Eye III & IV - Joseph D Klauer OD - PDF

EYE III & IV Joseph D Klauer OD  Objectives 1. Review the basic management of myopia, hyperopia, astigmatism, presbyopia, strabismus, and amblyopia. 2. Describe the diagnosis and management of orbital cellulitis. 3. Discuss the diagnosis and basic management of globe a...

EYE III & IV Joseph D Klauer OD  Objectives 1. Review the basic management of myopia, hyperopia, astigmatism, presbyopia, strabismus, and amblyopia. 2. Describe the diagnosis and management of orbital cellulitis. 3. Discuss the diagnosis and basic management of globe and orbital trauma including corneal abrasion, foreign body, hyphema, blowout fracture, & globe rupture.  How we see: Its complicated... Refractive Structures: Cornea Lens  Refractive errors and presbyopia are common, correctable causes of impaired vision worldwide. The Standard Eye creates clear images by bending light to focus on the retina. Refractive errors occur when components of the eye’s optical system fails to focus the optical image. Presbyopia (loss of near vision) occurs when the lens loses its normal accommodating power and can no longer focus on objects viewed at arm’s length or closer. Myopia (Nearsightedness) Myopia (near-sighted): long axial length, focal point of eye too close up. The patient can see near well, but has issues at distance. Over 40% of children aged 5-19 years are nearsighted—a prevalence that has approximately doubled in the past 25 years Prevalence decreases with age Image is focused in front of the retina Treatment: Corrective lenses (CONCAVE) LASIK- makes eyeball shorter Eyeball is too strong so negative prescription is given  Hyperopia (farsightedness) Hypermetropia (far-sighted): short axial length, focal point of eye too far back. The patient can see far away but has increased issues up close. Most common culprit in Refractive Amblyopia Treated with spectacle lenses (CONVEX), contact lenses. Plus powered scripts- CL is thickest in the middle and thin on the edges Not an ideal LASIK candidate.  Astigmatism: Aspherical Astigmatism shape of corneal surface causing visual blur. Especially noticeable at night, when it rains, and when working on screens. Treatment: Corrective lenses, glasses or contacts. Corneal Ectasia: Keratoconus (extreme astigmatism, associated findings)  Presbyopia (Loss of Near Vision) Non-refractive error issue Lens loses its normal accommodating power and can no longer focus on objects viewed at arm's length or closer Lens loses elasticity from continued growth Usually begins around age 40, maximum deficit by age 65 Treatment: Corrective lenses; Bifocals, Reading glasses, contact lenses.  Refractive/Binocular Vision Status Nystagmus: involuntary back and forth movement of one or both eyes that disrupt fixation. Occur secondary to pathology of the afferent visual pathway, disruption of ocular control, or abnormalities of eye muscles responsible for movement. Pursuits (smooth, slow) Saccades (jerk, fast) Strabismus: occurs when there is binocular misalignment of the visual axis of the eyes, resulting in diplopia, confusion, and suppression of the retinal image of the deviated eye. Unilateral and constant suppression can lead to amblyopia.  Strabismus “Cross-Eyed” Strabismus can be horizontal, vertical, torsional, or a combination of these. The eye misalignment can be congenital or acquired, latent (sometimes) or manifest (always), constant or intermittent, and fixed or variable, depending upon the position of gaze and other factors. Strabismus  Strabismus Cover/uncover test for diagnosis https://www.aao.org/pediatric-center- detail/strabismus-simulator Treatment: refractive correction, vision therapy, surgery. Depends on degree of strabismus  Amblyopia Defined as reduction in vision (20/30 or worse) in one eye or a difference of 2 or more lines in visual acuity between the two eyes that is not correctable with refraction (glasses). Amblyopia is not explained by structural abnormalities or pathology. Amblyopia occurs at the level of the visual cortex Develops from dissimilar retinal images during the critical period (birth to 7-9 years old). First 2-3 years of life most critical.  Amblyopia Form Deprivation Amblyopia (cataract, ptosis) Refractive Amblyopia (Rx) Anisometric (difference between two eyes) Isometric (high powers in both eyes) Meridional (astigmatism) Treatment: Correct Refractive error Remove obstacle from line of sight Patching, eye drop therapy THE EYE: Presenting Encounter What were they doing? Do they wear contacts? Is the eye red? Can they see? Does it hurt ? (1-10)  THE RED EYE Red Eye Differentials List Conjunctivitis Keratitis Episcleritis Scleritis Hypopyon Subconjunctival hemorrhage Corneal Abrasion Foreign body Hyphema  Conjunctiva Subconjunctival hemorrhage Ruptured episcleral blood vessel Benign, “bruise;” will resolve on its own Associated with ASA/blood thinner, strain, valsalva Look for posterior margins, especially following ocular surgery  Corneal Abrasion Common eye injury usually from foreign body, improper contact lens use Clinical Presentation Severe eye pain and tearing Red eye Foreign body sensation * Clinical evaluation Rule out vision threatening trauma Measure visual acuity Penlight exam (rAPD?) Fluorescein examination Lid eversion exam  Corneal Abrasion Fluorescein stain Tetracaine drops to anesthetize Touch eye with strip Cobalt blue filter Treatment Topical antibiotics Consider pain medications for large abrasions Foreign body removal if present Most heal within 24 hours NO topical steroids (initially!) Follow up daily until healed if: Abrasion is from contact lens Abrasions causing decreased vision Abrasions in young children Focal epithelial defect, likely corneal abrasion  Corneal Foreign Body Patient complains of “something in my eye” Foreign bodies are usually on the cornea or under the upper lid Apply anesthetic and examine with slit lamp if foreign body is not visible Fluorescein stain always to assess for abrasion Remove with sterile wet cotton tip or hypodermic needle Metallic foreign bodies leave rust stain that must be removed as well Prophylactic abx- high risk for infection first 24 hours Upper lid foreign bodies- use eyelid retractor and wet cotton tip  Cornea Foreign Body Most often metallic Can be removed with needle, may need to have rust removed with alger brush Determine depth Rule out penetrating injury Cover with antibiotics Normal tear film Scattered epithelial defects  Superficial Punctate Keratits Orbital Cellulitis Infection involving the contents of the orbit (fat and ocular muscles) IMPORTANT: distinguish from PRESEPTAL (aka preorbital) cellulitis Anterior eyelid infection Neither involves the globe itself Preseptal= infection of soft tissue anterior to orbital septum Orbital= infection of soft tissue posterior to orbital septum Orbital Cellulitis One of the leading causes of exophthalmos in children Ask about fever, sinus or dental infections, or trauma Through ethmoid sinusitis (lamina papyracea extremely thin) Orbital infection (dacryoadenitis, dacryocystitis) Staph A in adults most common, H Influenza in children most common Clinical Manifestations Ocular pain, eyelid swelling and erythema (BOTH preseptal and orbital) Pain with eye movement, proptosis (JUST orbital)  Orbital cellulitis Diagnosis Clinical Confirmed on CT orbit and sinus Treatment IV: broad-spectrum regimen aimed at S. aureus [MRSA], S. pneumoniae, other streptococci, gram-negative bacilli Why? Difficult to culture Vancomycin + Ceftriaxone or Ampicillin/Sulbactam Switch to oral? Afebrile/swelling improving Bactrim + Amoxicillin Orbital cellulitis Complications: orbital abscess, vision loss, cavernous sinus thrombosis, meningitis, and/or brain abscess These complications may develop rapidly; therefore, close monitoring is indicated, with daily checks of visual acuity and assessment of the pupillary light reflex. Diabetics and immunocompromised pts can develop mucormycosis; a life threatening fungal infection. Note necrotic tissue (black) in mouth and nose.  Orbital Trauma Eye injury includes trauma to the eye (ocular trauma) and/or the orbit (periocular trauma) Vision threatening injuries Caustic eye exposures, Orbital compartment syndrome (OCS), Hyphema, Retinal trauma Open globe injuries Foreign bodies Globe rupture Common injuries Eyelid lacerations (always refer/consult if margin is lacerated) Corneal abrasions and foreign bodies Orbital fractures Blowout fracture  Orbital Trauma Injuries should NOT be Exam manipulated. Visual Acuity Afferent exam APD (afferent pupillary defect) Afferent vs. Efferent Afferent transmits impulses from peripheral organs to CNS. Efferent (motor division) transmits from the CNS out to periphery to cause an action.  Orbital Trauma Chemical Burns Alkaline (cleaners, bleach) > Acid (toilet cleaner, rust remover) because they raise tissue pH, causing a breakdown in fatty acids for faster penetration. (Alkaline 2x as common!) Presentation: decreased vision, moderate to severe eye pain, blepharospasm (inability to open the eyelids), conjunctival redness, and photophobia. Steps: 1) Check pH, 2) IRRIGATE! 3) Refer. (Consider calling poison control) Orbital compartment syndrome (OCS) Orbit=confined space. Trauma and intraorbital hemorrhage can cause rapidly elevated intraorbital pressure. Symptoms= vision, diplopia, eye pain, and/or periorbital swelling Exam= Decreased visual acuity, afferent pupillary defect, proptosis, subconjunctival hemorrhage Tx: True ophthalmologic emergency! Requires lateral canthotomy. Refer and quickly!  Orbital trauma Alkal OCS i Burn  Orbital Trauma Hyphema Typically caused by blunt trauma. Associated injuries: head trauma, orbital fracture Blood in the anterior chamber, can result in permanent vision loss Bleeding results from tears in the vessels of the ciliary body or iris. Risk factor for poor outcome: bleeding disorders and complete vision loss on initial evaluation Emergency ophtho referral (consult) for B-SCAN if hyphema blocks view of posterior pole. Need to sleep elevated at 30-45 degree angle. Idiopathic Hyphema: ask aspirin, use of blood thinners. Order CBC, PT/PTT, & sickle cell screen to r/o sickle cell and/or clotting dz. Retinal trauma Result in loss of vision that may be partial, confined to a visual field, or complete Retinal detachment May cause light flashes, floaters, visual disruption (shadow or "like a curtain being pulled down"), visual field defect, and loss of peripheral and/or central vision Must be urgently repaired= urgent referral  Orbital Trauma Hyphem a  Orbital Trauma- Vision Threatening Open globe injuries Open globe rupture occurs following blunt eye injury Open globe laceration refers to a penetrating injury to the eye by an object Avoid any examination procedure that might apply pressure to the eyeball, such as eyelid retraction or intraocular pressure measurement by tonometry. Avoid placing any medication Identify and call ophthalmology STAT  Orbital Trauma- Vision Threatening Open globe injuries Clinical findings Markedly decreased visual acuity Relative afferent pupillary defect (rAPD) Eccentric or teardrop pupil Increased or decreased anterior chamber depth Extrusion of vitreous External prolapse of the uvea (iris, ciliary body, or choroid) or other internal ocular structures Tenting of the cornea or sclera at the site of globe puncture Low intraocular pressure (checked by an ophthalmologist only) + SEIDEL SIGN/TEST Orbital Trauma- Vision Threatening Open globe injuries 1. Stabilize the patient (usually significant trauma) 2. Identify 3. Call ophthalmology 4. Prophylactic parenteral antibiotic treatment 5. Tetanus prophylaxis  Orbital Fracture Occur more commonly in young adult males Assault or MVA most common reason in adults Usually associated with other injuries- ALWAYS rule out globe injury and intracranial injury in your evaluation How? Maxillary (posterior medial floor) most common bone Orbital floor fracture AKA “blowout fracture”  Orbital fracture Orbital floor fracture Most commonly from a ball striking the eye Direct blow to infraorbital rim Important to rule out inferior rectus muscle entrapment (most common complication) EOMs! Diagnosed on maxillofacial/orbital CT Ophthalmology follow up within 24 hours unless globe rupture (emergency consult) Orbital Fracture Exam findings Focal pain, swelling, or step-off on palpation of the bony prominences of the malar eminence, zygomatic arch, or orbital rim Crepitus suggesting fracture into a sinus Numbness of the forehead (supraorbital nerve damage with superior orbital roof or rim fracture) Numbness below the eye (infraorbital nerve damage with orbital floor fracture) Findings of secondary eye injury such as decreased visual acuity, diplopia or pain on eye motion, proptosis, orbital dystopia, or endophthalmos Eye IV Joseph Klauer OD  Objectives 1) Identify the epidemiology, signs and symptoms, diagnostic criteria and treatment options of ocular disease causing visual disturbances and/or redness 2) Describe the pathogenesis and appearance of diabetic retinopathy 3) Describe the pathogenesis and appearance thyroid-related ophthalmopathy 4) Describe the pathogenesis and appearance optic neuritis 5) Describe the pathogenesis and appearance papilledema  Diabetic Retinopathy One of the largest causes of vision loss worldwide Present in about 20% of type 2 diabetics Caused by tissue-damaging effects of chronic hyperglycemia Hyperglycemia leads to 2 main changes Abnormal permeability Occlusion with ischemia and subsequent neovascularization Two categories 1) Nonproliferative: diabetic retinopathy is present, but is reversible if diabetes gets under control 2) Proliferative: There will be vision loss  Diabetic Retinopathy Nonproliferative= microvascular changes are limited to the retina Mild (no vision loss), Moderate, severe Features: Cotton wool spots (nerve infarct) Intraretinal hemorrhage Hard exudates Microvascular abnormalities (microaneurysms, occluded vessels, dilated/tortuous vessels) Vision loss in NPDR primarily through macular edema Progresses to Proliferative with continued poor glycemia control. Proliferative New blood vessel growth on the surface of the retina, optic nerve, or iris Causes more severe vision loss, less common Complications of this growth includes hemorrhage, fibrosis, and retinal detachment Can arise without NPDR  Diabetic Retinopathy Presentation of diabetic retinopathy Most patients asymptomatic until it’s too late Can progress rapidly Important to screen yearly Macular edema cannot be corrected with refraction typically presents with the gradual onset of blurring of near and distant vision  Diabetic Retinopathy Prevention is key Good glycemic control Even a small decrease in A1C can be beneficial 1% decrease reduces incidence and progression of diabetic retinopathy by 35 and 15-25%, respectively Good blood pressure control Reduces vitreous hemorrhage Lipid-lowering therapy Possible reduction in macular edema- more studies need to be done  Thyroid-related Ophthalmopathy Female Predilection (8:1) most common in 4 th to 5th decade of life. Autoimmune Disorder: Thyroid eye disease is syndrome of clinical and orbital abnormalities caused by deposition of polysaccharides and infiltration with chronic inflammatory cells Thyroid stimulating (TSH) receptor antibodies are directed against EOMs and orbital tissue causing inflammation. Increased volume of orbital contents (muscles and connective tissue) resulting in optic nerve compression. Thyroid Eye Dz is most common cause of unilateral OR bilateral proptosis in middle-aged patients 20-25% of patients with Graves’ have clinically obvious orbitopathy Risk factors Smoking (strongest; 2-9x greater risk) Radioiodine therapy (treatment for Graves)  Graves Ophthalopathy Clinical Features Signs Proptosis (exophthalmos), lid retraction and lid lag Low TSH high T4 [run T3/T4/TSH labs] Diagnosis: Forced ductions to detect EOM restriction; CT/MRI to detect enlargement of EOMs (tendons will be spared), Exophthalmometry to measure proptosis, visual fields Treatment Systemic steroid Radiotherapy Surgery NO SPECS N: No signs/symptoms O: Only signs, no symptoms, (upper eyelid retraction) S: Soft tissue involvement (lid edema, conj chemosis) P: Proptosis E: EOM Involvement (”IM SLO”) [recti first] C: Corneal involvement (punctate keratitis, ulceration) S: Sight loss due to optic nerve compression. Disc edema, APD, reduced color vision, visual field loss [5%] IM SLO Inferior rectus Medial rectus Superior rectus Lateral rectus Obliques  Optic Neuritis Most common in young patients (20-45yo); females more than males (2:1) Caused by primary inflammation of the optic nerve; commonly associated with demyelinating disease Multiple sclerosis primarily. (15 year risk of dev. MS after ON is 50%) Presenting feature in 15-20% of patients Optic nerve inflammatory demyelination (white matter lesions on MRI; (to assess risk of developing MS) Clinical features Symptoms Monocular vision loss (acute) Pain on eye movement Signs Afferent pupillary defect Loss of color vision Flickering or flashes with EOM Swelling (papillitis)/paling of disc Treatment Steroids (mainstay of MS flares)