Advanced Eye Disorders PDF

Nystagmus Definition Pathophysiology 1. Movement is not smooth 1. vestibular & optokinetic stimulation symmetrical, full, & 2. caused by a variety of diseases maintained 2. Rhythmic oscillation of the eye Jerk Nystagmus Definition Gaze-Evoked Nystagmus 1. Slow drift off the target 1. Most common for...

Nystagmus Definition Pathophysiology 1. Movement is not smooth 1. vestibular & optokinetic stimulation symmetrical, full, & 2. caused by a variety of diseases maintained 2. Rhythmic oscillation of the eye Jerk Nystagmus Definition Gaze-Evoked Nystagmus 1. Slow drift off the target 1. Most common form of jerk nystagmus follow by fast 2. Holds gaze ® pt has tendency to drift corrective jerk back to primary position 2. Horizontal, vertical, or 3. Drugs ® sedative, anticonvulsants, alcohol torsional 4. Muscle paresis, myasthenia gravis, demyelinated dz, posterior brain lesions Planes of movement 1. Horizontal 2. Vertical 3. Rotary Downbeat Nystagmus 1. Lesions near craniocervial junction 2. Upbeat nystagmus assoc w/ damage to pontine from stroke, demyelination or tumor 3. Chiari malformation or MS 4. Brainstem or cerebellar stroke 5. Lithium meds, anticonvsulsant intoxication or, Alcoholism Pendular Nystagmus Definition Etiology 1. Continual oscillation w/o separate phases (slow/fast 1. MS correction) 2. Masses in brain or along optic tract Vestibular Nystagmus Definition Etiology 1. Dysfunction of the labyrinth (Meniere’s disease) , vestibular 1. Peripheral vestibular nystagmus ® attacks w/ nausea & nerve, or vestibular nucleus in the brainstem vertigo - Sudden shifts in head position may provoke this Optic Neuritis - Acquired abnormalities to optic disc ® disc responds in 3 Summary: ways to injury: 1. MS Pt 2. PAINful unilateral loss of vision 1. Cupping 3. Marcus Gun or RAPD on exam 2. Swelling 4. Steroids can help 3. Atropy Defintion Etiology Signs & symptoms 1. Common inflammatory 1. Multiple Sclerosis ® strong 1. Unilateral vision loss ® few days disease of optic nerve association 2. Marcus Gunn Pupil – RAPD - CN II 2. Viral infections - Unequal pupillary response to light 2/2 damage or 3. Sarcoidosis disease in the retina or optic nerve 4. Autoimmune disorders or 3. Pain w/ movement of eye regional inflammation 4. Loss of color vision Treatment 1. not necessary as it gradually recovers 2. IV or oral corticosteroids ® hasten recovery Papilledema Summary: 1. Intracranial pressures elevated 2. Brief visual changes 3. Disc enlarged, w/ margins obscured 4. Neuroimaging ® LP if imaging negative 5. Lower pressure w/ acetazolamide or treat underlying intracranial issue Epidemiology 1. Female - Mostly obese female Labs/ Imaging 1. Requires neuroimaging ® exclude intracranial lesions 2. Normal neuroimaging ® lumbar puncture next to identify & r/o causes Signs & symptoms 1. Bilateral optic disc swelling ® raised intracranial pressure 2. HA is common symptom 3. Complaint ® transient visual obscurations - bilateral or unilateral - lasts seconds or longer Treatment 1. Carbonic anhydrase inhibitor ® acetazolamide - Lowers intracranial pressure 2. Weight reduction is vital 3. Shunt placement ® sever or progressive vision loss Anterior Ischemic Optic Neuropathy (AION) Summary: 1. Older adults w/ GCA 2. SUDDEN Loss of half upper or lower field of vision 3. Unilateral w/ no pain Definition Epidemiology 1. Interrupted blood flow to the anterior 1. older adults portion of the optic nerve Etiology 1. Older adults w/ GCA 2. Congenitally crowded optic disk 3. HTN, DM, HLD, OSA 4. Vasculitis increase risk Treatment 1. Based on cause 2. Prompt ophthalmologist referral Symptoms 1. Sudden loss of half the upper or lower field of vision (altitudinal) 2. No pain & Unilateral ® can be bilateral Arteritic anterior ischemic optic neuropathy (AAION) 1. Requires urgent recognition ® steroids to prevent blindness Posterior Ischemic Optic Neuropathy Definition 1. Uncommon cause of acute vision loss Causes 1. Severe anemia 2. HTN (blood loss) most surgery Treatment 1. Treating the cause ® blood transfusions, reversal of hypotension LEBERS hereditary optic neuropathy Epidemiology 1. Yong men Signs & symptoms 1. Progressive & Painless 2. Severe central visual loss in one eye ® weeks to years later ® other eye pathophysiology 1. Point mutations 2. Maternally inherited by all children 3. Only 10% in female Toxic Optic Neuropathy Signs & Symptoms 1. Visual loss 2. Bilateral optic disc swelling Causes 1. Certain agents 2. Starvation & Malabsorption 3. Alcoholism Optic Disc Drusen Definition 1. Refractile, glittering particles in optic nerve 2. Not related to drusen or retina in macular degeneration Epidemiology 1. Northern European descent Treatment 1. No treatment available Causes Labs 1. Produce pseudopapilledema 1. B-ultrasound 2. Incidental & innocuoucs ® can 2. CT or OCT cause visual obscurations Cellulitis Orbital Summary: 1. SICK patients 2. Erythema/Edema + - Bug eye , PAIN WITH EOM , Systemic signs (fever) 3. Emergent referral 4. IV Vanco + 3rd gen cephalosporin + Flagyl - 2-4 wks abx Periorbital (preseptal cellulitis Summary: 1. No eye pain w/ EOM ® if any pain (mild) 2. cover for sinus if no trauma ® 1st line: Augmentin 3. + Bactrim if trauma likely as inciting event 4. no improvement 24-48 hrs ® inpatient needed Definition Definition 1. Infection of the eye muscles & fat around eye – FAT EOM 1. Redness of eyelid 2. Does NOT involve globe 2. Infection of the skin structures anterior to orbital septum Etiology Etiology 1. Underlying sinus infection 1. Mixed events, smaller amount due to sinus infection - Rhinosinusitis (staph or strep) most common cause 2. ophthalmic surgery Epidemiology Epidemiology 1. More common in pediatric population 1. More common than orbital cellulites Signs & Symptoms Signs & Symptoms Both: swelling, redness, fever, or pain 1. Pain with movement of eye 1. No pain w/ movement of the eye ® unliteral ocular pain 2. Double vision or blurry vision - Not triggered w/ movement 3. Decreased vision/vison loss 2. Vision is normal 4. Abscesses are possible 3. Eyelid swelling & erythema 5. Proptosis (budging of the eye) ® One “bug eye” ®CT 4. Chemosis occasionally scan - Swelling of conjunctiva to look jelly-like - CT scan may be necessary in patients w/o improvement Treatment Treatment 1. Emergent referral to ophthalmologist if suspected Inpatient vs outpatient: Uncomplicated orbital cellutlis 1. Ill appearing children < 1 yrs or Anyone fails 24-48 hrs abx 1. Initial Therapy Opt abx: 5-7 days total abx - IV abx ® prevent spread of infection & optic nerve 1. W/O evidence of skin trauma as inciting event damage - Cover for sinus infection - IV Vancomycin + IV Ceftriaxone or IV cefotaxime - 1st ® amoxicillin – clavulanic acid (Augmentin) 2. Anaerobic coverage - 2nd /3rd generation cephalosporin ® PCN allergy mild - ADD IV metronidazole to above regimen ® until - Levofloxacin for severe PCN allergy intracranial involvement R/O or cause is chronic sinusitis 2. W/ evidence of recent skin damage - PCN Allergy ® Vanco + metronidazole + levofloxacin - Cover for skin bugs - TMP-SMX (Bactrim) + one of the agents above 1. 2. 3. 4. 5. 6. Follow up Uncomplicated & improving ® transition to OP ABX 2-3 wks total abx 4 wks ® bony destruction of sinus MRSA: Bactrim or clindamycin Augmentin or cefpodoxime/cefdinir Levofloxacin for severe PCN allergies Referral for possible surgical drainage Follow up 1. 2. 3. 4. 5. Respond rapidly 24-48 hrs ® clear improvement Failure ® inpatient eval w/ imaging 5-7 days total abx Chronic sinusitis if recurs Macular Degeneration 1. Most common cause of blindness > 65 2. SMOKERS 3. Central vision loss 4. Dry – not much to do, drusen 5. Wet – faster, worse, hemorrahges, but can treat - VEGF inhibitors - Photocoagulation Definition Epidemiology Etiology 1. Breakdown of cells in the macula 1. 50 & 60 yrs 1. SMOKING resulting in: 2. Most common cause of 2. Toxic effect of drugs: - Gradual blindness in persons > 65 - Chloroquine - Irreversible 3. Slight female > male - Phenothiazine - Painless - Bilateral - Central vision loss w/ sparing of peripheral field Diagnosing VEGF-Inhibitors 1. Fundoscopic exam 1. Bevacizumab, Ranibizumab, Afilbercept, or Faricimab 2. Fluorescein angiography 2. VEGF- vascular endothelial growth factor 3. Amsler grid test 3. Promotes angiogenesis in subretinal space ® causes - Initially to identify affected area of eye edema &/or hemorrhage - Subsequently by pt for daily monitoring of dz progression 4. Early use changed outcome 5. Given once a month for 3-6 mo then reassess Atrophic (Dry), or Nonexudative Neovascular (Wet), or Exudative Definition Definition 1. Extracellular debris (drusen) deposits around macula under 1. Occurs between the retinal pigment epithelium & retinal pigment epithelium brunch membrane 2. Debris separates the retinal pigment layer disrupting the 2. Accumulation of serous fluid, hemorrhage & fibrosis photoreceptor function Signs & symptoms Signs & Symptoms 1. Gradual progressive bilateral vision loss 1. Vision loss is more rapid & severe than dry 2. Blurred central vision 2. Central blind spot 3. Visual distortion (straight lines are wavy) 3. Visual distortion (straight lines are wavy) Treatment Treatment 1. Slow disease progression 1. Intraocular injection of antagonists to vascular 2. STOP SMOKING endothelial growth factor (VEGF) 3. Add Mediterranean diet & antioxidants 2. Photocoagulation & photodynamic therapy is now 4. Visual assist devices falling w/ use of above Retinal Detachment 1. Floaters, flashing 2. Curtain drawn down 3. Urgent referral 4. Gas injection, PPV, buckling 5. Laser or Cryopexy Definition 1. Separation of the retina from its underlying supporting epithelium Etiology 1. Related to Retinal Tear - Spontaneous > 50 yrs old - Ocular trauma - Other predisposing conditions: DM retinopathy, wet macular degeneration Pathophysiology Signs & Symptoms 1. Elevated sheet of retinal tissue 1. Sudden visual field loss – often described as w/ folds “curtain being pulled across the eye” 2. Often preceded by floaters or shadow-like disturbance (flashing lights) - High degree of floaters 3. No pain 4. No redness 5. Can progress to blindness 6. Fundoscopic - Retina hanging in vitreous like a gray cloud - Horseshoe tear or U-shaped tear Prognosis 1. w/o tx ® total detachment can occur w/in 6 mo - poor prognosis if macula has detached 2. Prognosis is good: 80% will recover w/o recurrence 3. Watch the other eye ® detachment of contralateral eye occurs 25% Epidemiology 1. 1:10,000 annual incidence 2. Increased risk: significant myopia or cataract surgery Evaluation / Treatment 1. New onset S/S ® prompt referral to ophthalmology 2. See w/in 24 hrs Treatment: 1. Emergency consult/referral 2. Pneumatic retinopexy - gas 3. Pars plana vitrectomy 4. Scleral Bucling HTN Retinopathy Summary: 1. Chronic HTN 2. AV nicking 3. Copper Wiring 4. Papilledema (not dz specific) 5. Cotton wool spots (not dz specific) 6. Assess for elevated intracranial pressure 7. Treat underlying HTN Classification Based on fundoscopic exam: 1. Mild: retinal arteriolar narrow related to vasospasm, arteriolar wall thickening or opacification, arteriovenous (AV) nicking 2. Moderate: Hemorrhages, either flame or dot-shaped, cotton-wool spots, hard exudates, and microaneurysms 3. Severe: some, or all, of the above, plus optic disc edema. Presence of papilledema mandates rapid lowering of the BP Signs & symptoms MILD: 1. AV nicking 2. Copper wiring – vessel appears orange or yellow, not red 3. Focal arteriolar narrowing MODERATE: 1. Multiple retinal hemorrhages 2. cotton wool patches SEVERE: 1. swelling of the optic disk 2. cotton wool patch 3. retinal hemorrhage 4. hard exudate – yellowish, well-defined edges - more commonly seen in HTN retinopathy Treatment 1. Better management of HTN 2. Emergent management of pressure if papilledema present Diabetic Retinopathy Summary: 1. Diabetes 2. Leading cause of blindness in US 3. Multiple, nonspecific visual symptoms 4. Microaneurysms, cotton wool spots, exudates (soft>hard) on exam 5. Treatment for PRD - VEGF inhibitors - Laser - Surgical vitrectomy Definition Epidemiology Two types of Diabetic retinopathy 1. Complication of uncontrolled 1. Leading cause of blindness in 1. Non-proliferative diabetes that results from adults in US 2. Proliferative damage to the blood vessels 2. Proliferative Diabetic retinopathy & retinal structures & the 3. Present in 1/3 of pt w/ a dx of subsequent sequalae diabetes Signs & Symptoms 1. Spots floating in your vision Nonproliferative retinopathy: Proliferative diabetic retinopathy: 2. Blurred vision 1. Earliest stage of retinal 1. Advanced ® most severe type 3. Dark streaks on a read film involvement 2. Poor blood supply triggers retinal tissue to that blocks your vision 2. Retinal capillaries leak into retina produce GF leading to abnormal blood 4. Poor night vision leading to macular edema vessels to grow in the retina 5. Vision loss – central inf the - Proteins (Neovascularization) macula region is affected - Lipids 3. Small vessel occlusion retina seen as well- Red cells causing ischemia & soft exudates ® cotton wool spot – infarcted retina Characterized by: - Whitish/grey, cloud-like, w/ fimbriated 1. Microaneurysms (fringed) edges that appeared to float w/in 2. Dot & blot hemorrhages the substance of the inner retina 3. Hard (intra-retinal) exudates 4. New blood vessels then leak causing vitreous 4. Retinal edema hemorrhage & retinal detachment 5. Macular edema 5. More commonly seen in type 1 DM Prevention / Treatment 1. Prevention is key by having good glycemic control, BP control & lipid control 2. No cure right now 3. If macular edema present w/ visual acuity impairment: - Intravitreal injections w/ VEGF inhibitors agents as initial therapy + Focal laser photocoagulation 4. Surgery for advanced dz not responding to above treatments - Vitrectomy Blowout fracture 1. Trauma 2. Restricted EOM 3. Dropped eye/Enophthalmos 4. Crepitus 5. Evaluate for other structures damaged 6. Referral emergently General Historical clues Physical exam 1. Orbital floor bones ® thin & are 1. Reported numbness 1. Visual exam: composed of the maxillary, palatine, below eye - Double vision w/ upward gaze & zygomatic bones 2. Nausea & vomiting - Restricted EOM 2. Small round object strikes the eye are a concern - Decreased acuity 3. Causes floor to fracture ® trapping - Entrapped muscles 2. Severe pain orbital structures inferiorly stimulate vagal reflex 3. Severe swelling 4. Crepitus ® air leaked into skin possibly from sinus fracture 5. Floor fracture - Dropped eyd - Recessed posteriorly ® enophthalmos Imaging Treatment 1. CT requires for any of the above 1. Initial management ® surveil for other serious issues findings - Cervical spine injury 2. Coronal CT of orbit would be order - Globe injury 3. X rays are a poor test 2. Refer to ophthalmologist if any visual changes 3. Floor fractures ® specialized surgeon - Oculoplastic surgery - Facial & reconstructive surgery - Ophthalmologist that specializes in surgery Open Globe Fracture Summary: 1. High degree of blunt trauma or penetrating trauma 2. Pupil changes 3. Seidel Test + 4. Emergent imaging & referral 5. DO NOT INCREASE IOP Definition Signs & symptoms 1. Commonly after blunt eye injury 1. Obvious corneal or scleral laceration 2. Site of greatest structural weakness – 2. RAPD limbus 3. Peaked, eccentric, or tear dropped pupil 3. Blunt force 4. Intraocular or protruding foreign body 4. Object larger than orbital rim 5. Subconjunctival hemorrhage (posterior 5. Associated w/ orbital bony injury + rupture) open globe 6. Decreased visual acuity Treatment 1. Whenever globe injury suspected ® NEVER apply pressure to the eye or apply topicals 2. Immediate ophthalmology consult & comprehensive eye exam 3. Avoid increasing intraocular pressure - Cause extrusion of ocular contents & further wound contamination 4. Avoidance of any eye manipulation 5. Open globe ® avoid eye solutions (fluorescein, tetracaine, cycloplegics, & tonometry) 6. Eye shield placement over the affected eye 7. Bed rest 8. No oral intake 9. IV antiemetic therapy ® ondansetron 10. Empiric abx ® vanco & ceftazidime 11. Pain meds ® morphine& NSAIDS - Discouraged bc of platelet inhibiting properties 12. Sedation as needed 13. Consider giving Tetanus shot 2/2 open wound Labs & imaging 1. CT non-contrast 2. Seidel Test + - different than seidel sign - clearing of fluorescein that appears to be streaming away Hyphema 1. Blood in anterior chamber 2. B/O increases riks 3. Possible vision loss 4. Ophthalmologist consult ASAP 5. No aspirin Signs & Symptoms 1. Blood in the anterior chamber 2. Blunt or penetrating injury to the eye - After minior injury could suggest bleeding d/o ® sickle cell anemia 3. Can result in permanent vision loss Treatment 1. Ophthalmologist consult ASAP 2. No aspirin (avoid rebleed) 3. Head of bed elevated 4. Bed rest 5. Eye shield 6. Correct coagulopathy if present Signs & Symptoms 1. Layer of white cells in the anterior chamber 2. Suggestive of Fulminant ocular infection 3. Associated w/ sight-threatening infectious keratitis or endophthalmitis Grade scale 1. Microhyphema - Circulating red blood cells by slit lamp exam only - Prognosis: 90% 2. I - <. 33% - Prognosis: 90% 3. II - 33-50% - Prognosis: 70% 4. III - >50% - Prognosis: 50% 5. IV - 100% - Prognosis: 50% Hypopyon Treatment 1. Ophthalmologist w/in hours Central Retinal Artery Occlusion Summary: 1. Painless monocular vision loss 2. Vascular or cardiac patient 3. Cherry red spot or boxcar 4. Emergent – 90 min 5. tPA or massage 6. Look for underlying issues - Cardiac - GCA Definition 1. Occlusion of the central retinal artery or one of its branches by emboli Directed H&P 1. Cardiac - Afib, murumurs, HTN 2. Head - Temporal artery pulse, scalp tenderness, jaw claudication Etiology 1. Carotid disease 2. Cardiogenic emboli (A-fib) 3. Small artery dz from atherosclerosis - DM, HTN< smoking risk factors 4. Giant cell arteritis 5. Young patients: migraines, OPCs, systemic vasculitis, thrombophilia Signs & Symptoms 1. Sudden monocular visual loss - Visual acuity reduced to hand motions seen only 2. No pain 3. No redness 4. RAPD 5. Cherry-red spot @ fovea 6. “Boxcar” segmentation of blood in veins & arteries - Sign of sever obstruction 7. Emboli in retinal artery – seen in 20% of patients 8. Pale retina 9. Associated signs: - GCA - Trauma - Concurrent smoking symptoms Treatment 1. Emergent/Urgent referral to ophthalmology 2. IV or IA tPA 3. Those not tPA candidate: - Ocular massage - Hyperbaric oxygen - IV acetazolamide - CGA – high dose IV corticosteroids Labs/ Imaging 1. Checks ESR, CRP 2. Hypercoagulable workup 3. Duplex U/S carotids (carotids u/s) 4. ECG 5. Echocardiogram 6. Home rhythm monitoring Prognosis 1. Improvement is rare w/ CRAO the longer it occurs 2. Retina can only survive about 90 min w/o proper blood flow 3. Visual acuity @ onset highly predicts outcome – worse = only get temporary vision back Central Retinal Vein Occlusion Summary: 1. PAINLESS MONOCULAR LOSS 2. Vascular risk factors (DM, smoking, HTN) 3. Blood & thunder 4. Retinal hemorrhages 5. Urgent referral 6. VEGF inhibitors 7. Treat underlying issues Definition Risk Factors Signs & symptoms 1. Central retinal vein or one of its 1. DM 1. Painless unilateral vision loss branching becomes blocked 2. HTN 2. Normal EOM 2. Increased pressures cause macular 3. Cardiovascular dz 3. Blood & thunder appearance edema, neovascularization, & retinal 4. Glaucoma 4. Retinal hemorrhages ischemia 5. Smoking 5. Venous dilation & tortuosity 6. Yong patients: hypercoagulable 6. Cotton wool spots state 7. Optic disc swelling Labs Treatment 1. Screen for DM, HL 1. Urgent referral to Ophthalmologist 2. Hypercoagulable workup 2. Identify & treat any systemic conditions that may be associated 3. Macular edema - Intravitreal injections of VEGF inhibitors - Intravitreal corticosteroids are 2nd line 4. Neovascularization - Laser photocoagulation Amaurosis fugax Summary: 1. TIA of retina 2. SUDDEN vision loss ® 1+ visual fields 3. Hollenhorst plaque ® carotid dz 4. Carotid U/S 5. ASA & underlying cause Definition: 1. TIA (transient ischemic attack) of retina 2. Transient monocular visual loss 3. Rapid fading of vision pathophysiology 1. Same as CRAO & CRVO for vascular causes 2. Migraine 3. Glaucoma Symptoms & Signs 1. Sudden loss of vision in one or more visual fields 2. Evaluate retina for CRVO/ARAO changes 3. Hollenhorst plaque suggests carotid disease - Carotid Ultrasound should be ordered Treatment 1. Oral ASA 81 mg 2. Find underlying causes - W/U similar to CRAO here as well - Ischemia, Cardiac emboli, GCA are leads Definition 1. Reduced visual acuity not correctable by refractive means 2. Fixed ocular deviation Amblyopia Etiology 1. Strabismus ® most commonly 2. Uremia 3. Toxins ® alcohol, tobacco, lead, and other toxics Glaucoma Definition 1. Group of diseases characterized by damage to optic nerve, visual field loss, & associated w/ elevated intraocular pressure 2. Normal IOP: 8-21 3. Open angle 4. Angle closure Open Angle pathophysiology Damage to axons of retinal ganglion cells as they course thru optic nerve ® cell death & optic atrophy Summary: 1. Asymptomatic 2. Leading cause of blindness in AA 3. Found during routine exams 4. Dimmed/ Blurred vision 5. Lower IOP w/: - Betablockers - Prostaglandin drops 6. Laser or surgical options 2nd Summary: 1. Painful, red eye - Hazy “cloudy” cornea - Dilated fixed eye 2. Precipitated by pupillary dilation 3. URGENT referral 4. Lower IOP while u wait: - Timolol - Apraclonidine - Pilocarpine 5. Ophthalmologic procedure needed Epidemiology 1. Increased age 2. Pre-existing narrow anterior chamber angle - Asian & Inuit highest risk 3. Enlarged lens ( cataract) 4. Farsightedness 5. Precipitated by pupillary dilation Symptoms 1. Blurred vision/ Halos around light 2. PAIN 3. Red eye 4. N/V 5. HA Exam changes 1. Conjunctival redness 2. Ciliary Flush 3. Corneal edema/Hazy 4. Shallow anterior chamber 5. Mid dilated pupil that reacts poorly to light 6. MUCH more likely to have high IOP Epidemiology 1. 2nd leading cause of blindness in the world 2. Leading cause of blindness in AA pt 3. Elderly 4. FH 5. DM, HTN, Myopia, CV dz 6. Hx of of eye trauma, medications Symptoms 1. Asymptomatic 2. Found during routine exams 3. Dimmed/ blurred vision 4. Visual field loss (rare presentation) - Peripheral first ® central Exam changes 1. Cupping - Normal: diameter of the cup is 50% the diameter of the optic nerve head 2. Increase IOP present in 50-66% of patients 3. >90% of pt w/ pressures >21mmhg have no damage to optic nerve 4. Thin corenas are highest risk to progress Closed Angle Diagnosis 2 out of 3 need to be present to establish the diagnosis 1. Optic Disc abnormalities - Large cup/disc ratio - Narrowed optic disc neural rim - Asymmetric cupping 2. Increased IOP done using a Tonometer - Normal IOP is 8 to 21 mmHg - In acute episodes of closed-angle glaucoma, pressures are often 30 mmHg or higher on a Tonometer 3. Visual Field Loss - Automated perimeters Open angle treatment Closed Angle Treatment 1. All patients require IOP lowering agents ® regardless of pressure at time of 1. Urgent ophthalmology referral diagnosis 2. Apply a drop OF EACH if IOP >40 2. Laser or drops are first line – patient/ prover choice - Timolol (topical beta blocker 3. Drops - Apraclonidine (topical alpha2 agonist) - Topical prostaglandin analog (prosts) – Latanoporst, bimatoprost - Pilocarpine (topical cholinergic) - Increases aqueous outflow 3. IV carbonic anhydrase inhibitor co- SE: eye irritation, eyelash increase, iris darkening administration - Topical B-blockers (“-olol”) – timolo, betaxolol - Acetazolamide - Decreased production of aqueous humor 4. Osmotic Diuretics (mannitol) if - Cheaper option & Slightly less reduction in IOP refractory 4. Laser therapy = trabeculoplasty 5. Ophthalmology procedures: create - Improves drainage of aqueous humor through trabecular meshwork better flow for aqueous humor to 5. Surgery = trabeculectomy reduce pressure - First line if severe visual field deficits present - Laster peripheral iridotomy (tiny hole in - Cataracts, scarring, visual loss, are SE iris) - Create small flap in meshwork to improve outfow - Iridectomy (small piece of iris removed) - May scare over & need repeat work Medications that worsen glaucoma 1. Alpha/Beta agonists 4. Inhaled Beta 2 - Phenylephrine eye drops - Albuterol - Ephedrine 5. Psychiatric Drugs 2. Anticholinergics - SSRIs, TCAs, SNRIs - Atropine (any form) 6. Stimulants - Inhaled ipratropium (COPD/ Asthma treatment) - Amphetamine & derivatives 3. Antihistamines 7. Antibiotics - Benadryl, loratadine, Cimetidine (Zantac/H2) - Bactrim/ TMP-SMX Strabismus Summary: 1. Deviate from ocular alignment 2. Children 3. muscular imbalance 4. Association: cross eye, depth perception, & lazy eye 5. Tx: prevent/revert sensory effects Definition Etiology Epidemiology 1. Any deviation of perfect ocular 1. 2/2 muscular imbalance 1. 4% of children have strabismus alignment 2. Familial component 2. Eye movements are full & ocular 3. Trauma, brain tumor, intracranial misalignment is equal in all directions hemorrhage, infarct, elevated ICP of gaze Associated w/ Treatment 1. Amblyopia (lazy eye) 1. Goal: prevent/revert sensory effects (children especially) 2. Reduction of depth perception 2. Correct for cosmetic/psychosocial reasons 3. Crossed eyes 3. Options include: - Surgery to correct EOM muscle issue - Glasses/Prisms to train eyes - Patching of good eye can train the “bad” eye Endophthalmitis Summary: 1. Bacterial >>>> fungal infection 2. Emergent 3. Post eye procedure 4. Painful, swollen Definition 1. Bacterial or fungal infection of vitreous/ aqueous humor Bacterial Endophthalmitis Microbiology Procedure related 1. Coag-neg staph ~ 70% cases Trauma 1. Bacillus Cereus Symptoms Acute pain (or ache) & vision loss Exams 1. Chemosis 2. Hypopyon 3. Hazy view of retina Treatment 1. Medical Emergency - Culture of vitreous if possible B4 abx - Intravitreal abx = vanco + ceftazidime - Refractory cases or severe = vitrectomy - Debrides & Removes bad tissue = I&D 2. Traumatic cases: prognosis poor – aggressive - Vitrectomy - Intravitreal abx - Intravenous abx 5. Hypopon 6. Intravitreal abx required ® vanco + ceftazidime 7. Fungal occurs WITH fungemia: IV drug abusers - Systemic antifungals + intravitreal Etiology 1. Post procedure is common - Cataract surgery - Intravitreal injections 2. Post trauma & endogenous spread - Metal > other material Fungal Endophthalmitis Microbiology 1. Yeasts – Candida - Much more common in US 2. Molds – Aspergillus, Fusarium - Tropical climates - Surgery, trauma, ore extension of keratomycosis 3. RF: Fungemia w/ critical illness & IV drug abuse Symptoms 1. Vision loss, w/ or w/o pain or systemic signs 2. No anterior chamber changes w/ endogenous Exam 1. Fundoscopic exam ® chorioretinitis - White, mound-like lesions on retina - Chorioretinitis = 2nd to fungemia endogenous DX/ Treatment 1. DX - Hx clues ® IV drugs or concurrent dz (fungemia) 2. Request fungal culture specifically to improve yield 3. Blood culture in ALL pt once fungal suspected TX: 1. Systemic antifungals: fluconazole, voriconazole, or amphotericin B 2. PLUS Intravitreal antifungal: voriconazole or Amphotericin B 3. Vitrectomy possible Symptom ¯ visual acuity Photophobia Corneal opacity Severe HA w/ N Reasons for Urgent Ophthalmic Referral Possible disorder Symptom 1. Infectious keratitis Ciliary flush – ring @ the 2. Iritis limbus 3. Angle-closure glaucoma 1. Infectious keratitis Severe foreign body ® 2. Iritis can’t keep eye open 1. Infectious keratitis Fixed pupil 1. Angle-closure Suspicion for hyperacute glaucoma bacterial conjunctivitis or epidemic keratoconjunctivitis Possible disorder 1. Infectious keratitis 2. Iritis 3. Angle-closure glaucoma 1. Infectious keratitis 1. Angle-closure glaucoma 1. EKC Disease Nystagmus Summary of Diseases Disease Optic Neuritis Summary 1. Rhythmic oscillation of eye 2. Jerk Nystagmus - Gaze -Evoke: most common & drugs - Downbeat: damage to pontine ® stroke or tumor 3. Pendular nystagmus 4. Vestibular nystagmus: - Dysfunction of labyrinth - Peripheral caused by attacks w/ N & vertigo Papilledema 1. 2. 3. 4. 5. 6. AAION Intracranial pressure elevated Bilateral optic disc swelling HA common S/S Transient visual obscurations Neuroimage ® LP if – image Tx: weight loss or Acetazolamide - ¯ pressure Summary 1. Strong associated w/ MS 2. Unilateral vision loss 3. Marcus GUN pupil – Relative afferent pupillary Defect (RAPD) 4. Tx ® steroids (IV or oral) AION 1. Interrupt blood flow 2 anterior optic nerve 2. Older adults w/ GCA 3. Loss of ½ upper or lower field of vision 4. No pain 5. Unilateral usually 6. Tx: prompt referral & based on cause 1. Urgent recognition 2. Steroids ® prevent blindness PION LEBERS 1. 2. 3. 4. Young men Progressive Painless Severe central visual loss 1 eye ® other eye 5. Point mutation ® maternal inherited TON 1. 2. 3. 1. 2. Acute visual loss Anemia & HTN (surgery) Tx: based on cause Visual loss ® bilateral optic disc swelling Causes: certain agents/ starvation/ malabsorption/ alcohol ODD 1. 2. 3. 4. 5. Orbital Cellulits 1. 2. 3. 4. - SICK pt Erythema/Edema PLUS Bug eye PAIN W/ EOM Systemic signs (fever) Emergent referral TX: IV Vanco + 3rd gen ceph + flagyl 2-4 wks abx Refractile Glittering particles in optic nerve N. European Produce ® pseudopapilledema Cause ® visual obscurations Periorbital Cellulitis 1. 2. 3. 4. NO EYE PAIN W/ EOM ® pain = mild Cover for sinus if no trauma ® Augmentin + Bactrim ® trauma likely Improve 24-48 or inpatient Macular Degeneration 1. 2. 3. 4. 5. - Most common cause of blindness >65 SMOKERS Central vision loss Dry – not much to do, drusen Wet – faster, worse hemorrhages, can tx VEGF inhibitors Photocoagulation Retinal detachment 1. 2. 3. 4. 5. Floaters, flashing Curtain drawn down Urgent referral Gas injection, PPV, Buckling Laser or cryopexy Chronic HTN 1. 2. 3. 4. 5. 6. AV nicking Copper Wiring Papilledema ® not dz specific Cotton wool spots ® not dz specific Assess for elevated intracranial pressure Tx underlying HTN Diabetic retinopathy 1. 2. 3. 4. 5. 6. - Diabetes Leading cause of blindness ® AA Multiple, nonspecific visual symptoms Microaneurysm, cotton wool spots Exudates (soft>hard) on exam Tx for PRD VEGF inhibitors Laser Surgical vitrectomy Blowout Fracture 1. 2. 3. 4. 5. 6. Trauma Restricted EOM Dropped eye/Enophthalmos Crepitus Evaluate for other structures damaged Referral ® emergently Open globe rupture 1. High degree of Blunt trauma or penetrating trauma 2. Pupil change 3. Seidel Test + 4. Emergent imaging & referral 5. DO NOT INCREASE IOP Hyphema 1. 2. 3. 4. 5. Blood in anterior chamber Blunt or penetrating injury Bleeding D/O ® SCA Permanent vision loss TX: ophthalmologist ASAP & NO ASA Hypopyon 1. WBC in anterior chamber 2. Fulminant ocular infection 3. Assoc ® infectious keratitis or endophthalmitis 4. Ophthalmologist ASAP CRAO 1. 2. 3. 4. 5. 6. PAINLESS MONOCULAR VISION LOSS Vascular or cardiac pt Cherry red spot or boxcar EMERGENT – 90 min tPA or massage Underlying issue ® cardiac or GCA CRVO 1. 2. 3. 4. 5. 6. 7. PAINLESS MONOCULAR LOSS Vascular risk factors (DM, smoking, HTN) Blood & thunder Retinal hemorrhages Urgent referral VEGF inhibitors Tx: underlying issues Amblyopia 1. Fixed ocular deviation 2. Cause® strabismus, uremia, or toxins 3. ¯ visual acuity Angle closure 1. PAINFUL, red eye ® hazy “cloudy” cornea Strabismus & dilated fixed eye 2. Precipitated by pupillary 3. URGENT referral 4. Lower IOP while you wait: - Timolol - Apraclonidine - Pilocarpine 5. Ophthalmologic procedure needed Endophthalmitis 1. 2. 3. 4. 5. 6. Bacterial >>> fungal Emergent Post eye procedure Painful, swollen Hypopon Intravitreal abx required ® vaco + ceftazidime 7. Fungal = + fungemia - IV drug abusers - Systemic anti-fungals + Intravitreal Amaurosis Fugax 1. 2. 3. 4. 5. TIA of retina Rapid fading of vision in 1+ visual fields Patho: Glaucoma & migraine Hollenhorst plaque ® carotid dz ® U/S Tx: Oral ASA & find underlying cause Open angle glaucoma 1. 2. 3. 4. 5. 6. Asymptomatic Leading cause blindness in AA Found ® routine exams Dimmed / blurred vision Lower IOP w/: Betal blockers or prostaglandin drops Laser or surgical options 2nd 1. 2. 3. 4. 5. 6. - Cross-eyed Deviation from perfect ocular alignment 4% children Assoc ® reduction of depth perception Amblyopia (lazy eye) Tx: prevent/revert sensory effects Surgery® EOM muscle Glasses/Prisms Patch ® train bad eye