Ophthalmologic Disease 2023 PDF

Ophthalmology Patrick McNeal DMSc, PA-C Assistant Professor College of Health Professions, PAS Division By the end of this lecture, you should be able to: 1. Recognize and differentiate common pathological eye disorders and eye structures. 2. Review and discuss how to diagnose and treat frequently...

Ophthalmology Patrick McNeal DMSc, PA-C Assistant Professor College of Health Professions, PAS Division By the end of this lecture, you should be able to: 1. Recognize and differentiate common pathological eye disorders and eye structures. 2. Review and discuss how to diagnose and treat frequently encountered eye disorders. Learning Objectives - FCM Exam & PANCE preparation: • Amaurosis fugax • Hyphema • Amblyopia • Hypopyon • Blepharitis • Keratitis • Blowout fracture • Macular degeneration • Cataract • Nystagmus • Chalazion • Optic neuritis • Conjunctivitis • Orbital cellulitis • Corneal abrasion • Papilledema • Corneal foreign body • Pinguecula • Corneal ulcer • Pterygium • Dacryocystitis • Retinal detachment • Ectropion • Retinal vascular occlusion • Entropion • Retinopathy • Glaucoma • Scleritis • Globe rupture • Strabismus • Hordeolum • Subconjunctival hemorrhage PANCE Blueprint Conjunctival disorders • Conjunctivitis Corneal disorders • Cataract • Corneal ulcer • Infectious • Keratitis • Pterygium • Pinguecula Lacrimal disorders • Dacryocystitis Lid disorders •Blepharitis •Chalazion •Ectropion •Entropion •Hordeolum Orbital disorders •Orbital cellulitis •Retinal disorders •Macular degeneration •Retinal detachment •Retinopathy Vascular disorders Neuro-ophthalmologic disorders •Nystagmus •Optic neuritis •Papilledema Traumatic disorders •Blowout fracture •Corneal abrasion •Globe rupture •Hyphema • Glaucoma • Retinal vascular occlusion Vision abnormalities • Amaurosis fugax • Amblyopia • Scleritis • Strabismus Outline • Anatomy Review • Ophthalmology Terms • Ophthalmology History • Ophthalmology Exam • Eye Differentials (DDx) • Eye Disorders • Review External Eye Anatomy Anatomy Cross Section Posterior Eye Anything behind the corneal, conjunctiva, and eye lids. Ophthalmology History Main complaints being pain/redness & loss of vision acute vs chronic • Timeline – acute vs chronic • Unilateral or bilateral • Pain – rest, moving, sharp, dull, where…exactly • Discharge (color, consistency, amount) • Visual change – blurry, scotoma, central/peripheral, hazy/halos • Change around the eye – eyelids, eyelashes, skin around the eye • Systemic features (diabetes, cardiovascular risks, giant cell arteritis • Contact lenses/glasses - refractive error left contact lens in too long? Eye Terms You Need To Know • Aqueous humor: Clear fluid located between the cornea and lens of the eye. • Astigmatism: An irregularly shaped cornea resembling a football, causing both near and distant blurry vision. Correctable with glasses, contact lenses, or surgery. • Choroid: Vascular layer between the retina and sclera. • Cornea: Transparent outer layer of the eye that covers the iris. • Enucleation: Surgical removal of the eye. • Hyperopia: Difficulty focusing on nearby objects while distant objects appear clearer; also known as farsightedness. • Intraocular: Pertaining to the interior of the eye. • Iris: Colored membrane encircling the pupil, regulating light entry into the eye. • Iritis: Common uveitis type affecting the iris, often associated with autoimmune conditions. • Legal blindness: Vision in both eyes corrected to no better than 20/200, or visual field of 20 degrees or less. • Left eye = ocular sinister (o.s.), right eye = ocular dexter (o.d.), • Macula: Central part of the retina essential for high-resolution vision. • Myopia: Difficulty focusing on distant objects while near objects are clear; also called nearsightedness. • Night blindness: Difficulty seeing in low-light conditions, often due to vitamin A deficiency or retinal diseases like retinitis pigmentosa. • Optic nerve: Transmits light signals from the retina to the brain for image formation. • Peripheral vision: Side vision beyond the direct line of sight. • Presbyopia: Age-related loss of ability to focus on close objects. • Proptosis / Exophthalmos: forward protrusion of eye(s) as in Grave’s Disease or a mass /fluid behind the eye • Pupil: Central opening in the eye allowing light entry. • Refraction: Eye's bending of light for focused retinal imaging. • Refractive error: Vision issue caused by light not bending properly in the eye, often corrected with glasses, contacts, or surgery. • Retina: Thin nerve layer at the back of the eye detecting light and transmitting signals to the brain. • Retinoblastoma: Malignant tumor on the retina, frequently occurring in young children, lack of red-light reflex • Sclera: Eye's outer covering, forming the whites of the eyes. • Tunnel vision: Loss of peripheral vision, linked to conditions like retinitis pigmentosa or untreated glaucoma. • Visual field: Total range of sight, including peripheral vision. • Vitreous humor: Clear gel-like substance within the eye's center. Aqueous humor Iritis Legal Blindness Proptosis Retinoblastoma Tunnel vision Ophthalmology Exam • General Inspection • Well or unwell? • Inspect • Skin around the eye • Eyelid • Eyelashes, flip for foreign bodies (FB) • Conjunctiva/sclera • Fluorescein staining (FB/damage) • Pale • Cornea • Clarity, scars • Anterior Chamber and Iris • Slit lamp (hypopyon, hyphema, anterior uveitis) • Pupil • Shape, size, anisocoria • Palpate • Bones, eyelids, globes • Cranial Nerves CVII • Test red reflex • Optic disc • Pupil reflexes and accommodation • Direct, indirect • Snellen chart (visual acuity) • +/- pinhole • Color vision • Visual fields & blind spot CNIII,IV,VI • H-test (eye movements, or EOMS) • Diplopia Differentials (DDx) • • • Acute Vision Loss • Acute angle glaucoma • Retinal detachment • • Giant cell arteritis Amaurosis fugax • Optic neuritis • • Wet macular degeneration Vitreous hemorrhage • Atypical migraine Gradual vision loss • Cataracts • Chronic open angle glaucoma • • Diabetic retinopathy Cancer • Dry macular degeneration Foreign body sensation (FBS) • • Foreign body Corneal injury • Conjunctivitis • Entropion/ectropion • Dry eyes • Flashing lights • Retinal detachment or vitreous detachment • Migraine • Red eye + pain • Acute angle glaucoma • Corneal abrasion / ulcer • Scleritis / episcleritis • Keratitis • Conjunctivitis • Dry eyes • Endophthalmitis • Orbital cellulitis • Red eye + painless • Conjunctivitis • Pterygium • Subconjunctival hemorrhage Outline Conjunctival disorders • Conjunctivitis Conjunctivitis • Etiology • Inflammation or infection of the conjunctiva - thin tissue layer covering the inner eyelids and outer sclera. • Occurs as viral, bacterial, or allergic –mediated • Presentation • redness • foreign body sensation • discharge • normal visual acuity • normal pupil reactivity Bacterial Conjunctivitis • Presentation: - purulent discharge, injection (redness) - eye lashes “matted shut” in AM upon waking - unilateral • Pathogens: • Most common: strep, staph • Rarely: gonococcal or chlamydial • Treatment: • Hand hygiene and cool compresses • Topical antibiotics: • Polymyxin B and trimethoprim, Bacitracin, gentamicin, or erythromycin drops/ointment • Alternative treatment if suspecting gonococcus etiology or chlamydia • Contact lens wearers = broader coverage, i.e., Cipro/Moxi • Drops adults preferred peds depending on age prefer ointment, Follow-up – Routine / PRN Bacterial Conjunctivitis Viral Conjunctivitis Presentation - bilateral - most commonly adenovirus - commonly exposed to others with similar Very CONTAGIOUS - Watery discharge (usually non-purulent) - +/- pruritis - local (preauricular) lymphadenopathy Treatment: - cool compresses - artificial tears/saline drops as needed - hand hygiene Patient Education • Highly contagious for around 10-12 days from onset, if the eyes are red. • Avoid activities: touching their eyes, shaking hands, and sharing items like towels, napkins, and pillowcases. • Resolves on its own within 2-4 weeks. Viral Conjunctivitis Allergic Conjunctivitis • Etiology • Acute or chronic irritation from known allergen, chemical, smoke, etc. • Presentation • May appear like viral conjunctivitis • (bilateral, watery tearing, itchy/irritated) • Treatment • Allergy avoidance • Antihistamine, mast cell stabilizers, or anti-inflammatory drops (OTC is fine) • MAST CELL STABILIZERS - Cromolyn sodium (generic, Opticrom) • ANTIHISTAMINES - Olopatadine (Patanol, Pataday), azelastine HCl (Optivar) Chemosis • Collection of serous fluid within the substance of the conjunctiva and is a nonspecific sign of conjunctival irritation. • Can be seen in a wide range of conditions, including trauma, allergic reaction, inflammation, hypoalbuminemic states and infections Outline Corneal disorders • Cataract • Corneal ulcer • Infectious • Keratitis • Pterygium • Pinguecula Cataract • Opacification of the lens • Can occur unilateral or bilateral • Most common cause of blindness worldwide • Most common in elderly patients • Presentation: • Gradual painless worsening of vision, “halos” from on-coming car lights or streetlights, “glare”, needing brighter lights to read • Definitive treatment is surgical • If conservative measures fail (avoid excess UV light, wear sunglasses, control smoking/diabetes/alcohol abuse) Cataracts Arcus Senilis • This condition is essentially benign; but patient may be concerned • “Blue line”… This does not alter vision • May be a sign of hyperlipidemia • particularly in pts younger than 60 years old Hypopyon • Exudate in the anterior chamber • May be related to endophthalmitis or corneal ulcer • Treat underlying disease Endophthalmitis • Inflammation of the contents of the globe due to infection • Common etiologies: • Intraocular surgery • Penetrating trauma • Untreated corneal abrasion/ulcer • Presents with pain and loss of vision • Common to have recent Hx of surgery and not appropriately using prescribed prophylactic antibiotics • May have visible hypopyon • Treatment • Immediate referral • May need intravitreal antibiotics (via fine needle injection) • May need vitrectomy (vitreous humor is replaced w/ oil) Keratitis Inflammation of the cornea Causes: light exposure, infections Symptoms: moderate to intense pain and impaired vision, photophobia, redness, and a sensation of grittiness. Diffuse fluorescein stain uptake on Woods’ lamp or slit lamp exam. Herpes Keratitis Risk Factors • Immunosuppression or immunocompromised state, history of oral and genital ulcers, and recent infections Presentation: An acutely painful, injected eye, +/photophobia Diagnosis • Fluorescein staining shows dendrites (aka “lightening appearance” or “branching”) • Conjunctival scrapings, culture, PCR • Treatment: Antiviral drops (i.e., acyclovir) • Optho referral Pinguecula Yellow(ish), elevated conjunctival nodule, more commonly on the nasal side • Confined to the conjunctiva without corneal involvement. • It is a degenerative eye condition that is often confused with pterygium • It is common in persons over the age of 35 years. • Treatment • Eye lubrication for comfort • Avoid excess UV exposure (sunglasses) and avoid irritants as much as possible • Surgery is an option for chronic irritation or if becomes intrusive to central vision; or obscures large area of peripheral vision Pterygium Fleshy encroachment of the conjunctiva onto the of the cornea and is usually triangular shaped and associated with prolonged exposure to wind, sun, sand, and dust • More common in tropical climates • And often found in people who work outside frequently • Treatment / Management: • Key: • Eye lubrication for comfort (OTC okay); • Avoid excess UV exposure (sunglasses) and avoid irritants as much as possible • Surgery is an option for chronic irritation Corneal Ulcer • Etiology: Can be bacterial, viral or fungal • Often appears as a “white dot” on corneal exam • Ten-fold increase in risk for soft contact lens wearers • Treatment with antibiotic ointment/drop • Broader coverage for contact wearers • Refer for close follow up (w/in 24-48 hours) • After starting treatment to help prevent scarring and/or infection progression • Immediate referral necessary if ulcer is within central vision Corneal Ulcer Outline Lid disorders • Blepharitis • Chalazion • Ectropion • Entropion • Hordeolum BLEPHARITIS Chalazion • Chronic inflammation of a meibomian gland in the eyelid • painless • Treatment • Warm compresses, (key to treatment) • Topical antibiotics • When to Refer • For Incision & drainage or biopsy, if all treatment fails • May cure on own without intervention in some cases Hordeolum (Stye) Definition • Acute inflammation due to a small abscess of the meibomian gland or hair follicles of the eyelids • Two types: External- and Internal-type Signs/Symptoms: • Typically, acutely painful, redness, focal swelling of the eyelid Treatment: • Warm compresses - trying to remove oil that is likely blocking the outlet duct of the hair follicle • + Artificial tear lubrication • Topical antibiotics only if secondary infection develops or refractory symptoms / fail 1st line treatment Hordeolum - External Hordeolum - Internal An Internal stye may look worse, as granulation tissue is deposited over it as protection from the eye – may have FB / irritation sensation External Internal Entropion / Ectropion • Inward / outward irregular turning of the eyelid • Use magnifying glass, slit lamp • Often misdiagnosed as blepharitis • Causes • Older age (due to lid laxity), blepharitis, history of trauma, infection, stroke, or facial nerve palsies or paralysis. • Treatment • Lubricating drops • Surgical (if affecting daily life or vision) Entropion In Ectropion Out Outline Neuro-ophthalmologic disorders • Nystagmus • Optic neuritis • Papilledema Nystagmus • Rhythmic, involuntary, rapid eye movement • Types: Horizontal (side-to-side), vertical (up and down), rotary (circular). • Nystagmus in the primary position is classified according to trajectory: downbeat, upbeat, horizontal, torsional, or mixed. • Types of Nystagmus: • Down/Upbeat: CNS dysfunction. • Vestibular (horizontal): Labyrinth or vestibular nerve dysfunction. • Gaze-evoked: Common and often benign. Two Types: Congenital and Acquired. • Congenital: Develops in infancy, often 6 weeks to 3 months. • Sensory nystagmus: Linked to poor vision from conditions like cataract, strabismus, optic nerve issues. • Acquired: Develops later in life, various causes, associated with serious medical conditions. • Adults perceive shaky images • Investigation for visual abnormalities is required in patients with the congenital form. • MRI of the brainstem and cerebellum, with consideration of CSF exam if infection is suspected. Nystagmus • Non localizing – Drugs, toxins • Localizing • Down – Cervicomedullary • Up – Vermis • Convergence – Dorsal midbrain • See-saw – Third Para Sella • Rebound/periodic alternating nystagmus Copyrights apply See-Saw Nystagmus Optic Neuritis Etiology: • Demyelinating disease • • • Multiple sclerosis Infections / inflammation Viral, syphilis, tuberculosis, sarcoidosis • Exposure to toxins • (eg, arsenic, lead, others) • Idiopathic Presentation: • Sudden or rapidly progressing unilateral central vision loss • Frequently this is painful, often worse with eye movement. • The pupillary light response is diminished in the affected eye • afferent pupillary defect (or APD) • Patients are typically younger than 50 years old • Pts may complain that color vision is affected more than visual acuity (clarity) Diagnostics MRI evaluation (of brain/orbits) If there is suspicion for optic neuritis, consult ophthalmology AND neurology (or a neurophthalmologist) Treatment • Depends on underlying etiology • Intravenous corticosteroids may be helpful in cases associated with demyelinating disease. • **Do not start steroids without identifying etiology or being advised by a specialist to do so Afferent Pupillary Defect (APD) No response (either eye) to direct light accommodation (no constriction) Normal response to indirect accommodation (both eyes constrict) Afferent Pupillary Defect (APD) • “Pupil size is controlled in the midbrain, from which efferent nerves travel to both pupils, resulting in symmetric pupils, even with a unilateral light stimulus. The perception of the light stimulus, however, may be decreased by disease within anterior visual structures such as the retina, optic nerve, chiasm, optic tract, and midbrain pathways. With diminished afferent stimulation, less light is “perceived,” and pupil contraction diminishes (ie, dilates) as a result. In this situation, the affected side is said to demonstrate an afferent pupillary defect (APD). • Management and Disposition • The finding of an afferent pupillary defect is nonspecific. A fundoscopic exam may show occlusion of the central retinal vein or central retinal artery or a dense hemorrhage in the vitreous. Otherwise, a neurologic evaluation (history, physical examination, and computed tomography [CT] scan) is important to assess for treatable conditions. In the absence of gross ocular or neurologic disease, a clinically stable patient may be discharged from the ED with ophthalmology follow-up.” Singh M, Whitfield D. Afferent Pupillary Defect. In: Knoop KJ, Stack LB, Storrow AB, Thurman R. eds. The Atlas of Emergency Medicine, 5e. McGraw Hill; 2021. Accessed August 28, 2023. https://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2969&sectionid=250454399 Papilledema Definition: Swelling of optic disk due to increased intracranial pressure, almost always bilateral Symptoms Early visual symptoms often absent. • Brief vision disturbances may occur. Causes • Brain tumor or abscess • Cerebral trauma or hemorrhage • Meningitis • Cavernous or dural sinus thrombosis • Encephalitis • Idiopathic intracranial hypertension (pseudotumor cerebri): • Elevated cerebrospinal fluid (CSF) pressure without mass lesion Signs/Findings that can be seen on physical exam (fundoscopic exam): • Blurred margins of the optic disk • Hyperemic (erythema/redness) of the optic disk • Venules may be dilated and tortuous • The optic cup may be obscured by the swollen disk Diagnosis • Ophthalmoscopy to observe optic disk. • Further tests, including brain imaging. • Sometimes lumbar puncture to identify the cause. Treatment Approach • Targeted at addressing the underlying cause. • Addressing conditions causing elevated intracranial pressure is crucial. Fundoscopic Findings Outline Orbital disorders • Orbital cellulitis • Retinal disorders • Macular degeneration • Retinal detachment • Retinopathy Orbital Cellulitis • Pre-septal (periorbital) Cellulitis • Involves infection of the skin / tissue around the eye • Sx = Erythema / edema of the eyelids and surrounding • Tx = antibiotics: TMP/SMX, Clindamycin + Amox, Augmentin, or cefdinir for 10 days • Post-septal (orbital) Cellulitis • Involves infection posterior to the eye itself • Key findings to differential from preseptal type: • *Proptosis on exam, visual changes, or pain with eye movement* • In most patients, the affected eye is swollen closed • It is necessary to pry open the eye for examination • Chemosis Pre-septal Cellulitis (peri-orbital) No proptosis seen on CT Post-septal Cellulitis (orbital) Swelling or fat prolapse behind the 1st layer of the eye This is an example of postseptal (orbital) cellulitis Treatment: • Pre septal (periorbital) • Start oral antibiotics and consider referral • Follow closely, if unsure may need CT orbits • Post septal (orbital) • REFER immediately for ophthalmology consult • CT scan of orbits required to see how extensive and rule out other causes of proptosis (i.e., a mass) • Ultimately: Treatment = hospital admission, as IV antibiotics are required Retinal Detachment • Etiology • Trauma, previous ocular surgery, nearsightedness, family history of retinal detachment, and Marfan’s disease (a connective tissue disorder) • Presentation • Sudden unilateral, painless, decreased vision • May describe a “shadow” or “curtain coming down” • Others: “cloudy or smoky” vision, “floaters”, or momentary “flashes of light”. • Visual field defects may be noted, depending on the affected area of the retina Retinal Detachment Treatment • Emergent transfer to optho • Without treatment, many symptomatic retinal detachments progress to involve the entire retina and can lead to permanent loss of vision. • Surgery, laser, or cryotherapy Retinal Detachment- POCUS Retinopathies • Changes to the retina causing a subsequent change in vision • Causes: vascular changes and subsequent retinal injury and ischemia • Etiologies: • Diabetes (most common) hypertension, pre-eclampsia/eclampsia, HIV, sickle cell, some clotting disorders • Any microvascular/small vessel disease which could affect the small / delicate vessels of the retina. • Retinopathy can lead to blindness • This group of conditions are typically a slow and progressive process. • Unlikely for a retinopathy to cause a sudden loss of vision. Normal fundus (Inside, back surface of the eye = retina, macula, optic disc, fovea and blood vessels) Non-proliferative (NPDR) - Proliferative (PDR) Color fundus photograph of non-proliferative diabetic retinopathy showing retinal hemorrhages, yellow lipid exudates, and dull-white cotton wool spots (nerve fiber layer infarcts). Color fundus photograph of proliferative diabetic retinopathy displaying prominent neovascularization at the disc (NVD). Hypertensive Retinopathy Normal Hypertensive retinopathy with optic disc edema, cotton wool spots, flame hemorrhages, dot-blot hemorrhages, arteriovenous (AV) nicking, and exudates Macular Degeneration Also called age-related macular degeneration or “AMD” Etiology = a degenerative condition of the central portion of the retina (the macula) that results primarily in loss of central vision This is a gradual, painless, bilateral central vision loss that occurs in elderly patients, other symptoms: scotomas, night blindness 1.) “Dry” type- (most common form) – • Drusen present, pigment changes, and atrophy are also present, but there is no leakage of fluid into the sub-retinal space. • Usually, only mild - moderate visual loss is present although patients may complain of distorted vision 2.) “Wet” type• Characterized by the development of a choroidal neovascular membrane that leaks fluid and blood. • Can lead to profound vision loss. Treatment • Refer to ophthalmologist • Intravitreal injections, laser photocoagulation, photodynamic therapy, or even surgery. Amsler Grid 1. Normal 2. AMD Fundoscopic Findings Drusen are clustered in the center of the macula. “Dry type” Hemorrhage seen beneath the retina. Note the retinal Drusen bodies are extracellular deposits of lipids, proteins, and vessels are superficial to the hemorrhage, which lies cellular debris which are found within the layers of the retina and just beneath the retina. appear as small, yellow deposits on dilated eye exams “Wet Type” Outline Lacrimal disorders • Dacryocystitis Dacryocystitis • Inflammation of the nasolacrimal duct or sac, most commonly due to to duct obstruction • Excessive tearing • Infants may be born with it • Treatment: • • • • • warm compresses oral antibiotics pain control (i.e., acetaminophen, ibuprofen) irrigation if recurrent or infant REFER for surgical evaluation Outline Traumatic disorders • Blowout fracture • Corneal abrasion • Globe rupture • Hyphema Blowout Fracture • Fx to inferior and medial orbital wall • Typical hx: Punched in the face • Inferior Rectus entrapment • Impaired extraocular movements • Diplopia on upward gaze • CT orbits • Abx cephalexin, avoid head pressure changes • OMFS Corneal Abrasion Definition: Disruption of the corneal epithelium Presentation: • Pain, foreign body sensation (FBS), delayed presentation from initial inciting factor • Conjunctival injection (redness), +/- photophobia (if co-existing iritis) Evaluation: 1. Topical anesthetic (i.e., tetracaine 0.5%) drops to help exam, provide temp. relief • These can be harmful to the cornea if overused à Don’t provide these to a patient to take home 2. Fluorescein staining • Evaluate for extent, for ulcer, and exact location of injury- by Woodʼs Lamp or Slit Lamp 3. Evert the eyelid • To evaluate for retained foreign body Treatment: • Topical antibiotic drops and/or ointment- erythromycin ointment (preferred for lubricant function), basic artificial tears / lubricant drops PRN • F/U: 48 hrs with optho for recheck Corneal Abrasion Corneal Chemical Injuries • Call poison control • Measure Ph in Inferior Fornix • If Ph <6.5 or > 7.5 à chemical eye burn • Copious irrigation • Morgan lens • Consult • Attempt to bring pH back to normal • Of note, bleach-related exposures can cause significant chemical injuries of the cornea Globe Rupture Background: • Vision-threatening emergency: Full thickness disruption of sclera or cornea. Causes: • Blunt Eye Trauma • Penetrating trauma: Suspect with eyelid or periorbital puncture/laceration. • Often associated with metal-on-metal, machinery accidents. Clinical Features: • Globe rupture with protruding uveal tissue or deep orbital wounds. • Eye pain, possible visual acuity decrease. • Teardrop-shaped pupil, flat anterior chamber. • Extrusion of intraocular content, hemorrhagic chemosis. Evaluation: • Avoid tonometry. • Positive Seidel's test indicates globe rupture. Work-Up: • Non-contrast CT orbit: For intraocular foreign body or unclear diagnosis. Management: • Consult ophthalmology for surgical repair. • NPO, prevent further injury, no manipulation. • Use metal shield or paper cup for eye covering. • Consider antiemetics, IV pain meds, tetanus prophylaxis. IV Antibiotics Disposition: • Admission for surgical repair by ophthalmology. Globe Rupture Findings • Hyphema, subconjunctival hemorrhage, abnormal pupil shape, Limited OM, extrusion of globe contents, ↓visual acuity • Seidel Sign: Aqueous flow on fluorescein testing (streaming appearance). *pathognomonic Hyphema • Blood in the anterior chamber • Better assessed with pt upright • Significant Blunt trauma • Eye pain, vision changes, photophobia • Clinical diagnosis, consider CT orbits • Atropine for dilation to prevent pupillary movement • If penetrating trauma or suspect open globe – defer tonometry until open globe r/o • Shield, elevate HOB • Urgent ophthalmology consult • Usually resolves spontaneously Subconjunctival Hemorrhage Definition: Bright red blood between the conjunctiva and sclera Causes: Spontaneous or minor trauma, contact lens use, cough, sneeze, Valsalva, vomiting Risk Factors: elderly, hypertension, diabetes, advanced age, and the use of blood-thinning medication, think bleeding disorder if recurrent Treatment: Reassure patient, should not affect vision • Color changes and slow progression of resolution à 2-3 weeks) • Will change color as blood is broken down and reabsorbed Subconjunctival Hemorrhage Outline Vascular disorders • Retinal vascular occlusion Central Retinal Artery Occlusion (CRAO) • Retinopathy associated with central retinal venous obstruction • Most caused by an embolic / thrombotic event • Embolus, thrombus, or vasculitis • Embolus (e.g., is a clot formed remotely and travels to vessel site causing clot; such as atrial fibrillation or carotid stenosis embolism) • Thrombus (e.g., is a clot formed locally in a vessel which leads to occlusion of the vessel; commonly from atherosclerosis) • Vasculitis = giant cell arteritis, polyarteritis nodosa • Risk Factors= sickle cell disease, hypercoagulable states, leukemia and several others • (CRAO) and any branch retinal artery occlusion (BRAO) are disorders that are considered a form of stroke. Central Retinal Artery Occlusion (CRAO) Presentation • Onset will be sudden onset, painless, unilateral vision loss • partial or complete vision loss • Fundoscopic exam findings • “Cherry red spot” of fovea, “Box-carring” of smaller vessels (intermittent disruption of visualization of blood vessel), retinal swelling or edema, and finally, pale retina (late finding) Treatment Requires EMERGENT consult/transfer to an ER with ophthalmologist coverage for stroke-like evaluation (1) decreasing intraocular pressure with topical β-blocker eye drops or intravenous acetazolamide (2) ocular massage, applied with cyclic pressure on the globe for 10 seconds, followed by release and then repeated (3) Tissue plasminogen activator (TPA) may be considered for lysis of an occluding clot/thrombus. • Must weigh serious risks / benefits of such Tx with the patient Prognosis • Poor prognosis, commonly results in permanent vision loss CRAO - Fundoscopic Exam Findings “Cherry red spot” on fovea “Box-carring” of small vessels The retinal pallor caused by retinal edema is demonstrated here, contrasting with the "cherry red spot" Central Retinal Vein Occlusion (CRVO) Risk Factors: 90% over age 55, HTN, atherosclerosis, DM • Onset will be sudden, unilateral painless partial/full vision loss or blurred vision. • Fundoscopic exam findings: • “Blood and thunder” retina with dilated veins, hemorrhages, edema, exudates (see next slide) • Treatment • If Macular Edema, first line treatment for macular edema due to CRVO is antiVEGF (Vascular endothelial growth factor) therapy with intravitreal bevacizumab, ranibizumab, or aflibercept • No convincing evidence of medical treatment favorably altering the natural course • Prognosis • May resolve over time or cause some permanent disability of vision loss. CRVO Fundoscopic Exam Findings The hemorrhage is the most striking finding. Also note the blurred disk margin, the dilation and tortuosity of the venules, and the cotton wool spots. Outline Vision abnormalities • Amaurosis fugax • Amblyopia • Glaucoma • Scleritis • Strabismus Amaurosis Fugax Transient sudden complete loss of vision with complete sight restoration within a few minutes. • Can be unilateral or bilateral Etiology: • Embolic • Also consider: atherothrombosis, dissection, small artery occlusive disease (optic neuropathy, vasculitis), venous disease, cardiac disease, hypercoagulable disorders, and systemic hypoperfusion Treatment: Specialist consultation and ultimately, tx depends on etiology. These pts should be admitted for stroke “work up” to determine etiology. Amblyopia (lazy-eye) Definition Diagnosis • Poor vision primarily in one eye, sometimes in both • Routine vision screening for all kids aged 3 to 5 • Brain favors stronger eye, weakening the other over time Treatment Prevalence 1. Address underlying vision problem (glasses, contacts, surgery) • Most common cause of childhood vision loss, 3% of children Causes Symptoms 2. Strengthen weaker eye and retrain brain 1. Eye patch on stronger eye to encourage weaker eye use 2. Atropine eye drops in stronger eye to blur vision, favoring weaker eye • Symptoms can be subtle, such as poor depth perception Early Treatment is Crucial • Signs may include squinting, eye shutting, head tilting • Begin treatment as early as possible Risk Factors • Lifelong vision problems if untreated • Brain adapts due to a vision problem in one eye, Refractive errors (nearsightedness, farsightedness, astigmatism), Strabismus (misaligned eyes), Cataracts (cloudy eye lens) • Higher risk in premature, smaller birth weight babies • Family history, childhood cataracts, eye conditions, developmental disabilities Acute closed angle glaucoma (ACAG) Definition • Angle between iris/cornea closes, preventing drainage of aqueous fluid through trabecular meshwork • Increase intraocular pressure often >40mmHg normal 10-20 • Can lead to death of retinal cells = vision loss Etiology Age, female, PMH or FH, hyperopia (far-sighted, shallow AC) Triggered by pupil dilation Clinical Features • Decreased vision, Halos around lights, Headache, Severe or intense eye pain (usually unilateral), Nausea and vomiting. • Conjunctival redness, corneal hazy ,fixed dilated pupil, reacts poorly to light, hard globe on palpation Acute closed angle glaucoma (ACAG) • Diagnostics • Gonioscopy = gold standard, iris / cornea angle measurement • Slit lamp exam • Management • Medical emergency – do not dilate! • Supportive • Lie supine to avoid dilation • Analgesia + antiemetics • Medical • Timolol or pilocarpine • IV acetazolamide • IV Mannitol • Surgical • Laser iridotomy (definitive) Chronic open-angle glaucoma History • More common than ACAG, 2nd most common cause of legal blindness in the United States Risk Factors • Family History • Steroid use Symptoms • Bilateral, Painless • asymptomatic at first, occasionally described as tunnel vision. • gradual onset vision changes Physical examination • May present as loss of peripheral vision on exam • Elevated Intraocular pressure (IOP), when measured Treatment - Routine referral • β-blockers (timolol 0.5%), Prostaglandin analogs (latanoprost 0.005%), Carbonic anhydrase inhibitors (dorzolamide 2%), α-Agonists (brimonidine 1.0%) Scleritis inflammation in the episcleral and scleral tissues with injection in both superficial and deep episcleral vessels. Associated with an underlying systemic disease in up to 50% of patients: Polyangiitis, Rheumatoid Arthritis, Systemic Lupus Erythematous, Polyarteritis Nodosa: Symptoms • Severe Pain: Gradual, Dull and boring pain, exacerbated by eye movements, especially at night. Physical Examination Laboratory Testing • Laboratory workup includes assessment of blood pressure, renal function, acute phase response, CBC with differential, ESR/CRP, serum autoantibody screen, urinalysis, syphilis serology, uric acid, sarcoidosis screen, among others. Management • Minimize inflammation to reduce ocular damage. • Color and Appearance: unique violet-bluish hue, coupled with scleral edema and dilatation. • Distinguishing from Episcleritis - Episcleritis: Inflammation of the superficial episcleral tissue. Medical Therapy: • NSAIDs: • Globe Tenderness • Oral NSAIDs are first-line for mild-to-moderate scleritis. • Clinical Diagnosis Corticosteroids: • Diagnosis of scleritis primarily relies on clinical assessment. • Topical corticosteroids may help with ocular inflammation. • Laboratory testing is often essential to identify underlying connective tissue and autoimmune disorders. • Systemic corticosteroids are often necessary for treatment. Diagnostic Procedures • B-Scan Ultrasonography: Detects posterior scleritis, showing changes like scleral and choroidal thickening, optic nerve sheath distension, and retinal detachment. • Orbital MRI: Another tool for detecting posterior scleritis. • Side effects include elevated intraocular pressure, susceptibility to infection, gastric irritation, and more. Scleritis Strabismus Crossed eyes — is misalignment of the eyes, causing one eye to deviate inward (esotropia) toward the nose, or outward (exotropia), while the other eye remains focused. Epidemiology Strabismus prevalence: 2-4% of population Risk factors • Family history, Preterm birth, low birth weight, Ocular conditions like vision deprivation, hyperopia, amblyopia, Certain neuromuscular conditions. Symptoms Frequent blinking or squinting, diplopia Causes Congenital and acquired causes Evaluation • pupillary reactivity, eye movements, light reflex tests, cover/uncover tests. Treatment • Eyeglasses, prisms, vision therapy, or eye muscle surgery Complications • Amblyopia, Diplopia, Secondary contracture of extraocular muscles, limiting movement, • Psychosocial and vocational consequences. Copyrights apply Strabismus • Large-angle infantile-onset esotropia. EXTRA KNOWLEDGE • Test your knowledge • Vision Disorder Video • Slit lamp video • Wood’s lamp • FB rust-ring removal with Burr Diagnosis? Treatment? Case 1 Case 2: A 52-year-old woman presented with a 24-hour history of severe pain and blurred vision in her left eye. Let’s discuss physical exam steps & DDx 1. 2. 3. 4. 5. 6. 7. 8. 9. Visual acuity = vital sign of the eye Inspect external exam, lid flip if FB sensation EOMs Using light – pupil reflex, direct/indirect Fundoscopic exam Fluorescein stain IOP – tonopen Imaging – POCUS, vs CT orbits Consult ophthalmology Case 2 Continued • The patient described the pain as constant with a shooting character, lasting a few seconds. • Upon examination of her left eye, findings included a mid-dilated pupil unresponsive to light, conjunctival redness, and palpable hardening of the left orbit. • Her visual acuity in the left eye was measured at 20/125. • An elevated intraocular pressure of 55 mm Hg (normal range, 10 to 20) confirmed the diagnosis. Case 2 Continued • Acute angle-closure glaucoma is considered an ophthalmologic emergency. While the exact cause was not attributed to medication use or other identifiable factors, symptoms can be triggered by dim lighting and certain medications, such as anticholinergic and sympathomimetic drugs. • The patient was treated with intravenous acetazolamide, a topical carbonic anhydrase inhibitor, and an α2-adrenergic agonist. • She underwent a laser iridotomy, after which her symptoms quickly resolved. • This case highlights the importance of prompt intervention in cases of acute angle-closure glaucoma to alleviate the increased intraocular pressure and prevent potential vision loss. Likely History? Symptoms? Diagnosis? Treatment? Case 3 Symptoms? Diagnosis? Treatment? Case 4 Symptoms? Diagnosis? Treatment? Case 5 Symptoms? Diagnosis? Treatment? Case 6 Vision Disorder Video • https://twitter.com/HowThingsWork_/status/1589590567541149698?s=20 Slit Lamp Exam - Intro Click here for instructional video titled "Slit Lamp Exam" (24 mins) Please review this video prior to the end of this block. This video will provide a detailed explanation of how to use a slit lamp and important pathological findings associated with the eye. “Seidel’s Sign” -Used to assess for penetrating eye injuries. -Vitreous Fluid leaking on Fluorescein stain exam = emergent referral for OPEN Globe (globe penetration) Click this link to watch an example of +Seidel's Sign Diamond Burr / Removal of Corneal FB • Click this text to review removal of corneal FB's • View to 1 minute, then at 4:40 to end • This video covers the methods of corneal FB removal • Click this text to review needle corneal FB removal • This video covers the needle method of corneal FB removal Questions? Special acknowledgement to: Matthew Ewald, MSPAS, PA-C Thank You! References • https://eyewiki.aao.org • Greenberg RD, Daniel KJ. Chapter 31. Eye Emergencies. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment Emergency Medicine, 7e. New York, NY: McGraw-Hill; 2011. • Effron D, Forcier BC, Wyszynski RE. Chapter 3. Funduscopic Findings. In: Knoop KJ, Stack LB, Storrow AB, Thurman R. eds. The Atlas of Emergency Medicine, 3e. New York, NY: McGraw-Hill; 2010. • Riordan-Eva P. Disorders of the Eyes & Lids. In: Papadakis MA, McPhee SJ, Rabow MW. eds. Current Medical Diagnosis & Treatment 2015. New York, NY: McGraw-Hill; 2014. • Riordan-Eva P, Hoyt WF. Chapter 14. Neuro-Ophthalmology. In: Riordan-Eva P, Cunningham ET, Jr. eds. Vaughan & Asbury's General Ophthalmology, 18e. New York, NY: McGraw-Hill; 2011. • Ropper AH, Samuels MA, Klein JP. Chapter 13. Disturbances of Vision. In: Ropper AH, Samuels MA, Klein JP. eds. Adams & Victor's Principles of Neurology, 10e. New York, NY: McGraw-Hill; 2014. • Walker RA, Adhikari S. Chapter 236. Eye Emergencies. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011. • www.uptodate.com