Clinical Medicine and Surgery I · Exam 2

How to use this guide

Dr. Carter’s Clin Med Pro Study Tip (Hypotension deck, slide 7) lists what to learn for every condition. Each card below answers those ten fields:

Name of Condition
Definition
Etiology (cause)
Epidemiology (who)
Risk Factors
Pathology
Clinical Manifestation
Diagnosis
Treatment/Therapy
Mortality ★

Every field comes from the lecture slides only. Where a deck is silent the card says Not covered in the lecture rather than filling the gap from elsewhere (209 of 840 fields in this exam; Mortality alone: 79 of 84). Slide numbers follow each field. Cards open closed; tap one to read it.

The ★ on Mortality is on the original study-tip slide: fill it when a figure exists. A ★ highlighted phrase inside a field is a fact the professor emphasized in the lecture recording, carried over from this exam’s study guide.

Lecture 10 · Common Ophthalmological Disorders

Monique Jaquith, DMSc, PA-C · 31 conditions · source: CMS I Common Ophthalmological Disorders 2026 - Jaquith.pptx

Entropion2 not covered

Name of Condition: Entropion Slide 12
Definition: Eyelid margin turns inward, so lashes and skin rub against the surface of the eye. Slide 12
Etiology (cause): Aging; cicatricial (burn, surgery, trauma, chronic inflammation, scar); congenital. Slide 12
Epidemiology (who): Not covered in the lecture
Risk Factors: Aging; scarring from burn, surgery, trauma or chronic inflammation; congenital. Slide 12
Pathology: Lashes pushed onto the globe (trichiasis) cause irritation and corneal abrasion/potential corneal damage. Slide 12
Clinical Manifestation: Foreign body sensation, irritation, pain; conjunctival injection; inward-turned lid margin with lashes on the globe. Slide 12
Diagnosis: Clinical; slit lamp exam to check for corneal involvement. Slide 13
Treatment/Therapy: Preservative-free artificial tears by day, lubricating ointment at night; tape lid into place; surgery is definitive. Slide 13
Mortality ★: Not covered in the lecture

Ectropion2 not covered

Name of Condition: Ectropion Slide 12
Definition: Lower eyelid sags and turns outward, exposing the inner surface of the lid. Slide 12
Etiology (cause): Aging; cicatricial (burn, surgery, trauma, chronic inflammation, scar); congenital; facial nerve (cranial nerve VII) palsy (ectropion only). Slide 12
Epidemiology (who): Not covered in the lecture
Risk Factors: Aging; scarring; congenital; facial nerve (cranial nerve VII) palsy. Slide 12
Pathology: Everted lid margin leaves the eye exposed, causing exposure keratopathy. Slide 12
Clinical Manifestation: Tearing; conjunctival injection; outward-turned lid margin. Slide 12
Diagnosis: Clinical; slit lamp exam to check for corneal involvement. Slide 13
Treatment/Therapy: Preservative-free artificial tears by day, lubricating ointment at night; tape exposed lid into place; surgery is definitive. Slide 13
Mortality ★: Not covered in the lecture

Dermatochalasis3 not covered

Name of Condition: Dermatochalasis Slide 14
Definition: Excess, loose, sagging skin of the upper or lower eyelids. Slide 14
Etiology (cause): Aging. Slide 14
Epidemiology (who): Not covered in the lecture
Risk Factors: Aging. Slide 14
Pathology: Not covered in the lecture
Clinical Manifestation: Lid "heaviness", "looking through lashes", lid friction with blinking; bilateral excess flaps/folds of lid skin. Slide 14
Diagnosis: Examine visual fields for deficits. Slide 15
Treatment/Therapy: Blepharoplasty; often covered by insurance if a visual field defect is present. Slides 14–15
Mortality ★: Not covered in the lecture

Xanthelasma2 not covered

Name of Condition: Xanthelasma Slide 16
Definition: Harmless, soft, yellowish cholesterol deposit under the skin on or around the eyelids. Slide 16
Etiology (cause): Metabolic disorders with increased serum lipids. Slide 16
Epidemiology (who): Not covered in the lecture
Risk Factors: Elevated serum lipids (dyslipidemia), though many patients have normal lipid levels. Slides 16–17
Pathology: Cholesterol deposit under the eyelid skin. Slide 16
Clinical Manifestation: Typically asymptomatic; oval yellowish plaques on the eyelids. Slide 16
Diagnosis: Serum lipid profile and cardiovascular risk assessment; diabetes labs (fasting plasma glucose, hemoglobin A1C); liver function labs. Slide 17
Treatment/Therapy: Treat the underlying metabolic issue; local cryotherapy (liquid nitrogen), laser ablation, chemical peel or surgical excision; recurrences common despite effective local treatment. Slide 17
Mortality ★: Not covered in the lecture

Blepharitis / meibomitis2 not covered

Name of Condition: Blepharitis / meibomitis Slide 18
Definition: Blepharitis: common, non-contagious inflammation of the eyelid margins. Meibomitis: inflammation of the meibomian (lid-margin oil) glands. Slide 18
Etiology (cause): Rosacea, seborrheic dermatitis, colonization with Staphylococcus aureus. Slide 18
Epidemiology (who): Common; non-contagious. Slide 18
Risk Factors: Rosacea; seborrheic dermatitis; Staphylococcus aureus colonization. Slide 18
Pathology: Chronic lid-margin and meibomian gland inflammation with thickened lipid secretion; controlled rather than cured. Slides 18–19
Clinical Manifestation: Burning, dryness, grittiness, itching, foreign body sensation, tearing; crusting/scaling at lash bases (collarettes), red swollen lid margins, thick toothpaste-like meibomian secretion, frothy tear film; rosacea or seborrheic skin findings. Slide 18
Diagnosis: Not covered in the lecture
Treatment/Therapy: Lid hygiene (over-the-counter lid scrub); no improvement after 2 weeks: topical, then oral antibiotics; refer to ophthalmology if not improved after several weeks. Slide 19
Mortality ★: Not covered in the lecture

Chalazion2 not covered

Name of Condition: Chalazion Slide 20
Definition: Sterile obstruction of a meibomian gland producing a nontender eyelid nodule. Slide 20
Etiology (cause): Sterile meibomian gland obstruction. Slide 20
Epidemiology (who): Not covered in the lecture
Risk Factors: Blepharitis/meibomitis; rosacea. Slide 20
Pathology: Sterile obstruction of a meibomian gland. Slide 20
Clinical Manifestation: Focal eyelid swelling over days to weeks; visible/palpable subcutaneous lid nodule that is nontender. Slide 20
Diagnosis: Refer recurrent chalazia or those persisting more than 2 to 3 months to rule out sebaceous carcinoma. Slide 21
Treatment/Therapy: Warm compresses, gentle massage (improvement may take months); refer to ophthalmology for steroid injection or curettage if no spontaneous resolution; recurrent with rosacea needs ophthalmology. Slide 21
Mortality ★: Not covered in the lecture

Hordeolum3 not covered

Name of Condition: Hordeolum (also: stye) Slide 20
Definition: Acute inflammation of a meibomian gland (internal hordeolum) or of the glands of Zeis or Moll (external hordeolum). Slide 20
Etiology (cause): Usually staphylococcal infection. Slide 20
Epidemiology (who): Not covered in the lecture
Risk Factors: Blepharitis/meibomitis; rosacea. Slide 20
Pathology: Acute, usually staphylococcal, inflammation of a meibomian gland (internal) or Zeis/Moll gland (external). Slide 20
Clinical Manifestation: Eyelid pain, redness and swelling developing over 24 hours/overnight; visible/palpable subcutaneous lid nodule that is tender. Slide 20
Diagnosis: Not covered in the lecture
Treatment/Therapy: Warm compresses, gentle massage; refer to ophthalmology for incision and drainage if persistent (no improvement in 2 weeks); with associated pre-septal cellulitis, systemic antibiotics as for pre-septal cellulitis. Slide 21
Mortality ★: Not covered in the lecture

Dacryoadenitis3 not covered

Name of Condition: Dacryoadenitis Slide 22
Definition: Inflammation of the lacrimal gland (the tear-producing gland above the eye). Slide 22
Etiology (cause): Inflammatory (most common); bacterial (rare); viral (usually bilateral). Slide 22
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Inflamed, hyperemic palpebral lobe of the lacrimal gland. Slide 22
Clinical Manifestation: Unilateral pain, redness, swelling over the lateral one-third of the upper lid; tearing or discharge; possible ipsilateral preauricular lymphadenopathy, temporal conjunctival injection, fever, leukocytosis. Slide 22
Diagnosis: CT (computed tomography) of orbits and paranasal sinuses with contrast, especially if severe, orbital findings, chronic, atypical, suspected abscess/mass or not improving. Slide 23
Treatment/Therapy: As-needed acetaminophen; unclear cause: empiric oral antibiotics for 24 hours then reassess; inflammatory: oral corticosteroids (after excluding infection; respond within 48 hours); viral: cool compresses; monitor for orbital involvement. Slide 23
Mortality ★: Not covered in the lecture

Dacryocystitis3 not covered

Name of Condition: Dacryocystitis Slide 24
Definition: Infection or inflammation of the lacrimal (tear) sac, usually from a blocked tear duct. Slide 24
Etiology (cause): Nasolacrimal duct obstruction. Slide 24
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Obstructed nasolacrimal duct leads to infection/inflammation of the lacrimal sac. Slide 24
Clinical Manifestation: Red, painful, tense swelling over the lacrimal sac at the medial lower lid (below the medial canthal tendon); tearing, fever; mucoid/purulent discharge expressible from the lower punctum. Mass above the tendon: suspect lacrimal sac tumor. Slide 24
Diagnosis: Mainly clinical; CT (computed tomography) of orbits and sinuses with contrast if orbital extension, abscess, trauma, mass or atypical disease. Slide 25
Treatment/Therapy: Mild, afebrile: oral antibiotics for 10 days; febrile/ill: admit, intravenous antibiotics 48 to 72 hours then oral to 10 to 14 days with prompt ophthalmology consult; warm compresses; consider abscess drainage; later probing/irrigation or surgery. Slide 25
Mortality ★: Not covered in the lecture

Pinguecula2 not covered

Name of Condition: Pinguecula Slide 27
Definition: Non-cancerous yellowish or white deposit on the conjunctiva that does not involve the cornea. Slide 27
Etiology (cause): Chronic exposure to sunlight and wind. Slide 27
Epidemiology (who): Not covered in the lecture
Risk Factors: Chronic sunlight and wind exposure. Slide 27
Pathology: Conjunctival deposit confined to the conjunctiva, not crossing the limbus onto the cornea ("penguins can't fly"). Slide 27
Clinical Manifestation: Irritation, redness nasally and/or temporally, tearing; classic appearance almost always at 3 or 9 o'clock. Slide 27
Diagnosis: Clinical appearance; slit lamp exam of the adjacent cornea if referred. Slides 27–28
Treatment/Therapy: Protect eyes from sun, dust, wind; artificial tears; non-urgent referral to ophthalmology if growth or vision impairment. Conservative care will not make it resolve. Slide 28
Mortality ★: Not covered in the lecture

Pterygium2 not covered

Name of Condition: Pterygium (also: surfer's eye) Slide 27
Definition: Non-cancerous, raised, wedge-shaped fleshy conjunctival growth that extends onto the cornea. Slide 27
Etiology (cause): Chronic exposure to sunlight and wind. Slide 27
Epidemiology (who): Not covered in the lecture
Risk Factors: Chronic sunlight and wind exposure. Slide 27
Pathology: Triangular, insect-wing-shaped fleshy conjunctival growth invading the cornea ("pterodactyls fly into the cornea"). Slide 27
Clinical Manifestation: Irritation, redness nasally and/or temporally, tearing; sometimes decreased vision; almost always at 3 or 9 o'clock. Slide 27
Diagnosis: Clinical appearance; slit lamp exam to evaluate integrity of the adjacent cornea; differential: conjunctival intraepithelial neoplasia (more fan-like). Slides 27–28
Treatment/Therapy: Protect eyes from sun, dust, wind; artificial tears; non-urgent referral if growth or vision impairment; surgery if growing into the cornea and distorting vision. Slide 28
Mortality ★: Not covered in the lecture

Subconjunctival hemorrhage (atraumatic)2 not covered

Name of Condition: Subconjunctival hemorrhage (atraumatic) Slide 29
Definition: Harmless broken blood vessel producing a bright red patch of blood underneath the conjunctiva. Slide 29
Etiology (cause): Valsalva, bleeding disorder, antiplatelet/anticoagulant medications, hypertension. Slide 29
Epidemiology (who): Not covered in the lecture
Risk Factors: Valsalva; bleeding disorder; antiplatelet/anticoagulant medications; hypertension. Slide 29
Pathology: Bleeding beneath the conjunctiva. Slide 29
Clinical Manifestation: Red eye, often asymptomatic unless chemosis is present; blood under the conjunctiva. Differential: 360-degree traumatic hemorrhage, hyphema. Slide 29
Diagnosis: History is key; ocular exam; check blood pressure if no explanation; recurrent: medication review, blood pressure, targeted hematologic evaluation (may need hematology if no culprit medication). Slide 30
Treatment/Therapy: Reassurance; usually resolves spontaneously within 2 to 4 weeks (uncomplicated often about 1 to 2 weeks, larger ones longer); artificial tears for mild irritation; treat underlying bleeding disorder or hypertension. Slide 30
Mortality ★: Not covered in the lecture

Chemosis4 not covered

Name of Condition: Chemosis Slide 31
Definition: Swelling (edema) of the conjunctiva; more a sign/presentation than a diagnosis. Slide 31
Etiology (cause): Allergy, infection, thyroid eye disease, angioedema, trauma, orbital cellulitis, impaired orbital venous drainage. Slide 31
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Nonspecific conjunctival edema from eye irritation. Slide 31
Clinical Manifestation: Swollen conjunctiva; nonspecific sign of eye irritation. Slide 31
Diagnosis: Not covered in the lecture
Treatment/Therapy: Urgent when accompanied by proptosis, restricted eye movement, reduced vision or an afferent pupillary defect. Slide 31
Mortality ★: Not covered in the lecture

Acute allergic conjunctivitis4 not covered

Name of Condition: Acute allergic conjunctivitis Slides 32, 34
Definition: Non-infectious conjunctivitis: allergic inflammation of the conjunctiva ("pink eye"). Slides 32, 34
Etiology (cause): Reaction to a systemic allergen. Slide 34
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Allergic conjunctival inflammation forming papillae (red at surface, paler at base). Slides 33–34
Clinical Manifestation: Itchy, bilateral red eyes; swollen lids; watery/stringy discharge; preserved vision; chemosis, papillae, no preauricular node. Slide 34
Diagnosis: Not covered in the lecture
Treatment/Therapy: Avoid allergen; cool compresses, artificial tears, topical H1 (histamine-1) blocker with or without mast cell stabilizer (olopatadine does both), systemic H1 blocker; refer to ophthalmology if not relieved. Uncomplicated conjunctivitis: routine disposition. Slides 35, 70
Mortality ★: Not covered in the lecture

Acute viral conjunctivitis3 not covered

Name of Condition: Acute viral conjunctivitis Slides 32, 36
Definition: Infectious inflammation of the conjunctiva caused by a virus. Slides 32, 36
Etiology (cause): Most common: adenovirus; isolated ocular vs systemic infection; may follow or accompany an upper respiratory infection. Slide 36
Epidemiology (who): Not covered in the lecture
Risk Factors: Concomitant or preceding upper respiratory infection. Slide 36
Pathology: Viral conjunctival inflammation forming follicles (pale at surface, redder at base). Slides 33, 36
Clinical Manifestation: Diffusely red eye, profuse watery discharge, swollen tight lids but no pain; bilateral (often starts in one eye); inferior follicles; tender preauricular nodes. Slide 36
Diagnosis: Not covered in the lecture
Treatment/Therapy: Cool compresses, artificial tears; contagious precautions, hand hygiene; refer to ophthalmology if lasting more than 3 weeks or photophobia/decreased vision (uncomplicated: routine disposition). Self-limiting; worse over first week, resolves in 2 to 3 weeks. Slides 37, 70
Mortality ★: Not covered in the lecture

Autoimmune conjunctivitis4 not covered

Name of Condition: Autoimmune conjunctivitis Slide 38
Definition: Conjunctival inflammation associated with systemic autoimmune disease. Slide 38
Etiology (cause): Many autoimmune disorders, often already identified: ocular mucous membrane pemphigoid, Stevens-Johnson syndrome, Sjögren disease, graft-versus-host disease. Slide 38
Epidemiology (who): Not covered in the lecture
Risk Factors: Known systemic autoimmune disease. Slide 38
Pathology: Not covered in the lecture
Clinical Manifestation: Diffuse, often recurrent/chronic conjunctival hyperemia; minimal/no pain, no discharge; systemic complaints (malaise, fever, fatigue). Slide 38
Diagnosis: Not covered in the lecture
Treatment/Therapy: Routine referral to ophthalmology; ocular response depends on the underlying autoimmune disorder. Slide 39
Mortality ★: Not covered in the lecture

Acute bacterial conjunctivitis1 not covered

Name of Condition: Acute bacterial conjunctivitis Slides 32, 40
Definition: Infectious inflammation of the conjunctiva caused by bacteria. Slides 32, 40
Etiology (cause): Bacterial infection. Slide 40
Epidemiology (who): Seen in immunocompromised, elderly and pediatric populations and contact lens wearers. Slide 40
Risk Factors: Immunocompromise; elderly; pediatric; contact lens wear. Slide 40
Pathology: Bacterial conjunctival inflammation forming papillae. Slides 33, 40
Clinical Manifestation: Diffuse red eye, thick yellow or white purulent discharge, possible soreness; often unilateral; florid hyperemia, chemosis, papillae; usually no preauricular node. Slide 40
Diagnosis: Clinical; contact lens wearers need corneal assessment for microbial keratitis. Slide 41
Treatment/Therapy: Immunocompetent adult: topical broad-spectrum antibiotic (fluoroquinolone); hand hygiene. Referral: uncomplicated = routine; urgent ("immediate ophthalmology involvement") if immunocompromised, contact lens wearer, recent surgery, foreign body, corneal opacity/keratitis or no improvement in 24 hours. Slides 41, 70
Mortality ★: Not covered in the lecture

Gonococcal conjunctivitis (neonatal)2 not covered

Name of Condition: Gonococcal conjunctivitis (neonatal) Slides 40–41
Definition: Bacterial conjunctivitis from gonococcus; the major concern in neonates. Slides 40–41
Etiology (cause): Gonococcal bacterial infection. Slide 40
Epidemiology (who): Newborns. Slides 40–41
Risk Factors: Not covered in the lecture
Pathology: Risk if untreated: corneal perforation. Slide 41
Clinical Manifestation: Severe purulent discharge with a palpable preauricular node. Slides 33, 40
Diagnosis: Cultures/Gram stain; testing for chlamydia and disseminated infection. Slide 41
Treatment/Therapy: Emergent referral and hospitalization; immediate systemic ceftriaxone (intravenous/intramuscular, single dose); specialty consultation. Slide 41
Mortality ★: Not covered in the lecture

Adult chlamydial conjunctivitis2 not covered

Name of Condition: Adult chlamydial conjunctivitis (also: adult inclusion conjunctivitis) Slides 32, 42
Definition: Chronic (more than 4 weeks) conjunctivitis from Chlamydia trachomatis in adults. Slides 32, 42
Etiology (cause): Chlamydia trachomatis serotypes D to K by direct inoculation with infected genital secretions. Slide 42
Epidemiology (who): Not covered in the lecture
Risk Factors: Often concurrent asymptomatic urogenital infection. Slide 42
Pathology: Chlamydial conjunctival inflammation forming follicles; preauricular node enlargement. Slides 33, 42
Clinical Manifestation: Chronic hyperemia of the lower palpebral conjunctiva, stringy mucoid discharge, unilateral (sometimes bilateral), lasting a month or more and unresponsive to topical medications; follicles. Slide 42
Diagnosis: Conjunctival NAAT (nucleic acid amplification test) or DFA (direct fluorescent antibody) stain of conjunctival scraping confirms; diagnosis often delayed. Slide 43
Treatment/Therapy: Oral doxycycline for 7 days (avoid sun, full glass of water, stay upright, separate from antacids/minerals); evaluate for other sexually transmitted infections; notify partners. Resolves in weeks without permanent damage. Slide 43
Mortality ★: Not covered in the lecture

Neonatal chlamydial conjunctivitis2 not covered

Name of Condition: Neonatal chlamydial conjunctivitis Slide 44
Definition: Chlamydial conjunctivitis in newborns. Slide 44
Etiology (cause): Chlamydia trachomatis serotypes D to K by direct inoculation with infected genital secretions. Slide 44
Epidemiology (who): Neonates; those born to mothers with cervical infection may also have or develop pneumonia. Slide 44
Risk Factors: Direct inoculation with infected genital secretions (maternal cervical infection). Slide 44
Pathology: Not covered in the lecture
Clinical Manifestation: Conjunctivitis; may also have or develop pneumonia/pneumonitis. Slide 44
Diagnosis: Assess for pneumonia. Slide 44
Treatment/Therapy: Erythromycin for 14 days (monitor infants under 6 weeks for hypertrophic pyloric stenosis); azithromycin alternative; often treated in hospital because of concomitant pneumonia. Slide 44
Mortality ★: Not covered in the lecture

Trachoma2 not covered

Name of Condition: Trachoma Slide 45
Definition: Chlamydial eye infection; leading infectious cause of blindness worldwide. Slide 45
Etiology (cause): Recurrent infection with Chlamydia trachomatis serotypes A, B, C; highly infectious. Slide 45
Epidemiology (who): Transmitted rapidly in areas of poor hygiene; leading infectious cause of blindness worldwide. Slide 45
Risk Factors: Poor hygiene; recurrent infection. Slides 45–46
Pathology: Repeated infection: conjunctival inflammation, then eyelid scarring, then entropion, then trichiasis (lashes rubbing the eye), then blindness. Slide 46
Clinical Manifestation: Most active cases asymptomatic; if symptomatic: red eye, foreign body sensation, purulent discharge, follicles (especially upper lid). Slide 45
Diagnosis: Not covered in the lecture
Treatment/Therapy: Mass drug administration of single-dose oral azithromycin where prevalence is 5% or more; usually curative, reinfection common without better hygiene; trichiasis requires surgery. Slide 46
Mortality ★: Not covered in the lecture

Episcleritis3 not covered

Name of Condition: Episcleritis Slides 5, 47
Definition: Common, generally harmless inflammation of the episclera (thin layer of tissue between the white of the eye and its clear outer covering; deep subconjunctival tissue) Slides 5, 47
Etiology (cause): Often idiopathic; often no systemic association Slide 47
Epidemiology (who): Common Slide 47
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Acute-onset mild pain and focal, often sectoral redness; no discharge or photophobia; episcleral vessels move slightly with a cotton-tip applicator (after anesthesia); may recur in same or other eye Slides 47–48
Diagnosis: Phenylephrine 2.5% test: one drop in affected eye, wait 15 min, episcleral vessels should blanch Slide 48
Treatment/Therapy: Artificial tears + oral NSAID (nonsteroidal anti-inflammatory drug), taken with food; refer to ophthalmology if no response within 2 days; usually self-limited, resolves over 2–3 weeks Slide 48
Mortality ★: Not covered in the lecture

Scleritis3 not covered

Name of Condition: Scleritis Slides 5, 49
Definition: Painful, serious inflammation of the sclera (tough white outer layer of the eye) Slides 5, 49
Etiology (cause): Often a systemic autoimmune condition Slide 49
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Inflammation of scleral, episcleral and conjunctival vessels; scleral thinning lets the choroid show through (bluish, violaceous area); sclera at risk for perforation, greatest in necrotizing disease Slides 49–50
Clinical Manifestation: Severe boring eye pain, worse at night, radiating to face/periorbital region, may wake patient; pain with eye movement; diffuse conjunctival injection; violaceous hue of sclera; scleral vessels do NOT move with cotton-tip applicator (after anesthesia) Slides 49, 69
Diagnosis: Slit lamp exam and ophthalmoscopy (fundoscopy) by ophthalmology; work-up for underlying systemic condition Slide 50
Treatment/Therapy: Referral urgency, two stated: urgent referral to ophthalmology (scleritis management) and same day (red-eye referral timing); systemic corticosteroids or other immune-modulating agents (noninfectious anterior: often systemic NSAIDs (nonsteroidal anti-inflammatory drugs) first); may need surgical patch; less pain = first sign of response Slides 50, 70
Mortality ★: Not covered in the lecture

Pre-septal (periorbital) cellulitis2 not covered

Name of Condition: Pre-septal (periorbital) cellulitis (also: periorbital cellulitis) Slides 51–52
Definition: Bacterial infection of the eyelid and skin around the eye, in front of the orbital septum Slides 51–52
Etiology (cause): Direct extension from bacterial sinus, skin or dental infection; in diabetic, elderly or immunocompromised consider fungus (aspergillosis, mucormycosis) Slide 52
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetic, elderly, or immunocompromised: consider fungal cause Slide 52
Pathology: Preseptal soft-tissue inflammation on CT (computed tomography) Slide 51
Clinical Manifestation: Periocular pain, fever/chills, warmth; diffuse balloon-like edema, erythema, tenderness of lids and periorbital tissue; variable conjunctival injection; eye itself is white; vision, pupils and eye movements normal Slides 52–53
Diagnosis: CT (computed tomography) of orbits and paranasal sinuses with contrast (mild, clearly preseptal disease may be managed clinically without routine CT); complete eye exam with fundoscopy; Gram stain/culture of drainage; CBC (complete blood count) with differential; blood cultures Slide 53
Treatment/Therapy: Mild: outpatient oral antibiotics 10–14 days aimed at Staphylococcus (with or without MRSA (methicillin-resistant Staphylococcus aureus)) and Streptococcus; moderate-severe (toxic), poor compliance, age 5 or younger, or failing oral: admit + IV (intravenous) antibiotics 48–72 hours, then oral at least 1 week Slide 53
Mortality ★: Not covered in the lecture

Post-septal (orbital) cellulitis1 not covered

Name of Condition: Post-septal (orbital) cellulitis (also: orbital cellulitis) Slides 51–52
Definition: Dangerous bacterial infection of the tissues inside the eye socket, behind the orbital septum Slides 51–52
Etiology (cause): Direct extension from bacterial sinus (e.g. ethmoiditis), skin or dental infection; in diabetic, elderly or immunocompromised consider fungus (aspergillosis, mucormycosis) Slides 51–52
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetic, elderly, or immunocompromised: consider fungal cause Slide 52
Pathology: Inflammatory stranding of retrobulbar (intraconal and extraconal) soft tissue with proptosis and tenting of the posterior globe on CT (computed tomography); untreated may spread intracranially: meningitis, cavernous sinus thrombosis Slides 51, 53
Clinical Manifestation: Periocular pain, fever/chills, lid edema/erythema PLUS painful, decreased extraocular movement, reduced vision, diplopia, proptosis, significant conjunctival injection (eye itself red), possible afferent pupillary defect Slides 52, 68
Diagnosis: CT (computed tomography) of orbits and paranasal sinuses with contrast; complete eye exam with fundoscopy; Gram stain/culture of drainage; CBC (complete blood count) with differential; blood cultures Slide 53
Treatment/Therapy: Referral urgency, two stated: emergent (red-eye referral timing) and urgent ophthalmology/ENT (ear, nose, throat) involvement (cellulitis management); all cases: hospitalization + broad-spectrum IV (intravenous) antibiotics 48–72 hours, then oral at least 1 week; ENT, oral maxillofacial surgery and/or infectious disease consults Slides 53, 70
Mortality ★: Threatens vision and life Slide 68

Keratitis1 not covered

Name of Condition: Keratitis (also: microbial keratitis) Slides 5, 55
Definition: Inflammation of the cornea (clear, dome-shaped window covering the front of the eye) Slides 5, 55
Etiology (cause): Bacterial, viral, fungal infection; parasitic rare (Acanthamoeba, a free-living amoeba in soil, dust, water) Slide 55
Epidemiology (who): Acanthamoeba keratitis occurs primarily in contact lens wearers with poor lens hygiene (e.g. rinsing lens with tap water) Slide 55
Risk Factors: Corneal trauma, dry eyes, contact lens overwear (overnight wear increases risk), topical ocular corticosteroid therapy Slides 55, 71
Pathology: Ciliary flush from anterior ciliary artery branches signals corneal inflammation; undertreated: corneal scarring or perforation → endophthalmitis Slides 54, 56
Clinical Manifestation: Eye pain, foreign body sensation, tearing, photophobia, redness at edge of cornea, blurred vision; corneal opacity/haziness, “broken up” corneal light reflex, ciliary flush; Acanthamoeba: classic corneal ring infiltrate Slide 55
Diagnosis: Slit-lamp exam with fluorescein (epithelial defect, white infiltrate); culture/smear for large, central, deep, atypical or unresponsive ulcers (preserve lenses/case) Slides 56, 71
Treatment/Therapy: Referral urgency, two stated: urgent, within 24 hours (keratitis management) and same day (red-eye referral timing); treat underlying cause to prevent scarring; remove contacts, do not patch; no take-home topical anesthetic or corticosteroid Slides 56, 70–71
Mortality ★: Not covered in the lecture

Herpes simplex keratitis1 not covered

Name of Condition: Herpes simplex keratitis (also: dendritic keratitis) Slide 57
Definition: Herpetic keratitis from herpes simplex virus, showing a true dendrite on the cornea Slide 57
Etiology (cause): HSV-1 (herpes simplex virus type 1) much more common in the eye than HSV-2 Slide 58
Epidemiology (who): Patients often younger Slide 58
Risk Factors: Physical/emotional stress triggers recurrences Slide 59
Pathology: Recurrent disease can cause stromal scarring, neurotrophic keratopathy, glaucoma, need for corneal transplant, permanent visual loss Slide 59
Clinical Manifestation: Primary HSV-1 infection often not clinically apparent; facial vesicles lack dermatomal distribution and may not respect midline (only 10% of primary dermatitis bilateral); recurrences common Slides 58–59
Diagnosis: Fluorescein with cobalt blue light: true dendrite (“tree branching”, stained central bed, unstained raised edges, terminal end bulbs) = pathognomonic; slit-lamp + dilated fundoscopy by ophthalmology Slides 57, 59
Treatment/Therapy: Refer to ophthalmology; oral antivirals (acyclovir, valacyclovir, famciclovir) × 10 days; NO topical glucocorticoids by primary care with active epithelial disease, leave to ophthalmology Slide 59
Mortality ★: Not covered in the lecture

Herpes zoster keratitis2 not covered

Name of Condition: Herpes zoster keratitis (also: herpes zoster ophthalmicus (ocular involvement); pseudodendritic keratitis) Slide 57
Definition: Herpetic keratitis from herpes zoster with pseudodendrites on the cornea Slide 57
Etiology (cause): Herpes zoster virus Slide 58
Epidemiology (who): Patients often older; rare in children; also seen in immunosuppressed (e.g. HIV (human immunodeficiency virus), cancer) Slide 58
Risk Factors: Older age; immunosuppression; Hutchinson sign (tip of nose involved) = higher risk of ocular involvement Slide 58
Pathology: Not covered in the lecture
Clinical Manifestation: Pain/paresthesias of affected skin, may follow headache, fever, malaise; dermatomal vesicles (most often V1 (first trigeminal division)) respecting midline, unilateral, often spares lower lid; rash may precede eye involvement by days to months; postherpetic neuralgia Slides 58–59
Diagnosis: Fluorescein with cobalt blue light: pseudodendrites lacking tree-branch pattern, raised edges and terminal end bulbs; slit-lamp + dilated fundoscopy by ophthalmology Slides 57, 59
Treatment/Therapy: Refer to ophthalmology (ocular herpes zoster ophthalmicus: same day); oral antivirals × 10 days (ideally within 72 hours of rash), IV (intravenous) acyclovir if immunocompromised/severe; steroid drops per ophthalmology; retinitis/choroiditis/optic neuritis: corticosteroids + IV acyclovir; zoster vaccine prevention Slides 59, 70
Mortality ★: Not covered in the lecture

Corneal ulcer2 not covered

Name of Condition: Corneal ulcer Slide 60
Definition: Open sore on the cornea (clear front surface of the eye) Slide 60
Etiology (cause): Eye infection, corneal abrasion, severe dry eyes, eyelid closure problems, autoimmune diseases (e.g. rheumatoid arthritis: peripheral ulceration) Slide 60
Epidemiology (who): Not covered in the lecture
Risk Factors: Contact lens use = major risk factor Slide 60
Pathology: Corneal defect; heals with scar (may calcify); ciliary flush from anterior ciliary artery branches signals corneal inflammation Slides 54, 60
Clinical Manifestation: Painful eye, reluctance/resistance to opening eye (photophobia, foreign body sensation), tearing, blurred vision, red eye; ciliary flush; white spot with surrounding corneal irregularity Slide 60
Diagnosis: Slit lamp and fluorescein exam; swab for culture of central and/or large ulcers Slide 61
Treatment/Therapy: Referral urgency, two stated: emergent referral to ophthalmology (corneal ulcer management) and same day (red-eye referral timing); start broad-spectrum topical agent (4th-generation fluoroquinolone); steroid drops only per ophthalmology; next-day follow-up; severe/unresponsive may need corneal transplant Slides 61, 70
Mortality ★: Not covered in the lecture

Anterior uveitis3 not covered

Name of Condition: Anterior uveitis (also: iritis; iridocyclitis) Slides 5, 62
Definition: Inflammation of the front of the uvea: iris (iritis) or iris and ciliary body (iridocyclitis) Slides 5, 62
Etiology (cause): Idiopathic, autoimmune; may be infectious Slides 62–63
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: White cells in anterior chamber, keratic precipitates (white blood cell deposits on posterior surface of cornea); iris adheres to lens (posterior synechiae) giving irregular pupil Slides 62, 69
Clinical Manifestation: Eye pain, redness at edge of cornea, photophobia, vision often preserved; consensual photophobia (pain in affected eye when light shone in other eye); ciliary flush; variable IOP (intraocular pressure); irregular pupil Slides 62, 68
Diagnosis: Slit lamp exam (cells, “snowstorm” in anterior chamber, flare) and dilated fundoscopy; systemic evaluation if recurrent or signs of systemic autoimmune disease Slides 62–63, 69
Treatment/Therapy: Referral urgency, two stated: urgent, within 24 hours (uveitis management; delay risks vision loss) and same day (red-eye referral timing); infectious: treat organism; noninfectious: often topical corticosteroids; acute cases respond in days–weeks, chronic slowly Slides 63, 70
Mortality ★: Not covered in the lecture

Posterior uveitis3 not covered

Name of Condition: Posterior uveitis (also: choroiditis; retinitis) Slides 5, 64
Definition: Inflammation of the back of the eye: the choroid (vascular middle layer) and frequently the retina Slides 5, 64
Etiology (cause): Idiopathic, autoimmune, infectious (toxoplasmosis, cytomegalovirus) Slide 64
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Cells in posterior vitreous, vitreous haze, inflammation of retina or choroid; develops more slowly than anterior uveitis, may last years Slides 64–65
Clinical Manifestation: Blurred vision, floaters, scotomas, metamorphopsia; no pain if isolated posterior uveitis; may be acute and rapidly vision-threatening Slide 64
Diagnosis: Slit lamp exam and dilated fundoscopy; possibly fluorescein angiography (active vs inactive lesions) Slide 65
Treatment/Therapy: Refer to ophthalmology (long-term follow-up); by cause, like anterior uveitis, but not responsive to topical treatment: may need intraocular corticosteroid injection; exclude infection before immunosuppression Slide 65
Mortality ★: Not covered in the lecture

Lecture 11 · Neuro-Ophthalmology

Lauren Reynolds, MSPA, PA-C · 12 conditions · source: 11. Neuro-Ophthalmology STUDENT VERSION 2026.pptx

Nystagmus2 not covered

Name of Condition: Nystagmus Slide 3
Definition: Involuntary, biphasic, rhythmic, tremor-like oscillating movement of the eyes. Slide 3
Etiology (cause): Congenital (infantile or latent) or acquired; upbeat nystagmus is always abnormal (cerebellar or medullary lesion), less commonly drug intoxication; pendular type often congenital or after prolonged bilateral blindness beginning in childhood. Slides 3–4
Epidemiology (who): Most common form is horizontal jerk nystagmus. Slide 4
Risk Factors: Not covered in the lecture
Pathology: Jerk: slow drift then fast beat, named for the fast-phase direction (vertical, horizontal, torsional), worse gazing toward the fast phase; horizontal types: physiologic gaze-evoked, infantile, spasmus nutans, latent. Pendular: both phases equal velocity and amplitude, mostly horizontal. Slide 4
Clinical Manifestation: Usually symptomatic unless acquired before age 8: vertigo (often primary symptom, common with vestibular problems); oscillopsia (environment seems to move back and forth); blurred vision; abnormal compensatory head positioning. Slide 3
Diagnosis: Refer/work up: infants and young children with nystagmus; nystagmus acquired in adolescence or adulthood; concerning adult nystagmus (upbeat, monocular/asymmetric, non-physiologic horizontal). Complete ophthalmic exam, then initial imaging, then labs if relevant. Slide 5
Treatment/Therapy: Referral to ophthalmology; the underlying etiology must be addressed. Slide 5
Mortality ★: Not covered in the lecture

Opioid overdose (pupillary constriction)3 not covered

Name of Condition: Opioid overdose (pupillary constriction) Slide 12
Definition: Overdose of opioids, which act as parasympathomimetics on the pupil. Slide 12
Etiology (cause): Excess opioid intake. Slide 12
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Parasympathomimetic effect on the pupillary constriction pathway causes miosis. Slides 11–12
Clinical Manifestation: Decreased mental status, respiratory depression (under 12/min), decreased tidal volume, pupillary constriction; mental status and breathing are what matter clinically. Slide 12
Diagnosis: Monitor pupil size alongside breathing: pupils may re-constrict before respiratory depression returns, signaling need for another dose. Slide 12
Treatment/Therapy: Naloxone (preferably intravenous; intranasal available over the counter); lasts about 2 hours, so repeat if respiratory depression and coma return; can continue until pupils dilate. Slide 12
Mortality ★: Not covered in the lecture

Anisocoria2 not covered

Name of Condition: Anisocoria (also: asymmetric pupils; physiologic (benign) anisocoria) Slide 21
Definition: Unequal pupil size; pupils should be unequal only when the efferent pathways are not working properly. Slide 21
Etiology (cause): Most commonly physiologic. Small pupil abnormal: ocular condition preventing dilation, miotic drops (pilocarpine), sympathetic dysfunction (Horner). Large pupil abnormal: pharmacologic mydriasis (anticholinergics, sympathomimetics), trauma including prior eye surgery, Adie tonic pupil, cranial nerve III palsy. Slides 21–22
Epidemiology (who): Not covered in the lecture
Risk Factors: Ocular trauma; topical medications; toxin and drug exposure (atropine, ipratropium, scopolamine, glycopyrrolate, clonidine, phenylephrine, epinephrine). Slides 22–23
Pathology: Efferent limb is bilateral, so both pupils normally receive the same command. Anticholinergic pupil is usually 8 mm or more and nonreactive; sympathomimetic pupil only 1-2 mm larger than baseline. Slides 21–22
Clinical Manifestation: Physiologic: usually under 0.4 mm, equal in light and dark, no dilation lag, usually persistent, may switch sides. Small pupil abnormal if it dilates poorly in dim light; large pupil abnormal if it constricts poorly to light. Slides 20–22
Diagnosis: History (trauma, old photographs, topical drugs, toxins, neuro signs); compare pupils in light and dark. More in dark: apraclonidine (small pupil dilates = Horner). More in light: 0.1% pilocarpine constricts Adie pupil; no constriction to 1% pilocarpine = pharmacologic. Slides 20, 23
Treatment/Therapy: Physiologic anisocoria can be normal; note and document the difference so the cause can be worked out. Slide 20
Mortality ★: Not covered in the lecture

Relative afferent pupillary defect3 not covered

Name of Condition: Relative afferent pupillary defect (also: Marcus Gunn pupil) Slide 26
Definition: Pupil sign indicating an afferent defect, usually at the level of the retina or optic nerve. Slide 26
Etiology (cause): Lesion of the afferent limb of the pupillary reflex (retina or cranial nerve II), i.e. the pre-chiasmal visual pathway. Slide 26
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Diminished perception of light in the affected eye, so moving light from the normal eye to the affected eye makes both pupils dilate. Slide 26
Clinical Manifestation: Light in affected eye: no direct or consensual response; light in normal eye: both constrict; swinging light back to the affected eye: both pupils dilate at the same rate. Lid normal. Slides 24, 26
Diagnosis: Pupil exam moving a bright light from the normal to the affected eye. Differential: optic nerve lesion (glaucoma, optic neuritis/multiple sclerosis), retinal detachment, macular degeneration, CRVO (central retinal vein occlusion). Slide 26
Treatment/Therapy: Determined by the underlying cause. Slide 26
Mortality ★: Not covered in the lecture

Horner syndrome★ Professor emphasized3 not covered

Name of Condition: Horner syndrome (also: oculo-sympathetic paresis) Slide 28
Definition: Acquired condition following damage to the sympathetic nerve supply of the eye. Slide 28
Etiology (cause): Often idiopathic. 1st-order: brainstem stroke/tumor, spinal cord lesion above T1. 2nd-order: Pancoast tumor (superior pulmonary sulcus), thyroid cancer. 3rd-order: carotid dissection, cavernous sinus thrombosis. Slides 15, 30
Epidemiology (who): Not covered in the lecture
Risk Factors: Trauma (e.g. brachial plexus injury, carotid dissection); reported after COVID-19 with intubation/mechanical ventilation. Slides 15, 28
Pathology: Loss of the 3-neuron sympathetic pathway (hypothalamus, ciliospinal center of Budge C8-T2, superior cervical ganglion, along carotid) to the pupil dilator, facial sweat glands and Muller muscle. Slides 13, 30
Clinical Manifestation: ★ Classic triad: ptosis, miosis, anhidrosis (anhidrosis may be absent depending on lesion site). Hallmark: ★ dilation lag (anisocoria most evident 4-5 s after dimming lights). Normal levator function; usually unilateral. Slides 15, 24, 28–29, 49
Diagnosis: ★ Dilute apraclonidine drops: no effect on normal pupil, dilate the Horner pupil in most patients. Cocaine drops are an alternative (less sensitive, costly, special storage). Carotid dissection may add focal neurologic complaints. Slides 15, 28
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Argyll Robertson pupil★ Professor emphasized3 not covered

Name of Condition: Argyll Robertson pupil Slides 19, 32
Definition: Bilateral miosis with light-near dissociation: pupils do not constrict to light but quickly constrict with near accommodation. Slides 19, 32
Etiology (cause): Classically tertiary syphilis; also diabetes mellitus, chronic alcohol use, neurosarcoidosis, multiple sclerosis, encephalitis. Slide 32
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Exact mechanism unknown; suspected dorsal midbrain (pretectal) lesion interrupts the light reflex, while the near pathway skips that portion (★ basis of light-near dissociation). Slides 19, 32–33
Clinical Manifestation: Bilateral small, irregular pupils; weak or absent light response not improved by dark adaptation; normal or brisk near response; syphilis patients may have tabes dorsalis (posterior column involvement, sensory ataxia). Slides 24, 32
Diagnosis: Pupils slowly dilate with atropine drops; syphilis workup may be indicated. Slide 32
Treatment/Therapy: No treatment for the pupil itself; treat the underlying cause (syphilis: intramuscular penicillin G). Slide 32
Mortality ★: Not covered in the lecture

Adie tonic pupil2 not covered

Name of Condition: Adie tonic pupil (also: tonic pupil; Holmes-Adie syndrome) Slide 35
Definition: Dilated pupil with poor light reaction and slow, tonic constriction and re-dilation to near effort. Slide 35
Etiology (cause): Inflammation (infection vs autoimmune) damaging the ciliary ganglion or short ciliary nerves. Slide 35
Epidemiology (who): Often females in their 30s; often unilateral. Slide 36
Risk Factors: Not covered in the lecture
Pathology: Parasympathetic damage followed by aberrant reinnervation; pupil becomes supersensitive to cholinergic drops. Slides 35–36
Clinical Manifestation: Mydriasis, poor light reaction, slow near constriction then slow re-dilation; often asymptomatic or photophobia/blurring; sector paralysis on slit lamp; reduced corneal sensation; often absent Achilles/patellar reflexes; no ptosis or eye movement weakness. Slides 24, 35–36
Diagnosis: Dilute pilocarpine 0.1%: no effect on normal pupil, constricts the Adie pupil in most patients (unless acute phase); slit lamp; esthesiometer for corneal sensation. Slides 23, 36–37
Treatment/Therapy: Idiopathic Adie syndrome is largely benign: reassurance. Over time the pupil becomes smaller ("little old Adie"). Slide 36
Mortality ★: Not covered in the lecture

Cranial nerve III (oculomotor) palsy★ Professor emphasized1 not covered

Name of Condition: Cranial nerve III (oculomotor) palsy (also: third nerve palsy) Slides 39–40
Definition: Peripheral palsy of the oculomotor nerve (levator palpebrae, superior/inferior/medial rectus, inferior oblique, pupillary sphincter). Slides 39–40
Etiology (cause): Most common: microvascular disease (diabetes mellitus, hypertension). Most dreaded: compression by enlarging aneurysm, usually posterior communicating artery. Other: severe head trauma, migraine, uncal herniation. Slide 40
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetes mellitus; hypertension; severe head trauma (skull fracture and/or loss of consciousness). Slide 40
Pathology: Levator palpebrae inactivated (ptosis); sphincter pupillae tone lost (mydriasis); unopposed superior oblique and lateral rectus pull eye down and out. Slide 40
Clinical Manifestation: Ptosis, mydriasis, eye "down and out"; binocular horizontal, vertical, or oblique diplopia; reduced levator function, usually unilateral. Slides 24, 40, 49
Diagnosis: Classify complete vs incomplete and ★ pupil-involved vs pupil-spared. Pupil involved: immediate (STAT) CTA (computed tomography angiography) head/MRA (magnetic resonance angiography) brain. Pupil-sparing: reassurance and imaging, but not urgently. Slide 41
Treatment/Therapy: By etiology. Traumatic: observe about 6 months before corrective treatment; patch one eye for diplopia. Microvascular: good prognosis, improves within weeks, resolves by 3 months. Aneurysm pre-rupture: often endovascular coiling. Slide 41
Mortality ★: Aneurysm threatens rupture within hours or days; rupture is a cerebrovascular emergency. Slides 40–41

Cranial nerve IV (trochlear) palsy2 not covered

Name of Condition: Cranial nerve IV (trochlear) palsy (also: fourth nerve palsy) Slides 42–43
Definition: Peripheral palsy of the trochlear nerve, which supplies the superior oblique (intorts and depresses the eye); peripheral lesion gives ipsilateral deficits. Slides 42–43
Etiology (cause): Isolated palsy most commonly congenital (even in adults); acquired: trauma (even mild), microvascular disease (diabetes mellitus, hypertension). Slide 43
Epidemiology (who): Not covered in the lecture
Risk Factors: Trauma; diabetes mellitus; hypertension. Slides 43, 46
Pathology: Only nerve arising from the dorsal brainstem and crossing; with superior oblique weak, the inferior oblique is unopposed in medial gaze. Slides 42–43
Clinical Manifestation: Binocular vertical diplopia; deficit most apparent on adduction; compensatory head tilt to the opposite side improves hypertropia, ipsilateral tilt worsens it. Slide 43
Diagnosis: Isolated atraumatic palsy: MRI (magnetic resonance imaging) brain with and without contrast; hemoglobin A1C if risk factors and no known diabetes. Slide 46
Treatment/Therapy: Traumatic: observe about 6 months before corrective treatment; patch one eye for diplopia meanwhile. Congenital: patching in children (especially under 5) under an ophthalmologist. Microvascular: resolves by 3 months. Slide 46
Mortality ★: Not covered in the lecture

Cranial nerve VI (abducens) palsy2 not covered

Name of Condition: Cranial nerve VI (abducens) palsy (also: sixth nerve palsy) Slides 44–45
Definition: Peripheral palsy of the abducens nerve, which supplies the lateral rectus (abducts the eye). Slides 44–45
Etiology (cause): Children: most commonly intracranial tumors (brainstem, posterior fossa). Adults: most commonly microvascular disease (diabetes mellitus, hypertension); also major trauma (skull base fracture). Slide 45
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetes mellitus; hypertension; skull base fracture. Slides 45–46
Pathology: Lateral rectus weakness impairs abduction. Slide 44
Clinical Manifestation: Binocular horizontal diplopia. Slide 45
Diagnosis: Isolated atraumatic palsy: MRI (magnetic resonance imaging) brain with and without contrast; hemoglobin A1C if risk factors and no known diabetes. Slide 46
Treatment/Therapy: Traumatic: observe about 6 months before corrective treatment; patch one eye for diplopia meanwhile. Congenital: patching in children (especially under 5) under an ophthalmologist. Microvascular: improves within weeks, resolves by 3 months. Slide 46
Mortality ★: Not covered in the lecture

Ptosis2 not covered

Name of Condition: Ptosis (also: blepharoptosis) Slide 48
Definition: Drooping of the upper eyelid from a congenital or acquired abnormality of the muscles that elevate the eyelid. Slide 48
Etiology (cause): Cranial nerve III palsy, Horner syndrome, myasthenia gravis, myotonic dystrophy, pseudoptosis (dermatochalasis), mechanical (infection, inflammation, lid tumor), botulinum toxin injection, infectious botulism. Slide 49
Epidemiology (who): Not covered in the lecture
Risk Factors: Botulinum toxin injection of the eyelid or upper face; food or wound botulism exposure. Slide 49
Pathology: Lid elevators: levator palpebrae superioris (cranial nerve III) and sympathetic Muller muscle (extra 1-2 mm); orbicularis oculi (cranial nerve VII) closes the lids. Slide 48
Clinical Manifestation: Clues: cranial nerve III (reduced levator, mydriasis, eye movement deficit); Horner (normal levator, miosis); myasthenia gravis (variable through the day, fatigable, diplopia); botulism (bilateral palsies, symmetric descending weakness). Slide 49
Diagnosis: Assess levator function, laterality, pupil, eye movements and variability; myotonic dystrophy also has temporalis/sternocleidomastoid/distal weakness, cataracts, cardiac conduction issues, long hollow-cheeked face. Slide 49
Treatment/Therapy: Directed at the cause; botulinum toxin ptosis usually resolves in 3-4 weeks. Slide 49
Mortality ★: Not covered in the lecture

Pre- and post-chiasmal lesions (visual field defects)3 not covered

Name of Condition: Pre- and post-chiasmal lesions (visual field defects) Slides 51–52
Definition: Lesions along the visual pathway producing characteristic visual field defects depending on location. Slides 51–52
Etiology (cause): End-stage glaucoma (constricted field); optic neuritis in multiple sclerosis or macular degeneration (central scotoma); pituitary tumor (bitemporal hemianopia); stroke (homonymous hemianopia). Slide 51
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Pre-chiasm (optic nerve): single-eye loss. Chiasm: bitemporal hemianopia. Post-chiasm (tract, radiation, cortex): contralateral homonymous hemianopia; optic radiation lesions can give quadrantanopia; cortex may spare the macula. Slides 51–53
Clinical Manifestation: Constricted field (bilateral sometimes signifies hysteria), central scotoma, total monocular blindness, bitemporal hemianopia, homonymous hemianopia, superior quadrantanopia, macular-sparing hemianopia. Slides 51–53
Diagnosis: Thorough history and physical; labs and imaging (CT (computed tomography) head or MRI (magnetic resonance imaging) brain) if indicated. Slide 54
Treatment/Therapy: Ophthalmology referral; specialist referral as appropriate (neurology, vascular surgery, neurosurgery). Slide 54
Mortality ★: Not covered in the lecture

Lecture 12 · Acute Vision Loss

Monique Jaquith, DMSc, PA-C · 12 conditions · source: 12. Acute Vision Loss current - Jaquith.pptx

Amaurosis fugax2 not covered

Name of Condition: Amaurosis fugax (also: fleeting blindness) Slides 3–5
Definition: Transient, painless monocular vision loss lasting a few seconds to minutes; a group of disorders with benign to grave neurologic or ophthalmologic implications Slides 3–5
Etiology (cause): Retinal emboli of carotid (TIA, transient ischemic attack) or cardiac origin; retinal vascular spasm; also migraine or retinal artery occlusion Slides 3–5
Epidemiology (who): Not covered in the lecture
Risk Factors: Older age; diabetes; hypertension; atherosclerosis; cardiac valve disease; intravenous drug use; sickle cell; coagulation disorders; Raynaud phenomenon Slide 5
Pathology: Blockage in the blood vessels that supply the retina causes retinal ischemia Slides 4, 6
Clinical Manifestation: Transient "curtain" descending over the vision of one eye (less often ascending); mild blurring or fogging to complete blackness; part or all of the visual field; painless Slides 4, 6
Diagnosis: History: one or both eyes (cover each eye), duration, pain, exact symptoms; carotid Doppler if carotid source suspected; echocardiogram if cardiac source; MRA (magnetic resonance angiography) of all arteries for emboli Slides 4, 7
Treatment/Therapy: Treat the underlying cause; aspirin and clopidogrel to reduce stroke risk; carotid endarterectomy for carotid emboli; calcium channel blockers for Raynaud/vasospasm; early evaluation reduces vision loss (~85% fully recover, the rest progress to central retinal artery occlusion) Slide 8
Mortality ★: Not covered in the lecture

Acute angle-closure glaucoma1 not covered

Name of Condition: Acute angle-closure glaucoma (also: acute closed-angle glaucoma) Slides 9, 12, 14
Definition: Emergency: the iris blocks the drainage angle and intraocular pressure rises dramatically; can cause permanent blindness without prompt treatment Slides 9, 12, 14
Etiology (cause): Severe angle occlusion by the iris; obstruction may be secondary to tumor, scarring, or other mechanical causes Slides 9, 14
Epidemiology (who): Much less common than chronic open-angle glaucoma Slide 15
Risk Factors: Systemic anticholinergics (e.g. atropine); nebulized bronchodilators; history of anterior uveitis; lens dislocation; optic neuropathy; African American race Slide 14
Pathology: Closed angle: iris blocks outflow through the trabecular meshwork, so fluid builds up behind the iris and intraocular pressure rises Slides 9, 12, 14
Clinical Manifestation: Severe, sudden eye pain; decreased vision; colored halos around lights; headache, nausea, and vomiting common Slides 13, 16
Diagnosis: Dilated (fixed) pupil; hazy cornea; bilateral narrow or occluded angle; tonometry or gonioscopy shows intraocular pressure 40–80 mmHg Slides 11, 13, 17
Treatment/Therapy: Topical pilocarpine or topical beta-blocker (timolol); IV (intravenous) acetazolamide (carbonic anhydrase inhibitor), then mannitol or isosorbide; definitive: laser peripheral iridotomy 1–2 days after onset Slides 13, 20
Mortality ★: Not covered in the lecture

Chronic open-angle glaucoma1 not covered

Name of Condition: Chronic open-angle glaucoma (also: primary open-angle glaucoma) Slides 9, 15
Definition: Chronic, idiopathic optic nerve damage with an open angle and progressive peripheral visual field loss Slides 9, 15
Etiology (cause): Idiopathic; abnormal trabecular meshwork/canal of Schlemm secondary to aging Slides 9, 15
Epidemiology (who): Much more common than acute angle-closure; over 90% of glaucoma is primary open-angle Slides 12, 15
Risk Factors: African American race; Hispanic ethnicity; adults over 40 and increasing age; diabetes; family history; hypertension; myopia Slide 15
Pathology: Aging trabecular meshwork next to the canal of Schlemm becomes blocked → optic nerve damage and visual field loss, with or without elevated intraocular pressure; optic nerve cupping (widened, deepened cup from lost nerve fibers) Slides 12, 15, 19
Clinical Manifestation: Asymptomatic in most; may have persistently elevated bilateral intraocular pressure; gradual peripheral vision loss → "tunnel vision" → complete blindness Slides 13, 16
Diagnosis: Unobstructed open angle with optic nerve defects: increased cup-to-disc ratio, rim pitting/thinning, bayoneting (narrow angulations of vessels), splinter hemorrhages; visual field defects; intraocular pressure normal or high on tonometry/gonioscopy Slides 13, 18–19
Treatment/Therapy: Lower intraocular pressure; first-line drops: latanoprost, tafluprost, timolol (beta-blocker); if refractory/advanced: laser trabeculoplasty, then trabeculectomy with iridectomy Slides 12–13, 21
Mortality ★: Not covered in the lecture

Optic neuritis2 not covered

Name of Condition: Optic neuritis Slide 22
Definition: Inflammatory condition that damages the optic nerve Slide 22
Etiology (cause): Inflammation from multiple sclerosis, autoimmune disorders, postviral, or idiopathic Slide 23
Epidemiology (who): Usually 18–45 years old; 75% female Slide 23
Risk Factors: Not covered in the lecture
Pathology: Inflammatory, demyelinating damage to the optic nerve; recurrence carries a greater risk of developing multiple sclerosis Slides 22–24
Clinical Manifestation: Unilateral vision loss over hours to days; painful eye movement; RAPD (relative afferent pupillary defect; Marcus Gunn pupil); central vision and color vision loss; disc often normal-appearing; spontaneous recovery (near-normal vision at 1 year) Slides 23–24
Diagnosis: Clinical diagnosis from history and exam; full ophthalmic (slit lamp, dilated fundoscopy, color vision) and neurologic exam; MRI (magnetic resonance imaging) of brain and orbits with and without contrast (optic nerve enhancement; periventricular T2 FLAIR (fluid-attenuated inversion recovery) hyperintensities); may need labs Slides 23–24
Treatment/Therapy: Refer to ophthalmology; corticosteroids may quicken visual recovery and delay onset of multiple sclerosis; 2 or more demyelinating lesions on MRI → refer to neurology/neuro-ophthalmology Slide 24
Mortality ★: Not covered in the lecture

Retinal detachment1 not covered

Name of Condition: Retinal detachment Slides 25–26
Definition: Serious emergency in which the light-sensitive retina pulls away from its normal position; rhegmatogenous, traction, or serous/exudative types Slides 25–26
Etiology (cause): Commonly follows a retinal tear or hole Slide 26
Epidemiology (who): Most common after age 50 Slide 26
Risk Factors: Myopia; trauma; cataract extraction; diabetes; tumor; connective tissue diseases; family history Slide 26
Pathology: Age-related shrinkage of the vitreous humor causes traction on the retina Slide 26
Clinical Manifestation: New flashes and floaters (retinal tears); gray/black peripheral shadow, a "curtain or dark cloud" that may cover the whole field in days; sudden vision loss if the macula is involved; changes with head position Slide 27
Diagnosis: Direct and dilated ophthalmoscopy: elevated gray retina with folds, pigmented well-demarcated detachment, orange crescent-shaped tears; ultrasound determines type and is more sensitive than fundoscopy Slides 28–29
Treatment/Therapy: Emergency: refer immediately; surgical repair urgently or within a week by type: laser photocoagulation, cryotherapy, pneumatic retinopexy, vitrectomy, scleral buckle Slide 30
Mortality ★: Not covered in the lecture

Central retinal vein occlusion1 not covered

Name of Condition: Central retinal vein occlusion (also: CRVO) Slide 31
Definition: Blockage of the main retinal vein that prevents blood from draining, causing sudden blurry vision or vision loss Slide 31
Etiology (cause): Occlusion of the central retinal vein by a thrombus Slide 32
Epidemiology (who): More common than central retinal artery occlusion Slide 32
Risk Factors: Hypertension; diabetes; hyperlipidemia; Raynaud phenomenon; age over 50; hypercoagulable disorders; giant cell arteritis; endocarditis; atrial myxoma; obesity Slide 32
Pathology: Thrombus blocks venous drainage of the entire retina; neovascularization occurs weeks to months later Slides 32, 34–35
Clinical Manifestation: Sudden, painless vision loss, sometimes gradual over days to a week; more severe than branch occlusion Slides 33, 35
Diagnosis: Disc swelling, venous dilation, cotton wool spots, retinal hemorrhages: "blood and thunder" fundus; confirm with color fundus photography and fluorescein angiography; evaluate for underlying disorders Slide 34
Treatment/Therapy: Urgent referral to ophthalmologist to restore blood flow Slide 34
Mortality ★: Not covered in the lecture

Branch retinal vein occlusion6 not covered

Name of Condition: Branch retinal vein occlusion (also: BRVO) Slide 35
Definition: Blockage of a smaller side-branch retinal vein, affecting part of the eye Slide 35
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Occludes a branch vein rather than the main trunk, so only part of the retina is affected Slide 35
Clinical Manifestation: Vision loss limited to part of the eye; less severe than central retinal vein occlusion Slide 35
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Central retinal artery occlusion★ Professor emphasized1 not covered

Name of Condition: Central retinal artery occlusion (also: CRAO) Slide 36
Definition: Emergency that acts like a stroke in the eye, causing sudden, painless vision loss in one eye Slide 36
Etiology (cause): Arteriosclerosis; atherosclerosis; carotid or cardiac emboli Slide 37
Epidemiology (who): Less common than central retinal vein occlusion Slide 32
Risk Factors: Hypertension; diabetes; hyperlipidemia; Raynaud phenomenon; old age; hypercoagulable disorders; giant cell arteritis; endocarditis; atrial myxoma; obesity; atrial fibrillation Slide 37
Pathology: Blocked central retinal artery: ★ irreversible retinal damage may occur after 90 minutes; ★ risk of stroke increases at onset of the occlusion; neovascularization weeks to months later Slides 37, 39
Clinical Manifestation: Painless, profound vision loss over seconds; acuity counting fingers to light perception; temporal "island" of vision; ★ pupil slow to direct light but brisk when the other eye is illuminated Slide 38
Diagnosis: Pale retinal swelling with cherry-red spot at the fovea; blocked arteries, segmented venous blood, emboli; color fundus photography and fluorescein angiography show absent perfusion Slide 39
Treatment/Therapy: Prompt treatment: high-concentration inhaled oxygen and digital massage over the eyelid; IV (intravenous) acetazolamide to lower intraocular pressure; anterior chamber paracentesis; thrombolytic into the ophthalmic artery within 8 hours Slide 40
Mortality ★: Not covered in the lecture

Branch retinal artery occlusion5 not covered

Name of Condition: Branch retinal artery occlusion (also: BRAO) Slide 41
Definition: Sudden, painless blockage of a smaller branch retinal artery in one eye Slide 41
Etiology (cause): Embolus or clot Slide 41
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Blocks a branch vessel rather than the main arterial trunk, so ischemia is localized Slide 41
Clinical Manifestation: Sudden, painless, partial, localized vision loss in one eye (vs severe, widespread loss in central occlusion) Slide 41
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Papilledema3 not covered

Name of Condition: Papilledema Slides 42–43
Definition: Swelling of the optic disc caused by increased intracranial pressure Slides 42–43
Etiology (cause): Tumor; trauma; intracranial infection; hemorrhage; vitamin A toxicity Slide 43
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Raised intracranial pressure swells the optic disc; acute: hemorrhages, cotton wool spots; chronic: elevated disc, blurred margins; atrophic: optic nerve axons die Slides 43, 45
Clinical Manifestation: Non-specific vision changes (flickering, blurry, double vision); signs of raised intracranial pressure: nausea, vomiting, headache Slide 44
Diagnosis: Ophthalmoscopy: engorged retinal veins, swollen disc, ± hemorrhages; lumbar puncture: raised opening pressure confirms it; MRI (magnetic resonance imaging) and/or CT (computed tomography) of the head to rule out mass lesion Slide 46
Treatment/Therapy: Treat the underlying disorder Slide 46
Mortality ★: Not covered in the lecture

Non-arteritic anterior ischemic optic neuropathy2 not covered

Name of Condition: Non-arteritic anterior ischemic optic neuropathy (also: NAION) Slides 47–48
Definition: Sudden loss of blood flow to the front of the optic nerve (optic disc) causing rapid, painless vision loss; the non-arteritic type Slides 47–48
Etiology (cause): Not covered in the lecture
Epidemiology (who): 90–95% of cases; age 40–60 Slide 48
Risk Factors: Small, crowded optic disc ("disc at risk"); hypertension; diabetes; high cholesterol; sleep apnea Slides 48, 52
Pathology: Optic disc ischemia; optic nerve edema resolves within 8 weeks, leaving atrophy Slides 47, 52
Clinical Manifestation: Sudden, painless loss of side or central vision; swollen, pale optic nerve head; usually one eye first, the other at risk; mild visual improvement in some over months Slides 50, 52
Diagnosis: Diagnosis of exclusion: same workup as arteritic to exclude giant cell arteritis; medical evaluation (hypertension, diabetes, anemia); neuroimaging if unclear Slide 52
Treatment/Therapy: Observation and cardiovascular risk factor modification; consider avoiding bedtime antihypertensives (nocturnal hypotension); counsel on risk to the other eye Slide 52
Mortality ★: Not covered in the lecture

Arteritic anterior ischemic optic neuropathy2 not covered

Name of Condition: Arteritic anterior ischemic optic neuropathy (also: AAION; giant cell (temporal) arteritis) Slides 47, 49
Definition: Sudden loss of blood flow to the front of the optic nerve from giant cell arteritis; medical emergency to prevent vision loss in the other eye Slides 47, 49
Etiology (cause): Giant cell arteritis (temporal arteritis), an inflammation of blood vessels Slide 49
Epidemiology (who): Age 55 and older Slide 49
Risk Factors: Not covered in the lecture
Pathology: Arteritic inflammation cuts blood flow to the optic disc; biopsy shows thickening of the media and endothelium Slides 47, 49, 51
Clinical Manifestation: Sudden, painless vision loss; swollen, pale optic nerve head; one eye first; systemic: malaise, weight loss, fever, temporal/occipital headache, scalp tenderness (hair combing), jaw claudication (pain with chewing) Slides 49–50
Diagnosis: ESR (erythrocyte sedimentation rate) and CRP (C-reactive protein); temporal artery biopsy is the gold standard (may wait up to 1 week after starting steroids); color Doppler ultrasound may be suggestive Slide 51
Treatment/Therapy: Refer emergently any patient over 50 with sudden vision loss; early IV (intravenous) methylprednisolone x3 days, then slow oral taper for 6–12+ months; famotidine for ulcer prophylaxis; tocilizumab as steroid-sparing option; osteoporosis prevention Slide 51
Mortality ★: Not covered in the lecture

Lecture 13 · Chronic Vision Loss and Tumors of the Eye

Valerie Beck, DMSc, PA-C · 15 conditions · source: Chronic Vision Loss & Tumors - Dr Rappa.pptx

Idiopathic intracranial hypertension★ Professor emphasized2 not covered

Name of Condition: Idiopathic intracranial hypertension (also: pseudotumor cerebri) Slides 4–5
Definition: Elevated intracranial pressure (elevated lumbar puncture opening pressure) of idiopathic cause; also called pseudotumor cerebri. Slides 4–5
Etiology (cause): Idiopathic. Slide 4
Epidemiology (who): Primarily overweight females of childbearing age. Slide 4
Risk Factors: Overweight; obesity-related metabolic syndrome is often associated. Slides 4, 6
Pathology: Not covered in the lecture
Clinical Manifestation: Intractable headaches of variable features · transient visual loss · pulsatile tinnitus (intracranial noises) · pain behind the eyes · mild pain with eye movement or globe compression · signs: ★ papilledema, visual field loss, abducens (sixth cranial nerve) palsy. Slide 4
Diagnosis: MRI (magnetic resonance imaging) of brain with and without contrast plus magnetic resonance venography (rules out cerebral venous sinus thrombosis) · lumbar puncture: elevated opening pressure · systemic blood pressure · ophthalmology: perimetry, dilated fundoscopy, optic nerve photography. Slides 5–6
Treatment/Therapy: Start acetazolamide promptly + weight reduction program with a dietitian; followed by ophthalmology and neurology · failure/intolerance of medical therapy: surgical cerebrospinal fluid diversion (optic nerve sheath fenestration or ventriculoperitoneal shunt). Slide 5
Mortality ★: Not covered in the lecture

Primary open-angle glaucoma★ Professor emphasized1 not covered

Name of Condition: Primary open-angle glaucoma Slide 8
Definition: The most common form of glaucoma: progressive optic nerve damage and visual field loss, typically with normal (open) anterior chamber angles and elevated intraocular pressure. Slide 8
Etiology (cause): Optic nerve damage from elevated intraocular pressure; "primary" = no known secondary cause of open-angle glaucoma. Slides 9, 40
Epidemiology (who): Adult onset; many patients do not know they have it. Slide 9
Risk Factors: Elevated intraocular pressure · age · race · family history of glaucoma. Slide 8
Pathology: Open angle at the trabecular meshwork (versus closed in angle-closure) · excavation (cupping) of the optic nerve: cup-to-disc ratio 0.2 normal, 0.7 to 0.99 in glaucoma. Slides 7–8
Clinical Manifestation: Often asymptomatic at onset, then slowly progressive, painless vision loss · peripheral loss with ★ central acuity initially spared · optic cupping, characteristic field loss on perimetry, may have elevated intraocular pressure. Slides 8, 40
Diagnosis: Annual ophthalmology exam · optic nerve damage on fundoscopy and/or perimetry, adult onset, normal-appearing angles on gonioscopy, no secondary cause. Slide 9
Treatment/Therapy: Goal: preserve vision · eyedrops that lower pressure by reducing aqueous production or increasing outflow: beta blockers (timolol), alpha-2 agonists (brimonidine), carbonic anhydrase inhibitors (dorzolamide), prostaglandin analogs (latanoprost) · laser trabeculoplasty · surgery · damage is irreversible, but treatment preserves vision. Slide 9
Mortality ★: Not covered in the lecture

Myopia2 not covered

Name of Condition: Myopia (also: nearsightedness) Slide 18
Definition: Refractive error with excessive refractive power: distant objects focus in front of the retina. Slide 18
Etiology (cause): "Long eyeball", generally from an overly protruding cornea. Slide 18
Epidemiology (who): Not covered in the lecture
Risk Factors: Family history (genetic) · prolonged periods of reading · ocular trauma displacing the lens forward. Slide 18
Pathology: Excess refractive power places the focal point anterior to the retina. Slide 18
Clinical Manifestation: Reduced clarity of distance vision (refractive error is the most common cause of reduced visual acuity); blur improves with corrective lenses. Slides 17–18, 40
Diagnosis: Snellen chart in primary care · pinhole occluder overcomes most refractive errors · confirmed by an optometrist with a phoropter. Slide 17
Treatment/Therapy: Refer suspected isolated refractive error to an optometrist · concave spherical lens (negative diopter) scatters light and moves focus back onto the retina · first line: spectacles, contact lenses, laser refractive surgery. Slides 17–18
Mortality ★: Not covered in the lecture

Hyperopia2 not covered

Name of Condition: Hyperopia (also: farsightedness) Slide 19
Definition: Refractive error with insufficient refractive power: distant objects focus behind the retina. Slide 19
Etiology (cause): "Short eyeball", generally from a flat cornea. Slide 19
Epidemiology (who): Not covered in the lecture
Risk Factors: Anything that shortens the eye's axial length: ocular trauma displacing the lens backward, mass effect of an orbital tumor behind the retina. Slide 19
Pathology: Insufficient refractive power places the focal point posterior to the retina. Slide 19
Clinical Manifestation: Reduced clarity of vision (refractive error is the most common cause of reduced visual acuity); blur improves with corrective lenses. Slides 17, 40
Diagnosis: Snellen chart in primary care · pinhole occluder overcomes most refractive errors · confirmed by an optometrist with a phoropter. Slide 17
Treatment/Therapy: Refer suspected isolated refractive error to an optometrist · convex spherical lens (positive diopter) converges light and moves focus forward onto the retina · first line: spectacles, contact lenses, laser refractive surgery. Slides 17, 19
Mortality ★: Not covered in the lecture

Astigmatism2 not covered

Name of Condition: Astigmatism Slide 20
Definition: Refractive error with uneven curvature of the cornea or lens, so no point focus forms on the retina: multiple focal points. Slide 20
Etiology (cause): Uneven (oval) curvature of the cornea or lens. Slide 20
Epidemiology (who): Not covered in the lecture
Risk Factors: Largely unknown; possibly genetic or developmental. Slide 20
Pathology: Oval-shaped cornea produces multiple focal points instead of one. Slide 20
Clinical Manifestation: Blurry image; blur improves with corrective lenses. Slides 20, 40
Diagnosis: Snellen chart in primary care · pinhole occluder overcomes most refractive errors · confirmed by an optometrist with a phoropter. Slide 17
Treatment/Therapy: Refer suspected isolated refractive error to an optometrist · corrected with a toric lens · first line: spectacles, contact lenses, laser refractive surgery. Slides 17, 20
Mortality ★: Not covered in the lecture

Presbyopia2 not covered

Name of Condition: Presbyopia Slide 21
Definition: Not a refractive error: age-related loss of the lens's normal accommodation for near vision. Slide 21
Etiology (cause): With age the lens grows larger, thicker and much less elastic, so it can no longer round up when the zonular fibers loosen. Slide 21
Epidemiology (who): Starts around age 45; essentially zero accommodation by age 65 to 70. Slide 21
Risk Factors: Increasing age. Slide 21
Pathology: Lost ability to increase focusing power at reading distance, so the near image focuses behind the retina. Slide 21
Clinical Manifestation: Cannot focus on objects at arm's length or closer. Slide 21
Diagnosis: Not covered in the lecture
Treatment/Therapy: Convex lens for near only: a half-glass, or the bottom part of bifocals if distance correction is also needed. Slide 21
Mortality ★: Not covered in the lecture

Strabismus2 not covered

Name of Condition: Strabismus Slides 25, 30
Definition: Misalignment of the eyes: esotropia (in), exotropia (out), hypertropia (up), hypotropia (down). Slides 25, 30
Etiology (cause): Many causes: disorder of the brain, cranial nerves, neuromuscular junction or extraocular muscles · children: congenital (infantile esotropia, Duane, Mobius, Brown syndromes) or acquired (accommodative esotropia, sensory esotropia from cataract, tumors, thyroid eye disease, myasthenia gravis, raised intracranial pressure). Slides 25, 27
Epidemiology (who): Not covered in the lecture
Risk Factors: Down syndrome (higher prevalence of esotropia) · cerebral palsy · thyroid eye disease (restrictive, muscle inflammation). Slide 29
Pathology: Neurologic causes include cranial nerve palsies: third (ptosis, pupil involvement, exotropia with vertical deviation), fourth (vertical diplopia worse on downgaze), sixth (horizontal diplopia, esotropia). Slides 25, 29
Clinical Manifestation: Adult: diplopia that disappears when either eye is covered · one eye fails to track, fixate or move fully in a gaze direction · complications: amblyopia (up to 50% of younger children), diplopia (acquired, age 4+), extraocular muscle contracture. Slides 25, 28
Diagnosis: History, pattern of misalignment, associated findings · confirm with the cover test (elicits fixation movement of the misaligned eye) · displaced corneal light reflex in moderate to large deviations. Slides 25, 28
Treatment/Therapy: Refer to ophthalmology at any age for comprehensive exam; prognosis depends on the underlying cause. Slide 28
Mortality ★: Not covered in the lecture

Amblyopia★ Professor emphasized1 not covered

Name of Condition: Amblyopia (also: lazy eye) Slide 33
Definition: Developmental vision disorder: one eye fails to reach normal acuity even with glasses or contact lenses. Slide 33
Etiology (cause): Abnormal early visual development; the brain favors one eye · causes: strabismus (most common), anisometropia (large prescription difference between eyes; seen with eyelid hemangioma, congenital ptosis), deprivation (cataract, ptosis, corneal opacity). Slides 30, 33
Epidemiology (who): ★ The most common cause of vision loss in children; up to 3 to 5% of children. Slide 33
Risk Factors: Strabismus (up to 50% of younger children with strabismus develop amblyopia) · significant refractive difference between eyes · congenital ptosis, cataract. Slides 28, 30, 33
Pathology: Brain ignores input from the weaker eye, which develops poor vision; unequal vision develops in the first decade. Slides 30, 33
Clinical Manifestation: Usually the same signs as strabismus · unequal vision between the eyes · occlusion objection: child unbothered when the amblyopic eye is covered, fussy when the good eye is covered. Slides 30, 32
Diagnosis: Screen all children under 5 (USPSTF (US Preventive Services Task Force), American Academy of Pediatrics) · preverbal: fixation reflex, occlusion objection, vertical prism tests · verbal (usually over 3): optotypes; unilateral = 2 or more lines difference. Slides 30–32
Treatment/Therapy: Refer all to ophthalmology · patch the good eye (or dilate it with atropine drops) · outcome good for most if treated before age 7, though many do not reach normal vision; better if started under age 5, with better baseline acuity and good compliance. Slide 34
Mortality ★: Not covered in the lecture

Cataract★ Professor emphasized1 not covered

Name of Condition: Cataract (also: acquired and pediatric (congenital)) Slide 36
Definition: Lens proteins break down and clump, clouding the lens and impairing vision; most develop slowly and are age-related. Slide 36
Etiology (cause): Aging (most common overall) · secondary to other eye disease · trauma · medications · systemic disease · pediatric: most commonly idiopathic. Slide 36
Epidemiology (who): Mostly age-related · posterior subcapsular: ★ more rapid onset, classically under 50. Slides 36–37
Risk Factors: Diabetes · corticosteroid use · cigarette smoking · UV (ultraviolet) exposure. Slide 36
Pathology: Acquired: nuclear (central yellow-brown), posterior subcapsular (plaque near back of lens), cortical (peripheral spoke-like) · pediatric: ★ zonular is the most common, polar, nuclear, posterior lenticonus. Slides 37–38
Clinical Manifestation: Slowly progressive blur, glare (bright sun, night headlights) · nuclear: myopic shift, distance worse than near · posterior subcapsular: trouble reading · pediatric: inattentive if bilateral, smaller eye, nystagmus · ★ a cataract alone does NOT cause a relative afferent pupillary defect. Slides 36–37
Diagnosis: Early: slit lamp exam · advanced: loss of red reflex on ophthalmoscopy, leukocoria (white pupil) · non-urgent ophthalmology referral for slit lamp and dilated fundoscopy (urgent if secondary uveitis or glaucoma). Slides 36, 39
Treatment/Therapy: Surgery only (extraction with lens implant), deferred until it impairs daily activities unless neonatal (amblyopia risk) or it hinders or causes other eye disease · full visual recovery in 99% · declines surgery: trial of mydriasis (cyclopentolate), annual review · posterior capsule opacification after surgery: YAG (yttrium aluminum garnet) laser. Slide 39
Mortality ★: Not covered in the lecture

Retinoblastoma★ Professor emphasized

Name of Condition: Retinoblastoma Slide 41
Definition: Rare eye cancer, primarily of young children, developing in the retina. Slide 41
Etiology (cause): Caused by a mutation. Slide 41
Epidemiology (who): Primarily young children; rare in adults. Slides 41, 47
Risk Factors: Family history. Slide 41
Pathology: Unilateral or bilateral retinal tumor; calcifications on imaging; metastasis usually within 1 year of diagnosis. Slides 41–42, 47
Clinical Manifestation: Poor vision or strabismus · ★ leukocoria if the tumor is large and near the back of the lens · smaller tumors seen only on ophthalmoscopy. Slide 41
Diagnosis: Screen red reflex and alignment; refer suspected cases within weeks (family history: within the first 8 weeks of life, exam under anesthesia) · dilated ophthalmoscopy + imaging · biopsy contraindicated (tumor seeding). Slide 42
Treatment/Therapy: Ocular oncologist: multimodal therapy, or enucleation if very large · genetic counseling · best outcomes with early diagnosis, small tumors, no metastasis. Slide 42
Mortality ★: Death nearly 100% if untreated; treated 5-year survival over 95%; no recurrence 5 years after diagnosis = cured. Slide 42

Primary uveal melanoma★ Professor emphasized

Name of Condition: Primary uveal melanoma (also: includes iris, ciliary body and choroidal melanoma) Slide 45
Definition: ★ The most common eye cancer in adults, arising from melanocytes of the uveal tract (choroid, ciliary body or iris). Slide 45
Etiology (cause): Melanocytes of the uvea; distinct from cutaneous and conjunctival melanoma. Slide 45
Epidemiology (who): Adults. Slide 45
Risk Factors: Cutaneous or iris nevi · cutaneous freckles · ocular melanocytosis. Slides 45, 50, 54
Pathology: Melanotic or amelanotic; iris (anterior uvea), ciliary body or choroid (posterior uvea); ciliary body tumors may show a sentinel vessel and extrascleral extension. Slide 44
Clinical Manifestation: Usually asymptomatic, found on routine surveillance · iris melanoma: slow-growing dark brown or translucent mass, usually inferior, unilateral, over 3 mm base and 1 mm deep, prominent feeder vessel, corectopia (pupil pulled out of shape). Slides 45, 50
Diagnosis: Refer to ophthalmology for fundoscopy and testing (ocular oncologist) · clinical diagnosis: history, exam, imaging · FNA (fine needle aspiration) biopsy for molecular prognostic testing · differential: iris nevus, congenital heterochromia. Slides 45–46
Treatment/Therapy: Most common treatment: radiation therapy; surgical resection now less common; local treatment effective. Slide 46
Mortality ★: High metastatic risk, often present at diagnosis; ★ liver is the most common site · 10-year mortality 32%; iris melanoma far better (about 4 to 10%). Slide 46

Iris nevus3 not covered

Name of Condition: Iris nevus (also: nevus of the iris) Slide 48
Definition: Small, pigmented, benign spot on the iris; typically harmless. Slide 48
Etiology (cause): Not covered in the lecture
Epidemiology (who): Often clinically apparent around puberty. Slide 48
Risk Factors: Not covered in the lecture
Pathology: Pigmented or nonpigmented; typically does not grow; usually not vascular; low risk of transformation to melanoma. Slides 48–49
Clinical Manifestation: Asymptomatic · usually inferior half of iris · flat or minimally elevated (under 1 mm), uncommonly over 3 mm · may cause corectopia (pupil pulled out of shape) or iris ectropion (iris pigment epithelium on the anterior iris surface). Slides 48–49
Diagnosis: Refer to ophthalmology to rule out melanoma · ABCDEF growth predictors: Age 40 or under, Blood in anterior chamber, Clock-hour inferior, Diffuse, Ectropion, Feathery margins. Slides 49, 51
Treatment/Therapy: Ophthalmology surveillance, more frequent at first, then annual with dilated fundoscopy · ocular oncologist for concerning lesions. Slide 49
Mortality ★: Not covered in the lecture

Conjunctival melanoma2 not covered

Name of Condition: Conjunctival melanoma Slide 52
Definition: Rare but potentially fatal eye cancer of the conjunctiva. Slide 52
Etiology (cause): More similar to cutaneous and mucosal melanoma than to uveal melanoma. Slides 45, 52
Epidemiology (who): Typically middle-aged to elderly patients. Slide 52
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Usually asymptomatic, found on routine surveillance · nodular, well-vascularized, dark brown or translucent conjunctival mass · prominent conjunctival feeder vessel. Slide 52
Diagnosis: Refer to ophthalmology (ocular oncologist) · clinical diagnosis: history, exam, imaging · wide excisional biopsy · differential: conjunctival nevus (stable, cysts, well-defined borders), primary acquired melanosis. Slides 52–54
Treatment/Therapy: Wide excision (orbital exenteration if advanced) + adjunctive radiation · sentinel lymph node biopsy to detect early metastasis. Slide 53
Mortality ★: Potentially fatal; 10-year mortality 39%. Slides 52–53

Squamous cell carcinoma7 not covered

Name of Condition: Squamous cell carcinoma Slide 55
Definition: Not covered in the lecture
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Non-pigmented lesion that may appear gelatinous or leukoplakic (white patch). Slide 55
Diagnosis: Can be mistaken for amelanotic melanoma. Slide 55
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Lecture 14 · Ocular Trauma

Chand Shah, MPAS, PA-C · 14 conditions · source: CMS I Ocular Trauma - Shah Fallsv.pptx

Open globe injury3 not covered

Name of Condition: Open globe injury Slide 14
Definition: Ocular injury with a full-thickness defect in the cornea and/or sclera; divided into full-thickness eye wall laceration and globe rupture Slide 14
Etiology (cause): Sharp object or high-velocity projectile (eye wall laceration) or severe blunt trauma (globe rupture) Slides 14–15, 17
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Intraocular compartments are exposed to the external environment Slide 14
Clinical Manifestation: Pupil distorted (usually toward the wound); flat anterior chamber; extruding uveal tissue; massive hemorrhagic chemosis; soft eye; deep eyelid laceration; intraocular blood (hyphema, vitreous hemorrhage) Slide 14
Diagnosis: CT (computed tomography) without contrast for eye penetration; with metal or organic penetration: CT of the orbit, no MRI (magnetic resonance imaging); never dilate the eye when trauma is suspected Slide 6
Treatment/Therapy: Tape a protective shield over the eye and consult ophthalmology immediately; antiemetic, analgesics, tetanus vaccine; do not remove a penetrating object; immediate surgical repair Slides 6, 17
Mortality ★: Not covered in the lecture

Full-thickness eye wall laceration4 not covered

Name of Condition: Full-thickness eye wall laceration Slide 15
Definition: Open globe injury that cuts completely through the cornea, sclera, or both Slide 15
Etiology (cause): Sharp object or high-velocity projectile (e.g., fishing hook, knife) Slide 15
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Object may be withdrawn/extruded before evaluation, retained in the wound, or pass through (entry and exit wound); cut lens capsule makes the lens hydrated, edematous, opaque; lens fragments in the anterior chamber cause inflammation Slides 15–16
Clinical Manifestation: Not covered in the lecture
Diagnosis: Fundoscopic exam, always checking the anterior compartments Slide 16
Treatment/Therapy: Lensectomy required but may be delayed past globe repair (to treat hyphema/inflammation and plan intraocular lens placement); leave posterior-segment foreign bodies alone at initial evaluation Slide 16
Mortality ★: Not covered in the lecture

Globe rupture3 not covered

Name of Condition: Globe rupture Slide 17
Definition: Splitting or tearing of the cornea and/or sclera at a weak point Slide 17
Etiology (cause): Severe blunt ocular trauma (e.g., car airbag, fist, baseball) Slide 17
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Common sites: posterior to the extraocular muscles (especially superonasal quadrant), along prior intraocular surgery incisions, lamina cribrosa Slide 17
Clinical Manifestation: Suspect with any blunt trauma causing massive hemorrhagic chemosis or a soft eye Slide 17
Diagnosis: CT (computed tomography) may be done to rule out a foreign object Slide 17
Treatment/Therapy: Protective shield taped over the eye and immediate ophthalmology consult; antiemetic, analgesics, tetanus vaccine; immediate surgical repair (wound exploration and repair) Slide 17
Mortality ★: Not covered in the lecture

Corneal abrasion2 not covered

Name of Condition: Corneal abrasion Slide 18
Definition: Scratching or scraping away of some of the corneal epithelium Slide 18
Etiology (cause): Injury such as a fingernail or contact lens manipulation Slide 18
Epidemiology (who): One of the most common ophthalmic injuries Slide 18
Risk Factors: Not covered in the lecture
Pathology: Loss of epithelium exposes the basement membrane, which takes up fluorescein Slide 18
Clinical Manifestation: Severe foreign body sensation, tearing, light sensitivity, blurred vision Slide 18
Diagnosis: Slit-lamp exam with fluorescein (stains the exposed basement membrane) shows the extent Slide 18
Treatment/Therapy: Topical broad-spectrum antibacterial: erythromycin ointment (no contact lens, or organic source); ciprofloxacin, ofloxacin or tobramycin (contact lens wear); no patching (slide 18 suggests it; it neither speeds healing nor eases pain); periodic re-exam; never prescribe topical anesthetic drops (delay healing, mask worsening, cause corneal ulcer) Slides 18, 20
Mortality ★: Not covered in the lecture

Corneal/conjunctival foreign body3 not covered

Name of Condition: Corneal/conjunctival foreign body Slide 21
Definition: Object with too little momentum to pass through the eye wall becomes embedded in the cornea or conjunctiva Slide 21
Etiology (cause): History of grinding or striking metal Slide 21
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Iron or copper foreign bodies leave a rust ring Slide 22
Clinical Manifestation: Foreign body sensation, light sensitivity, excessive tearing Slide 21
Diagnosis: Slit lamp shows small bodies; larger ones visible on diffuse light exam; linear vertical corneal epithelial defects mean a foreign body under the upper lid (tarsal conjunctiva): evert the lid promptly Slide 21
Treatment/Therapy: Topical anesthetic, slit-lamp exam, remove with sterile 27-gauge needle (upper-lid body: cotton-tipped applicator); rust ring: battery-operated burr drill; antibiotics + abrasion care; ophthalmology if it may have passed through the cornea Slides 21–22
Mortality ★: Not covered in the lecture

Hyphema2 not covered

Name of Condition: Hyphema Slide 24
Definition: Hemorrhage/blood in the anterior chamber from trauma injuring its blood vessels Slide 24
Etiology (cause): Blunt or penetrating trauma Slide 24
Epidemiology (who): Not covered in the lecture
Risk Factors: Sickle cell anemia and aspirin/antiplatelet drugs raise the risk of secondary hemorrhage Slide 25
Pathology: High risk of secondary hemorrhage causing permanent visual loss; most rebleeding occurs in the first 72 hours Slide 25
Clinical Manifestation: Blurred vision, eye pain, light sensitivity; can be a sign of open globe Slide 24
Diagnosis: Diffuse light exam (gross hyphema), slit lamp, comprehensive ophthalmic exam; measure IOP (intraocular pressure) unless penetrating injury is suspected Slides 24–25
Treatment/Therapy: Goal: prevent rebleeding; bedrest, head of bed slightly up; antiemetics; corticosteroids; cycloplegic drops; oral aminocaproic acid (antifibrinolytic); avoid aspirin/antiplatelets; treat high pressure (beta blockers, pilocarpine, acetazolamide, osmotic agents) Slide 25
Mortality ★: Not covered in the lecture

Lid laceration4 not covered

Name of Condition: Lid laceration (also: eyelid laceration) Slide 26
Definition: Laceration of the eyelid; full-thickness or partial-thickness Slide 26
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Unrepaired deep medial-third laceration (canalicular system transection) causes chronic tearing Slide 27
Clinical Manifestation: Full-thickness lid laceration accompanies corneal laceration or globe rupture in about 2/3 of cases Slide 26
Diagnosis: Determine whether it goes through the tarsal plate of the upper lid; check margin, medial canthus, lacrimal system, inner lid surface, ptosis, levator Slides 26–27
Treatment/Therapy: Ophthalmology consult: lid margin, within 6-8 mm of medial canthus, lacrimal duct/sac, inner lid surface, ptosis, tarsal plate or levator; partial-thickness: emergency room repair, ophthalmology in 2-3 days; face may be left open 24 h before closure Slides 26–27, 30
Mortality ★: Not covered in the lecture

Orbital and lid contusion4 not covered

Name of Condition: Orbital and lid contusion Slide 31
Definition: Eye trauma causing soft tissue swelling within the orbit without hemorrhage Slide 31
Etiology (cause): Eye trauma Slide 31
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Tarsal plate and orbital septal margin act as a wall that keeps blood in the anterior tissues Slide 31
Clinical Manifestation: Preseptal ecchymosis or hematoma Slide 31
Diagnosis: Not covered in the lecture
Treatment/Therapy: Supportive to surgical depending on status; must rule out brain trauma Slide 31
Mortality ★: Not covered in the lecture

Periorbital hematoma6 not covered

Name of Condition: Periorbital hematoma Slide 33
Definition: Bleeding within the orbit, around the eye Slide 33
Etiology (cause): Trauma; orbit/eyelid surgery; peribulbar injections; orbital varices; lymphangiomas and arteriovenous malformations; anticoagulants; sickle cell anemia; orbital pseudotumor; idiopathic Slide 33
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Lateral canthotomy with cantholysis (expose lateral canthal tendon, incise its inferior branch) to drain the blood Slide 33
Mortality ★: Not covered in the lecture

Rhegmatogenous retinal detachment2 not covered

Name of Condition: Rhegmatogenous retinal detachment Slide 35
Definition: Retinal detachment from one or more full-thickness breaks in the sensory retina Slide 35
Etiology (cause): Retinal breaks + vitreous traction let liquefied vitreous pass into the subretinal space; usually spontaneous and age-related Slide 35
Epidemiology (who): Most common type of retinal detachment Slide 35
Risk Factors: Myopia, cataract surgery, ocular trauma; usually preceded by posterior vitreous detachment Slides 35, 37
Pathology: Not covered in the lecture
Clinical Manifestation: Shadow or curtain descending over vision; cloudy/smoky vision, floaters, flashes; monocular field defects; reduced central acuity if macula involved Slide 36
Diagnosis: History and dilated eye exam; refer immediately, seen by ophthalmology within 24 hours Slide 36
Treatment/Therapy: Surgical; immediate ophthalmology; pain control, antiemetics, head of bed at 30-40 degrees Slide 35
Mortality ★: Not covered in the lecture

Traction retinal detachment5 not covered

Name of Condition: Traction retinal detachment Slides 35, 39
Definition: One of the three types of retinal detachment; typically more localized, with a concave shape Slides 35, 39
Etiology (cause): Most commonly proliferative diabetic retinopathy Slide 39
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: More localized, concave detachment; starts along the vasculature, then spreads to the retina and macula Slide 39
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Surgical Slide 39
Mortality ★: Not covered in the lecture

Exudative (serous) retinal detachment6 not covered

Name of Condition: Exudative (serous) retinal detachment (also: serous retinal detachment) Slide 39
Definition: Detachment without a retinal break or vitreoretinal traction Slide 39
Etiology (cause): Systemic vascular or inflammatory disease, or intraocular tumors Slide 39
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Manage the underlying condition Slide 39
Mortality ★: Not covered in the lecture

Orbital floor (blowout) fracture4 not covered

Name of Condition: Orbital floor (blowout) fracture (also: blowout fracture; orbital fracture) Slide 40
Definition: Fracture of the orbital floor (most often) or medial wall Slide 40
Etiology (cause): Blunt object (fist, ball) raises orbital pressure and blows out the floor; or a blow to the infraorbital rim buckles the floor Slide 40
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Periorbital ecchymosis, lid edema, infraorbital numbness, subcutaneous emphysema; diplopia on upward gaze (inferior rectus entrapment) or lateral gaze (medial rectus); severe pain, bradycardia, vomiting on attempted eye movement (entrapment); children: white-eyed blowout (entrapment without orbital soft tissue signs) Slides 41–42
Diagnosis: CT (computed tomography) of orbits and midface Slide 43
Treatment/Therapy: No entrapment/eye injury: ice, analgesics, follow up 2-3 days; sinus blood: antibiotics; true blowout: ophthalmology (30% globe injury); entrapment: immediate facial trauma surgeon (muscle necrosis); surgery may wait 1-2 weeks Slide 43
Mortality ★: Not covered in the lecture

Basilar skull fracture5 not covered

Name of Condition: Basilar skull fracture Slide 44
Definition: Linear fracture of the skull base (cribriform, orbital plate of frontal, temporal, sphenoid or occipital bone) Slide 44
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Often asymptomatic; Battle sign (bruising behind the ear), raccoon eyes (periorbital bruising); hemotympanum (blood in the middle ear); CSF (cerebrospinal fluid) leak: clear or pink rhinorrhea, otorrhea Slides 44–46
Diagnosis: CSF (cerebrospinal fluid) may be dextrose-positive; halo/double ring sign (inner ring of blood, outer ring of cerebrospinal fluid) on filter paper or bedsheet; CT (computed tomography) of orbits, though fractures may not show Slides 44, 46–47
Treatment/Therapy: CSF (cerebrospinal fluid) leak: neurosurgery consult and admission; admission based on condition, associated injuries, brain injury on CT (computed tomography); antibiotics controversial (resistant organisms) Slide 47
Mortality ★: Not covered in the lecture