Download Inner Eye Disorders. and more Exams Ophthalmology in PDF only on Docsity!
Inner Eye Disorders
Choroid - middle layer Retina - inner layer, senses light Vitreous Humor - gel inside the eye Optic Disc - head of optic nerve Physiologic Cup Center of optic disc 50% of disc diameter Macula - no vessels, keenest central vision Fovea - center of macula (cones) - Refractive errors - Myopia (near sighted) Hyperopia (far sighted)) Presbyopia Astigmatism What is being described? -Difficult seeing far away -Near-sighted -Light rays focus in front of the retina -Distance image is blurred -Eye is "too long" - Myopia What is being described? -Difficulty seeing close up -Far-sighted -Light rays focus behind the retina -Close image is blurred -Eye is "too short" -Cornea is flat - Hyperopia
Emmetropia - • Condition of the normal eye
- Vision perfect
- Parallel light rays fall on retina Presbyopia (old people vision) - -Lens becomes hardened w/ age (after 40 yrs.) -Less pliable/elasticity and decreased strength in ciliary muscle >> decrease in accommodation -Patient losses the ability to make lens rounder >> progressive decrease in near vision -Bifocals needed Astigmatism - -Error in focusing ability of eye -Light is not uniformly focused in all directions -Caused by unequal curvature of the front surface of the cornea (not spherical) Retinopathy - Macular Degeneration Retinal Detachment CRAO CRVO Retinoblastoma Optic Neuritis Papilledema Diabetic and Hypertensive Changes Permanent central vison loss due to atrophy of the outer retina. SX: -Dry: painless, gradual progressive bilateral VL -Drusen bodies -Wet: sudden vision loss due to leakage of serous fluid and blood from neovascularization -Both: Distortion of images with Amsler Grid - Macular degeneration Dry macular degeneration - painless, gradual progressive bilateral VL -Drusen bodies (lipid, protein and cellular debris deposits)
Etiology Central Retinal Artery Occlusion (CRAO) - -If >50 >> giant cell arteritis must be considered -Carotid/cardiac sources of emboli must be investigated >> duplex US, ECG, echo -RF: DM, HTN, HLD, oral contraceptive use, systemic vasculitis Treatment CRAO - -Lay patient flat >> ocular massage & high concentration O -IV acetazolamide, Anterior chamber paracentesis -GCA >> high dose steroids and temporal artery biopsy -Retinal embolization (a-fib) or anticoagulation Occlusion of the central retinal vein. Sx: Monocular visual loss often upon waking in the a.m. PE: Disc swelling, venous dilation, retinal hemorrhages "blood and thunder", cotton-wool spots - Central Retinal Vein Occlusion (CRVO) Treatment CRVO - -macular edema w/ laser treatment or intravitreal injection of VEGF -Initial visual loss severity is a good guide to outcome What is used to detect CRVO? - Fluroescein angriography Rare cancer that starts in the retina. PE : Abnormal red reflex, leukocoria, decreased visual activity Imaging; CT or MRI
- Usually developes early childhood - Retinoblastoma Retinoblastoma etiology - -Usually develops early in childhood, typically 12-18 months of age -Early detection is important or the disease can be fatal ~1/2 of children have a hereditary genetic defect; can be congenital mutation in chromosome 13 gene (13q14) Treatment retinoblastoma - -Priority: preserve the life of the child then preserve the vision -Enucleation of the eye
-External beam radiotherapy -Brachytherapy-radioactive implant -Thermotherapy -Laser photocoagulation -Systemic chemotherapy -Prognosis: 95-98% cure rates with early detection -Extraocular retinoblastoma: CA spreads to brain, spinal cord, bone marrow, and LN Inflammation of the optic nerve. Sx: -Unilateral vision loss and pain with EOMS -Vision ususally returns in 2-3 weeks -Loss of color vision, blurry, sudden PE: flame-shaped hemorrhage, Relative afferent pupillary defect (Marcus Gunn Pupil): swinging flashlight test - Optic Neuritis Optic neuritis Etiology - -Associated with: Multiple Sclerosis -Viral infections: Measles, Mumps, Varicella How is optic neuritis diagnosed - MRI: Enhancement of optic nerve Tx optic neuritis - -IV steroids -Should not receive PO steroids as it increases the recurrence rate. Optic disc swelling due to inc intracranial pressure Sx: Enlargement of blind spot, +/- loss of acuity - Papilledema Etiology papilledema - -Due to increased intracranial pressure -Pseudotumor cerebri -Tumors, inflammation, edema, encephalitis Intracranial HTN/Hypertensive emergency
-Microaneurysms -Retinal hemorrhages -Retinal edema -Hard exudates - Non-proiferative Diabetic retinopathy What is the telltale factor of Proliferative retinopathy? - Neovascularization Treatment Diabetic retinopathy - -pan retinal laser photocoagulation to prevent blindness -Injection of anti VEGF (vascular endothelial growth factor) Transient vision loss , Latin for fleeting blindess, not a disease but a sign of other disorder. SX: Painless, transient and complete unilateral or bilateral blindness lasting seconds to minutes with spontaneous recovery Described as "blind being pulled down" - Amaurosis Fugax Etiology Amaurosis Fugax - Blood clot or plaque blocks blood flow to retina (retinal ischemia following transient occlusion of central retinal artery) RF: Heart disease Dysrhythmias Alcohol/cocaine use Diabetes Family history of stroke High blood pressure High cholesterol Increasing age Smoking Related disorders to Amaurosis Fugax - Brain tumor Head injury History of MS and SLE
Migraine headaches Optic neuritis Polyarteritis nodosa Treatment amarosis fugax - -Treat the underlying cause -Give Aspirin Collection of blood between the conjunctiva and sclera Sx: does not affect vision, minimal sx, painless, stops at limbus - Subconjunctival Hemorrhage Etiology Subconjunctival Hemorrhage - -Transient increase in venous pressure (Valsalva, cough, vomiting) -Can be from trauma -Consider HTN, coagulopathy/meds Treatment Subconjunctival Hemorrhage - No treatment - spontaneous improvement modalities of globe injury - Closed -Anterior vs posterior segments Open Anterior segment - conjunctival abrasion, corneal abrasion*/foreign body, hyphema, lens dislocation, iris prolapse Posterior segment - vitreous hemorrhage, scleral laceration, retina detachment Open globe injury - Penetrating trauma (globe laceration) High velocity blunt trauma (globe rupture) Blood in anterior chamber causing cililary flush, pain, photophobia. - Hyphema
Occurs when the integrity of the outer membranes of the eye is disrupted by blunt or penetrating trauma.
- Full thickness injury of cornea and/or sclera - Globe rupture MC site of rupture - Under rectus muscle where eyewall is thinnest Red flags of globe rupture - -Deformity of the eye -full thickness laceration -prolapse of contents -afferent pupillary defect -teardrop pupil -decreased visual acuity -chemosis -low IOP Dx Globe rupture - -slit lamp, fundoscopy, fluorescein -Seidel Test -CT Orbits Tx Globe rupture - -eye shield -surgical repair in 12-24 hours -TDAP -vancomycin AND ceftazidime OR -ciprofloxacin Orbital wall trauma- medial wall and orbitoal floor causing muscle and fat to become trapped. Sx: Enophthalmos, ptosis, resisted EOMs Diplopia with upward gaze Dx : Teardrop sign on CT - Elevated head of bed, ice packs, consider antibiotics, nose blowing precautions, surgery ENT/Opthalmology/OMFS
Treatment Orbital Blow Out Fracture - -Elevated head of bed, ice packs, consider antibiotics, nose blowing precautions, surgery -ENT/Opthalmology/OMFS What must you avoid in orbital blow out fractures due to possibility of emphysema resulting in orbital compartment syndrome? - Blowing nose w/ mouth closed Valsalva maneuvers
