cortex
- neither the entire retina nor the visual pathway need to be completely normal to have visual
acuity
        - measured by snell chart
                 - Pt at 20 feet
                 - 20/40 means from 20' Pt sees what a normal person could see from 40 feet
                 - 5/400 means from 5' Pt sees what normal person sees from 400'
        - snell chart
        - bedside: use glasses, 14"
(b) visual field
        = visual space where objects are simultaneously visible while fixating on a target
        - check by confrontation
        - image is inverted and reversed on the
        - review visual pathway
                 - constant retinotopic distribution o f fibers in the pathway
                 - lesions in and behind the chiasm produce defects in both eyes
(C) color perception
(d) contrast sensitivity
- it measures the way we really see thing as contrasts of form and shape and not as black letters
on a white background which represents 100 percent of contrast
        - optic neuritis – may recover acuity but not contrast sensitivity thus they
complain of the view being “washed out”
        - greatest contrast sensitivity b/w 3-5 cycles per degree of arc

2. OCULAR MOTILITY
- binocular single vision (BSV) provides stereopsis which is the ability to view the env. In
three dimensions
- initiation of gaze mvmts
         -
         - parietal-occipital lobes also contribute
- EOM
         - MR = ADduction
         - LR = ABduction
         - SR = elevation and ABduction
         - IR = depression and ABuction
         - SO = depression and ADuction
         - IO = elevation and ADduction

3. PUPILLARY FUNCTION
(a) light reflex pathway
(b) ocular sympathetic pathway
        - stimulus = load noise, fear
        - hypothalamus – BS – T1 SC – paravertebral symp chain (second order) – synapse
In the superior cervical ganglion – postgangl fibers (third order) run w ICA – enter    orbit
– dilator of pupil
(c) near reflex and accomodation
        - near synkinesis = convergence + accomodation + miosis (constriction) with
conscious visual effort at a near object
(d) anisocoria
        = unequal pupils
        - never due to optic n. disease b/c of dual crossover and always implies an efferent
defect of either the occulomotor n. or sympathetic paresis

THE NEUROPTHAMOLOGICAL PATIENT
- problems are afferent visual symptoms or s/s of ocular motility disorders
1. Afferent System Disorders
- history - visual loss Hx, one or both eyes, onset and progression, duration, pain, past Hx?
- examination
        - the most important test is the pinhole test
        -
        - visual acuity does not improve
                - exclude a large media opacity (appear black w red reflex)
                - visual loss or optic nerve disease? Do a swinging flashlight test
                                 1. shine in good eye and see direct and consenual response
                                 2. Shine in poorer eye
                                 3. Shine in good eye again (keep there for 5sec until stabile)
                                 4. Rapidly swing the light across the nose bridge
                                         - if poor eye constricts and then returns to the
                                  previously stabile size the vision loss is solely retinal
                                  in origin
                                         - if poor eye dilates instead of constricts the visual loss
                                  is due to optic nerve disease
                                         - opthalmoscpe exam also helps (atropy vs macular deg

2. DISORDERS OF OCULAR MOTILITY
- less than 10
         - usu present with strabissimus
         - require full opthamological exam b/c dev’p into amblyopia
- adults
         - usu present with diplopia
         - note: monocular diplopia is possible
                 - small opacities, lens hardening can cause it
                 - usu reported as “ghosting”
                 - pinhole relieves the diplopia and makes the Dx
         - binocular diplopia
                 - horizontal or vertically displaced?\
                 - maximal displacement in what direction?
                 - onset acute or chronic, constant or intermittent
                 - pain, headache
                 - worse at near or far
- examination
         - look for ptosis, dilated pupil in examination
         - forced duction test (FDT)
               = attempt to move the eyeball in the direction of the paralyzed muscle
               - if you cannot move the eyeball it implies that there is restriction by the
antagonistic muscle
               - seen in Grave’s disease (MR restriction thus you cannot abduct)
- exclude....
        - MG by tensilon test
        - decompensated latent strabismus
               - deviation is constant and full EOMs




GLAUCOMA
** affects 2% of population
** key to prevention is early Dx and Tx, it can be controlled but not cured
= group of diseases characterized by an IOP of sufficient degree to cause optic nerve     damage
and visual field changes
- not all have high IOP
         - normal IOP = 10-21mmHg w/ ave = 17mmHg
- normal (low) tension glaucoma
         = optic nerve change is consistent with glaucomatous neuropathy and visual field
changes are found in a Pt that has never had an IOP > 21
- occular HTN
         = IOP is contiually > 21 but has a normal optic nerve head and visual fields
- optic nerve and cup to disc ratio
         - normal cup:disc ratio is 0.3
         - 0.3 - 0.7 should be investigated
         - >0.2 assymetry b/w eyes should be investigated
         - progressive enlargement of ratio is an indicator
         - can lose up to 50% b/f any visual field loss detectable
- visual field
- sharp vision preservation = glaucoma commonly causes loss of the peripheral     field with
preservation of the central field
         - thus, often present late with significant damage
- risk factors
         - IOP                   - positive family Hx
         - age                   - diabetes
         - HTN                   - race (B>W)
- screening
         - most Pts are asymptomatic at time of diagnosis
         - IOP is a poor indicator alone
         - best screen for glaucoma is the optic nerve head

OPEN ANGLE GLAUCOMA:
        -Primary open angle glaucoma = IOP > 21 w/ optic nerve damage and visual field
changes, usu bilateral
- Normal (low) tension glaucoma = IOP <21 but w/ optic n. damage and visual field change
- Ocular hypertensives = IOP > 21 w/ no problems
- incidence = 60%
- pathology
        - drainage doesn’t work thus inc IOP
- treatment
        - FIRST LINE
                - beta-blockers (topical)
                - do not use in heart block or COPD
        - SECOND LINE
                - adrenalin (propine is a prodrug)
                        - s/es = stinging, headache, allergic conjunctivitis
                - pilocarpine (mitotic)
                        - s/es = difficult night vision, myopia, headache (ciliary bd spasm)

        -THIRD LINE
                - carbonic anhydrase inhibitors (diamox)
                - dec IOP by 50%
- limited use b/c of s/es – malaise symptom complex, GI symptom complex,
             Renal calculi, stevens-Johnson syndrome, blood
                                            dyscrasias
        -FOURTH LINE
                - argon laser trabeculoplasty
                - used w/ uncontrolle IOP on full meds
                - burns the trabecular meshwork to inc drainage
        -SURGERY
                - last resort, makes a new drainage

CLOSED ANGLE GLAUCOMA: - 12%
= Due to mechanical obstruction by the peripheral iris
- F>M, 1in 1000 after 40yo
- precipitated by mydriasis (watching TV in dark room)
- presentation
        - periocular pain + rapid, progressive vision loss + eye congestion + N + V
        - halos around the eye are due to corneal edema
- Tx
        1. Miotics - constrict the pupil and pull iris away from angle
        2. Diamox - dec the IOP
        3. Hyperosmotic agents - dec IOP by drawing water out of eye
                - oral glycerol, iv mannitol (better),
        4. Laser iridotomy - definitive Tx, done to both eyes b/c other eye has 50% chance
of developing CA glaucoma as well

CONGENITAL GLAUCOMA: - 3%
- autosomal recessive w/ incomplete penetrance, 1/10,000 births
- 70% bilateral
- signs
        - classic triad = tearing + photophobia + blepharospasm
        - corneal edema, enlargement, and clouding
        - Haab’s striate = tears in descemet’s mem
- treatment
        - surgery is preffered
        - topical drops and po CA-Is used until surgery
- prognosis
        - better if they present in first 1-24 mnths
        - more difficult to ctrl if present at birth or w/i first month


SCREENING = OPTIC NERVE HEAD + IOP
MEASURE IOP IN THOSE > 55yo IN ROUTINE PHYSICAL




RETINAL DETACHMENT

= separation of neurosensory retina from the underlying retinal pigment epithelium
resulting in the loss of oxygen supply to the outer retina which is dependent of diffusio   from
the choriod

CLASSIFICATION:
     1. rhegmatogenous = spontaneous detachment secondary to a retinal tear/break
     2. Tractional = any process putting traction on the retina (fibrous tissue in PDR, or
     penetrating trauma) may separate the retinal from the RPE
     3. Exudative = tumor, inflam, etc. results in fluid accumulation

POSTERIOR VITREOUS DETACHMENT:
= separation of the vitreous from the retina: increases with age b/c the hyaluronic acid       In the
vitreous decreases w/ age :. collagen fibrils shift and small pockets of liquid       vitreous
develop and eventually gain access to the space b/w the vitreous and the         retina
- most rhegmatogenous detachments are preceded by a PVD
- vitreous base = firm vitreous attachment of collagen fibers to the retina and pars plana at each
side of the ora serrata

SYMPTOMS OF PVD:
         1. Photopsia = sensation of flashing lights due to mechanical traction on retina
         2. Floaters = black spots or wavy lines in the visual field due to vitreous   aggregates,
avulsed epipapillary glial tissue, or limited vitreous hemorrhage
         3. Blurred vision = due to a shower of floaters or diffuse vitreous hemorrhage
            Vitreous hemorrhage results from a break or avulsion of a retinal bv as the PVD
occurs.
- significance of symptomatic PVD
         - 15% have a retinal tear
         - must be referred imediately for dilated fundic exam
         - may be possible to Tx w/ laser photocoagulation or externalcryotherapy which
will usu prevent retinal detachment

CONDITIONS PREDISPOSING TO RETINAL DETACHMENT:
- occurs spontaneously, w/o trauma in 10/100,000 per year
- associated conditions
         1. myopia – more PVDs, more lattice degeneration, thined retina b/c of inc length
         2. aphakia/pseudophakia – cataract extraction
                 - general popn rate of retinal detachemnt = .05%
                 - phacoemulsification or extracapsular extraction = 0-2% develop RD
                 - intracapsular extraction = 2-5% develop retinal detachment
         3. Trauma – blunt trauma is the leading cause in children
         4. Lattice degeneration – inner retinal degeneration :. retinal thinning that shows
a lattice resulting in retinal holes and tears; direct cause of 21% of Rds,
More common in myopics
         5. Other – inflam, degen, ....


SYMPTOMS OF RETINAL DETACHMENT:
1. Symptoms of PVDs – flashers + floaters + blurred vision
2. Visual field loss – peripheral scotoma (shadow) that is constant in location, of constant     or
increasing size, that enlarges from the periphery toward fixation, and extends to        the
peripheral extent of the visual field – cannot see around it
3. Unilaterl blurred vision
**URGENT REFERRAL
        - outer retinal layers have lost their direct O2 supply
        - inner retinal layers retain supply from the central retinal aa.

				
DOCUMENT INFO
Shared By:
Categories:
Tags:
Stats:
views:45
posted:10/15/2011
language:English
pages:47