Clinical Medicine II: Acute & Chronic Vision Loss; Eye Trauma PDF

CLINICAL MEDICINE II: ACUTE & CHRONIC VISION LOSS; EYE TRAUMA Rachel Elbing MPH, PA-C Clinical Assistant Professor Augsburg Physician Assistant Studies © 2025  OBJECTIVES 1. Summarize the etiology, pathophysiology, clinical f...

CLINICAL MEDICINE II: ACUTE & CHRONIC VISION LOSS; EYE TRAUMA Rachel Elbing MPH, PA-C Clinical Assistant Professor Augsburg Physician Assistant Studies © 2025  OBJECTIVES 1. Summarize the etiology, pathophysiology, clinical features, how diagnosis is established, potential complications and treatment for the conditions listed below: Glaucoma (acute & chronic) Amaurosis fugax Uveitis Diabetic retinopathy Iritis Hypertensive retinopathy Cataract Optic neuritis Retinal detachment Papilledema Vitreous hemorrhage Ruptured globe (in lecture) Macular degeneration Retinal vein occlusion Retinal artery occlusion  OBJECTIVES 2. Review common causes of eye trauma and discuss important physical examination techniques in the setting of eye trauma 3. Differentiate between acute angle closure and chronic glaucoma. 4. Differentiate amblyopia and strabismus (in lecture) 5. Define nystagmus, describe its features and its common causes (central and peripheral) 6. Establish parameters for which ocular conditions are vision threatening, and whether the condition requires emergent or non-emergent referral. GLAUCOMA…ANATOMY REVIEW https://www.aafp.org/pubs/afp/issues/2003/0501/p1937.html  GLAUCOMA: OVERVIEW Glaucoma = rise intraocular pressure sufficient to damage optic nerve → vision loss Obstruction or reduced flow of aqueous humor in anterior chamber at angle where iris meets corneal-scleral junction Different nomenclature… Based on angle Open-angle Normal tension Angle-closure Primary vs Secondary causes Acute vs Chronic  GLAUCOMA: ESSENTIALS Open-Angle Glaucoma Most common form – accounting for at least 90% of all cases More chronic, insidious onset Acute Angle-Closure Glaucoma A “Do Not Miss” diagnosis → leads to permanent blindness if not treated w/i 24 hours Primary vs Secondary causes  OPEN-ANGLE GLAUCOMA Reduced aqueous fluid through trabecular meshwork Most common Insidious onset Often bilateral 60-70% of cases have no identifiable cause Risk factors: age (generally >40yo), fhx, African ethnicity, systemic HTN, DM, myopia  OPEN ANGLE GLAUCOMA SYMPTOMS Sxs: Initially none to minimal (detected on routine eye test) Progressive → Peripheral vision loss Scotomas Central vision is spared until late disease Visual field loss = complaints of impaired… Night driving Near vision Reading speed Outdoor mobility  OPEN ANGLE GLAUCOMA PHYSICAL EXAM Physical Exam: Visual acuity (can be normal!) Visual field defects Optic disc cupping IOP elevation nl = 10-21mmHg Could be normal early in dz Optho: Measurement of anterior chamber angle Slit-lamp: optic disc atrophy, optic nerve cupping  OPEN ANGLE GLAUCOMA DIAGNOSIS Suspect if any of the following conditions present Consistently elevated IOP Suspicious-appearing optic nerve Abnormal visual field Diagnosis if presence of progressive optic neuropathy in 1+ eye characterized by Acquired typical structural damage to optic nerve Open anterior chamber angle as measured by gonioscopy © 2025 UpToDate, Inc.  OPEN ANGLE GLAUCOMA: TREATMENT Pharmacologic Increase aqueous outflow → Prostaglandin analogs “Latanoprost” Cholinergic agonists “Pilocarpine” Decrease production/inflow of aqueous humor → Beta blockers: “Timolol” Alpha-2 adrenergic agonists “Brimonidine” Carbonic anhydrase inhibitors “Acetazolamide” (PO/IV) Reduction of vitreous volume w/ hyperosmolar agents Laser trabeculoplasty Surgical - more for refractory cases  CLOSED ANGLE GLAUCOMA Obstruction of angle by iris Adhesion may be reversible or permanent if inflammation & scarring have occurred Risk Factors: older age, hyperopia, Asian or Inuit descent Drug-induced Adrenergic agents - phenylephrine Anticholinergic drugs Periocular botulinum toxin Sulfa-based drugs  CLOSED ANGLE GLAUCOMA SYMPTOMS Sxs: Severe ocular pain Facial pain Sudden vision loss Blurred vision (typically UNILATERAL) Halos around lights Headache Eye redness Nausea and vomiting  CLOSED ANGLE GLAUCOMA PHYSICAL EXAM PE: Conjunctival hyperemia/injection Hazy cornea Slit lamp & IOP measurement May see pale central depression of optic disc May see increased ratio of physiologic cupping diameter to disc diameter Decreased visual acuity and visual field loss Pupil (to evaluate optic nerve status) Size and shape Reactivity – fixed mid-dilated pupil  CLOSED ANGLE GLAUCOMA DIAGNOSIS Initial diagnosis based on history and physical exam EMERGENT optho consult! Gonioscopy is gold-standard though (ophthalmologist!)  CLOSED ANGLE GLAUCOMA TREATMENT EMERGENT Optho consult Avoid: ______________ Place patient supine Reduce IOP! Timolol - Topical BB Apraclonidine - alpha agonist Pilocarpine - muscarinic/cholinergic agonist Acetazolamide IV and PO - carbonic anhydrase inhibitor Systemic osmotic agent (oral glycerol, mannitol, isosorbide) if not response to acetazolamide Optimal treatment Laser peripheral iridotomy: opens another pathway for fluid to pass from posterior to anterior chamber  UVEITIS: ESSENTIALS Intraocular inflammation or inflammation of the uvea (middle portion of the eye) Frequently occurs in association with other systemic medical conditions, especially infections and autoimmune disease Autoimmune cx → Spondyloarthritis, sarcoidosis, psoriatic arthritis, IBD, MS, HLA-27 allele Potential infectious causes → bacterial, viral, fungal, parasitic (herpes, CMV, toxoplasmosis, syphilis, TB, zika) Genetic predisposition  Sxs depend on portion of uveal involved UVEITIS: SIGNS AND SYMPTOMS Anterior uveitis - aka “iritis” (Most cm.) Pain, redness, “ciliary flush” Constricted pupil Visual loss is variable Leukocytes “cells and flare” in the anterior chamber on slit lamp exam Hypopyon Posterior uveitis Painless Can result in nonspecific visual changes such as floaters and/or reduced visual acuity  UVEITIS: DIAGNOSIS If suspected, referral to ophthalmology for slit-lamp examination and a dilated fundus examination is required for diagnosis Leukocytes in the anterior chamber of the eye on slit lamp (anterior uveitis) Direct visualization of active chorioretinal inflammation and/or by detection of leukocytes in the vitreous humor (posterior uveitis) Panuveitis is diagnosed when inflammation is detected simultaneously in the anterior chamber, vitreous and retina or choroid  UVEITIS: TREATMENT Approach depends on etiology, location and severity of inflammation Management requires Ophthalmologist consult Therapy should be initiated within 24 hours of the onset Anterior: usually response to topical corticosteroids Posterior: commonly requires systemic, periocular or intravitreal corticosteroid therapy Infectious cx: specific antimicrobial therapy  CATARACT: ESSENTIALS Clouding/opacity of the lens → vision loss Senile: age-related structural changes to lens fibers → rearrangement necessary to maintain optical clarity (most common cx) Acquired: trauma, radiation, heat Congenital Metabolic: diabetes (alters refractive lens properties), steroid use RF: Age, DM, tobacco use, systemic corticosteroids, obesity  CATARACT: DIAGNOSIS Often asx initially Patient may report gradual painless loss of vision at distance and/or near in one or both eyes Gradually reduced contrast Reduced color intensity Distance vision more affected than near vision Difficulty in recognizing faces Difficulty in working outdoors at dusk  CATARACT: PHYSICAL EXAM/DIAGNOSIS PE: Lens opacities often detected during routine eye exam in asymptomatic patients Dark shadow against red reflex or absent fundus reflex (red reflex) White pupil Decreased visual acuity  CATARACT: TREATMENT Consult ophthalmology Surgical intervention Removal and placement of an intraocular lens Indicated when visual function no longer meets patient’s needs and surgery is likely to improve vision Phacoemulsification is procedure of choice and most commonly used method in US to remove lens https://www.youtub e.com/watch?v=6hg vjigs2_E (start at 2:10)  RETINAL DETACHMENT: ESSENTIALS = separation of retina from underlying retinal pigment epithelium Two types: “Rhegmatogenous” retinal detachment - MOST CASES Detachment that occurs due to holes, tears or breaks in retina or vitreous detachment “Non-rhegmatogenous” retinal detachment Exudative or serous retinal detachment d/t fluid in subretinal space secondary to systemic diseases Tractional retinal detachment (mechanical forces on retina, usually mediated by fibrotic tissue resulting from previous disease) but NO break  RETINAL DETACHMENT: ESSENTIALS Risk factors: age, hx cataract surgery, retinal atrophy, myopia, trauma  RETINAL DETACHMENT: SYMPTOMS Rapid, painless vision loss Usually in periphery with progression toward center Early sx: Acute onset floaters & flashes Once detachment occurs → “dark curtain” over visual field  RETINAL DETACHMENT: DIAGNOSIS Detection of retinal detachment made with ophthalmologic visualization If ophthalmoscopy cannot be performed, ophthalmic ultrasound may be used for diagnosis https://www.youtube.com/watch?v=gNLTZipajwM https://journals.sagepub.com/doi/full/10.1177/10249079177350 85  RETINAL DETACHMENT: TREATMENT Emergent Optho referral If immediate referral is not possible, instruct patient to lie down with the face on the side of the detachment to the pillow (opposite the field defect) to minimize the detachment extending toward the macula Surgical repair: Visual acuity outcome may be improved in patients having macular reattachment if surgery performed 50: obtain CRP and ESR - r/o “________” https://www.youtube.com/watch?v=uiIRvn11cAE  RETINAL ARTERY OCCLUSION: TREATMENT Emergent Optho consult (Permanent vision loss in 90m!) Acute management Recumbent position Ocular massage → attempt dislodge clot to smaller branch High concentrations of inhaled O2 Decrease pressure if elevated IOP (think glaucoma meds) Vasodilator medications Hyperbaric oxygen tPA - used some centers, not standard of care  AMAUROSIS FUGAX: ESSENTIALS Transient monocular or binocular visual loss Varied terminology: Some suggest term implies vascular cause for visual loss OR visual loss from any origin and involving one or both eyes Etiology: MC = ischemia d/t retinal embolus from ______ or _______) Other ischemic cx: GCA, hypercoagulable states, hyperviscosity Other monocular cx: include papilledema, optic nerve compression, idiopathic Binocular visual loss implies a process posterior to the optic chiasm and may include migraine, seizure, vertebrobasilar ischemia AMAUROSIS FUGAX  AMAUROSIS FUGAX: SYMPTOMS AND PHYSICAL EXAM Sxs: Transient vision loss one or both eyes Additional history helps narrow on cx Duration Mono/binocular Specific description of symptoms and associated sx Commonly described as curtain effect descending over field of vision lastly a few minutes PE: Most commonly PE is _______ Test visual acuity and visual fields and examination of optic fundus  AMAUROSIS FUGAX: MANAGEMENT Most cases - similar to _________________ Common diagnosis testing for amaurosis fugax… Ophthalmology consult Neuroimaging ESR/CRP Carotid imaging EKG Identify source of emboli Hypercoagulable testing Brain MRI EEG Referral to stroke center or hospital admission if two or more episodes in preceding week  AMAUROSIS FUGAX: TREATMENT Tx dependent on etiology… Etiology Duration Visual loss Assoc Sx Mechanism Carotid disease, 1-10 minutes Monocular, rapid Hemispheric Retinal embolism embolic source onset symptoms Giant cell arteritis Variable Usually monocular Headache, Ischemia of optic neck/jaw pain nerve Papilledema Seconds Graying or blurring Headache, Elevated ICP diplopia Idiopathic retinal 5-60 minutes Varied HA Vasospasm vasospasm Migraine 10-30 minutes Usually binocular, Migraine HA Cortical with spread depression or retinal vasospasm Vertebrobasilar 1-10 minutes Homonymous Other brainstem Embolic ischemia hemianopia deficits Seizure 3 minutes Binocular visual Altered Epileptic discharge field loss consciousness, motor symptoms  DIABETIC RETINOPATHY: ESSENTIALS = microvascular complication of diabetes that is a leading cause of preventable blindness in adults At 20 years after dx of DM 99% w/ Type I and 60% w/ Type II have Pathophysiology: chronic exposure to hyperglycemia → microvascular damage and retinal dysfunction Two main categories Non-proliferative: mild, moderate and severe Capillaries of retina leak proteins, lipids, or RBCs into retina → macular edema, ↓ visual acuity Proliferative: less common, but more severe vision loss Growth of new vessels and fibrous tissue d/t severe capillary occlusion and retinal ischemia  DIABETIC RETINOPATHY: ESSENTIALS Risk factors: Duration of diabetes mellitus Younger age T2DM onset → increased risk Hyperglycemia Dyslipidemia Cataract surgery HTN  DIABETIC RETINOPATHY: SYMPTOMS Sxs: often asx, even with severe diabetic retinopathy If sx: Blurred or double vision Narrowed field of vision Seeing dark spots, floaters, shadows Feeling of pressure or pain in eyes Difficulty seeing in dim light  DIABETIC RETINOPATHY: PHYSICAL EXAM Non-proliferative: microaneurysms, retinal hemorrhages, retinal edema, hard exudates, nerve fiber layer infarcts = cotton wool spots Proliferative: neovascularization arising from disc and/or retinal vessels → hemorrhages, fibrosis, retinal detachment DIABETIC RETINOPATHY: DIAGNOSIS  DIABETIC RETINOPATHY: TREATMENT Slow progression… Optimize glycemic control Optimize serum lipid control Strictly control blood pressure/hypertension Optho referral Initially eye exam q3-4 months, then yearly VEGF therapy Laser photocoagulation therapy to reduce risk of vision loss in patients with high-risk proliferative diabetic retinopathy  HYPERTENSIVE RETINOPATHY: ESSENTIALS Vascular changes visualized directly Determine extent/severity of vascular disease RF: hypertension, other vascular disease  HYPERTENSIVE RETINOPATHY: CLINICAL FEATURES Sxs: usually asx PE: Arteriolar narrowing “Copper/Silver wiring” A-V nicking Exudates Cotton-wool spots Hemorrhages Papilledema HYPERTENSIVE RETINOPATHY: TREATMENT Routine eye exams Good BP control  OPTIC NEURITIS: ESSENTIALS = disorder of inflammation of optic nerve that results in visual loss Etiology: idiopathic or MS In adults, viral etiology in peds Pathophysiology: thinning of the retinal nerve fiber layer  OPTIC NEURITIS: SYMPTOMS Sxs: subacute unilateral loss of vision – ranging from blurring of vision to no light perception Usually gradually progresses over days to about 2 weeks before spontaneous improvement occurs Reduced color vision Periocular pain exacerbated w/ movement Occurs in >90% of patients, of varying intensity, can precede onset of visual symptoms, usually only lasts a few days  OPTIC NEURITIS: PHYSICAL EXAM & DIAGNOSIS Often clinical dx based on hx and PE ↓VA, ↓ color vision, ↓ contrast RAPD Central scotoma typically Papillitis (only in ⅓) Swollen, pale Small flame-shaped hemorrhages may be seen MRI of brain and orbits w/ contrast can help confirm dx and provide assessment risk of MS  OPTIC NEURITIS: TREATMENT Corticosteroids High-dose IV corticosteroids May hasten visual recovery but may not improve long- term visual acuity or visual field If an episode of isolated optic neuritis is confirmed by an ophthalmologist, refer patient to neurologist for further assessment Improvement in vision can be seen up to 1 year after acute optic neuritis  PAPILLEDEMA: ESSENTIALS = optic disc swelling that is due to raised intracranial pressure ICP → transmitted to the optic nerve sheath Any entity that ↑ ICP can → papilledema Intracranial lesions (tumor, hematoma) Cerebral edema (encephalopathy, cerebral infarction, TBI) Increased CSF production Decreased CSF absorption Obstructive hydrocephalus Obstruction of venous outflow Idiopathic intracranial hypertension (pseudotumor cerebri)  PAPILLEDEMA: SYMPTOMS Headache = cardinal symptom of ↑ ICP Positional, usually worsening w/ recumbency & early AM Nausea, vomiting Binocular horizontal diplopia d/t lateral rectus paresis CN 6 is believed to be more vulnerable to the effects of increased intracranial pressure because of its long course in the subarachnoid space and its bend to enter the cavernous sinus Pulsatile machinery-like sound in the ear  PAPILLEDEMA: PHYSICAL EXAM Fundoscopic findings Early Loss of spontaneous venous pulsations Splinter hemorrhages Fully- developed Optic disc becomes elevated, cup is obliterated and the disc margins become obscured Chronic Central cup remains obliterated but hemorrhagic and exudative components resolve  PAPILLEDEMA: DIAGNOSIS Neuroimaging: Brain MRI If neuroimaging is normal, lumbar puncture should be done for opening pressure and analysis Formal visual field testing  PAPILLEDEMA: TREATMENT Treatment of increased intracranial pressure is specific to the underlying etiology Permanent loss of vision is a common consequence of papilledema that is untreated or unresponsive to treatment  RUPTURED GLOBE/OPEN GLOBE: ESSENTIALS Integrity of the outer membranes of the eye is disrupted by blunt or penetrating trauma Any full-thickness injury to the cornea, sclera, or both is considered an open globe injury Pathophysiology: mostly d/t blunt trauma → globe compression → increased IOP → frank rupture in “inside-out” mechanism Risk factors: males, prior ocular surgery Ophthalmologic emergency © 2025 UpToDate,  RUPTURED GLOBE: CLINICAL FEATURES Sx: Pain, loss of vision/blurred vision, diplopia PE: VISUAL ACUITY! Teardrop pupil Positive Siedels test AVOID putting pressure on the globe to prevent further extrusion of intraocular contents Diagnosis: Clinical CT scan for further assessment Can detect ocular rupture, associated optic nerve injury and small FB  RUPTURED GLOBE: TREATMENT Ophthalmology consult and transfer if needed → NEEDS SURGERY Protect eye from any pressure Leave impaled FB - avoid further trauma Antiemetics (oral) to prevent valsalva, sedation and analgesics PRN Avoid topical eye solutions Prophylactic antibiotics (IV) Tetanus  STRABISMUS: ESSENTIALS = condition of misalignment of the eyes – can be horizontal, vertical or torsional Terms used to describe strabismus depend upon direction of eye deviation Congenital vs. acquired RF: fhx, low birth weight, optho dx  STRABISMUS: DIAGNOSIS Physical exam Corneal light reflex: shining a light onto patient’s eyes from a distance and observing the reflection of the light on the cornea with respect to the pupil Cover test Cover/uncover test  STRABISMUS: TREATMENT Initial management addresses vision impairment caused by amblyopia Refractive error correction with prescription of glasses or contacts and/or occlusion therapy or pharmacologic or optical penalization Alignment Surgical and non-surgical interventions are used to correct ocular alignment Spectacles or contacts, miotic drops to manipulate accommodation, occlusion therapy, visual training exercises Surgery on the extraocular muscles  AMBLYOPIA: ESSENTIALS Commonly referred to as “lazy eye” Reduction secondary to neurological deficits in visual output caused by abnormal brain stimulation during critical periods of visual development Usually unilateral Most common cause of vision loss and mononuclear blindness in children 90% of amblyopia is caused by strabismus (ocular misalignment) and/or anisometropia (significant difference in refractive error between 2 eyes)  AMBLYOPIA: PRESENTATION Chief complaint: Visual loss Usually unilateral PMH: Strabismus Congenital cataract Ptosis (from Horner syndrome) Lesion obstructing vision  AMBLYOPIA: DIAGNOSIS PE: Evaluation for intermittent or fixed strabismus Eye fixation pattern and ability to follow Fundoscopy Pupil reaction Red reflex in infants Retinal evaluation in older children Perform vision testing using Snellen eye chart when child is able (usually age 3-4 years)  AMBLYOPIA: TREATMENT Occlusion of better-seeing eye while forcing use of amblyopic eye Initial treatment includes Refractive correction of visual impairment in affected eye(s) with glasses Correction of any strabismus with glasses or surgery if severe Removal of any obstacle to vision, such as cataract or local hemangioma  NYSTAGMUS OVERVIEW Rhythmic regular oscillation of the eyes “Jerk”: slow drift in one direction w/ corrective jerk - more common “Pendular”: slow, sinusoidal oscillations Continuous or paroxysmal Can be vertical, horizontal, torsional, or mixed  NYSTAGMUS Horizontal: Most common Often associated with ________________ Can be central Vertical: CENTRAL cause What could these be?? _______________ Rotatory (Torsional): Peripheral vestibular disorders MC  BOARD QUESTION: 45 y/o female presents with onset of visual loss in left eye over the past 2 days. Fundoscopic exam reveals hyperemia and swelling and blurring of the optic disc. No history of headache. Patient describes pain with eye movement. Which of the following is most likely diagnosis? A. Pseudotumor cerebri B. Ophthalmic migraine C. Retinal detachment D. Optic neuritis QUESTIONS?