PHAS 608 Clinical Medicine I Fall 2024 Ophthalmology Lecture cont. PDF

PHAS 608 Clinical Medicine I Fall 2024 Ophthalmology cont. Tamarah Thompson, DSc, MSHS, MS, PA-C  Agenda o Ophthalmology (Eye ) Lecture  Objectives By the end of the ophthalmology module, students will be able to: o Discuss and descri...

PHAS 608 Clinical Medicine I Fall 2024 Ophthalmology cont. Tamarah Thompson, DSc, MSHS, MS, PA-C  Agenda o Ophthalmology (Eye ) Lecture  Objectives By the end of the ophthalmology module, students will be able to: o Discuss and describe the following common ophthalmic (eye) diseases and disorders that are observed in primary medical care with respect to epidemiology, etiology, pathophysiology, clinical presentation (signs and symptoms), diagnostic findings, and treatment: a. Conjunctival disorders b. Corneal disorders c. Lacrimal disorders d. Lid disorders e. Neuro-ophthalmic disorders f. Orbital disorders g. Retinal disorders h. Traumatic disorders i. Vascular disorders j. Vision abnormalities k. Neoplasms l. Foreign Bodies  Objectives o Apply knowledge of ophthalmic anatomy in addition to physiology of sight when taking a patient’s history and performing a physical examination. o Differentiate and analyze normal and abnormal ophthalmic and otolaryngologic exam findings, using the information to guide and support medical decisions and treatment plans. o Differentiate and analyze urgent and non-urgent ophthalmic conditions. o Apply pathophysiology concepts regarding ophthalmic and otolaryngologic diseases, using the information to guide and support medical decisions and treatment plans. o Recognize and distinguish relevant differential diagnoses utilizing a system based pathophysiological model. o Recognize and distinguish relevant differential diagnoses utilizing a system based pathophysiological model. o Choose and interpret common ophthalmic and otolaryngologic laboratory and diagnostic tests/screenings.  Objectives o Develop a patient-centered treatment plan to include non- pharmacologic and pharmacologic interventions using evidence- based medicine o Provide patient education and referrals in addition to developing a monitoring plan to optimize short- and long-term patient health outcomes. o Recognize indications for immediate referral to an ophthalmologist for various types of eye trauma: o Conjunctival injury o Cornea injury o Chemical burns o Blunt and penetrating trauma o Iris injury o Anterior chamber injury o Lens injury o Globe rupture Ophthalmic (Eye) Disorders o Lid disorders o Orbital disorders o Lacrimal disorders o Retinal disorders o Conjunctival disorders o Vascular disorders o Corneal disorders o Vision abnormalities o Neuro-ophthalmic o Traumatic (ER) disorder disorders o Neoplasms o Other disorders- Foreign Body Orbital Disorders o Orbital Cellulitis Orbital Cellulitis o Definition: an acute infection of the soft tissues (orbit posterior to the orbital septum) surrounding the eye o Ocular adnexal and orbital tissues o Pathophysiology/Etiology: o Infection of the paranasal sinuses → extends to the deep orbital structures o Sinusitis (ethmoid) – 90% of cases o Dental, facial, globe/eyelid, lacrimal infections o Direct inoculation of the orbit from trauma or surgery o Inflammation noted within 48-72 hours o Spread from bacteremia o Infecting organisms: Strep pneumoniae (the incidence reduced by pneumococcal vaccine); Staph Aureus; H. influenzae; and Gram- bacteria o Fungal pathogens: Mucor and Aspergillus species – high mortality in immunocompromised o Winter; Children (M > F) more commonly affected; adults (F> M with MRSA infections) Orbital Cellulitis o Signs and symptoms: o Fever, edema and redness of eyelid and surrounding skin, ptosis, and restricted (paralysis/weak) EOM o Orbital pain and tenderness o Exophthalmos (bulging eye), purulent d/c; conjunctivitis o Decreased vision and sluggish pupillary response o Elevated intraocular pressure o DDx: Exophthalmos; Preseptal cellulitis; Orbital pseudotumor; Rhabdomyosarcoma; conjunctivitis, retinoblastoma o Diagnostic Evaluation: PROMPT CLINICAL Dx. o Labs- CBC to check for leukocytosis; o Blood culture (prior to antibx.) o Gram stain if purulent d/c o CT scan with contrast to determine extent of disease  Orbital Cellulitis o Treatment/Management: o MEDICAL ER = Hospitalization and immediate treatment with IV antibiotics – Broad spectrum until pathogen identified o Ticarcillin-clavulanate; Nafcillin and Ceftazidime o If penicillin sensitivity, use Cefazolin or Vancomycin o Vancomycin and clindamycin for MRSA infection or suspicion o Cephalosporin (ceftriaxone; cefazolin) for trauma related ds. o covers S. aureus and group A beta-hemolytic streptococci o IV antifungal tx. (Amphotericin) and surgical debridement – Fungal infections o Surgery may be required to drain the paranasal sinuses or an orbital abscess o Other tx.: intranasal decongestants and corticosteroids o Patient Education: o Take antibiotics as directed for sinus infections, especially young children o Refer all patients with orbital cellulitis or suspicion to an Ophthalmologist IMMEDIATELY Retinal Disorders o Retinopathy o Diabetic o Hypertensive o Retinal Detachment o Macular Degeneration (Age-Related = ARMD) Retinopathy  Diabetic Retinopathy o Definition: Damage to the retina due to diabetes mellitus (DM) o Leading cause of new blindness in 25-74 y.o. in the United States o Present in about 28.5% of diabetics > 40 y.o. o Annual incidence of 65,000 o Pathophysiology/ Etiology: Unclear o Classified as Proliferative or Nonproliferative o Proliferative - retinal ischemia → neovascularization (ie. new blood vessel formation) at the optic disc or elsewhere leading to vitreous hemorrhage and acute vision loss o less common but causes more severe visual loss o Nonproliferative – commonly due to diabetic macular edema (focal or diffuse) or macular ischemia o Macular involvement is the most common cause of legal blindness in type 2 diabetes. o Can be mild, moderate, or severe Diabetic Retinopathy o Signs and Symptoms: o Initially asymptomatic o Advanced stages: floaters, blurred vision, progressive, decreased visual acuity o Fundoscopic Examination: microaneurysms, venous loops/beading; scattered dot and blot hemorrhages; macular edema; flame-shaped hemorrhages, cotton-wool spots, retinal exudates, microaneurysms, venous bleeding  Diabetic Retinopathy o Differential Diagnosis: Retinal vein occlusion; ocular ischemic syndrome; macular edema (diabetics) o Diagnostic Evaluation: Clinical o Eye exam: visual acuity, fundoscopic exam of retina o Imaging: Fluorescein angiography, optical coherence tomography, B-scan ultrasonography o Labs: fasting glucose/A1C o Treatment/Management: o Triamcinolone (corticosteroid); VEGF inhibitors : Afibercept, Ranibizumab- helps manage macular edema and neovascularization o Glycemic control (A1C 6-7%) is the most important modifiable factor o Optimize blood pressure, kidney function, and serum lipids o Laser photocoagulation and vitrectomy o Refer to ophthalmology o Patient Education/Maintenance/Prevention: o Advise the need for diabetic (glycemic control) = slows ds. progression o In patients with type 1 and 2 diabetes, eye examination is needed at the time of diagnosis , then every 5 years or Type 1 and annually for Type 2 DM o Report visual sx. immediately o Smoking cessation and management of HTN, kidney ds, and HLD)  Hypertensive Retinopathy o Definition: Retinal changes due to hypertension that may affect vision o Etiology/Pathogenesis: o Commonly associated with chronic hypertension → retinal vascular occlusions including branch retinal vein and central retinal vein occlusion. o Acute hypertension may produce optic nerve edema and serous retinal detachment o Pheochromocytoma, malignant hypertension (hypertensive emergency), or preeclampsia-eclampsia (pregnancy) Hypertensive Retinopathy o Signs and Symptoms: o Vary based on the degree and rate of BP elevation as well as the underlying state of ocular circulation o usually asymptomatic o +/- decreased vision o Fundoscopic exam: arterial narrowing, AV nicking, nerve fiber layer infarcts, and intraretinal hemorrhages o Moderately sclerosed arterioles demonstrate “copper wiring” o Severely sclerosed vessels demonstrate “silver wiring” o Acute hypertension emergency - papilledema with disc swelling, hemorrhages, and exudates  Hypertensive Retinopathy o Differential Diagnosis: branch retinal vein occlusion, central retinal vein occlusion, central retinal artery occlusion; diabetic retinopathy o Diagnostic Evaluation: o Fundoscopic examination o Physical examination including blood pressure o Rule out other end organ damage if hypertensive emergency (› 180/120 with end organ damage) o Treatment/Management: Control blood pressure o Emergency management → Only indicated in acute hypertension emergency o Refer to the emergency department o Patient Education: o Advise need for blood pressure control o Follow up with ophthalmology as directed for examinations Age-Related Macular Degeneration  Macular Degeneration o Definition: eye disease of macula that affects central vision → a breakdown / destruction of the retina o Age-Related Macular Degeneration (AMD) = Leading cause of permanent central visual loss in adults 50+ y.o. o Pathophysiology/Etiology: o Age-related or toxic drug effects o Drusen deposits in Bruch membrane → degenerative loss of nutritional supply, atrophy, and neovascular degeneration → hemorrhage and fibrosis o Types: nonexudative (dry/atrophic form) and exudative (wet form) o Dry - atrophy of the retinal apparatus (outer retina, the retinal pigment epithelium, and the choriocapillaris, which supplies blood to both the outer retina and the retinal pigment epithelium) o Wet - choroidal new vessels grow under either the retina or the retinal pigment epithelial cells, leading to accumulation of exudative fluid, hemorrhage, and fibrosis o Risk Factors: o Individuals 50+; Caucasians, Females (earlier age), hereditary, HTN, HLD, CVD, DM, smoking, farsightedness, UV light, poor nutrition, sedentary lifestyle Atrophic (dry) AMD Wet AMD  Macular Degeneration o Signs and Symptoms: o Retinal drusen → Hard drusen (yellow subretinal deposits - hyaline nodules) and soft drusen (larger, pale deposits that are less distinct) o Loss of central vision o Dry → gradual, progressive, bilateral visual loss of moderate severity; spares periphery. +/- drusen o Wet → rapid, severe visual loss (accounts for 90% of legal blindness due to AMD) o +/- retinal mottling, leaks, and hemorrhage o Scarring in end-stage ds. o Differential Diagnosis: Peripheral drusen; Myopic Degeneration; Toxic retinopathies; Ocular histoplasmosis syndrome o Diagnostic Evaluation: Clinical by optometrist o Comprehensive eye exam with fundoscopy and visual acuity o Amsler Grid – home screening Macular Degeneration Amsler Grid: Macular Degeneration Screening Tool Amsler Grid  Macular Degeneration o Treatment/Management: o Early ds.- laser therapy and intravitreal injections of monoclonal antibody drugs = slows progression o Oral treatment with antioxidants (vitamins C and E), zinc, copper, and omega-3-fatty acids = slows progression o Telescopic/Microscopic lenses – maximizes vision o Dry – No CURE or specific treatment o Older patients with sudden visual loss → Urgent referral to Ophthalmology o Wet - inhibitors of vascular endothelial growth factors (VEGF): anibizumab (Lucentis), bevacizumab (Avastin), and aflibercept (VEGF Trap-Eye, Eylea) o Patient Education: o Sunglasses with ultraviolet protection o Advise vitamin supplementation o Advise Mediterrean diet and smoking cessation Retinal Detachment  Retinal Detachment o Definition: separation/tearing of the retina from the back of the eye (posterior vitreous detachment) resulting in vision loss o Starts in superior temporal retinal area o Pathophysiology/Etiology: o Separation of retina from pigmented epithelial layer = tissue appears as if it is flapping in vitreous humor o Inflammatory changes in the vitreous, retina, or choroid o persons over 50 years of age o Nearsightedness (myopia), glaucoma, and cataract surgery o penetrating or blunt ocular trauma o Rhegmatogenous retinal detachment (RRD) - most common form of retinal detachment associated with vitreous hemorrhage o Tractional (TRD): preretinal fibrosis associated with proliferative retinopathy due to diabetic retinopathy or retinal vein occlusion; a complication of rhegmatogenous retinal detachment o detachment occurs when scar tissue on the retina’s surface contracts and causes the retina to pull away from the back of the eye  Retinal Detachment o Pathophysiology/Etiology: o Exudative (ERD): accumulation of subretinal fluid secondary to neovascular age-related macular degeneration or secondary to choroidal tumor o No tears or breaks in the retina o Signs and Symptoms: o RRD: Flashes of lights, floaters, Curtain or shadow moving over the field of vision, painless, peripheral or central visual loss; retina may be seen elevated in the vitreous cavity with an irregular surface o TRD: May be asymptomatic; visual loss or visual field defect with irregular retinal elevation adherent to scar tissue on the retinal surface, sometimes extending into the vitreous o ERD: Minimal to severe visual loss or visual field defect; dome-shaped retina with shifting subretinal fluid with changes in posture  Retinal Detachment o DDx: Neoplastic process; scleritis; retinal vein occlusion; age-related macular degeneration; cataract; optic neuritis o Diagnostic Evaluation: o Comprehensive eye exam including fundoscopy and visual acuity o Treatment: Definitive Tx- Surgical Repair o Emergent ophthalmology consult (laser or cryosurgery) o In transport, patient should remain supine with head to side of retinal detachment o Other surgical options: Vitrectomy (replace vitreous- jelly-like material); Scleral buckle; Air/Silicone oil injection o Eye patching may help prevent eye movement until surgery is performed o Patient Education: o Prognosis depends on degree of retinal involvement o Encourage annual eye exams Vascular Disorders o Retinal Vascular Occlusion  Retinal Vascular Occlusion o Definition: Occlusion of the vessels of the eye o Etiology/Pathogenesis/Risk Factors: o Central and branch retinal vein occlusion: associated with thrombosis often due to uncontrolled, chronic hypertension → arteriosclerosis o Risk Factors: o DM, HLD, Glaucoma o Hyperviscosity states : Smoking, HTN, and obesity o Estrogen therapy o Central and branch retinal artery occlusion: An Ophthalmic ER o Risk Factors: o carotid and cardiac emboli from an arrhythmia like atrial fibrillation; Vasculitides o Young patients → Migraine, oral contraceptives, Central Retinal Vein Occlusion o Signs and symptoms: - sudden, unilateral, painless loss of vision (blurred/complete) -may be asymptomatic in early stages - widespread hemorrhages (“ blood and thunder” retina); dilated veins, exudates, optic disk swelling, afferent pupillary defect; cotton-wool spots Branch Retinal Vein Occlusion o Signs and symptoms: - Painless loss of vision with fovea involvement - Gradual visual loss with development of macula edema - Peripheral vision loss; blurred or distorted central vision - hemorrhages, vein dilation and tortuosity - cotton-wool spot Central Retinal Artery Occlusion o Signs and symptoms: - Sudden, painless, unilateral vision loss (Amaurosis Fugax) with poor visual acuity - restricted to temporal field - Retinal pallor and edema with a cherry- red spot at the fovea - “Box-carring”- separation of arterial flow and arterial narrowing - Retinal opacity - Occasionally, emboli are seen in the central retinal artery or its branches Branch Retinal Artery Occlusion o Signs and symptoms : - Sudden, unilateral loss of vision if the fovea is involved - Common for sudden loss of a discrete area in the visual field -Retinal swelling +/- adjacent cotton-wool spots  Retinal Vascular Occlusion o Diagnostic Evaluation: o Vein occlusion: Comprehensive eye examination - check intraocular pressure and assess for signs of open- or narrow-angle glaucoma o Check blood pressure and ask about tobacco use and history of glaucoma o Ask women about estrogen therapy o Artery occlusion: Urgent ophthalmology referral; refer to ER urgently → stroke manifestations and tx. o Erythrocyte sedimentation rate and C-reactive protein will be elevated o Duplex ultrasonography of the carotid arteries, ECG, and echocardiography → identify carotid or cardiac sources ASAP to aid in early treatment to prevent stroke o Screen all patients for diabetes mellitus and hyperlipidemia o Younger patients → antiphospholipid antibodies, lupus anticoagulant, inherited thrombophilia, and plasma homocysteine should be evaluated  Retinal Vascular Occlusion o Treatment/Management: o Treat underlying condition o Central Retinal Artery Occlusion o ER ophthalmology referral o Thrombolytics and anticoagulants o Vessel dilation and paracentesis (to attempt to save eye) o Keep recumbent with gentle ocular massage (to decrease extent of damage) o Manage atherosclerosis or arrhythmia to reduce recurrence o Central Retinal Vein Occlusion o Vision typically resolves with time (partially) o Workup for thrombosis o VEGF inhibitors and photocoagulation (laser therapy) o Patient Education: o Advise blood pressure and glycemic control; o Encourage annual physical examination to include comprehensive eye exam  Vision Abnormalities & Refractive Errors o Vision Abnormalities o Refractive Errors o Amaurosis Fugax o Myopia o Amblyopia o Hyperopia o Glaucoma o Astigmatism o Open Angle o Presbyopia o Angle-Closure o Scleritis o Strabismus  Amaurosis fugax (Transient monocular vision loss) o Definition: temporary unilateral vision loss o Pathophysiology/Etiology: o retinal embolus from ipsilateral carotid disease or the heart o Risk Factors: o Giant cell arteritis, hypercoagulable state (such as antiphospholipid syndrome), hyperviscosity, and severe occlusive carotid disease o Signs and Symptoms: o Unilateral temporary loss of vision lasting seconds to hours o Curtain passing vertically across the visual field  Amaurosis fugax (Transient monocular vision loss) o Diagnostic Evaluation: o Assess for connective tissue diseases o Coagulopathy studies (prothrombin, factor Va, thrombin, CBC, protein C & S) o Carotid artery ultrasound (checking circulation) o R/o Giant cell arteritis o DDX: optic disk swelling, central and branch artery occlusion, optic neuritis, giant cell arteritis o Treatment/Management: early ophthalmology consult, treat underlying disorder; anticoagulation o All patients with possible embolic, transient visual loss should be treated immediately with oral aspirin (at least 81 mg daily) or another antiplatelet drug until the cause has been determined o Urgent carotid endarterectomy or angioplasty with stenting for ipsilateral carotid artery stenosis o Patient education: o Follow treatment plans to aid in control of underlying disease Amblyopia o Definition: commonly referred to as “lazy eye;” unilateral or bilateral decreased vision due to abnormal vision development o Pathophysiology/Etiology: improper stimulation of nerve pathways between the brain and an eye, causing the brain to favor the unaffected eye o Large difference in degree of myopia (nearsightedness) or hyperopia (farsightedness) o Children(< 6 y.o.)- commonly affected o Risk Factors: family hx., premature birth, developmentally disabled, strabismus; large refractive errors; no eye exam at scheduled intervals o Signs and symptoms: o wandering eye → favor one eye more o Bump into things on affected side  Amblyopia o DDx: strabismus o Diagnostic Evaluation: Eye exam o Assess visual acuity → better with using single letter rather than a line of letters (crowding phenomenon) o Normal eye exam – consider an organic cause → CT scan; MRI; fluorescein angiography o Treatment: o Prescription lenses, prisms, eye patch o Vision therapy (learn how to use the eyes together) o Surgery o Patient education o Educate parents about the importance of regular eye exams, treatment, and compliance  Strabismus o Definition: also referred to as “crossed eyes; ”a misalignment of one eye relative to the other eye in one or more position of gaze o may be a sign of a more serious ocular or systemic ds.: Hurler syndrome, Gaucher syndrome, Fetal alcohol syndrome, an intracranial process affecting CN 3, 4, or 6 , retinoblastoma o Pathophysiology/Etiology: poor eye muscle control, problems with nerves or the brain, extreme hyperopia (farsightedness), or other eye injuries /medical conditions o Classified based on the characteristic of the misalignment (direction of the eye deviation) or the presumed etiology o Esotropia: inward or medial misalignment of one eye relative to the other; usually congenital (onset in the first 6 months of life) o Acquired esotropia –accommodative: associated with moderate or severe hyperopia (farsightedness); onset is between 2 - 4 y.o. o Acquired esotropia –nonaccommodative (rare)- must rule out brainstem tumors or Arnold-Chiari malformation; constant deviation with little or no farsightedness. No specific age. o Exotropia: outward or lateral deviation of one eye relative to the other. Onset usually 2 - 5 y.o. o Vertical strabismus (hyper/hypotropia): an incomitant deviation due to a paresis or restriction of one or more extraocular muscles. Most common cause is paresis of the 4th cranial nerve  Strabismus Classifications o Other classifications: o Frequency of occurrence- constant vs. intermittent o Eye involved-unilateral vs. bilateral and alternating (different eye is involved at different times) Strabismus o Risk Factors: o Family history, refractive error, Downs Syndrome, cerebral palsy, stroke/head injury o Signs and symptoms: deviation (misalignment) of eyes; decrease vision; frequent blinking/squinting; head tilting; diplopia; faulty depth perception o Esotropia: large and constant misalignment of eyes. Limitation of abduction of one or both eyes, nystagmus and vertical deviation o Acquired esotropia: accommodative: when the child tries to accommodate to overcome the hyperopia and the eyes converge. o Exotropia: intermittent, eyes point beyond object being viewed; HA, reading difficulty, and eye strain o Vertical strabismus: patients will often have hypertropia that may improve by tilting the head, usually to the side opposite of the palsied muscle  Strabismus o DDx: pseudostrabismus; amblyopia, retinoblastoma, trauma, cranial nerve palsy, brainstem tumor, Arnold-Chiari formation o Diagnostic Evaluation: o Comprehensive eye exam including visual acuity, refraction, and cover/uncover test o Examination of Cranial Nerves 3, 4 and 6 o Rule out any other underlying causes o Treatment/Management: o Eyeglasses or contacts; prism lenses (thicker on one side- helps eliminate eye turning) o Vision therapy o Surgery o Patient education: o Encourage compliance with corrective lenses o Encourage pediatric eye exams as indicated Glaucoma  Glaucoma o Definition: increased pressure within the globe → optic nerve damage o Pathophysiology/Etiology: o Primary Acute Angle-Closure Glaucoma: Ophthalmologic emergency o Closure of an already narrow anterior chamber angle = OUTFLOW Obstruction o Risk factors: farsighted individuals ; increased age o Secondary acute angle closure glaucoma: does not require a preexisting narrow angle, may occur in anterior uveitis, dislocation of the lens, or various drugs o Chronic Angle-closure glaucoma: flow of aqueous fluid into the anterior chamber angle is obstructed o Inuit's, Chinese, and eastern Asians – commonly affected o Risk factors: Increasing age, diabetes mellitus (DM), obesity, ocular trauma o Chronic Primary Open-angle glaucoma: MORE COMMON- elevated intraocular pressure due to reduced drainage of aqueous fluid through the trabecular meshwork o Afro-Caribbeans, Africans, and Hispanics/Latinx – commonly affected at an earlier age and results in more severe optic nerve damage Glaucoma o Signs and symptoms: o Acute angle-closure glaucoma: o Rapid onset of red, painful eye with tearing and profound visual loss with “halos around lights.” fixed, mid-dilated pupil, +/- diaphoresis, nausea, and abdominal pain o Cloudy cornea, fixed mid- dilated pupil; photophobia, firm globe on palpation o Intraocular pressure usually greater then 50mm Hg (normal limit is 10-20 mm Hg) o Open-angle glaucoma = Chronic glaucoma: o No symptoms in early stages. o Insidious progressive bilateral loss of peripheral vision resulting in tunnel vision; preserved visual acuities until ds. advances; o ocular HTN with pathologic cupping of the optic disks and elevated intraocular pressure Glaucoma o DDx: Conjunctivitis; Corneal disorders; Ophthalmicus; Iritis and Uveitis; Orbital Infections o Diagnostic Evaluation: o Open-Angle (chronic)Diagnosis requires 2/3 o Abnormal optic disk or retinal nerve fiber o Visual field impairment o Elevated IOP o Ophthalmologic examination o Tonometry (measure intraocular pressure) Glaucoma o Treatment/Management: o Angle-Closure Glaucoma: Ophthalmic emergency o REFER ASAP for reduction of intraocular pressure o Start IV Acetazolamide + topical Beta blocker (Timolol) - lower intraocular pressure o Osmotic diuretics → oral glycerin and intravenous urea or mannitol → if no response to Acetazolamide o once the intraocular pressure has started to fall, topical 4% pilocarpine, 1 drop every 15 minutes for 1 hour and then four times a day, is used to reverse the underlying angle closure o Definitive treatment requires peripheral iridotomy (other eye is treated prophylactically on an elective basis) o Patient Education: o Encourage annual eye examinations to check intraocular pressure  Glaucoma o Treatment/Management: o Open- Angle (Chronic) Glaucoma: o Medical treatment is directed toward lowering intraocular pressure = ↓ < 16 mm Hg o First-line therapy = Prostaglandin analog eye drops (Latanoprost 0.005% (Xalatan) or Bimatoprost 0.03% (Lumigan) QHS) o Topical beta-adrenergic blocking agents may be used alone or in combination with a prostaglandin analog o Topical Beta blockers (Timolol 0.25%)or carbonic anhydrase inhibitors( Brinzolamide 1% (Azopt) or Dorzolamide 2% (Trusopt)- when prostaglandin analogs and beta blockers are contraindicated o Laser trabeculoplasty (adjunct to topical meds); peripheral iridotomy o Refer to ophthalmology for chronic tx. and monitoring o Patient Education:  Scleritis o Definition: inflammation of the sclera o Pathophysiology/Etiology: Often associated with an autoimmune disorder (RA; vasculitis/connective tissue diseases) o Signs and symptoms: o unilateral or bilateral, focal or diffuse redness or violaceous discoloration; initial scleral thickening; late scleral thinning o pain is a hallmark symptom → severe, penetrating pain that radiates to the forehead, brow, jaw, or sinuses; awakenings during the night o DDx.: conjunctivitis, episcleritis, herpes zoster o Diagnostic evaluation: o Slit-lamp o CT or MRI to test for suspected autoimmune disorders o Treatment: Corticosteroids, NSAIDs, immunosuppressives, and biologics o Patient education: Advise regarding medication compliance and side effects  Refractive Errors o Definition: reduced vision clarity o Most common cause of decreased vision o Pathophysiology/Etiology : the shape of the eye; problem with accurately focusing light on the retina; curvature of the cornea or lens o Types of refractive errors: o Myopia (nearsighted) o Hyperopia (farsighted) o Astigmatism o Presbyopia o Signs and symptoms: blurry vision o Diagnostic evaluation: Eye exam - Visual acuity test o Treatment/management: o Contact lens, glasses, or surgery  Myopia (Nearsightedness) o Definition: able to see things close up (near) clearly but items farther away appear blurred o Etiology/Pathophysiology: Unknown o Longer eyeball; steeply-curved cornea o light rays converge together in front of the retina o Risk factors/groups: inherited, DM, visual stress/eyestrain, cataracts inherited; school-aged children o Signs and symptoms: blurred vision that improves when object becomes nearer (i.e. nearsighted); squinting the eyelids to better focus on distant objects; headaches; eyes that hurt or are tired o Differential diagnosis(DDX): astigmatism; trauma o Treatment/management: corrective lenses (glasses and contacts); laser corrective surgery (Lasik) o Patient education: Advise regular eye exams, eye protection; good  Hyperopia (Farsightedness) o Definition: ability to see distant objects more clearly than close objects o Pathophysiology/Etiology: the eye does not bend light properly o Shorter eyeball shorter or insufficiently curved cornea o Visual images focuses behind the retina o Risk groups/factors: inherited o Signs and symptoms: cant’s maintain clear focus on close (blurry); eyestrain; squinting; headache o DDX: presbyopia o Treatment: Glasses or contact lens; laser surgery o Patient education: o Advise regular eye exams and eye protection o Good lighting  Astigmatism o Definition: blurred or distorted vision at any distance o Etiology/Pathophysiology: irregularly shaped cornea or lens has mismatched curves; light rays don’t bend the same with mismatched curves (uneven focus) o Risk groups/factors: hereditary; eye injury, surgery, or disease; frequently occurs with other vision conditions o Signs and symptoms: o blurred distant and near vision, difficulty with night vision headaches, squinting o Diagnostic Evaluation: Comprehensive eye exam o Visual acuity and refraction o Keratometry/topography (measures corneal curvature) o Treatment/management: o Glasses, contact lens, or surgery o Patient education: Advise routine eye exams  Presbyopia o Definition: Gradual loss of the ability to focus on near objects o Etiology/Pathophysiology: shape of lens changes (hardening that occurs with age); lens becomes less flexible making it harder to change shape to focus on close images o Risk groups/factors: aging adult (early-mid 40’s), diabetes, CVD, multiple sclerosis, drugs o Signs and symptoms: o blurred near vision; eyestrain- holding reading material further away; headaches o DDX: Hyperopia o Treatment/management: o Glasses, contacts, surgery; lens implants o Monovision: (1 contact for near vision in 1 eye and a contact for distant vision if needed); 40+ y.o. o Patient education: Encourage regular eye exams and eye protection; Manage any disease; use good lighting, eat healthy  Learner’s Check A 12 –year-old girl presents complaining of increasing difficulty seeing the white board at school. She was sitting in the back of the class but had to move up front in order to take notes well. Her mother also notices that she sits closer to the TV than the rest of the family. What is the MOST likely refractive error? A. Hyperopia B. Myopia C. Emmetropia D. Presbyopia Traumatic Eye Disorders o Blowout fracture o Globe rupture o Hyphema o Foreign Body o Corneal o Intraocular Blowout Fracture Blowout Fracture o Definition: the most common orbital fracture and involves a disruption or break in thin orbital bones o Etiology/Pathogenesis: o Blunt trauma → fracture of orbital floor , trapping structures below o A direct blow to the globe or orbital rim  Blowout Fracture o Signs and symptoms: o Trauma to the eye (i.e.. a fist fight, object hitting eye) o Swelling and ecchymosis around eye o Restricted eye movement (can’t look up) o Vision loss o Diplopia that is worse with a downward gaze o Numbness of cheek and gum on the affected side o When a large section of the globe is fractured patient may have enophthalmos or a sunken globe o If the infraorbital nerve is contused or compressed anesthesia of the maxillary teeth and upper lip may be noted o Step-off deformity palpated over the intraorbital rim o Subcutaneous emphysema is pathognomonic for fracture into a sinus or nasal antrum  Blowout Fracture  DDx: Traumatic optic neuropathy; nasal fracture; ruptured globe  Diagnostic Evaluation:  X-ray:  “hanging teardrop” sign is seen with herniation of orbital fat into the maxillary sinus;  “open bomb-bay door” results from bone fragments that protrude into the sinus  CT scan with coronal sections to determine the surface area of the broken floor  Blowout Fracture o Treatment/Management: o Referral to ophthalmologist, plastic surgeon, oral maxillofacial surgeon, or ear/nose/throat specialist ASAP o Surgical repair may be necessary and will be determined by surgical consult o Nasal decongestants, ice packs/cold compress, and antibiotic during transport o Patient Education/maintenance/prevention: o Advise to stay calm o Avoid sneezing or anything that with ↑ pressure Globe Rupture  Globe Rupture o Definition: disruption of the outer membranes of the eye due to blunt or penetrating trauma o Damage to the posterior segment of the eye is associated with a very high frequency of permanent visual loss o Etiology/Pathogenesis: o Blunt object impacts the orbit, compressing the globe along the anterior- posterior axis causing elevation in IOP → scleral tears o Sharp objects or those traveling at high velocity may perforate the globe directly o Small foreign bodies may penetrate the eye and remain in the globe o Signs and symptoms: o Eye/eyelid pain and swelling with vision loss or blurred vision, diplopia, bleeding  Globe Rupture o DDx: Corneal laceration; retinal detachment; vitreous hemorrhage o Diagnostic Evaluation: o Based on history, maintain a high index of suspicion of an occult injury → diagnosis may not be that obvious o Careful and detailed ocular examination o CT of the obits and adjacent structures o X-ray rarely used o Treatment/Management: Ophthalmic Emergency = Requires definitive management by an ophthalmologist o Protect the eye from any pressure or inadvertent contact by covering the eye with a rigid shield while in transport o Impaled foreign bodies should be left undisturbed o Eye patches are contraindicated o Prophylactic antibiotic treatment to prevent infection o Patient Education/maintenance/prevention: Encourage close follow-up Hyphema  Hyphema o Definition: A collection of blood (microhyphema = suspended RBCs, to massive hemorrhage) in the anterior chamber of the eye → rise in intraocular pressure o Pathophysiology/Etiology: o Usually a result of blunt or penetrating trauma to the eye o May have other ocular injuries o Can occur spontaneously in patients with sickle cell disease o Common in athletes o Signs and symptoms: o “Bleeding” in the anterior portion of the eye (iris) = Injection o Eye pain with decreased/ blurry vision o Increased intraocular pressure o Sluggish pupil, iris tears  Hyphema o DDx.: Subconjunctival hemorrhage, conjunctivitis, ocular injury o Diagnostic Evaluation: o Eye exam with visual acuity o Tonometry (measure intraocular pressure) o Treatment/Management: o Goals: Accelerate absorption of the blood to prevent rebleeding and other complications o Immediate ophthalmology referral o Elevate patient’s head and administer atropine 1% , prednisolone acetate 1% o If globe is intact →measure intraocular pressure (IOP) o if IOP is elevated, give topical beta blocker and oral or IV acetazolamide o if no response → add mannitol IV o Carbonic anhydrase inhibitor (acetazolamide) should be avoided in patients with sickle cell disease  Hyphema o Patient Education: o Advise that rebleeding can occur 3 to 5 days later (30 percent of cases) o Encourage rest to prevent rebleeding o Advise close follow-up due to glaucoma risk Foreign Body  Foreign Body o Definition: Any material that becomes embedded in the eye o Etiology/Pathogenesis: o Small particles become embedded into the conjunctiva or cornea of eye o Windy weather may cause dirt, sand, dust to fly into eye; occupational hazard o Signs and symptoms: o Foreign body sensation; eye pain; tearing; photophobia; hyperemia o +/- injection/ erythema o Decreased visual acuity; visualization of a foreign body either in the conjunctiva or cornea; o Subsequent corneal abrasion after foreign body removal o Subsequent rust ring after removal of a metal foreign body  Foreign Body o DDx: Corneal abrasion; Conjunctivitis; Keratitis o Diagnostic Evaluation: o Detailed history is important o Always check visual acuity if foreign body suspected o Fluorescein stain o Plain films (X-ray) –if suspicion for metallic foreign body o Order CT if plain film is negative and high suspicion of embedded foreign body o Treatment: o REFER patients with suspected intraocular foreign body, laceration, or globe trauma to an ophthalmologist IMMEDIATELY o Remove foreign body under slit magnification using topical anesthesia (Tetracaine 0.4% 1 ggt) o Irrigate with saline and use a moist cotton-tipped applicator to remove conjunctival foreign bodies and some corneal foreign bodies o If unable to remove corneal foreign body with a cotton-tipped applicator, try using a 30 to 25 gauge needle o Assess antibiotic and tetanus vaccine needs o Patient Education: o Wear protective eye wear when working with metal  Neoplasms o Basal Cell Carcinoma o Squamous Cell Carcinoma o See section on Lid tumors)