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USMLE Step 2 (Fach) / Ophthalmology (Lektion)

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• Age-related macular degeneration Degenerative disease of the retina. Epidemiology:- Leading cause of blindness in individuals > 65 years in developed countries.- Sex: ♀ > ♂ Risk factors:- Advanced age- Family history - Cardiovascular disease- Smoking- Obesity Pathophysiology:- Dry AMD (∼ 90%): deposition of yellow-whitish material (i.e., consists of lipids, vitronectin, proteins) in and under the retinal pigment epithelium (drusen) → slow progressive atrophy of the local retinal pigment epithelium- Wet AMD (∼ 10%): choroidal neovascularization → leaking of intravascular serous fluid and blood → sudden localized elevation of the macula and/or detachment of the retinal pigment epithelium Clinical features:- Painless central or pericentral visual impairment → reduced visual acuity, difficulty adapting to changes in lighting- Dry AMD: slow progressive visual impairment (usually over decades) - Wet AMD: acute or insidious onset (over weeks to months) and usually manifests in one eye first- Metamorphopsia- Scotoma (blind spot) Diagnostics: - Amsler grid: detection of metamorphopsias and scotomas- Fundoscopy→ Dry AMD: Drusen, retinal pigment epithelium atrophy/hypertrophy→ Wet AMD: Grayish-green retinal discoloration; serous detachment of the retina; subretinal and intraretinal hemorrhage and/or exudate- If wet AMD is suspected:→ Fluorescence angiography (intravenous injection of fluorescein dye, followed by serial photographs of the retina to visualize vessels)→ Color fundus photography: enables evaluation of disease progression and interpretation of fluorescein angiography→ Optical coherence tomography (OCT)  Treatment:- Patient education, visual and reading aids, cessation of smoking, improve diet - Antioxidants therapy: vitamins A, C, and E, beta-carotene, zinc- Treatment of wet AMD→ First-line: injection of VEGF inhibitors (ranibizumab, bevacizumab, pegaptanib) into the vitreous body→ Second-line: Laser coagulation
• Cataract Clouding of the lens of the eye. Epidemiology:- Leading cause of visual impairment and blindness in the world- Sex: ♀ > ♂ Etiology:- Congenital cataracts (< 1%)→ Caused by congenital infections (rubella, hepatitis, mumps, toxoplasmosis)→ Galactosemia (reversible)- Acquired cataracts (> 99%)→ Age-related (> 90%)→ Associated with syndromes: Diabetes mellitus, renal insufficiency, myotonic dystrophy, Wilson's disease, Trisomy 21, neurofibromatosis type 2→ Drug-induced: Glucocorticoids → Traumatic→ Physically related conditions: Radiation, excessive sunlight or UVB exposure Clinical features:- Reduced visual acuity: blurred, clouded, or dim vision- Painless and often bilateral- Glare: in daylight, in low sunlight, and from car headlights; associated with halos around lights- Opacities within the red reflex or obscuration of ocular fundus detail during opthalmoscopy- Grey, white, yellow, or brownish clouding of the lens - Congenital cataracts: Leukokoria, strabismus, nystagmus Treatment: - Extracapsular cataract extraction (ECCE) = Removal of the lens nucleus by anterior capsulotomy (a surgical opening in the anterior capsule) with retention of posterior capsular integrity, and placement of the intra-ocular lens (IOL) in the posterior chamber
• Diabetic retinopathy Epidemiology:- After 15 years with disease, approx. 90% of type 1 diabetic patients and approx. 25% of type 2 diabetic patients develop diabetic retinopathy.- The most common cause of visual impairment and blindness in patients aged 25-74 years in the US Symptoms: - Asymptomatic until very late stages of disease- Visual impairment- Progression to blindness Nonproliferative retinopathy (mild, moderate, severe): accounts for most cases of diabetic retinopathy- Findings: intraretinal microvascular abnormalities (IRMA), including microaneurysms; caliber changes in venous vessels; intraretinal hemorrhage; hard exudates, retinal edema, and cotton-wool spots - Visual loss, most commonly due to macular edema Proliferative retinopathy- Findings: Preretinal neovascularization is the hallmark, fibrovascular proliferation, vitreous hemorrhage, traction retinal detachment, rubeosis iridis → secondary glaucoma. Additionally, findings of nonproliferative retinopathy are usually present.- Visual loss may be due to vitreous hemorrhage, retinal detachment, or neovascular glaucoma. Macular edema- Findings: clinically significant retinal thickening and edema involving the macula, hard exudates, macular ischemia- May occur in all stages of NPDR and PDR Treatment:- Nonproliferative retinopathy→ Laser treatment: focal photocoagulation→ Intravitreal anti-vascular endothelial growth factor (VEGF) injection- Proliferative retinopathy and severe nonproliferative retinopathy→ Laser treatment: panretinal photocoagulation over the course of numerous appointments→ Vitrectomy in case of traction retinal detachment and vitreal hemorrhage- Macular edema→ VEGF inhibitors→ Focal photocoagulation
• Ectopia lentis Displacement of the lens of the eye. Etiology:- Trauma (most common)- Simple ectopia lentis: A hereditary disorder in which zonular fibers degenerate, leading to lens dislocation.- Marfan syndrome- Homocystinuria Clinical features:- Can be subluxated or completed luxated- Marfan syndrome: superior, temporal subluxation of the lens (upward and outwards)- Homocystinuria: inferior, medial subluxation of the lens (downward and inwards) Diagnostics: - Ophthalmological assessment: Visual acuity testing, slit lamp examination, retinoscopy, ultrasound of the eye, and tonometry- Iridodonesis: tremors of the iris during eye movement- Lentodonesis: tremors of the lens during eye movement- The equator of the lens may be visible in the pupil- The lens may dislocate into the vitreous or the anterior chamber- Features of glaucoma (e.g., raised intraocular pressure) due to pupillary block- Evaluation for underlying Marfan syndrome or homocystinuria Treatment:- Refractive correction- Lensectomy/vitrectomy = Removal of the lens and vitreous body and concurrent use of contact lenses
• Retinal detachment Detachment of the inner layer of the retina (neurosensory retina) from the retinal pigment epithelium. Rhegmatogenous retinal detachment- Mechanism: Retinal tears → retinal fluid seeps into the subretinal space → retinal detachment- Pathological myopia- Previous intraocular surgery (e.g., cataract surgery)- Posterior vitreous detachment- Trauma Tractional detachment- Mechanism: Traction on the vitreoretinal band during eye movements → retinal detachment- Proliferative diabetic retinopathy- Retinopathy of prematurity Exudative detachment- Systemic diseases: Pre-eclampsia, hypertension, bleeding disorders- Tumor growth: Retinoblastoma, melanoma of the choroid Clinical features:1. Prodromal symptoms- Floaters- Flash of light (photopsia)2. Localized retinal detachment: scotoma (visual field defect)- Depending on the location of the detachment, a rising wall/dark shadow may appear- The visual field defects may begin in either the nasal or temporal visual field.3. Extensive retinal detachment and/or macular involvement- Sudden, painless loss of vision in the affected eye- Relative afferent pupillary defect Diagnostics:- Opthalmoscopic findings: A freshly detached retina has a grey color instead of the normal pink color.- Rhegmatogenous retinal detachment: → A retinal tear may potentially be visible (e.g., horseshoe, linear, or round retinal tears).→ The detached retina floats freely in the vitreous body, and moves with eye movements.- Non-rhegmatogenous retinal detachment: No retinal tear is observed. Treatment:- For retinal holes/retinal tears with little or no retinal detachment: laser photocoagulation or cryoretinopexy- In the case of extensive retinal detachment: prompt surgical treatment- Tractional retinal detachment: Vitrectomy followed by internal tamponade and laser photocoagulation/cryoretinopexy.- Exudative retinal detachment: → Due to sub-retinal fluid accumulation: spontaneous reabsorption of fluid; no treatment is required→ Due to tumors: enucleation
• Retinal artery occlusion Etiology:- Emboli as a result of carotid artery atherosclerosis (most common)- Emboli from the atria (usually as a result of atrial fibrillation)- Thrombosis of the retinal vessels (usually as a result of atherosclerosis)- Rare causes: vasculitis (e.g., temporal arteritis), fibromuscular dysplasia Clinical features:- Sudden, painless loss of vision in one eye (often described as a “descending curtain”)- A past history of amaurosis fugax may be present.- Relative afferent pupillary defect- Grayish-white discoloration of the entire retina- Cherry-red spot at the fovea centralis Diagnostics:- Carotid doppler (to look for atherosclerotic plaques)- Echocardiography (to look for potential sources of emboli)- Tests to rule out temporal arteritis: Inflammatory markers (e.g., ↑ ESR), temporal artery biopsy Treatment: Ophthalmologic emergency!- Eyeball massage- Carbogen therapy: inhaling a mixture of 5% CO2 to vasodilate arteries- Decrease intraocular pressure with drugs and/or surgical therapy (e.g., paracentesis of the anterior chamber)- Hemodilution- Vasodilators (e.g., calcium channel blockers, sublingual nitroglycerine)- High-dose glucocorticoid therapy if temporal arteritis is suspected
• Retinal vein occlusion Etiology:- Systemic diseases: atherosclerosis, hypertension, diabetes mellitus- Hypercoagulable/prothrombotic states (e.g., polycythemia vera, sickle cell disease, oral contraceptive use)- Ocular diseases: Glaucoma, Vasculitis of the retinal artery Clinical features:- Sudden, severe loss of vision in the affected eye- Relative afferent pupillary deficit- Many dot-and-blot and/or flame-shaped hemorrhages in all four retinal quadrants- Cotton wool spots- Severe macular edema- Severe papilledema Diagnostics:- Fluorescein angiography: in order to differentiate ischemic from non-ischemic forms of retinal vein occlusion Treatment:- Laser therapy: Panretinal photocoagulation (in order to prevent neovascularizations)- Intravitreal injection of VEGF inhibitors and/or steroids
• Open-angle glaucoma Generally bilateral, progressive loss of optic nerve fibers with open chamber angles (often with increased IOP), not caused by another systemic or local condition. Pathophysiology: Secondary clogging of the trabecular meshwork or reduced drainage → gradual ↑ in IOP → vascular compression → ischemia to the optic nerve → progressive visual impairment. Etiology: Secondary clogging due to- Inflammatory cells (e.g., uveitis)- Red blood cells (e.g. vitreous hemorrhage)- Material from retinal detachment in the aqueous humor Clinical features:- Initially often asymptomatic- Bilateral, progressive visual field loss Diagnostics:- Slit lamp examination of the anterior segment: normal appearing anterior chamber angle- Tonometry: measure IOP (standard values range between 10-21 mm Hg)- Gonioscopy: to rule out angle-closure glaucoma- Fundoscopy: cupping and pallor of optic disc Treatment:- First-line: Topical prostaglandins (e.g., latanoprost)→ Adverse effects: epithelial keratopathy, iris hyperpigmentation, eyelash lengthening- Reduce aqueous humor production:→ Topical beta blockers (e.g., timolol)→ α2 agonists (e.g., apraclonidine)- In refractory cases: surgical trabeculectomy
• Angle-closure glaucoma Sudden and sharp increase in intraocular pressure caused by an obstruction of aqueous outflow (most commonly as a result of an occlusion of the chamber angle). Etiology/Risk factors:- Shallow anterior chamber (e.g., hyperopia, short eye)- Advanced age- Asian/Inuit ethnicity- Eye injury with scarring and adhesions- Rubeosis iridis- Mydriasis→ Drug-induced: anticholinergics (e.g., atropine) , sympathomimetics, decongestants→ Darkness→ Stress/fear response Clinical features:- Sudden onset- Unilateral red, hard, and severely painful eye- Frontal headaches- Vomiting, nausea- Steamy cornea and blurred vision- Dilated, nonreactive pupil Diagnostics:- Rock-hard globe on palpation- Slit lamp examination of the anterior segment: narrow anterior chamber angle, shallow anterior chamber- Gonioscopy (gold-standard)- Tonometry (if gonioscopy is unavailable): ↑ IOP Treatment:- Topical timolol, apraclonidine, and IV acetazolamide- Topical cholinergics (e.g., pilocarpine) can be added once IOP is < 40 mm Hg - Curative treatment: laser peripheral iridotomy- No mydriatic drugs!
• Bacterial keratitis Epidemiology: Most common form of keratitis (∼ 90%) Etiology:- Staphylococcus aureus- Streptococcus pneumoniae- Pseudomonas aeruginosa Risk factors:- Contact lens use- Recent eye surgery or injury- Immunodeficiency- Lacrimal duct stenosis Clinical features:- Progressive pain- Foreign body sensation- Purulent discharge- Photophobia- Excessive tearing- Blurry vision- Eye redness- Conjunctival injection Special form: Pseudomonas keratitis- Most common cause of bacterial keratitis in contact lens users- Characterized by a fulminant course with severe ulceration and corneal destruction/perforation within 2–5 days Diagnostics:- Slit lamp examination: Hypopyon- Fluorescein staining: round corneal infiltrate or ulcer - Cultures Treatment: Topical broad-spectrum antibiotics- Cefazolin with tobramycin/gentamicin or- Ofloxacin or- Ciprofloxacin
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• Herpes simplex keratitis Etiology: Infection due to reactivated herpes simplex virus (HSV) type 1 from the trigeminal ganglion Clinical features:- Similar to viral conjunctivitis, but usually unilateral- Eye redness- ± Eye pain- Foreign body sensation- Photophobia- Blurry vision; can lead to vision loss if untreated Diagnostics:- Fluorescein staining: superficial corneal erosions (dendritic ulcers) that resemble the branches of a tree- Direct fluorescein antibody test (HSV antigen detection) or polymerase chain reaction (PCR) test Treatment:- Topical trifluridine or ganciclovir- Refractory cases: Oral antiviral (e.g., acyclovir)
• Acanthamoeba keratitis Characteristics- Rare condition- Primarily occurs in immunocompetent contact lens wearers- Progressive course for several weeks despite an attempt of antibiotic treatment Clinical features:- Severe pain- Eye redness- Photophobia- Epiphora- Decrease in vision- Corneal ring infiltrate (late-stage) Diagnostics:- Slit-lamp examination and/or fluorescein staining: features of epithelitis and stromal disease- Culture and microscopy of eye scraping- Pathogen detection is often difficult. Treatment:- Topical antiseptic (e.g., chlorhexidine) with propamidine
• Herpes zoster keratitis Etiology: reactivated herpes zoster virus (involvement of the ophthalmic nerve ) Clinical features:- Prodrome: headache, malaise, fever- Impaired vision- Eye irritation (foreign body sensation)- Photophobia- Eye pain- In the innervation area of the ophthalmic nerve (forehead, bridge, and tip of the nose): Vesicular eruption; Anesthesia dolorosa Diagnosis:- Slit-lamp examination and fluorescein staining→ 1-2 days: punctate lesions on the corneal surface→ 4-6 days: dendritic lesions on the corneal surface Treatment: oral acyclovir, valacyclovir, or famciclovir
• Sympathetic ophthamia ("spared eye injury") Immune-mediated inflammation of one eye (the sympathetic eye) after penetrating injury to the other eye. Clinical features:- Anterior uveitis- Panuveitis, papillary edema, and blindness may develop Pathophysiology: Uncovering of "hidden" antigens. An immune response against these antigens can involve autoantiboies as well as a cell-mediated reaction
• Vitreous hemorrhage The extravasation of blood in and around the vitreous body Etiology: - Rupture of neovascular vessels in ischemic changes of the retina→ Proliferative diabetic retinopathy (most common cause)→ Retinal vein occlusion- Rupture of physiological vessels→ Lesions of the retina in symptomatic posterior vitreous detachment→ Retinal tear→ Blunt or penetrating traumatic injuries to the sclera or retina→ Increased intracranial pressure, e.g., in subarachnoid hemorrhage (Terson syndrome) Clinical features:- Sudden onset of symptoms: usually unilateral and painless- Floaters and/or visual loss: typically worse after sleep Diagnostics- Slit lamp examination→ Blood between the posterior vitreous base and internal limiting membrane→ Can determine the source of vitreous hemorrhage (e.g., retinal neovascularization) Treatment:- Since hemorrhage may resolve spontaneously, a wait-and-see approach is recommended at the beginning of treatment.- If severe disease progression/retinal detachment occurs: vitrectomy
• HIV-associated ocular manifestations HIV retinopathy:- Caused by a microvascular disorder- Fundoscopic findings: cotton wool spots, microaneurysms, retinal hemorrhages- Not painful- Vision unaffected Herpes simplex keratitis:- Slit-lamp examination: dendritic corneal lesions- Fundoscopic findings are normal- Painful, watery eyes- Blurry vision Varicella zoster retinitis:- Fundoscopic findings: retinal necrosis (starting from periphery)- Painful- Severe loss of vision Cytomegalovirus retinitis:- Fundoscopic findings: Hemorrhage, perivascular white opacities resembling cotton-wood spots (larger than HIV retinopathy!), "pizza pie" appearance, retinal detachment- Not painful- Vision initially unaffected- Later: Blurred vision, floaters, and photopsia (sensation of flashing lights); Lesions near the fovea may cause blindness Toxoplasma retinitis:- Fundoscopic findings: raised yellow-white cottony lesions- Lesions are nonvascular (meaning their distribution is not related to the vessels) DD: CMV- Painful- Visual impairment
• Allergic conjunctivitis Epidemiology: common in young adults Pathophysiology:IgE-mediated hypersensitivity (type I) against specific allergens (e.g., cat dander) Subtypes and key features: - Seasonal allergic conjunctivitis → Seasonal → Less acute onset and severe than the other types- Perennial allergic conjunctivitis → Seasonal or occurs all year round → Similar features to SAC- Giant papillary conjunctivitis → Chronic mechanical irritation (often by contact lenses) in combination with exposure to allergens→ Giant papillae at the tarsal conjunctiva of the upper lid - Atopic keratoconjunctivitis → Associated with atopic dermatitis of the eyelids→ Papillary reaction in the inferior tarsal conjunctiva- Vernal keratoconjunctivitis (VKC) ♂ > ♀, especially with atopic disease Clinical features:- General signs and symptoms of conjunctivitis- Itching - Excessive tearing Sneezing (In SAC and PAC) Treatment:- Avoid chronic irritation (contact lenses, allergens)- Cold compresses- Artificial tears- NSAIDs (e.g., ketorolac)- Antihistamines and mast-cell stabilizers (e.g., ketotifen) - Corticosteroids (e.g., fluorometholone): second-line treatment for SAC- Systemic: oral antihistamines (e.g., cetirizine)
• Bacterial conjunctivitis Etiology: Staphylococcus aureus (most common in adults), Streptococcal pneumoniae, Haemophilus influenzae, Pseudomonas, Haemophilus, and Moraxella catarrhalis  Clinical features: - Usually unilateral- Thick purulent discharge (yellow, white or green) - Reduced vision and risk of blindness (if cornea is involved)- Extraocular signs of bacterial infection  Diagnosis: Clinical diagnosis- Conjunctival scrapings and culture (or PCR) required if persistent or severe disease (i.e., multiple or large corneal lesions), if the diagnosis is uncertain, and in newborn conjunctivitis Treatment: - Topical broad-spectrum antibiotics (e.g., erythromycin or trimethoprim-polymyxin B)
• Strabismus Etiology:- Genetic- Uncorrected refractive error (particularly hyperopia and anisometropia) - Unilateral visual impairment/amblyopia (e.g., organic causes, retinaldisease, retinoblastoma)- Other: perinatal lesions (e.g., preterm birth, asphyxia), cerebral damage (e.g., trauma, encephalitis) Types:- Congenital or infantile concomitant strabismus→ Evident at birth or onset within 6 months of age; does not resolve spontaneously → May manifest as esotropia or exotropia- Latent strabismus: usually no clinical significance; the deviation is compensated by fixation (fusion); decompensation and manifestation occur in situations of physical stress. Diagnostics- Hirschberg test: a test for determining if the eyes are in alignment. A light is shone at the eyes and the location of the light reflex on the cornea is observed in reference to the pupil. Asymmetrical corneal reflections on examination of the eyes indicate that the visual axes are not aligned (strabismus). - Cover tests Treatment: - The main goals in strabismus management are to optimize visual acuity and achieve binocularity.1. Correction of refractive errors2. Visual training therapy3. Occlusion treatment- Initiate as early as possible!- Cover the unaffected eye using a patch (occlusion) → training of the weaker eye4. Penalization therapy (cyclopentolate drop therapy): apply cyclopentolate drops to the unaffected eye → blurs vision → encourages monocular use of the affected eye5. Strabismus surgery- Transposition or repositioning of muscles- Tucking or advancement to tighten muscles- Myectomy or tenectomy to loosen extraocular muscles
• Hordeolum Common acute inflammation of the tear gland or eyelash follicles (Zeis or meibomian glands) Etiology:- Mainly Staphylococcus aureus, rarely Streptococcus - Increased occurrence in individuals with acne vulgaris and diabetes mellitus Clinical features:- Painful, erythematous, tender pus-filled nodule - Spontaneous perforation and purulent discharge after a few days  Diagnostics: usually a clinical diagnosis Treatment: - Most styes are self-limiting and resolve spontaneously after 1–2 weeks. - Warm compress and massage - Eyelid margin hygiene - Topical antibiotic treatment, e.g., gentamicin, amoxicillin, erythromycin- In the case of non-response to medical therapy or severe symptoms: incision and curettage, with systemic antibiotics (e.g., cephalexin)  Complications:- May present as a chalazion over a few months - Abscess of the eyelid and orbital cellulitis are rare.
• Chalazion A focal granulomatous swelling of the meibomian gland, a lipid-secreting gland of the eyelid. Etiology:- Poor eyelid hygiene, stress, or immunodeficiency- Systemic conditions: tuberculosis, rosacea, seborrheic dermatitis- Local anatomical abnormalities: complications of chronic blepharitis, malignancy, eyelid trauma, or post surgery Clinical features:- Chronic (slow-growing), firm, rubbery nodule on the eyelid - Heaviness of the eyelid- Can cause visual disturbances, if large enough  Diagnostics:- Usually a clinical diagnosis - Everting the eyelid may allow for better visualization of the lesion.- Biopsy: for a persistent or recurrent chalazion (may indicate an underlying sebaceous carcinoma of the eyelid) Treatment:- Conservative: wait and watch, warm compresses , and eyelid hygiene - In secondary infection: local antibiotics, e.g., tetracycline, doxycycline, minocycline, or metronidazole - In case of persistent chalazia (once a malignancy has been ruled out): Incision and curettage
• Open globe injuries Full-thickness perforation or laceration of the ocular globe  Mechanism of injury: sharp objects or high-velocity blunt objects  Clinical features:- Gross deformity of the eye (ocular rupture with fluid volume loss) or prolapsing uvea (full-thickness laceration)- Afferent pupillary defect and impaired visual acuity- All sequelae of ocular contusion are possible Diagnosis:- Careful investigation of the anterior and posterior segment of the eye (by slit lamp and fundoscopy, respectively)- Fluorescein stain if inconclusive: corneal abrasions and foreign bodies - Nonenhanced CT can be used if the eye cannot be directly visualized or to exclude the possibility of an intraocular foreign body.- Culture of the vitreous if a foreign body or infection is suspected Treatment:- Urgent stabilization and resuscitation- Analgesia (e.g., IV morphine), antiemetics (e.g., IV ondansetron), and tetanus vaccine or booster- Systemic antibiotic therapy for foreign bodies - Urgent ophthalmologic consultation for surgical repair Complications:- Permanent vision loss- Loss of eye- Endophthalmitis: inflammation of the tissues or fluid inside the eye(especially with retained intraocular foreign bodies), often presenting with deep ocular pain, a red eye, and reduced visual acuity - Sympathetic ophthalmia: bilateral granulomatous panuveitis after unilateral penetrating injury (and rarely after intraocular surgery) → bilateral blindness may occur
• Acute dacryocystitis Acute inflammation of the lacrimal sac Etiology: Congenital/acquired dacryostenosis → stasis of tears → secondary bacterial infection → lacrimal sac inflammation Clinical features:- Erythema, edema, warmth, and significant pain below the medial canthus of the eye- Pressure on the swelling causes pain and purulent discharge from the punctum.- Epiphora- Fever (may be present) Diagnostics:- Clinical- Pus culture- Blood culture: in patients with systemic symptoms (fever)- Dacryocystography (DCG) : in patients with dacryostenosis secondary to trauma (altered anatomy) or suspected tumors (to locate the tumor) Treatment:- Symptomatic: warm compresses, NSAIDs- Systemic antibiotics: Oral clindamycin, IV or oral amoxicillin + clavulanic acid, and IV vancomycin can be used empirically; culture-specific antibiotics are used once the report is ready- Incision and drainage if lacrimal sac abscess occurs- DCR (treatment of the NLD obstruction): after treating the infection

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