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Ocular Emergencies

Ocular Emergencies for the Disclosure Statement Primary Care Optometrist

. Honorarium, Speaker, Consultant, Research Grant:  Aerie, Alcon, Allergan, B+L, Carl Zeiss, Glaukos, Heidelberg, Novartis, Topcon,

Michael Chaglasian, OD, FAAO Associate Professor Illinois Institute Illinois College of [email protected]

What is a “True” Emergency? “True” Emergency

. Pain (vs. discomfort) . History is key to differentiating emergency versus urgency . Current or potential for:  Phone or in person  Vision loss  Proper triage is essential  Structural damage  After hours protocol  Needs immediate (same day) attention  Your office and your specialists  Medico-legal implications

History Emergency Exam

 Vision  Recent ocular disease or  One or both ? surgery . Acuity . External examination  Visual field  Other diseases . Visual fields . SLE  Sudden or gradual  cardiac, vascular, or .  Blurred or lost? autoimmune . IOP  ?  viruses . Ocular Motility . Fundus exam  Mono or Bino  Medications or recent  Pain changes to medications  Redness  Nausea/vomiting  Onset  Trauma  Contact lenses

M. Chaglasian, OD 1 Ocular Emergencies

Emergency Kit “True” Emergency

. Chemical Burns . Eye shield . pH paper  Alkaline . Pressure patch . Bandage CL’s . Sterile eye wash . Diamox . Central Retinal Artery Occlusion . Alger brush . Topical drops . Forceps  Antibiotics  NSAID’s . Golf spud . Both have extremely high risk of severe and permanent  Steroids vision loss which can be prevented via immediate  Cycloplegics intervention and treatment

Chemical Trauma Chemical Burns . Copious irrigation  anesthetic . Acid exposure  speculum  Only penetrate through epithelium  sterile saline v tap water  car battery, vinegar, and some refrigerants . Contacts can be removed after irrigation . Sweep fornices – repeatedly . Alkaline exposure  Penetrates tissues more easily and . Examination after irrigation and neutralization of pH have a prolonged effect . Debride necrotic tissue  lime, (plaster, cement) lye, ammonia found in household . Want neutral pH of 7.0 – cleaners, fertilizers, and pesticides check q15min with pH paper . Have patient bring agent if possible

Chemical Burns Roper Hall Classification of Ocular Burns

. Determine area of involvement  Assessed by extent of FL staining Grade Prognosis Limbal Ischemia Corneal Damage  Assess depth of conjunctival penetration 1 Good None Epithelial Damage  Vascular ischemia, necrosis of limbal and bulbar 2 Good Less than 1/3 Haze but detail  Loss of limbal vascular plexus is key indicator to severity of visible permanent vision loss 3 Guarded 1/3‐1/2 Total haze that obscures iris . Check IOP 4 Poor >1/2 Opaque  Tonopen  IOP meds

M. Chaglasian, OD 2 Ocular Emergencies

Alkali Chemical Burn Alkali Chemical Burn

. 50 yo CM bricklayer . Needs more irrigation and debridement . Mortar splashed in eyes 1 day prior . Emergency amniotic membrane transplant (AMT) . Went to ER, eyes rinsed, given drops and Augmentin . c/o FBS, OD; OS feels fine . VA: OD HM; OS 20/20-2 . pH: 10 OD, 7.4 OS

Chemical Burn Management Chemical Burn - Ocular Sequelae

. Cycloplegic . Tarsorraphy . Advanced . Chronic Dry Eye . AB or AB/steroid combo ung  Glue/permanent . destruction . Persistent epithelial defects/ RCE . Pain control . Symblepharon . Infectious  Cyclo, steroids, NSAIDs . AMT . Cicatricial - months . Stromalysis . Artificial tears . Limbal stem cell transplant . Pressure patch  Uninjured eye - autograft . . Perforation  . . Irreversible intraocular damage BCL not tolerated  Close relative – allograft . Oral narcotics/NSAID . . . Topical sodium ascorbate 10% . Corneal transplant . Descemet membrane . and Citrate Oral . Artificial . Doxycycline detachment . Diamox . Retinal detachments

Amniotic Membrane Transplant (not Bandage) AMT

. Used as a surgical graft, where the tissue is integrated into the host. Amniotic membrane provides the scaffold for re-epithelialization. . When used as a graft, AM is typically glued or sutured in place, and epithelium is expected to grow over it. . Amniotic membrane is the innermost layer of the placenta, with 3 layers: . AMT has an low immune response, so few rejections  Epithelium . Shown to:  thick basement membrane: supports epi call migration and inhibits apoptosis 1.  epithelialization  Avascular stromal matrix: rich in growth factors & protease inhibitors 2.  fibrosis,  inflammation,  scarring 3. provides an anti-inflammatory and anti-scarring effect that AM applied with epithelial-basement minimizes the buildup of scar tissue side facing UP, stroma DOWN . Other uses: Acts as basement membrane for corneal epithelium to grow over  Stevens-Johnson syndrome  Bullous /, pterygia  Prevent post-op adhesion of conj/ in

16. Sippel KC, et al. Amniotic membrane surgery. Curr Opin Ophthalmol 2001;12:269-281

M. Chaglasian, OD 3 Ocular Emergencies

CRAO CRAO

. Sudden, painless, unilateral loss of vision . 47yoCF with 3 day h/o blur, OS, with severe loss . (+) APD yesterday . Swollen, pale posterior pole . Had been seen twice in previous week . “Cherry red” spot  1 MD, 1 OD • Vascular attenuation &/or boxcarring of flow  Dx: Dry eyes in arteries & veins  Tx: Artificial tears  Spoke to tech yesterday • May see an embolus in vessel on . Casual about coming in

Patient findings CRAO

OD OS . In office AC paracentesis & digital massage  ASA 20/20 Distance Acuity CF 1’ . To Cardiologist (+) APD  Echocardiogram 12 TA 12 . To ER BP 128/79  Blood work  ESR: rule out Temporal Arteritis

WNL SLE WNL . To PCP  Hematology workup . To  Brimonidine Vision Never Improved

CRAO CRAO Causes

. Echocardiogram  Dilated aortic root . Emboli . In patients of 70 years of  associated with connective tissue dx  74% cholesterol age and older, . Blood work:  10.5% calcific giant cell arteritis is more  ESR: minimally elevated  15.5% platelet-fibrin likely to be the cause than  Elevated homocysteine level . Thrombosis in younger patients.  amino acid in blood derived from the digestion of . Vasculitis protein-rich foods  GCA  Elevated PTT (Partial thromboplastin test) . Post-trauma  Other hypercoagulability factors negative  Negative CT, MRI, MRA

M. Chaglasian, OD 4 Ocular Emergencies

CRAO CRAO Testing

 ESR & CRP . Incidence . Risk Factors  Carotid Doppler –  r/o GCA r/o emboli from  3.5/10,000 in general  Age >40 population  CBC/lipid profile carotid  Systemic conditions  Cardiology referral  Auto-immune . 92% of patients have  HTN, DM, CV dx, prior MI,

CRAO CRAO & Mortality

. Retina suffers no detectable damage up to 97 . Patients with emboli have a 56% mortality rate over 9 years, minutes compared to 27% for an age-matched population without emboli . BUT sustains massive, irreversible damage after 4 hours . Life expectancy of patients with CRAO is 5.5 years compared to 15.4 years for an age-matched population without CRAO

 Hayreh SS, Zimmerman MB, Kimura A, et al. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723‐36.

CRAO – Acute treatment CRAO – Acute treatment • Lower IOP • Anterior chamber paracentesis • remove 0.1 to 0.4 ml of aqueous fluid within the first 24 hours.  Move occlusion • Digital ocular massage  Carbon/carbogen inhalation • Some use 3‐Mirror  CO dilates arterioles & increases O delivery to ischemic • IOP lowering agents 2 2 tissues  Paper bag – dilate retinal vessel  Remove embolus  Local intraarterial fibrinolysis (LIF) was associated with similar visual outcomes but increased rate of adverse reactions when compared to observation in the EAGLE study.  The study did not recommend LIF for acute CRAO.

M. Chaglasian, OD 5 Ocular Emergencies

CRAO Urgencies

. Risk of neovascularization . Giant Cell Arteritis . Penetrating injury  NVD, NVI, NVG . . Ruptured  Reports from 2.5-35% . CRVO . Lacerations  18.2% @ an average of 8.5 weeks post CRAO . . Corneal foreign body . . . . . Iritis  Ocular neovascularization following central retinal artery occlusion: prevalence and timing of onset. Eur J Ophthalmol. 2010 . Nov‐Dec;20(6):1042‐6.

Giant Cell Arteritis / Temporal Arteritis Background on GCA

. Giant cell arteritis (GCA) is the most common primary vasculitis in adults. . Histopathologically, GCA is marked by generalized granulomatous inflammation of medium- to large-sized vessels that occurs in the elderly. . Patients commonly note associated symptoms such as headache, jaw claudication, diplopia, myalgias, and constitutional symptoms. . The most commonly feared sequela of GCA is permanent visual loss secondary to arteritic anterior ischemic (AAION). . Since the vision loss from AAION can progress rapidly, and can involve the fellow eye within a matter of days, GCA is considered an ophthalmologic emergency.

Giant Cell Arteritis / Temporal Arteritis GCA Exam Findings

. Inflammation of medium & large sized arteries of the . CRAO body, restricting blood flow & causing pain . VA loss usually unilateral, but risk of loss in other eye if . AION not treated within 1 week . Flame hemes, cotton wool spots . Elderly (>60), white, female . Scalp tenderness, jaw claudication, HA, loss of appetite, . Pale, swollen disc weight loss, fatigue . 6th nerve palsy . Need stat ESR & temporal artery biopsy  Normal Sed Rate:  F= (age+10)/2  M= age/2

M. Chaglasian, OD 6 Ocular Emergencies

Treatment Ocular Urgencies

. High dose systemic steroids  60-100mg qd . Trauma . Retinal detachment  IV methylprednisone  Penetrating/non- . Orbital Cellulitis penetrating  250 mg q6h x 3 days . Iritis  . Aspirin . Corneal ulcer  Blowout fractures . Optic neuritis  Ruptured Globe . Referrals: Neurology, Rheumatology, . Acute exophthalmus  Lacerations  Temporal Artery Biospy  Corneal Abrasions  Color duplex ultrasonography  Foreign Bodies

Trauma Ocular Trauma

. 2,500,000 traumatic eye injuries /yr in US  40,000-60,000 lead to visual loss . 40% of all new cases of monocular blindness Closed Globe Open Globe . 80% occur in men . 75% are work related Burn LacerationRupture Laceration . Average age 30 Contusion

Penetrating Perforating

Hyphema Grading Traumatic hyphema

. Grade 1 - Layered blood occupying <1/3 of the anterior . r/o rupture . r/o sickle/sickle trait chamber . Fox shield . 10-20% re-bleed rate . Restrict activity/head elevation  More common w/Gr. 3-4  >50%  Hospitalization?  corneal staining, glaucoma, . Grade 2 - 1/3-1/2 of the anterior chamber . D/C blood thinners optic atrophy  Systemic aminocaproic acid  ASA, NSAID’s . Grade 3 - Layered blood filling 1/2 to less than total of the (ACA) anterior chamber . . Grade 4 - Total (100%) clotted blood, aka 8-ball hyphema . Pred Forte qid . ~30% have elevated IOP  <10%  Beta blocker  Gonio ~ 1 month later

M. Chaglasian, OD 7 Ocular Emergencies

Angle Recession Traumatic Glaucoma

. Blunt trauma which causes a hyphema is more likely . patients with damage to greater than two-thirds of angle are also more likely to develop glaucoma to also cause an angle recession

. glaucoma associated with angle recession may develop months to years . Between 2 and 20% of patients with angle recession following the injury will go on to develop glaucoma . Glaucoma is related to magnitude of hyphema,  Only 13% get when hyphema is less than half of AC

. Bed rest (head elevated) or very limited activity along with patching are usually recommended.

Management Hyphema

. Early Phase Glaucoma and Acute Trauma . Measure the percent of hyphema in AC  Acute Inflammation / Iritis . Measure the IOP  Hyphema  may have very high IOP  red blood cells in the anterior chamber . NO ,  results from a tear in the angle that breaks a blood  must wait 7 days to prevent causing a rebleed vessel  rebleeds occur up to 7 days after trauma . Check sickle cell status  Those with SC may need AC wash out

Medications: Early Phase Elevated IOP from Hyphema

. For Inflammation: . PGAs:  Not an option for early phase  :  Good option b/c uveoscleral outflow  w/ atropine 1% BID, 5% . Beta Blockers  Timoptic XE, Betagan, etc. . Alphagan  Topical steriods: . Topical or Oral CAI’s  prednisolone acetate 1% QID . Cosopt or Combigan= good option . The usual duration of an uncomplicated hyphema is 6 days  NO aspirin products: rebleed . Anterior Chamber “Wash Out”

M. Chaglasian, OD 8 Ocular Emergencies

Trauma - Penetrating Injury Trauma - Laceration

If rupture- STOP exam . Fox shield and to hospital for exam under . Corneal anesthesia . Conjunctival . CT if foreign body can’t be seen . Lid . Systemic antibiotics . Compromise protective outer layers, increasing the risk of infection . Be alert with high velocity injuries for intraocular foreign  Risk of endophthalmitis bodies . Intraocular contents may be outside the globe . Seidel’s sign: (+) full thickness laceration

Corneal Lacerations Corneal Laceration

. 41yoCM- construction foreman  Full thickness . Nail ricocheted off a wall and hit his OD 1 day prior – felt OK  protect w/ shield & immediate referral . Today, 5/10 pain, , FBS . h/o metallic FB 10 ya  Partial thickness . Recent tetatnus shot  treat as abrasion

Corneal Laceration Corneal Laceration

. Va OD: 20/20; OS: 20/25 . + Ocuflox . 1 day follow up, feels 50% better . (+) epi defect . + Cyclogyl . Va 20/30 . (+) AC rxn . No epithelial defect . (-) Seidel’s sign . Get CT to r/o intraocular foreign body . + stromal haze . TA 9 mmHg, OU . Lid eversion negative . Fundus exam WNL . Decrease Ocuflox . Start Pred-Forte

M. Chaglasian, OD 9 Ocular Emergencies

Conjunctival Lacerations Blow Out Fracture

. SLE . Direct trauma to the globe causes an increase in intra-orbital pressure & decompression via orbital  Subconj heme floor fracture  (+) Fl stain  Maxillary bone & posterior medial wall . DFE . Periorbital swelling, ecchymosis & restricted eye movement  Mild . Diplopia, hypesthesia of cheek & teeth, orbital pain  Majority are self-limiting . Most common sign is limited upward or downward  Antibiotic, patch, follow up 1 day gaze due to entrapment of IR or IO  Severe . Crepitus  Antibiotic, patch & refer  palpate the bony rim of the or lid  small bubbles of air "pop" when compressed.

Management Blow Out Fracture

. Ice packs 24-48 hours, no nose blowing . When should surgical repair of blowout fractures be considered? . Recovery can be spontaneous - 2-3 days  Fractures with persistent symptoms (typically double vision or pain) are . Systemic antibiotics usually candidates for surgical repair. Timing of the repair varies, but most often is within two weeks of the injury. Initial repair may consist of any of . Can trigger orbital cellulitis, angle recession glaucoma, & RD. the following: . Prompt surgery if poor cosmesis, persistent diplopia, enophthalmus,  • exploration of fracture site and repositioning of bone pediatric patient with entrapment • release of trapped tissue from fracture site • covering of fracture site with synthetic material . What long-term problems may develop following blowout fractures?  Most fractures heal without long-term effects. However, surgery (eye muscle surgery) is sometimes necessary for persistent double vision. Occasionally, persistent double vision can be treated with non-surgical methods (prism glasses or botulinum toxin injections)

Corneal Abrasion Corneal Abrasion

. 44yoCM . Acute pain & photophobia . CC: Pocked in OS with belt buckle . May need anesthetic to perform exam 1 day prior . : S/P PRK OU . Debride loose epi if necessary . (+) FBS, photophobia, redness . Antibiotic/cycloplegic/NSAID . Pressure patch v. Bandage CL . Antibiotics . RCE issues . Cycloplegic . Treat any associated anterior chamber reaction . BCL? . Debridement of loose tissue . RCE issues  Fingernail, paper, fingernail, pre‐existing EBMD

M. Chaglasian, OD 10 Ocular Emergencies

Corneal/Conjunctival Foreign Body Rhegamatogenous Retinal Detachment

• History important • ? object . Symptoms: . Separation of neurosensory • High speed?  Flashes retina from the underlying • DFE  Vitreous separates from the retinal pigment RPE, by fluid from the • SLE epithelium vitreous cavity and into the • Lid eversion  sub-retinal space.  Separation at retinal vessel may leak blood 1) Removal: into the vitreous irrigation, moistened cotton . Time course of retinal break swab, spud, needle, forceps,  Decreased VA from or defect to time of Alger brush macular involvement can lead to severe, permanent detachment is highly 2) Antibiotic/cyclo/patch/BCL vision loss variable and unpredictable 3) Steroids for scar modulation after defect healed

Rhegamatogenous RD Retinal Detachment

. Develop from Retinal Defect: • 51yo AAM presents to Urgent Care @ IEI  Hole or Break in sensory retina • CC: Sudden blurry vision superiorly OS  Frequently from Posterior Vitreous Detachment (PVD) • x1 week, painless & progressive (-) trauma (-) flashes . Other Forms of Retinal Detachments: • POH: extraction, OU  Exudative • LEE: 2 years ago at IEI, no SRx  Tractional • PMH: HTN, NIDDM (controlled)

Entrance Examination Slit-Lamp Examination

OD OS

• VA sc: OD 20/60+1 PH: 20/60+2 Adnexa/Lids: 1+ MGD 1+ MGD • OS 20/50-1 PH: 20/40+2 Conjunctiva/Sclera: W&Q W&Q • Pupils: PERRL 1+APD(OS) Cornea: Unremarkable Unremarkable Angles: 4+T/4+N 4+N/4+T • EOMs: FROM OU Anterior Chamber: D&Q D&Q

• CVF: FTFC OD Iris: Unremarkable, (‐)NVI Unremarkable, (‐)NVI PCIOL in place, intact, PCIOL in place, intact, • Constricted superiorly OS Lens: clear clear

IOP (Goldmann): 14 12 Anterior Vitreous: Unremarkable (+)Shafer’s sign

M. Chaglasian, OD 11 Ocular Emergencies

Rhegmatogenous Retinal Detachment RRD Statistics

Prevalence: RRD 10-15/100,000 . Patient education: • 70%: Non-Traumatic • 50% myopic . risk of permanent vision, • 1-3D: 4x risk, >3D: 10x risk need for IMMEDIATE retinal referral. • 10% increased risk in fellow eye • 10%: Trauma • 20%: Post- . Patient Treatment and Outcome: • S/P Cataract Extraction • 10 year risk: 6x risk • S/P Refractive lens exchange • 2-8% RRD within 1 month • 20 - 30% have lattice degeneration

SYMPTOMATOLOGY Key Findings for Referral

. Finding a retinal break . Often asymptomatic and thus detected on routine examination . Finding subretinal fluid . Inferior and temporal location from atrophic holes  May not find break, but it’s likely there as that’s how the fluid got  Patients less aware of these slowly progressive RDs as superior and nasal fields of view are less sensitive in

. Flashes/Floaters. Yes or No? . Other Signs:  Not noticed while sleeping  Unilateral symptoms often masked  Acute PVD  Not affecting central vision  Pigment cells in vitreous or vitreal heme  Slow progression/change  Frequent “Red Herring”  TIA, acephalgic migraine, PVD w/o detachment . Techniques to help:  PVD Follow Up: 6-8 weeks of exam detection or with increased  Scleral depression and 3-Mirror retinal exam symptoms  OCT

OCT for RD Treatment

. Use Wide-field Mode . Laser . Helpful in Differential diagnosis  or Laser Indirect LIO for more peripheral breaks . Helpful in determining macular  status  For subclinical holes and breaks with limited SRF and areas of contact between the retina and RPE remain  “on or off”  Laser is applied at the border of the attached and detached retina, the photocoagulation creates “seal” that prevent further progression of the break/detachment

. Monitor Asymptomatic Breaks?  Low (~5%) risk for progression

M. Chaglasian, OD 12 Ocular Emergencies

Treatment Clinical Pearls - Urgency

. Pneumatic Retinopexy (62-78%) Macula On Status Timeframe  Oil/Gas bubble with laser Progressive/large Immediate/next day . Pars Plana : small incision Stable/small/inferior <5 days  Fluid-Air, air-gas exchange, silicone oil injection with laser Macula Off Duration Mean Postoperative VA† . Scleral Buckle: for larger RDs . Thin scleral band placed under conjunctiva to indent ≤10 days 20/41 sclera towards retina followed by laser or cryotherapy 11 days to 6 weeks 20/121 . Decreased in utilization in favor of PPV due to >6 weeks 20/178 numerous SEs †Scleral buckle repairs

Endophthalmitis Endophthalmitis Vitrectomy Study (1995)

. Incidence 0.13% . 420 patients < 6 weeks post CE or 2o IOL c s/s of endophthalmitis  ( review of 215 articles from 1963-2003) . Randomized to +/- systemic antibiotics . Randomized to ParsPlanaVitrectomy (PPV) v AC tap & vitreous injection with antibiotics . Symptoms: . Pain, decreased vision, photophobia, redness . Results: . Signs:  Patients with > LP: Tap and inject (no need for immediate PPV)  Corneal edema, hypopyon, vitritis,  Patients with < LP: Immediate PPV, and inject  3 fold increase in the frequency of achieving 20/40 or better acuity

Acute Angle Closure Glaucoma When can the angle close?

. Classic Symptoms:  Unilateral, painful eye  Blurred vision, halos  Nausea, vomiting

. Characteristics:  Older, white, hyperopic females age > 30 yrs  Peak age 55-70  First-degree relative with ACG  History - previous episodes, medications, surgeries, etc.

M. Chaglasian, OD 13 Ocular Emergencies

Acute Angle Closure Glaucoma CLINICAL FEATURES:

. Symptoms: Pain, halos around lights, redness, nausea, . Acute Angle Closure Attack: vomiting  diffuse conjunctival hyperemia . Signs: Corneal edema, fixed,oval mid-dilated , ciliary flush, AC inflammation, glaukomflecken  cloudy, edematous cornea  . Extremely elevated IOP fixed, oval, mid‐dilated pupil  VA often significantly reduced . Gonioscopy  IOP ranges 40‐70+ mm Hg  Indentation  inflammation / aqueous  Both eyes cell/flare

“CLASSIC” PATIENT SYMPTOMS: GONIOSCOPY

. These symptoms are associated with “Acute” Angle Closure Look for PAS (peripheral anterior )  deep, aching pain (high IOP) as evidence of angle closure  redness, tearing, photophobia  blurred vision, halos (edema) Gonioscopy of both eyes to  nausea, vomiting (pain) confirm a narrow angle approach  Headache (symmetry) Note: Only Indentation gonioscopy . Many patients do NOT have these symptoms shows this, not three mirror.

Indentation Gonioscopy Gonioscopy Lenses Posner 4 mirror » Handle

Sussman 4 mirror » No handle A. = Appositional angle closure » www.ocular-instruments.com B. = Synechial angle closure

M. Chaglasian, OD 14 Ocular Emergencies

Gonioscopy on the Web! When can the angle close?

www.gonioscopy.org

Management - Acute Angle Closure Glaucoma Corneal Ulcer

. Oral CAI’s (250 - 500 mg Diamox) . Peripheral vs Central  Tablet form only, not Sequel form  Sequel takes too long to act . Infection . Topical fixed combination:  Staph, strep, moraxella, pseudomonas  Combigan / Cosopt . Pain, redness, photophobia  Iopidine (if available) . Topical steroids . CL wear . When IOP < 45, add 1-2% pilocarpine . Chronic eyelid disease . SLE: focal accummulation of inflammatory cells in excavation . Definitive Treatment: Laser Peripheral Iridotomy (LPI) with overlying epi defect  Eliminates pupillary block  Prophylactic LPI of fellow eye

Corneal Ulcer Differential Dx

. 15yoCF . Infiltrate . Being treated elsewhere . Ulcer for Corneal ulcer, OS  Pseudomonas  > 1 week with fortified  Fungal antibiotics, oral AB’s  Acanthamoeba . SCL wearer  Fell asleep on a road trip . VA sc: OD 20/20, OS 20/400 PH NI

M. Chaglasian, OD 15 Ocular Emergencies

Corneal Ulcer Treatment Corneal Ulcer Treatment

. Discontinue CL wear . Fortified agents?  subconjunctival loading dose injection of 0.3 cc gentamicin . Antibiotic mixed with 0.3 cc lidocaine at the time of presentation  BESIVANCE (besifloxacin) 0.6% . Steroids when defect is closed to modulate scarring  1 gtt q15minX 2 hrs, then hourly while awake  The SCUT study (Steroids for Corneal Ulcers Trial), a large series involving 500 patients that was published in the Archives of . Cycloplegic Ophthalmology, found no overall difference in three-month BSCVA and no safety concerns with adjunctive therapy for bacterial . Culture if available, if central, if >3mm corneal ulcers

If NI, consider fungal or acanthamoeba….

Optic Neuritis Optic Neuritis: Signs and Symptoms

. Unilateral, acute loss of vision . Varying degrees of vision reduction: . Women, 20-45yo, AA  Ranging from a mild decrease in visual acuity to complete . Strong association with MS vision loss, which is often monocular but can be binocular . The patient’s history may reveal the following signs and symptoms of optic neuritis:  , ocular or orbital pain, worse on EOM’s  Preceding viral illness  Rapidly developing impairment of vision in 1 eye or, less commonly, both eyes: During an acute attack . (+) APD, color vision & VF loss  Dyschromatopsia in the affected eye: Occasionally may be more prominent than the decreased vision [4]  Abnormal contrast sensitivity and color vision:  Retro-orbital or ocular pain:  In almost all patients with adult optic neuritis who have  In association with the vision changes and usually exacerbated by eye movement; the pain may precede vision loss decreased visual acuity  Uhthoff phenomenon, in which vision loss is exacerbated by heat or exercise

Optic Neuritis: Signs and Symptoms Evaluation and Workup

. Field defects: . Magnetic resonance imaging (MRI) is highly sensitive for and specific in the assessment of inflammatory changes in the optic nerves,  May include altitudinal, arcuate, nasal step, central and for central nervous system white matter lesions. , cecocentral scotoma  MRI also helps to rule out structural lesions.

. Initially, the optic nerve head may appear normal. . Labs. Only if other forms of neuritis are possible  Erythrocyte sedimentation rate  Papillitis (swollen disc) may be seen in one third of  Thyroid function tests patients with optic neuritis  Antinuclear antibodies  Angiotensin-converting enzyme  Rapid plasma reagin  Mitochondrial deoxyribonucleic acid (DNA) mutation studies

M. Chaglasian, OD 16 Ocular Emergencies

Management Optic Neuritis Treatment Trial

. Visual function begins to improve 1 week to several weeks after onset, . 448 pts even without any treatment  Oral placebo, IV steroids with placebo orals, or oral steroids . Permanent residual deficits in color vision and contrast and brightness  The primary goal was to determine whether oral or IV steroids altered sensitivity are common the visual outcome in patients with acute optic neuritis. . Pharmacologic therapy in optic neuritis (ON) is directed at ameliorating  IV steroids accelerated recovery of VA initially, the acute symptoms of pain and decreased vision caused by but provides no longterm benefit. demyelinating inflammation of the nerve; varying regimens of  Oral steroids provided no visual benefit and was associated have been used for this purpose. with a higher rate of recurrence. . IV steroids do little to affect the ultimate visual acuity in patients with  Initial MRI result, if abnormal with white matter abnormalities, was the single most important predictor of the optic neuritis, but they do speed the rate of recovery; future risk of MS  Some clinicians advocate IV steroids in patients with either severe or  Routine blood tests of no value bilateral vision loss

If Possible MS Papilledema

. For patients with optic neuritis whose brain lesions . Bilateral optic nerve head edema, secondary to increased on MRI indicate a high risk of developing clinically ICP definite MS, treatment with immunomodulators: . Decreased acuity may not be  interferon [INF] beta-1a, presenting symptom  Headache  INF beta-1b, . Need imaging to rule out space  glatiramer acetate occupying lesion . Lumbar tap/CSF studies . Pseudotumor Cerebri - Dx. of (may be considered) exclusion

Central Retinal Vein Occlusion Neovasculogenesis:

. Non-ischemic v. Ischemic

 Ischemic – less common, more severe with poorer prognosis . Chronic retinal hypoxia is theorized to initiate the production of an  NVG/NVI angiogenic substance / vasoproliferative substance which elicits new  q1month x 6months, q2-3 months x 6 months, q4-6 months x 3 blood vessel growth. years  Vascular Endothelial Growth Factor (VEGF) . Men > 50 . Iris tissue is the primary site for developing neovascularization.  Progresses through several stages: . <40: Needs systemic workup  antiphospholipid antibody syndrome . Poor acuity, possible APD . Hemes, dilated vessels, CWS, retinal & macula edema . Lower IOP

M. Chaglasian, OD 17 Ocular Emergencies

Angle Closure Stage First Step= Medical treatment.

. Time frame for development to this . Features: . Medical therapy is directed at lowering the IOP, reducing the stage:  pain, photophobia anterior segment inflammation and making the patient more   can be variable, from days to decreased Va comfortable. months  increased IOP, high  Note the similarities and differences to the management of  . NVG is known as the: conj. congestion primary acute angle closure  "Ninety day glaucoma“, because of  iritis its rapid onset  corneal edema   ectropian  synechial angle closure

Rapid IOP Reduction: Central Retinal Vein Occlusion

. Acetazolamide: 250 mg x 2 . Prompt referral to PCP . Beta blocker and Alphagan  FBS, ESR, CBC, lipid profile, FTA-ABS . Strong association with HTN, DM, POAG . Anti-inflammatory:  Check BP and IOP in office  prednisolone acetate 1% . Hyperlipidemia, hyperviscosity

. Atropine 1% . Macula edema treatment:  For pain and inflammation  Avastin  Ozurdex  Kenalog . Referral for Avastin and PRP  PRP

Orbital Cellulitis Patient “Emergencies”

. Usually results from spread of infection from paranasal sinuses . Ocular Migraine  CT . Redness/itching/burning/discharge  ENT consult . Subconjunctival hemorrhage . Tx with IV antibiotics . Gradual change in visual acuity . Must distinguish from Preseptal . Lid bumps (non- painful)  Both present with lid edema, pain, redness . Refractive changes  FEVER  PROPTOSIS  PRECIPITATING EVENT  ANY AGE, SEX, RACE

M. Chaglasian, OD 18 Ocular Emergencies

Take Home Message

. Be prepared  Have appropriate equipment/ referrals in place . Take the time to train your staff  You are ultimately responsible Thank you! . Be methodical in your thinking & your examination . Know when it’s OK to treat, and when you must refer

M. Chaglasian, OD 19