Disclosures and Special Request. What questions to ask? What Classifies an Emergency? Visual Loss

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Clifford Turner
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1 Diagnosing and Managing Ocular Emergencies and Urgencies: Part I SRC 2013 Melbourne, Australia Blair Lonsberry, MS, OD, MEd., FAAO Diplomate, American Board of Optometry Clinic Director and Professor of Optometry Pacific University College of Optometry blonsberry@pacificu.edu Disclosures and Special Request Paid consultant for: Alcon Pharmaceuticals, Bausch and Lomb, Carl Zeiss Meditec, Merck Pharmaceuticals, NiCox, SARcode Commitment to change: write down three clinical pearls that you learned from this presentation that you can incorporate into your practice to improve patient care revisit these points a month from now, in 3 months and again in 6 months and see if you have adopted them make a commitment to change how you care for patients 1 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. Onset Visual Loss What questions to ask? suddenly noticed or sudden onset? 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) 10) Redness Associated Factors is there any redness? location? 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 1

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, Inflammatory

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

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

2 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, Inflammatory Infiltrative Mechanical central retinal artery occlusion, vitreous heme optic neuritis 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 2

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

3 (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.

3 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 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 Entrance Skills/Health Assessment Physical Presentation VA: OD: finger count OS: 6/12 (20/40) 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 viewer.php?cisoroot=/ehsl- WFH&CISOPTR=159 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 Imaging/Surgery 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 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 ituitary%20program/craniopharyngio ma/cranio_sag_preop_fullylabeled.jp g 3

Craniopharyngioma Craniopharyngioma: slow-growing, epithelial-squamous origin, calcified cystic tumor arises from remnants of the craniopharyngeal duct Craniopharyngiomas have a benign histology but

4 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 h 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 6/12 (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. 4

$Gradual Onset Vision Loss: Cataracts Most common non refractive cause of visual impairment S&S include: misting/blurring of vision colors seem faded poor night vision glare, change in refractive$ surgery.

5 Gradual Onset Vision Loss: Cataracts Most common non refractive cause of visual impairment S&S include: misting/blurring of vision colors seem faded poor night vision glare, change in refractive error (typically myopic shifts) Most common are age related (though congenital, metabolic and traumatic possible) By age 80, more than half of all patients either have a cataract or have had cataract surgery. Gradual Onset Vision Loss: 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 mg QID for 5-7 daysy 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. 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) 5

Dendritic Ulcers 3 1 Herpes Simplex Keratitis Tx: Topical aciclovir ointment 5

ointment 5 times/day for 3 days after fluorescein staining i has resolved Oral

without the toxicity Valtrex (valacyclovir)) 500 mg TID for 7-10 days Famvir

prophylaxis of 400 mg acyclovir BID for 1 year to decrease recurrence Valtrex

Forte QID until inflammation reduced and then slowly taper.

vision in the right eye PMHx: HTN for 15 years, takes water tr pill VA s: 6/18

6 Dendritic Ulcers 3 1 Herpes Simplex Keratitis Tx: Topical aciclovir ointment 5 times/day for 3 days after fluorescein staining has resolved Vidarabine ointment 5 times/day for 3 days after fluorescein staining i has resolved Oral acyclovir (2 g/day) has been reported to be as effective as topical antivirals without the toxicity Valtrex (valacyclovir)) 500 mg TID for 7-10 days Famvir (famciclovir) 250 mg TID for 7-10 days Herpes Simplex Keratitis Consider prophylaxis of 400 mg acyclovir BID for 1 year to decrease recurrence Valtrex 500 mg qd If stomal keratitis present, after epi defect has healed, add Pred Forte QID until inflammation reduced and then slowly taper. Case 65 year old Caucasian patient presents with sudden onset loss/blurring of vision in the right eye PMHx: HTN for 15 years, takes water tr pill VA s: 6/18 (20/60) OD, 6/7.5 (20/25) OS Pupils: PERRL APD CVF: Inferior defect right eye, no defects noted in the left eye 6

$Vision Loss Without Pain: Diabetes/Diabetic Retinopathy Microvascular complications resulting in capillary closure & abnormal permeability S&S include; blurring of vision (maculopathy and refractive$ 10, 2012: FDA approves Lucentis to treat diabetic macular edema The drug s safety and effectiveness to treat DME were established in two clinical studies involving 759 patients who were treated and

10, 2012: FDA approves Lucentis to treat diabetic macular edema The drug s safety and effectiveness to treat DME were established in two clinical studies involving 759 patients who were treated and

7 Vision Loss Without Pain: Diabetes/Diabetic Retinopathy Microvascular complications resulting in capillary closure & abnormal permeability S&S include; blurring of vision (maculopathy and refractive error shifts), sudden drop in vision (vitreous heme), dot and blot hemes, exudate, cotton wool spots, neovascularization (iris, retina and disc) VEGF and DME Aug. 10, 2012: FDA approves Lucentis to treat diabetic macular edema The drug s safety and effectiveness to treat DME were established in two clinical studies involving 759 patients who were treated and followed for three years. patients were randomly assigned to receive monthly injections of Lucentis at 0.3 milligrams (mg) or, or no injections during the first 24 months of the studies after 24 months, all patients received monthly Lucentis either at 0.3 mg or Results: 34-45% of those treated with monthly Lucentis 0.3 mg gained at least three lines of vision compared with 12-18% of those who did not receive an injection. Vision Loss Without Pain: Vein Occlusion Associated with: hypertension, coronary artery disease, DM and peripheral vascular disease. Usually seen in elderly patients (60-70), slight male and hyperopic predilection. Second most common vascular disease after diabetic retinopathy. Branch Retinal Vein Occlusion: Signs/Symptoms BRVO: sudden, painless, visual field defect. patients may have normal vision. quadrantic VF defect, dilated tortuous retinal veins with superficial hemes and CWS typically occurs at A/V crossing (sup/temp) BRVO BRVO more common than CRVO and has more favorable prognosis Overall 50-60% of BRVO patients will maintain VA of 6/12 (20/40) or better Visual loss results from: Macular edema Foveal hemorrhage Vitreous heme Epiretinal membrane RD Macular ischemia Neovascularization complications 7

Question Study Design (n=397) BRVO BRAnch retinal Vein Occlusion study safety/efficacy Macular Edema Secondary to BRVO What would you recommend to a patient with a nonischemic BRVO who has decreased

Monitor for 5-6 months then initiate anti-vegf if not resolved 5. Initiate anti-vegf treatment immediately 12M Sham (n=132) 1:1:1 Randomization 0.

8 Question Study Design (n=397) BRVO BRAnch retinal Vein Occlusion study safety/efficacy Macular Edema Secondary to BRVO What would you recommend to a patient with a nonischemic BRVO who has decreased vision secondary to macular edema? 1. Monitor as will resolve on its own 2. Monitor for 5-6 months then macular grid laser if not resolved 3. Macular grid laser immediately 4. Monitor for 5-6 months then initiate anti-vegf if not resolved 5. Initiate anti-vegf treatment immediately 12M Sham (n=132) 1:1:1 Randomization 0.3 mg (n=134) (n=131) Monthly Injections (last at 5M) Rescue Laser (if eligible beginning at Month 3) PRN ranibizumab for all patients Rescue Laser (if eligible beginning at Month 9) 0.3 mg Month 6 Primary Endpoint from Baseline RS Letters) Mean Change f BCVA (ETDR Mean Change from Baseline BCVA BRVO Sham/ (n=132) 0.3 mg (n=134) (n=131) * * Day 0 Month 5 Monthly Treatment Month Months 6 11 PRN Treatment The gain of additional 3 lines occurred at a rate of 61% of 0.5 AVT grp, 55% for 0.3 AVT & 29% placebo Central Retinal Vein Occlusion: Signs/Symptoms CRVO: thrombus occurring at lamina is classical theory but new evidence indicates that the occlusion is typically in the optic nerve posterior to the lamina cribrosa decreased VA ranging from near normal to hand motion with majority 6/60 (20/200) range dilated tortuous vessels, with numerous retinal hemes and CWS Central Retinal Vein Occlusion Visual morbidity and blindness are primarily from: persistent macular edema, macular ischemia and neovascular glaucoma Central Retinal Vein Occlusion CRVO s can be ischemic or non. Classical definition of ischemic is 10-disc area of non-perfusion found on angiography RAPD and ERG maybe better predictor RAPD and ERG maybe better predictor VA s typically worse in ischemic Increased number of cotton wool spots with decreased VA maybe predictive 8

Central Retinal Vein Occlusion Ischemic CRVO may lead to iris neovascularization and neovascular glaucoma Estimated apprx 20% of CRVO s are ischemic with 45% of those developing neo Traditional

(n=392) CRVO Central Retinal vein occlusion Study: Efficacy & safety Macular Edema Secondary to CRVO Sham (n=130) 1:1:1 Randomization 0.

3 mg Month 6 Primary Endpoint om Baseline BCVA Letters) Mean Change fro (ETDRS Mean Change from Baseline BCVA +12.7* +14.9* CRVO Sham/ (n=130) 0.3 mg (n=132) (n=130) 18 16 14 12 10 8 6 4 2 0 2 07 +0.

3 Vision Loss Without Pain: Artery Occlusion Primarily embolic in nature from cholesterol, calcifications, plaques.

9 Central Retinal Vein Occlusion Ischemic CRVO may lead to iris neovascularization and neovascular glaucoma Estimated apprx 20% of CRVO s are ischemic with 45% of those developing neo Traditional treatment for iris neo has been PRP Regular examinations (1-2 wks) to monitor for ischemia or neo development should include gonio as angle neo can precede iris rubeosis 12M trial Study Design CRUISE (n=392) CRVO Central Retinal vein occlusion Study: Efficacy & safety Macular Edema Secondary to CRVO Sham (n=130) 1:1:1 Randomization 0.3 mg (n=132) (n= 130) Monthly Injections (last at 5M): 6M tx period PRN Lucentis available for for all patients: 6M tx period 0.3 mg Month 6 Primary Endpoint om Baseline BCVA Letters) Mean Change fro (ETDRS Mean Change from Baseline BCVA +12.7* +14.9* CRVO Sham/ (n=130) 0.3 mg (n=132) (n=130) Day 0 Month 5 Months 6 11 Monthly Treatment Month PRN Treatment Pts with >/= 3 line improvement was noted in 48% of.5 AVT, 26 of.3 AVT & 17% of sham Vision Loss Without Pain: Artery Occlusion Primarily embolic in nature from cholesterol, calcifications, plaques. Usually occurs in elderly associated with: hypertension (67%), carotid occlusive disease (25%), DM (33%) and cardiac valvular disease. Sudden loss of unilateral, painless vision defect dependent upon location of occlusion Vision Loss Without Pain: Artery Occlusion BRAO typically located in temporal retinal bifurcations. CRAO CRAO has profound vision loss with history of amaurosis fugax. Vision is usually CF (count fingers) to LP (light perception) with positive APD. Diffuse retinal whitening with arteriole constriction, cherry red macula. 9

10 Ophthalmic Emergency Treatment is controversial due to poor prognosis and questionable benefit. Treat immediately before workup, if patient presents within 24 hours of visual loss: Digital ocular massage, systemic acetozolamide (500 mg IV or po), topical ocular hypertensive drops (Iopidine, B blocker), anterior chamber paracentesis, consider admission to hospital for carbogen Tx (high carbon dioxide) 10

Interactive Grand Rounds

Interactive Grand Rounds Blair Lonsberry, MS, OD, MEd., FAAO Professor of Optometry Pacific University College of Optometry blonsberry@pacificu.edu CASE 1 Case History 38 black male, complaining that the