Info
🌱 來自: Huppert’s Notes
Vision loss🚧 施工中
Vision loss
• Physical exam: Perform a fundoscopic exam, pupillary exam, test visual acuity, extraocular motions, and peripheral vision. See anatomy of the eye in Figure 10.1.
FIGURE 10.1: Anatomy of the eye. The eye has three aspects: the anterior segment, the posterior segment, and the surrounding tissues. The anterior segment includes the conjunctiva, sclera, cornea, iris, ciliary body, and crystalline lens. The posterior segment includes the vitreous humor, retina, choroid, and optic nerve. The eyelids, extraocular muscles, and lacrimal drainage system are other important structures relevant to eye anatomy.
• Differential diagnosis:
- Age-related macular degeneration (ARMD)
• Symptoms: Loss of central vision and visual acuity
• Etiologies:
- Nonexudative “dry” (more common)
• Pathophysiology: Poorly understood; potentially primary senescence of the retinal epithelium
• Symptoms: Gradual loss of unilateral or bilateral vision; often causes difficulty reading or driving
• Physical exam: Slit-lamp exam with yellow/white deposits (called “drusen”) that form under the retinal pigment epithelium
• Treatment: Smoking cessation, supplementation with zinc/antioxidant vitamins
- Exudative “wet”
• Pathophysiology: Choroidal neovascularization, likely due to isoforms of vascular endothelial growth factor (VEGF)
• Symptoms: Sudden vision loss due to neovascularization which can be rapidly progressive; one of the earliest signs is when straight lines appear wavy (metamorphopsia)
• Physical exam: Slit-lamp exam with subretinal leakage of serous fluid/blood
• Treatment: Anti-VEGF intraocular injections (e.g., ranibizumab), supplementation with zinc/antioxidant vitamins
- Glaucoma
• Symptoms: Loss of peripheral vision, tunnel vision with central sparing; both open-angle and closed-angle (“angle-closure”) glaucoma may be primary or secondary (e.g., due to elevated intraocular pressure [IOP] from uveitis, trauma, glucocorticoid therapy, etc.)
• Subtypes:
- Open-angle glaucoma (more common)
• Description: Progressive neuropathy of the optic nerve, due to poorly understood causes, but typically associated with elevated IOP
• Symptoms: Painless, progressive peripheral vision loss; often initially undetected by patient
• Physical exam: Fundus exam with evidence of nerve damage (“cupping” = enlargement optic disc)
• Diagnosis: 1) Evidence of optic disc abnormalities, 2) Adult onset, 3) Open anterior chamber angles, 4) Absence of another known cause for glaucoma (i.e., would result in diagnosis of secondary glaucoma); tonometry with increased IOP can be suggestive but is not always present
• Treatment:
- Medical: 1) Increase aqueous outflow (prostaglandin analogues, alpha-agonists), 2) Decrease aqueous production (topical beta-blocker: timolol, alpha-agonist, carbonic anhydrase inhibitor)
- Interventional: Laser therapy, surgery (trabeculectomy)
- Closed-angle glaucoma
• Description: Narrowing or closure of the anterior chamber angle, which normally allows drainage of aqueous humor; thus causing an elevation in IOP and damage to the optic nerve
• Symptoms: Painful red eye, sudden blurred vision with “halos,” associated nausea/vomiting; can be precipitated by dilation with atropine (if a shallow anterior chamber was not recognized)
• Physical exam: Mid-dilated, minimally reactive pupil; conjunctival redness; corneal edema/cloudiness; shallow anterior chamber
• Approach: Patients with symptoms and signs of acute closed-angle glaucoma require emergent evaluation by an ophthalmologist, including evaluation of acuity, IOP, slit-lamp examination, and gonioscopy
• Diagnosis: Gonioscopy to measure the anterior chamber angle is the gold-standard; requires slit lamp with special lens to visualize the angle
• Treatment: Requires emergent surgical intervention
- Prior to surgery, attempt to decrease IOP with eye drops (0.5% timolol, 1% apraclonidine, 2% pilocarpine); IV acetazolamide or IV mannitol may be used with specialist assistance
- Avoid atropine
- Cataracts
• Pathophysiology: The lens of the eye is transparent due to highly organized cytoplasmic proteins called crystallins but cannot shed nonviable cells, which occur with age or due to secondary causes (inflammation, trauma) and become cataracts
• Symptoms: Slowly progressing loss of visual acuity, blurry vision with glare (e.g., difficulty with night driving due to oncoming headlights). Patients become progressively more near-sighted and may no longer require reading glasses (“myopic shift” or “second sight”)
• Physical exam: Clouding of lens
• Treatment: Surgery (if cataract interferes with patient functioning)
- Central retinal vein occlusion (CRVO)
• Pathophysiology: Thrombus in the central retinal vein results in venous obstruction, causing retinal capillary nonperfusion and ischemia
• Symptoms: Subacute painless unilateral vision loss of variable time course (hours to weeks); sometimes preceded by positive visual phenomenon (e.g., scintillations)
• Physical exam: Optic disc swelling, may also have venous dilation/tortuosity with intraretinal hemorrhage (“blood and thunder” fundus)
• Treatment: Anti-VEGF intraocular injections, laser surgery
- Central retinal artery occlusion (CRAO)
• Pathophysiology: Occlusion of the central retinal artery (considered a form of stroke), typically due to carotid artery atherosclerosis or cardiogenic embolism, and rarely due to other vascular, hematologic, or inflammatory causes
• Symptoms: Sudden, painless, unilateral vision loss
• Physical exam: Pallor of the optic disc, cherry red fovea, boxcar segmentation
• Treatment: Requires emergent ophthalmology referral for consideration of advanced therapy such as revascularization. Temporizing measures: Instruct the patient to breathe into a paper bag and hold their eye, ocular massage, high-flow O2, medical therapy for reduction of IOP
- Retinal detachment
• Pathophysiology: Separation of the retina from the underlying retinal pigment epithelium and choroid; vision loss occurs if separation progresses to include the central retina
• Symptoms: Painless, unilateral vision loss often associated with floaters, black spots, or flashes; symptoms progress at variable pace
• Physical exam: Elevated retina with folds or tear, abnormal red reflex
• Treatment: Requires emergent ophthalmology referral and surgical spot welding; if vision is still intact, it is even more emergent to try to save the patient’s vision
- Transient monocular visual loss (aka Amaurosis Fugax)
• Etiologies: Carotid pathology, cardioembolic, giant cell arteritis, vasospasm, retinal migraine
• Symptoms: Sudden transient unilateral vision loss; vision returns when reperfused
• Physical exam: May have normal exam
• Diagnosis: Carotid ultrasound, lipids, consider TIA/stroke work-up or evaluation for GCA based on patient risk factors
• Treatment: Attempt to identify etiology and reduce risk factors
- Arteritic anterior ischemic optic neuropathy (AAION)
• Pathophysiology: Typically, occlusion of the posterior ciliary artery (branch of the ophthalmic artery from the internal carotid, which supplies the optic nerve). Can be associated with giant cell arteritis.
• Symptoms: Sudden vision loss, jaw claudication, scalp tenderness
• Physical exam: Pallor and edema of the optic disc
• Diagnosis: Temporal artery biopsy, elevated ESR/CRP
• Treatment: High-dose steroids as soon as possible (don’t wait for biopsy!)