Transcript Diagnosing and Managing Ocular Emergencies and Urgencies

Diagnosing and Managing Ocular
Emergencies and Urgencies
Blair Lonsberry, MS, OD, MEd., FAAO
Diplomate, American Board of Optometry
Clinic Director and Professor of Optometry
Pacific University College of Optometry
[email protected]
1
Disclosures and Special Request
Paid consultant for:
– Alcon Pharmaceuticals, Bausch and Lomb, Carl Zeiss
Meditec, NiCox, Sucampo
Special Request:
Interactive remotes don’t work on your TV, so please don’t
take them home! 
Commitment to change:
- write down three things that you “learned” from this
presentation that you can incorporate into your practice
to improve patient care
What Classifies an Emergency?
• Any condition in which the patient has the
potential for:
– vision loss,
– currently experiencing vision loss,
– permanent structural damage,
– pain or discomfort,
– or is an “emergency” for the patient.
• It is important to be able to triage a walk-in
patient and, more importantly, a call-in patient.
What questions to ask?
Onset
suddenly noticed or sudden onset?
Visual Loss
any loss of vision?
loss vs. blurry vision
one eye or both
part of visual field or all
transient vs. permanent
Pain
is there pain? constant? scale (1-10)
Redness
is there any redness? location?
Associated
Factors
contact lens wear? trauma?
discharge?
photophobia? medical history (eg.
DM)
Common Types of Ocular Emergencies
• Vision Loss:
– Gradual vs. sudden onset
– Vision loss with or without pain
• Trauma
• Red eyes
Visual Loss
• Visual loss varies greatly in meaning from patient
to patient
– ranging from blur to complete blindness and may affect
one or both eyes
• Components include:
– acuity,
– visual field,
– color and brightness may be affected jointly or
separately
• Detailed history and extent of vision loss crucial
Profound Loss of Vision
• Referring to a complete or greatly diminished
vision affecting the whole field
• Common causes of severe vision loss:
Vascular
central retinal vein occlusion,
central retinal artery occlusion,
vitreous heme
Inflammatory
optic neuritis
Infiltrative
Mechanical
optic neuropathy
retinal detachment
Monocular vs. Binocular
• Ocular or optic nerve pathology causes monocular vision
loss
• lesion at or posterior to chiasm causes binocular vision loss
– VF defects become more congruous the further back in
the visual pathway
– Homonymous VF defects noted posterior to chiasm
• Difference between mono vs. bino usually straightforward,
keeping the following in mind:
– Patients occasionally mistake homonymous
hemianopsia (similar loss of visual field in both eyes) for
a monocular loss
Visual Defects
Monocular
• Differentiate between eyes that have lost all
useful vision and those that have blurred vision
• Blurring of vision is not localized and may be
caused by pathology anywhere from cornea to
optic nerve
• Need to get anatomical diagnosis first before
considering the cause
General Appearance
• Level of consciousness
– When introducing yourself be
aware of the patient’s gross level
of consciousness?
• Is the patient awake, alert and
responsive?
• Personal Hygiene and Dress
– Is it appropriate for the
environment, temperature, age
and social status of the patient?
– Is the patient malodorous or
disheveled?
General Appearance
• Posture and Motor control
– What posture does patient assume while sitting in
the exam chair
– Are there any signs of involuntary motor activity
such as tremors
• E.g. damage to the cerebellum may produce a tremor that
usually worsens with movement of the affected limb
Case Example
• 48 yr old white female presented for
diabetic eye exam on referral from her
PCP
– She was scheduled 2 weeks previously but had fallen
and was unable to make that appointment
– She reports that her vision in her right eye seems to
be getting worse over the past several weeks.
– Was diagnosed with diabetes 1.5 years ago
• BS control has been erratic with range between
120-240
• Last A1C: 9.1
Blood Sugar
• Throughout a 24 hour period blood sugar typically
maintained between 3.9-7.8 mmol/L (70-140 mg/dL)
– Diabetes is diagnosed with a fasting BS of > 7.0 mmol/L
(126 mg/dL)
– or an A1c value of > 6.5
• Hypoglycemia is typically defined as plasma glucose 3.9
mmol/L (70 mg/dL) or less
– patients typically become symptomatic of hypoglycemia at
2.8 mmol/L (50 mg/dL) or less
• [A1c (%) x 1.59] – 2.59 = average Blood Glucose (in
mmol/L)
VEGF and DME
Entrance Skills/Health Assessment
VA: OD: finger count
OS: 20/40 (6/12)
CVF: OD: unable to assess
OS: temporal
hemianopsia
Pupils: sluggish reactivity with a
2+ RAPD OD
SLE: corneal arcus noted, no
other significant findings
IOP: 16, 16 mmHG OD, OS
DFE: see photos
Note: not patient photos
http://content.lib.utah.edu/cdm4/item_
viewer.php?CISOROOT=/EHSLWFH&CISOPTR=159
Physical Presentation
• Upon entering the room I noted that her right hand
was twitching
– I asked her how long that had been going on and
she said about 2-3 weeks
– I asked her if she experienced headaches, to which
she said she had bad headaches that even woke her
up at night
Referral
• Contacted her PCP who reported that she had
examined the patient 3 weeks prior and had not
noted any of these findings
• Referred the patient for an immediate MRI
– wasn’t able to be scheduled until the next day
Imaging/Surgery Referral
• MRI revealed large mass in
her brain
– Patient was diagnosed with
a Craniopharyngioma
– She was referred for
immediate surgery
– Neurosurgeon reported that
she removed a tangerine
sized Craniopharyngioma
– was the largest tumor she
has ever removed
Note: not patient MRI
http://neurosurgery.ucla.edu/images/P
ituitary%20Program/Craniopharyngio
ma/Cranio_Sag_Preop_fullylabeled.jp
g
Craniopharyngioma
• Craniopharyngioma:
–
–
–
–
slow-growing,
epithelial-squamous origin,
calcified cystic tumor
arises from remnants of the craniopharyngeal duct
• Craniopharyngiomas have a benign histology but
malignant behavior
– they have a tendency to invade surrounding structures
and recur after what was thought to be total resection
Craniopharyngioma
• Visual field examination
may reveal various patterns
of visual loss
– most frequently
bitemporal
hemianopsia
• suggestive of
compression of the
optic chiasma
and/or tracts
Our Patient
• Patient had a complete resection of the tumor in
addition to radiation therapy
• She developed several significant perioperative
complications:
– Leakage of CSF which resulted in her having to have
a shunt
• She subsequently developed an infection post surgically
– She is NLP in her right eye, but did regain 20/40
vision in her left eye
• Retains a temporal hemianopsia OS
– Diabetes control became erratic and was put on
several hormone replacement medications
Neurological Screening: Cerebrum
• Frontal lobe
– Emotions, drive, affect,
self-awareness, and
responses related to
emotional states
– Motor cortex associated
with voluntary skeletal
movement and speech
formation (Broca)
Right vs Left Brain Injury
• So what happens if one side of the brain is injured?
– People who have an injury to the right side of
the brain "don't put things together" and fail to
process important information.
• As a result, they often develop a "denial
syndrome" and say "there's nothing wrong with
me.“
Right vs Left Brain Injury
• The left side of the brain deals more with language and
helps to analyze information given to the brain.
– If you injure the left side of the brain, you're aware that
things aren't working (the right hemisphere is doing its
job) but are unable to solve complex problems or do a
complex activity.
– People with left hemisphere injuries tend to be more
depressed, have more organizational problems, and have
problems using language.
Gradual Onset:
Cataracts
• The decreased acuity must correlate with the
severity of the cataract…
– ie if cataract doesn’t correlate with the amount of vision
loss (or afferent pupillary defect present) then you need to
find another reason for the vision (or other test results)
Preseptal Cellulitis
• infection and inflammation
anterior to the orbital septum
and limited to the superficial
periorbital tissues and eyelids.
– Signs and Symptoms include:
• eyelid swelling,
• redness,
• ptosis,
• pain and
• low grade fever.
Preseptal Cellulitis Treatment
Treatment:
• Mild:
– Keflex or Ceclor 250-500mg
QID for 5-7 days
– Augmentin 500 mg TID
– or 875 mg BID for 5-7 days
• Moderate to severe:
– IM Rocephin (ceftriaxone) 12 grams/day or
– IV Fortaz (ceftazidime) 1-2 g
q8h.
Question
A 65 year old white male
patient presents with this
lesion on his forehead. States
it is “itchy” and is flaky in
appearance. What is this?
1. Seborrheic keratosis
2. Keratoacanthoma
3. Basal cell carcinoma
4. Actinic keratosis
Question
Actinic keratosis if left untreated has a 20%
chance of converting to which of the following?
1
3
2
4
Pre-Malignant Eyelid Lesions: Keratoacanthoma
• Appears as a solitary,
rapidly growing nodule on
sun exposed areas of
middle-aged and older
individuals
• Nodule is usually
umbilicated with a
distinctive crater filled with
keratin
• Lesion develops over
weeks and undergoes
spontaneous involution
within 6 mo to leave an
atrophic scar
Pre-Malignant Eyelid Lesions: Keratoacanthoma
• Lesion on the eyelids may
produce mechanical
problems such as ectropion
or ptosis.
• Differential SCC, BCC,
verruca vulgaris and
molluscum
• Many pathologists consider
it a type of low grade SCC
• Complete excision is
recommended as there are
invasive variants
Pre-Malignant Eyelid Lesions: Actinic
Keratosis
• Also known as solar or
senile keratosis
• Most common premalignant skin lesion
• Develops on sunexposed areas and
commonly affect the
face, hands and scalp
(less commonly the
eyelids)
Pre-Malignant Eyelid Lesions: Actinic
Keratosis
• Appear as multiple, flattopped papules with an
adherent white scale.
• Development of SCC in
untreated lesions as
high as 20%
• Management is surgical
excision or cryotherapy
(following biopsy)
Orbital Blowout Fracture
• Signs & Sx’s:
– Enophthalmos
– Diplopia
– Impairment of eye
movement 20 to EOM
entrapment, orbital
hemorrhage or nerve
damage
– Infraorbital n. anesthesia
• CT should include axial
and coronal cuts
Orbital blowout fracture
Disposition - If no diplopia, minimal displacement, and
no muscle entrapment, discharge with follow up within a
week.
Consider Surgery - For enophthalmos, muscle
entrapment, or visual loss.
Management:
– Ice packs beginning in clinic and for 48 hrs will help
decrease swelling associated with injury.
– Elevate head of bed (decrease swelling).
– If sinuses have been injured, give prophylactic
antibiotics and instruct patient not to blow nose.
– Treat nausea/vomiting with antiemetics.
Case
• 20 year old male presents with a red
painful eye
– complains about red/painful
right eye
– Started that morning when he
woke up
– reports a watery discharge, no
itching, and is not a contact lens
wearer
• SLE:
– See attached image with NaFl
stain
Herpes Simplex Keratitis: Clinical
Features
• Characterized by primary outbreak and subsequent
reactivation
• Primary outbreak is typically mild or subclinical
• After primary infection, the virus becomes latent in
the trigeminal ganglion or cornea
• Stress, UV radiation, and hormonal changes can
reactivate the virus
• Lesions are common in the immunocompromised
(i.e. recent organ transplant or HIV patients)
Dendritic Ulcers
3
Herpes Simplex Keratitis
• Topical:
– Viroptic (trifluridine) q 2h until epi healed then taper
down for 10-14 days.
• Viroptic is toxic to the cornea.
– Zirgan (ganciclovir) available in USA, use 5 times a
day until epi healed then 3 times for a week
• Oral acyclovir (2 g/day) has been reported to be as
effective as topical antivirals without the toxicity
– Valtrex (valcyclovir)) 500 mg TID for 7-10 days
– Famvir (famciclovir) 250 mg TID for 7-10 days
• If stomal keratitis present, after epi defect has healed,
add Pred Forte QID until inflammation reduced and then
slowly taper
Prophylaxis??
• Prophylaxis of 400 mg acyclovir BID vs placebo for 1 year
resulted in a lower recurrence in the treatment arm (19%
vs 32%)
– Valtrex 500 mg qd was found to be equivalent to
acyclovir BID
• Pitfalls to Prophylaxis:
– Reduction of recurrence does not persist once drug
stopped
– Resistance????
• van Velzen, et. al., (2013) demonstrated that longterm ACV prophylaxis predisposes to ACV-refractory
disease due to the emergence of corneal ACVR HSV-1.
Case
• 27 year old pharmacy student presents to the
clinic on emergent basis
– complains about red/painful eyes for the past 2 days
– started OD then transferred to OS
– reports a watery discharge, no itching, and is not a
contact lens wearer
– reports that others in his class have had a similar red
eye
– no seasonal, food or drug allergies
– has taken Visine 4-5 times/day since eyes became red
but hasn’t helped much
Question
Which of the following best represents your patient?
1
2
3
4
Conjunctivitis
Bacterial Conjunctivitis
Viral Conjunctivitis
Allergic Conjunctivitis
Blepharo-conjunctivitis
Viral Conjunctivitis
• Most common infectious
keratitis presenting on
emergent basis
• 62% caused by adenovirus
• Two major types:
– Pharyngoconjunctival
fever
– Epidemic
keratoconjunctivitis
Viral Conjunctivitis
• PCF: history of recent/current upper respiratory
infection
• EKC: highly contagious with a history of coming
in contact with someone having a red eye.
– Adenovirus 8 common variant leading to “rule of 8’s”
• First 8 days red eye with fine SPK
• Next 8 days deeper focal epithelial lesions
• Following 8 potential development of infiltrates
• Resolution
• RPS Adeno Detector available to use for
adenoviral confirmation
– AdenoPlus is currently being marketed and distributed by NiCox
AdenoPlus
• Have you heard about this?
www.nicox.com
Interpreting the results
NEGATIVE RESULT
•
Only a BLUE line appears in the control zone.
–
A negative result is indicative of an absence of
Adenovirus Antigens.
POSITIVE RESULT
•
The presence of both a BLUE line in the control
zone and a RED line in the result zone
indicates a positive result.
•
Even if the RED line is faint in color, incomplete
over the width of the test strip, or uneven in
color, it must be interpreted as positive.
•
A positive result indicates the presence of
Adenovirus antigens.
www.rpsdetectors.com
Interpreting the results
Invalid Result
• If a BLUE line does not appear,
the test may be invalid.
– Reimmerse the absorbent tip
into the buffer vial for an
additional 10 seconds.
– If a BLUE line still does not
appear after 10 minutes, the
test must be discarded and the
subject retested by resampling
the eye using a new AdenoPlus
test kit
www.rpsdetectors.com
JOURNEY OF THE “RED EYE”
“Red Eye”
Protocol
Patient has “Red Eye”
Front Office IDs & Isolate
the “Red Eye”
Patient is taken to “Red
Eye Room”
“Red Eye” Patient history
& work up
Tech performs
AdenoPlus™ test to rule
out Adenovirus
Dr. starts clinical evaluation
with Adenoviral conjunctivitis
confirmed, or rule out
Dr. proceeds with
evidence based treatment
History Signs Symptoms
Pink eye exposure, spread from one eye to the other, recent upper respiratory
symptoms
Itching, burning, foreign body sensation, tearing, discharge, eyelash matting
Pre-auricular adenopathy, chemosis
No significant pain, light sensitivity, or visual loss
AdenoPlus
POSITIVE
Education: hygiene and hand
washing
Supportive care: artificial
tears, cool compresses and
antihistamines
Antiviral medication
No antibiotics
NEGATIVE
Consider topical
antibiotics or
antihistamines
Viral Conjunctivitis:
Signs and Symptoms
•
•
•
•
•
•
•
•
•
Gritty sensation
Watery discharge
Sticky in mornings
Follicular response
Chemosis
Injection
SPK
Infiltrates possible
Positive lymph nodes


Pseudomembranes in
severe cases
Subconjunctival hemes
Management
• Consider the use of anti-inflammatory treatment
to relieve patient symptoms and improve comfort
– Alrex QID OU
– Lotemax QID OU
– FML QID OU
• EKC patients are typically very uncomfortable and
would benefit from anti-inflammatory treatment
– especially if infiltrates or pseudomembrane present
Management
• Betadine (Melton-Thomas Protocol):
– Proparacaine
– 4-5 drops of Betadine 5%
• Get patient to close eye and gently roll them around
– After one minute, lavage the eye
– Lotemax/FML 4 times a day for 4 days
• Alternative: Betadine swabsticks.
– 5% Betadine solution only comes in 30 ml bottles cost
$14.00.
– Case of 200 Betadine swabsticks apprx. 45 dollars.
Management
• Antivirals used in HSV keratitis are
ineffective in treatment of viral
conjunctivitis
– New Update: in conversation with several
colleagues, Zirgan 4-5 times/day has shown
significant improvement in patients over a 710 time period.
• Important to stress limited contact with
others, frequent hand washing, not
sharing of towels, etc.
Sinusitis Red Eye
• With a sinus infection or
inflammation
– the sinuses swell and mucus cannot
properly drain.
• The increase in mucus and the narrow
passage through which it tries to escape
creates pressure in the sinuses that
leads to pain.
• The sinuses surround the ocular region
– pressure from sinuses may feel like
eye pressure.
– swollen sinuses and nasal
membranes can push against ocular
nerves resulting in pain.
• Pooled mucus can result in infection
that increases the pain in the sinus and
ocular region even
Sinusitis Treatment
• The infection is likely bacterial and should be
treated with antibiotics if:
– symptoms last for 10 days without improvement, or
– include fever of 102 degrees or higher,
– nasal discharge and facial pain lasting three to four days
• Because of increasing resistance to the antibiotic
amoxicillin — the current standard of care — the
ISDA recommends Augmentin
• Augmentin 250/500 TID for 5-7 days for adults,
10-14 days for children
– Alternative is Keflex 500 mg QID
Flashes and Floaters
• Patients often present complaining of “spots” or
“cobwebs” in front of their eyes
• Causes of floaters include: posterior vitreous
detachment (PVD), retinal tear, vitreous heme,
uveitis.
• Since PVD and retinal tears present the same way, a
RT has to be eliminated
• Ask the patient whether spots move with eye and
continue to move after the eye has stopped
• Large spots could be blood clots
Posterior Vitreous Detachment (PVD)
Vitreous Heme
Retinal Tear
Flashes and Floaters
• Sudden onset typically means a PVD, retinal tear or
heme
• If the spots appear after flashing light, then retinal tear
must be eliminated
• Myopes tend to have floaters and will notice them for a
long time
• Key is to rule out potentially sight threatening
condition for the floaters, ie retinal tear.
• Patients with retinal condition such as lattice
degeneration and myopes need to be educated about
S&S of RD (flashes and floaters)
– 5-10% population has lattice
– Risk of RD with lattice is approx 1%
– 30-50% of patients with a RD have lattice
Flashes and Floaters:
Management
• A patient who presents with a sudden onset PVD
without retinal breaks or hemorrhage requires
repeat peripheral examination in six weeks, as the
risk of retinal complications is highest within the six
weeks following vitreous detachment.
• If no retinal breaks are seen at that point, routine
yearly examination is all that is needed
• Lid nevi:
Lid Nevi
– congenital or acquired
– occur in the anterior lamella of the
eyelid and can be visualized at the
eyelid margin.
• The congenital eyelid nevus is a
special category with implications
for malignant transformation.
• With time, slow increased
pigmentation and slight
enlargement can occur.
• An acquired nevus generally
becomes apparent between the
ages of 5 and 10 years as a small,
flat, lightly pigmented lesion
Congenital Nevus
• The nevus is generally well
circumscribed and not
associated with ulceration.
• The congenital nevus of the
eyelids may present as a
"kissing nevus" in which the
melanocytes are present
symmetrically on the upper and
lower eyelids.
– Presumably this nevus was
present prior to eyelid separation
Congenital Nevus
• Most nevi of the skin are not considered to be
at increased risk of malignancy.
– However, the large congenital melanocytic
nevus appears to have an increased risk of
malignant transformation of 4.6% during a
30 year period
Acquired Lid Nevi
• Acquired nevi are
classified as:
– junctional (involving the
basal epidermis/dermis
junction), typically flat in
appearance
– intradermal (involving
only the dermis), tend to
be dome shaped or
pedunculated
– compound (involving
both dermis and
epidermis) tend to be
dome shaped
Corneal Ulcers
•
•
Infective bacterial and fungal corneal lesions cause severe
pain and loss of vision
Signs and Symptoms:
– Pain, photophobia, tearing
– Mucopurulent discharge with generalized conjunctival
injection
– Decreased VA (esp if on visual axis)
– Possible AC reaction and hypopyon
– Dense infiltrate
– Satellite lesions around main lesion may indicate fungal
infection
Sterile vs Infectious Infiltrates
Peripheral (Sterile) Corneal Ulcer
Infectious Corneal Ulcer
Corneal Ulcers
• The Steroids for Corneal Ulcers Trial (SCUT)
• Conclusions:
– no overall difference in 3-month BSCVA and no safety
concerns with adjunctive corticosteroid therapy for
bacterial corneal ulcers
– researchers did find significant vision improvement for one
specific subgroup of the study by using steroid therapy on
patients with severe ulcers
• Application to Clinical Practice:
– Adjunctive topical corticosteroid use does not improve 3month vision in patients with bacterial corneal ulcers
unless in the severe category
Corneal Ulcers
•
•
Infective bacterial and fungal corneal lesions cause severe
pain and loss of vision
S and S:
– Pain, photophobia, tearing
– Mucopurulent discharge with generalized conjunctival
injection
– Decreased VA (esp if on visual axis)
– Possible AC reaction and hypopyon
– Dense infiltrate
– Satellite lesions around main lesion may indicate fungal
infection
Associated Factors
• Contact lens wear, especially soft and extended wear
lens
• Recent history of corneal trauma
• Topical steroid use
• History of exposure to vegetative matter (fungal
etiology)
Protein Synthesis Inhibitors
• These antibiotics work by targeting the bacterial
ribosome.
– they are structurally different from mammalian
ribosomes,
– in higher concentrations many of these antibiotics
can cause toxic effects.
• This group includes:
– (a) tetracyclines, (b) aminoglycosides, (c) macrolides,
– (d) chloramphenicol, (e) clindamycin, (f)
quinupristin/dalfopristin and (g) linezolid
Tetracyclines
• Nonresistant strains concentrate this antibiotic intracellularly
resulting in inhibition of protein synthesis.
• Broad spectrum, bacteriostatic,
– effective against gram (+) and (-) bacteria and against nonbacterial organisms
– widespread resistance has limited their use.
• Drug of choice for Rocky Mountain Spotted Fever, Cholera,
Lyme disease, mycoplasma pneumonia, and chlamydial
infections.
• Side effects include gastric discomfort, phototoxicity, effects
on calcified tissues, vestibular problems, pseudotumor.
Tetracyclines
• This group includes:
– Tetracycline (250mg - 500 mg cap BID-QID) needs
to be taken 1 hour before or 2 hours after a meal.
– Minocycline (100 mg cap BID)
– Doxycycline (20mg - 100 mg cap or tab BID)
Tetracyclines: Acne Rosacea
• Acne rosacea:
– affects females>males after 30 with peak
incidence 4-7th decade of Celtic/Northern
European descent. Males more disfigured.
• 4 subtypes with classic signs of flushing,
papules or pustules usually in crops,
telangiectasia.
– secondary ocular complications (85% of
patients) and often precede other skin
manifestations include erythema, itching and
burning.
• Mainstay oral Tx is Oracea (40 mg in
morning) or
– tetracycline 500 mg po BID or doxycycline
100 mg po BID or minocycline 100 mg po
BID for 4-12 wks.
– NOTE: Oracea is subantimicrobial therapy
Acne Rosacea Treatments
Oral Antibiotics
Topical Treatments
Non-Prescription
Erythromycin
metronidazole (Metrogel)
Rosacea-Ltd III
Tetracycline
BenzaClin (Clindamycin 1% &
benzoyl peroxide 5%)
ZenMed
Doxycycline
BenzaMycin (Erythromycin 3% &
benzoyl peroxide 5%)
Neova Therapy
Minocycline
tretinoin (Retin-A)
Kinerase
Clindamycin 1% lotion/gel
Rosacare
Plexion Cleanser/Lotion (Sulfa 10%
& sulfur 5%)
www.internationalrosaceafoundation.org
Anti-inflammatory effects
•
•
•
Degrade extracellular proteins
Tetracyclines inhibit MMPs
Anti-inflammatory
Question
75 white female complains of sudden decreased vision left
eye. From picture above what is most likely cause?
1. BRVO
2. Ischemic optic neuropathy
3. Papilledema
4. Low tension glaucoma
Epidemiology
• Nonarteritic: usually seen in
younger patients
– Fellow eye involved in 2540% of cases
– Associated with
hypertension and diabetes
Epidemiology
 Arteritic: usually seen in >55 yrs old (mostly over 70)
◦ fellow eye involved in 75% of cases within 2 weeks without
treatment
Symptoms
• Acute visual loss (arteritic>non)
• dyschromatopsia
• Arteritic may also have associated:
– Headache, fever, malaise,
– weight loss, scalp tenderness, jaw claudication,
– amaurosis fugax, diplopia, and eye pain.
Ocular Signs
• Sudden, unilateral, painless
decreased vision and color
vision
• Positive RAPD
• Altitudinal visual field defect
(usually inferior and large)
• Swollen optic disc
• Fellow nerve often crowded
with small or absent cup
(“disc at risk”)
Additional Testing
• Lab tests:
– STAT ESR (rule out arteritic form)
– CBC (low hematocrit, high platelets)
– Fasting blood sugar
– C reactive protein,
– VDRL/FTA-ABS
– ANA
• Check blood pressure
Management
• Arteritic:
– Systemic steroids to prevent fellow eye involvement
• methylprednisolone 1 g IV qd in divided doses for 3 days
then,
• prednisone 60-100 mg po qd with a slow taper
– Check PPD, blood glc and chest radiographs before
starting systemic steroids
• Non-arteritic:
– Consider daily aspirin
Vision Loss Without Pain:
TIA/TMB/Amaurosis Fugax
 Refers to temporary visual impairment of variable
duration (seconds to hours)
◦ TIA: transient ischemic attack-can be cerebral or retinal
◦ TMB: transient monocular blindness secondary to a
retinal TIA
◦ Amaurosis Fugax: same as TMB
 Abrupt onset, progression to involve all or part of
visual field, sight usually returns
 Within affected area, visual acuity maybe dimmed or
completely lost
TIA’s
• Stroke is 3rd leading cause of mortality in developed
countries and most common cause of neurological
disability
• 15-20% of patients with stroke have a preceding TIA,
though guidelines for referral and evaluation are
debated
– Traditional guidelines suggested that assessment
should be complete within 1 week of TIA
TIA’s
• Risk of stroke after TIA has traditionally been
considered relatively low, but
– new studies indicate that the risk is much
higher than previously thought and the time
window for prevention is short.
• Effective secondary prevention depends on
reliable identification of those at high risk and
targeting treatment.
TIA’s: High Risk Factors
 Five (5) risk factors are associated with a high
risk (30%) of recurrent stroke at 3 months:
◦ Age over 60
◦ Symptom duration greater than 10 minutes
◦ Motor weakness
◦ Speech impairment
◦ Diabetes
 Isolated sensory of visual symptoms were
associated with low risk of stroke!
TIA: Early Treatment
 Several treatments are likely to be effective in
preventing stroke in the acute phase after a TIA:
◦
◦
◦
◦
◦
Aspirin
Anticoagulants
Statins
Endarterectomy (for >50% carotid stenosis)
Further research needed for:
 Lowering blood pressure acutely after TIA
 Prophylactic use of neuroprotective drugs
Amaurosis Fugax:TMB
• Most common cause is:
– thromboembolic disease (eg carotid artery disease throwing
emboli) or
– vasospasm
• Described as “curtain falling over vision”
• Risk of stroke or death is about 3-5%,
– which is significantly lower than for a cerebral TIA (15-20%)
• Px still require work-up to determine cause:
– e.g. carotid doppler
Alkali Chemical Burns
•
Alkali exposure results in:
–
–
–
–
Loss of corneal and conjunctival
epi, stromal keratocytes and
endothelium
Loss of clarity is secondary to
stromal hydration
Damage to the vascular
endothelium of conjunctival and
episcleral vessels
Intraocular structures such as iris,
lens and ciliary body are rapidly
damaged if alkali penetrates cornea.
Acidic Chemical Burns
•
•
Epithelium provides
effective barrier to weak
acids. Stronger acids cause
protein precipitation in
epithelium and stroma
which creates a barrier to
further penetration.
Very strong acids penetrate
as quickly as alkalis
Chemical Burn Treatment
• Immediate irrigation is of paramount importance
• Most patients are disabled by severe blepharospasm
and disorientation so require assistance away from
harm and to initiate irrigation.
• Make sure to remove any solid particulate matter
prior to beginning irrigation
• Minimum of 15 minutes constant irrigation (some
recommend 30 minutes)
Chemical Burn Treatment
• Water is commonly recommended however it is
hypotonic to corneal tissue and can result in
increased water intake into the corneal and
subsequent diffusion of corrosive materials
deeper into cornea.
• Recommend fluids of higher osmolarity such as
sterile lactated Ringers and balanced saline
solution.
Chemical Burn Treatment
• Effectiveness of irrigation can be assessed using
pH paper and continued as long as pH outside
of the normal range.
• For grade I and II burns will typically heal
without permanent damage.
– Topical steroid/antibiotic drops/ung recommended
and daily follow up.
– Cycloplegia for pain and further reduction of
inflammation.
Chemical Burn Treatment
• Severe ocular burns are difficult to treat and
may require months of healing
• Basic treatment of these eyes is to reduce
inflammatory response caused by necrotic tissue
– Corticosteroid use
– Prophylactic antibiotics (consider doxycycline as it
inhibits proteinase activity)
– May require surgical intervention with debridement
of necrotic tissue and possibly reconstructive
surgery.