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Disease Cause Symptoms Diagnosis Treatment Picture Dacryocystitis Infection of the lacrimal sac due to obstruction of the nasolacrimal duct Infection in infants: Streptococcus pneumonia, Staphylococcus sp., H. influenza, and Enterobacteriaceae sp.
Infection in adults: S. aureus, S. epidermidis, Pseudomonas aeruginosa, anaerobic organisms
- Often unilateral
- Tearing and discharge Redness, swelling, pain in the area of the lacrimal sac
- Warm, moist compresses PO Abx (mild: Clindamycin, severe: Vancomycin plus Ceftriaxone)
Chronic or Severe Cases: Correction of obstruction- Dacryocystorhinostomy
Preseptal Cellulitis Infection of the soft tissues anterior to the orbital septum Trauma, insect/animal bite, or foreign body of surrounding tissues of the face and eyelids
- Sinusitis S. aureus, S. pneumonia, beta-hemolytic streptococci
More common in children than adults
- Unilateral ocular pain
- Eyelid swelling/erythema ** Will NOT cause pain w/ EOMs, proptosis, or ophthalmoplegia w/ diplopia Trimethoprim-sulfamethoxazole OR Clindamycin PLUS Amoxicillin or Amoxicillin-clavulanic acid or Cefpodoxime or Cefdinir x 5- days Pinguecula Develop when eye is irritated (dry, windy, sunny conditions; trauma)
- Common in persons > Small, yellow, raised conjunctival nodule at the temporal or nasal (more common) limbus No treatment; can resect Pterygium Usually associated with prolonged exposure to wind, sun, sand, and dust Conjunctival fleshy, triangular growth that crosses the limbus and encroaches on the corneal surface; usually on nasal side If threatens vision can be excised but recurrence is common Cataracts Cloudy or opaque area in the lens and leads to partial or total blindness Risk factors: 90% Age related (senile cataracts) most common (>60 y/o )
Congenital (rubella, CMV intrauterine infection)
- Smoking/ETOHuse
- Sunlight/UV exposure
- Trauma related Systemic disease (ex. DM)
Certain meds (ex. statins, steroids)
Patho: Lens is composed of specialized stratified epithelia that have a high content of cystoplasmic protein (crystallins) > Lens doesn’t shed nonviable cells > susceptible to degenerative effects of cell structure aging
- Painless
- Progressive blurred vision
- Decrease in visual acuity
- Glare from lights
- Decreased night vision
- Decreased color perception
- Usually bilateral Impaired red reflex (lens opacity, darkening of red reflex, obscured ocular fundus) Non-urgent referral for a comprehensive ophthalmic exam
Removal of the entire lens and replacement with an intraocular artificial lens
Surgery typically saved until vision can no longer be corrected (functional visual impairment)
Chronic Open Angle Glaucoma Most common type and after cataracts the second leading cause of blindness
Risk factors: Increases with age (>40); more prevalent in African Americans; FHx
Patho: IOP is elevated d/t either increased aqueous production and/or reduced drainage of aqueous fluid through the trabecular meshwork > eventually damages optic nerve
- Usually bilateral
- Painless No symptoms at first and often found on routine eye exam
Gradual progressive cupping and corresponding pallor of the optic disk
Progressive peripheral visual field loss (tunnel vision) followed by central field loss and blindness
Tonometry is best screening test followed by visual field testing
Evidence of optic nerve damage (thinning, cupping), visual field abnormalities in absence of other causes, open/normal anterior chamber angles
Prostaglandin analog gtts (ex. Iatanoprost) 1st line Increases aqueous outflow
Beta adrenergic blocking agents (ex. timolol) Decreases aqueous production
Laser trabeculoplasty
- If medical therapy fails Increases aqueous outflow by improving drainage of through the trabecular meshwork
Surgery (last line) Creates a filtration bleb as an alternative route to drain aqueous humor
Chronic Angle Closure Risk factors: Asian, FHx, >60y/o, Female,
- Typically symptom free
- Slow progression of peripheral Screening should target Inuits and Asians as it is more common in these
- Laser peripheral iridotomy 1st step
Other Eye Diseases
Wednesday, April 5, 2023 8:06 AM latanoprost
damage
Closure Glaucoma FHx, >60y/o, Female, farsightedness Patho: Flow of aqueous fluid into the anterior chamber angle is partially obstructed Anterior: Abnormal tissue bridges the anterior chamber angle and undergoes contraction, pulling the peripheral iris into the angle
Posterior: Pressure behind the iris, lens, or vitreous causes the peripheral iris to be pushed into the anterior chamber angle
Slow progression of peripheral vision loss followed by central vision loss
- Asians as it is more common in these populations
- Tonometry and full eye exam step
- Surgical peripheral iridectomy ***Untreated chronic glaucoma that begins at 40-45 y/o will probably cause complete blindness by 60-65 y/o. Refer all patients with suspected glaucoma Dry Macular Degeneration Degenerative disease of the macula that results primarily in loss of central vision
- Most common Begins with accumulation of extracellular deposits called “drusen” - appear as small discrete yellow lesions clustered in the macula
Focal or widespread atrophy and detachment of the retinal pigment epithelium (RPE)
Thinning and loss of tissue in and around the macula
Cell atrophy occurs causing visual loss by affecting photoreceptor function
Gradual, bilateral, central vision loss
- Metamorphopsia First noticed as difficulty reading or driving, scotomas, or reliance on brighter light or a magnifying lens
Vitamin Supplement (ex. Ocuvite, PreserVision, AREDS2) Vitamin C, Vitamin E, Zinc, Lutein, Zeaxanthin, Copper
Followed by ophthalmology Monitored by Amsler grid, Snellen chart, Optical coherence tomography, and/or fundoscopic exam
Wet Macular Degeneration
- More rapid and severe Patho: Strong correlation with genetic polymorphisms predisposing to disease; Involves proliferation of abnormal choroidal vessels under the retinal pigment epithelium which leak and bleed causing retinal detachment
- Rapid progression (days-weeks) Acute visual distortion or loss of central vision
Distortion of straight lines (metamorphopsia)
Dark patch in central vision (scotoma)
Intravitreal injection of a vascular endothelial growth factor inhibitor (VEGF)
Bevacizumab, ranibizumab, aflibercept: 1st line
Laser photocoagulation- reserved for those who can’t be treated with VEGF
Vitamin supplementation with zinc and antioxidant vitamins
Hypertensive Retinopathy HTN affects retinal and choroidal circulation causing vascular damage
Acute BP elevation typically causes reversible vasoconstriction in retinal blood vessels, and hypertensive crisis may cause optic disc edema
Prolonged or severe hypertension leads to exudative vascular changes, a consequence of endothelial damage and necrosis.
HTN accelerates the development of atherosclerosis
DBP 90-110: Retinal arteries become more tortuous and narrower and develop abnormal light reflexes (silver wiring- vascular wall hyperplasia/thickening and copper wiring-arteriosclerosis)
There is increased venous compression at the AV crossing (AV nicking) d/t arteriolar wall enlargement from arteriosclerosis, predisposing to vein occlusions.
Flame shaped hemorrhages from increased intravascular pressure
Cotton-wool spots: small, white, superficial foci of retinal ischemia
Yellow hard exudates: intraretinal lipid deposits from leaking vessels
DBP 130- 140 : Optic disc edema (papilledema)
Mild: Retinal arteriolar narrowing d/t vasospasm (copper wiring, silver wiring), arteriolar wall thickening, and AV nicking
Moderate: Hemorrhages (flame or dot), cotton wool spots, hard exudates, and microaneurysms
Severe: Some or all of the above, plus optic disc edema (papilledema)
Diabetic Retinopathy Leading cause of blindness in the US in 20-74 y/o
- Takes years to develop Increases in prevalence and severity with increasing duration and poorer control of DM
Not detected for at least 3 years after diagnosis of DM 1
Present in about 20% of patients at diagnosis of DM 2
Patho: Chronic hyperglycemia
Increases retinal blood flow: increased stress on vessels > stimulates vasoactive substance production, vascular leakage, increased fluid accumulation resulting in edema
Accumulation of sorbitol within retinal cells > leads to oxidative stress,
Nonproliferative Nerve fiber layer infarcts (cotton wool spots)
Intraretinal hemorrhages (blot/dot, flame)
- Microaneurysms
- Venous bleeding
- Retinal edema
- Hard exudates Can progress to proliferative- Leak fluid into retina, vessels swell and distort decreasing blood flow, deprives retina of blood supply which can lead to growth of new blood vessels
Proliferative Neovascularization- arising from either the optic disc or the retinal vessels
Sequela- preretinal and vitreous hemorrhage, fibrosis, and retinal detachment
Annual dilated fundus exams in all DM patients & all newly diagnosed DM 2 patients should be screened
- DM, BP, Hyperlipidemia control
- Nonproliferative: Intravitreal anti-vascular endothelial growth factor (Anti- VEGF)
Focal photocoagulation to treat macular edema
- Proliferative
- VEGF inhibitors (Bevacizumab)
- Panretinal photocoagulation Vitrectomy: vitreous hemorrhage or retinal detachment and vision loss
Nonproliferative Proliferative
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