1. 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

2. 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

3. 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.

4. What questions to ask? Onset Visual Loss Pain Redness
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)

5. Common Types of Ocular Emergencies
Vision Loss:
Gradual vs. sudden onset
Vision loss with or without pain
Trauma
Red eyes

6. 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

7. 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
optic neuropathy
Mechanical
retinal detachment

8. 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

9. Visual Defects

10. 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

11. 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?

12. 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

13. 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
Last A1C: 9.1

14. Blood Sugar
Throughout a 24 hour period blood sugar typically maintained between mmol/L ( 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)

15. VEGF and DME

16. 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

17. 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

18. 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

19. 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

20. 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

21. 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

22. 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

23. 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)

24. 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.“

25. 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.

26. 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)

27. 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.

28. Preseptal Cellulitis Treatment
Mild:
Keflex or Ceclor mg QID for 5-7 days
Augmentin 500 mg TID
or 875 mg BID for 5-7 days
Moderate to severe:
IM Rocephin (ceftriaxone) 1-2 grams/day or
IV Fortaz (ceftazidime) 1-2 g q8h.

29. 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?
Seborrheic keratosis
Keratoacanthoma
Basal cell carcinoma
Actinic keratosis

30. Question
Actinic keratosis if left untreated has a 20% chance of converting to which of the following? 1 2 3 4

31. 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

32. 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

33. Pre-Malignant Eyelid Lesions: Actinic Keratosis
Also known as solar or senile keratosis
Most common pre-malignant skin lesion
Develops on sun-exposed areas and commonly affect the face, hands and scalp (less commonly the eyelids)

34. Pre-Malignant Eyelid Lesions: Actinic Keratosis
Appear as multiple, flat-topped papules with an adherent white scale.
Development of SCC in untreated lesions as high as 20%
Management is surgical excision or cryotherapy (following biopsy)

35. 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

36. 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.

37. 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

38. 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) 38

39. Dendritic Ulcers

42. Herpes Simplex Keratitis
Topical:
Viroptic (trifluridine) q 2h until epi healed then taper down for 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

43. Prophylaxis?? Pitfalls to 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 long-term ACV prophylaxis predisposes to ACV-refractory disease due to the emergence of corneal ACVR HSV-1.

44. 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

45. Question
Which of the following best represents your patient? 1 2 3 4

46. Conjunctivitis Bacterial Conjunctivitis Allergic Conjunctivitis
Viral Conjunctivitis
Blepharo-conjunctivitis

47. Viral Conjunctivitis
Most common infectious keratitis presenting on emergent basis
62% caused by adenovirus
Two major types:
Pharyngoconjunctival fever
Epidemic keratoconjunctivitis

48. 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

49. AdenoPlus
Have you heard about this?

50. 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.

51. 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

52. JOURNEY OF THE “RED EYE”
Patient has “Red Eye”
“Red Eye” Protocol
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

53. 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
NEGATIVE
Education: hygiene and hand washing
Supportive care: artificial tears, cool compresses and antihistamines
Antiviral medication
No antibiotics
Consider topical antibiotics or antihistamines

54. Viral Conjunctivitis: Signs and Symptoms
Pseudomembranes in severe cases
Subconjunctival hemes
Gritty sensation
Watery discharge
Sticky in mornings
Follicular response
Chemosis
Injection
SPK
Infiltrates possible
Positive lymph nodes

55. 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

56. 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.

57. 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 7-10 time period.
Important to stress limited contact with others, frequent hand washing, not sharing of towels, etc.

58. 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

59. 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, days for children
Alternative is Keflex 500 mg QID

60. 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

61. Posterior Vitreous Detachment (PVD)

62. Vitreous Heme

63. Retinal Tear

64. 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

65. 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

66. 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

67. 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

68. 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

69. 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

70. 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

71. Sterile vs Infectious Infiltrates

72. Peripheral (Sterile) Corneal Ulcer

73. Infectious Corneal Ulcer

74. 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 3-month vision in patients with bacterial corneal ulcers unless in the severe category

75. 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

76. 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)

77. 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

78. Tetracyclines
Nonresistant strains concentrate this antibiotic intracellularly resulting in inhibition of protein synthesis.
Broad spectrum, bacteriostatic,
effective against gram (+) and (-) bacteria and against non-bacterial 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.

79. Tetracyclines This group includes:
Tetracycline (250mg mg cap BID-QID) needs to be taken 1 hour before or 2 hours after a meal.
Minocycline (100 mg cap BID)
Doxycycline (20mg mg cap or tab BID)

80. Tetracyclines: 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

81. 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%)

82. Anti-inflammatory effects
Degrade extracellular proteins
Tetracyclines inhibit MMPs
Anti-inflammatory

83. 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

84. Epidemiology Nonarteritic: usually seen in younger patients
Fellow eye involved in 25-40% of cases
Associated with hypertension and diabetes

85. Epidemiology
Arteritic: usually seen in >55 yrs old (mostly over 70)
fellow eye involved in 75% of cases within 2 weeks without treatment

86. 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.

87. 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”)

88. Additional Testing Lab tests: Check blood pressure
STAT ESR (rule out arteritic form)
CBC (low hematocrit, high platelets)
Fasting blood sugar
C reactive protein,
VDRL/FTA-ABS
ANA
Check blood pressure

89. Management Arteritic: Non-arteritic:
Systemic steroids to prevent fellow eye involvement
methylprednisolone 1 g IV qd in divided doses for 3 days then,
prednisone mg po qd with a slow taper
Check PPD, blood glc and chest radiographs before starting systemic steroids
Non-arteritic:
Consider daily aspirin

90. 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

91. 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

92. 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.

93. 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!

94. 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

95. 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

96. 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.

97. 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

98. 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)

99. 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.

100. 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.

101. 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.