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PAJ 5500 · Class of 2028

Clinical Medicine and Surgery I · Exam 2

Ophthalmology block — everything that has to be recallable cold

How to use this: this is a condensed, night-before-the-exam reference, not a replacement for the full study guide — it assumes you've already learned the material and just need the highest-yield facts at a glance. If a term feels unfamiliar, go back to the full guide for the explanation.

★ HER OWN INSTRUCTION — MAKE THIS CHART

TermWhat you need to know
What she said, verbatim“My recommendation to you guys for those is again, use your resources, MAKE A CHART — which ones cause PAIN, which ones don’t cause pain? Which ones are UNILATERAL, which ones are BILATERAL? Which ones will cause which PHYSICAL EXAM ABNORMALITIES, like FIXED PUPILS, for example. That’s how you’re gonna differentiate these.”
How hard she committed to it“Particularly your PINK EYE — know the difference and how to differentiate those. That’s a thousand percent on the exam because that’s on your boards. So that’s definitely gonna be on your exam. AT LEAST TWO QUESTIONS MINIMUM. Haven’t made those questions yet, but I guarantee you those are gonna be on the exam.”
PAINLESSENTROPION · ECTROPION · DERMATOCHALASIS · XANTHELASMA · BLEPHARITIS / MEIBOMITIS · CHALAZION · PINGUECULA · PTERYGIUM · SUBCONJUNCTIVAL HEMORRHAGE · ALLERGIC CONJUNCTIVITIS · VIRAL CONJUNCTIVITIS · CHLAMYDIAL CONJUNCTIVITIS - ADULT INCLUSION · TRACHOMA · AUTOIMMUNE CONJUNCTIVITIS · POSTERIOR UVEITIS.
PAINFULHORDEOLUM · DACRYOADENITIS · DACRYOCYSTITIS · GONOCOCCAL CONJUNCTIVITIS · EPISCLERITIS · SCLERITIS · PRE-SEPTAL CELLULITIS · POST-SEPTAL CELLULITIS · KERATITIS · HERPES SIMPLEX KERATITIS · HERPES ZOSTER KERATITIS · CORNEAL ULCER · ANTERIOR UVEITIS. Note EPISCLERITIS is MILD pain and SCLERITIS is SEVERE, BORING and WORSE AT NIGHT — that contrast is the whole point of the pair. POST-SEPTAL cellulitis adds PAIN ON EYE MOVEMENT.
PAIN VARIES / dependsCHEMOSIS · BACTERIAL CONJUNCTIVITIS. BACTERIAL conjunctivitis is soreness rather than true pain; CHEMOSIS depends entirely on its cause.
BILATERALDERMATOCHALASIS · XANTHELASMA · BLEPHARITIS / MEIBOMITIS · ALLERGIC CONJUNCTIVITIS · VIRAL CONJUNCTIVITIS · CHLAMYDIAL CONJUNCTIVITIS - NEONATAL · TRACHOMA · AUTOIMMUNE CONJUNCTIVITIS. VIRAL starts in ONE eye and spreads to the other — do not let the first day fool you.
UNILATERALCHALAZION · HORDEOLUM · DACRYOADENITIS · DACRYOCYSTITIS · SUBCONJUNCTIVAL HEMORRHAGE · BACTERIAL CONJUNCTIVITIS · CHLAMYDIAL CONJUNCTIVITIS - ADULT INCLUSION · EPISCLERITIS · SCLERITIS · PRE-SEPTAL CELLULITIS · POST-SEPTAL CELLULITIS · KERATITIS · HERPES SIMPLEX KERATITIS · HERPES ZOSTER KERATITIS · CORNEAL ULCER · ANTERIOR UVEITIS. DACRYOADENITIS is unilateral EXCEPT the viral form, which is usually bilateral.
EITHER / not defined by sideENTROPION · ECTROPION · PINGUECULA · PTERYGIUM · CHEMOSIS · GONOCOCCAL CONJUNCTIVITIS · POSTERIOR UVEITIS.
PUPIL abnormalities — she named theseANTERIOR UVEITIS: pupil small and IRREGULAR, may be stuck to lens or cornea. POST-SEPTAL CELLULITIS: possible AFFERENT PUPILLARY DEFECT. ACUTE GLAUCOMA (on the red-eye chart): DILATED and FIXED. Everything else on the list leaves the pupil alone — and that is itself the discriminator.
PINK EYE — the one she guaranteedALLERGIC: ITCH, bilateral, watery/stringy, PAPILLAE (“looks like a strawberry”), NO node. VIRAL: adenovirus, profuse WATERY, FOLLICLES, TENDER preauricular node, one eye then the other. BACTERIAL: thick YELLOW/WHITE, often UNILATERAL, PAPILLAE, usually NO node. GONOCOCCAL: SEVERE purulent WITH a palpable node. CHLAMYDIAL: CHRONIC >1 month, stringy mucoid, FOLLICLES, failed topicals.
Findings are SUGGESTIVE, not definitiveHer caveat about papillae and follicles: “There are some findings that could be suggestive, but they’re NOT DEFINITIVE.”

How This Exam Is Written

TermWhat you need to know
Almost all vignettes“Pretty much all clinical vignettes… recognize conditions by the vignette.” Read for the DEFINING FEATURE, not the disease name.
What the lead-in asks“SOME diagnosis, but A LOT are next management plan, first line treatment, patient education.” The lead-in decides the answer — read it before the options.
Pictures“Way more non-pictures than pictures.” Do not bank on recognizing a photograph.
Which half is this?CMS = MANAGEMENT. Clin Path I Lecture 4 = MECHANISM, on the same condition list. If the question asks WHY the tissue fails, that is the other course.

★ THE RED EYE — Before You Name It

TermWhat you need to know
The first 60 secondsVISUAL ACUITY each eye with correction · PUPILS (shape, reactivity, afferent defect) · EXTRAOCULAR MOVEMENTS (pain? restriction?) · CORNEAL CLARITY + FLUORESCEIN · pattern of INJECTION and DISCHARGE · history of CONTACT LENS, TRAUMA, SURGERY, STEROIDS.
THE TWO RED FLAGSREDUCED VISION or an ABNORMAL PUPIL. “Do not let obvious redness substitute for an eye examination.”
Danger signs — NOT conjunctivitisModerate-severe pain or CONSENSUAL PHOTOPHOBIA · reduced acuity/RAPD/abnormal pupil · corneal opacity, infiltrate, ulcer or DENDRITE · CILIARY FLUSH, hypopyon, high pressure · proptosis, diplopia, painful restricted movement · chemical or penetrating injury, recent surgery · CONTACT LENS WEARER WITH PAIN.
Localize by patternCONJUNCTIVA: itch/discharge, diffuse, VISION PRESERVED. CORNEA: pain/photophobia, fluorescein defect. ANTERIOR CHAMBER: CONSENSUAL photophobia, ciliary flush, irregular pupil. SCLERA/ORBIT: deep pain or painful movement, violaceous, proptosis. ANGLE CLOSURE: pain+headache+halos+nausea, cloudy cornea, MID-DILATED pupil.
TWO EXCEPTIONS TO THE SEQUENCECHEMICAL — IRRIGATE FIRST, before history or exam, then check pH normalized. OPEN GLOBE — rigid shield, NO pressure, NO TONOMETRY, nil by mouth, emergency consult.
Referral timingEMERGENT NOW: chemical injury, open globe, angle closure, ORBITAL cellulitis, endophthalmitis. SAME DAY: keratitis/corneal ulcer, ANTERIOR UVEITIS, SCLERITIS, ocular herpes zoster. URGENT 24–48h: unexplained vision loss, persistent pain/photophobia, atypical red eye. ROUTINE: uncomplicated conjunctivitis, chronic lid disease.

Eyelids

TermWhat you need to know
ENTROPION vs ECTROPIONENTROPION turns IN → foreign body sensation → TRICHIASIS → corneal abrasion. ECTROPION turns OUT → tearing → EXPOSURE KERATOPATHY. CN VII palsy causes ECTROPION only. SURGERY IS DEFINITIVE for both.
DERMATOCHALASISExcess loose skin + orbital fat prolapse, from AGING. “Heaviness,” “looking through lashes.” EXAMINE VISUAL FIELDS — a deficit is what gets BLEPHAROPLASTY covered by insurance.
XANTHELASMAOval YELLOWISH plaques, asymptomatic. WORK UP THE METABOLISM: lipid profile + fasting glucose/HbA1C + liver function. Treat the underlying issue. Local: cryotherapy, laser, peel, excision. RECURRENCES ARE COMMON. Caveat: many patients have NORMAL lipids.
BLEPHARITIS / MEIBOMITISROSACEA · SEBORRHEIC DERMATITIS · STAPH AUREUS. Crusting/scaling at LASH BASES, thick TOOTHPASTE-LIKE meibomian secretion, decreased or frothy tear film. LID HYGIENE FIRST → if no better at 2 WEEKS, topical abx → then oral. CHRONIC: CONTROLLED, NOT CURED.
CHALAZION vs HORDEOLUMCHALAZION: STERILE meibomian obstruction, days–weeks, NON-TENDER. HORDEOLUM: acute INFECTION (staph), 24h/overnight, TENDER. Both: warm compresses + massage.
When to refer a lid lumpHORDEOLUM: no better in 2 WEEKS → ophtho for I&D. CHALAZION: no resolution → ophtho for steroid injection or curettage; IMPROVEMENT MAY TAKE MONTHS. RECURRENT, or persisting >2–3 MONTHS → REFER TO RULE OUT SEBACEOUS CARCINOMA.

Lacrimal

TermWhat you need to know
DACRYOADENITIS = GLANDLATERAL ⅓ of the UPPER lid. INFLAMMATORY MOST COMMON (bacterial rare, viral usually bilateral). ± ipsilateral PREAURICULAR node, temporal injection, fever, leukocytosis. Inflammatory → CORTICOSTEROIDS, response in 48h.
DACRYOCYSTITIS = SACNASAL aspect of the LOWER lid, BELOW the medial canthal tendon. From NASOLACRIMAL DUCT OBSTRUCTION. Mucoid/purulent discharge EXPRESSIBLE FROM THE LOWER PUNCTUM.
A mass ABOVE the tendonNOT dacryocystitis — suspect a LACRIMAL SAC TUMOR (rare).
Dacryocystitis managementAfebrile, well, reliable → OUTPATIENT ORAL ABX ×10 DAYS. Febrile, ill, unreliable → ADMIT, IV 48–72h then oral to complete 10–14 days. Improvement expected 24–48h. Afterwards: PROBING AND IRRIGATION often needed, may need surgery.
THE HEDGESImaging is NOT automatic for either — reserve CT for severe disease, orbital findings, chronicity, atypical presentation, suspected abscess/mass, or failure to improve. DO NOT START STEROIDS until infection is reasonably excluded.

Conjunctiva & Surface

TermWhat you need to know
PINGUECULA vs PTERYGIUMBoth from SUN and WIND, almost always at 3 or 9 O’CLOCK. PTERYGIUM EXTENDS ONTO THE CORNEA; PINGUECULA DOES NOT. “Pterodactyls fly (into cornea), penguins can’t.”
Pterygium managementSun/dust/wind protection + lubricating drops — but CONSERVATIVE MANAGEMENT WILL NOT RESOLVE IT. NON-URGENT referral if GROWING or VISION AFFECTED. Surgery if distorting vision.
SUBCONJUNCTIVAL HEMORRHAGEVALSALVA · bleeding disorder · ANTIPLATELET/ANTICOAGULANT · HYPERTENSION. Painless, vision/pupil/cornea NORMAL. HISTORY IS THE WORKUP — CHECK THE BP if unexplained. Reassurance; resolves 2–4 WEEKS.
Recurrent hemorrhage — the hedgeNOT automatic hematology referral. Medication review, blood pressure, TARGETED evaluation for hematologic disease.
CHEMOSISConjunctival SWELLING — a SIGN, not a diagnosis. Allergy, infection, thyroid eye disease, angioedema, trauma, orbital cellulitis, impaired venous drainage. URGENT if with PROPTOSIS, RESTRICTED MOVEMENT, REDUCED VISION or an AFFERENT PUPILLARY DEFECT.

Conjunctivitis — All Of It

TermWhat you need to know
Acute vs chronicACUTE ≤ 4 WEEKS. CHRONIC > 4 WEEKS.
PAPILLAE vs FOLLICLESPAPILLAE: RED at surface, PALER at base → BACTERIAL (except chlamydia) and ALLERGIC. FOLLICLES: PALE at surface, REDDER at base → CHLAMYDIAL and VIRAL. PREAURICULAR NODE → chlamydial, GONOCOCCAL, viral.
ALLERGICITCH · bilateral · watery/stringy · chemosis · papillae · NO NODE · vision preserved. Avoid allergen, cool compresses, artificial tears, topical H1 ± mast cell stabilizer — OLOPATADINE DOES BOTH — plus systemic H1.
VIRALADENOVIRUS. Profuse WATERY discharge, FOLLICLES, TENDER PREAURICULAR NODE, starts one eye then the other, recent URI. Cool compresses, artificial tears, CONTAGIOUS PRECAUTIONS. Often WORSE OVER WEEK ONE, resolves 2–3 WEEKS. Refer if >3 wks, or photophobia/vision loss after onset.
BACTERIALTHICK YELLOW/WHITE discharge, often UNILATERAL, papillae, usually NO node. Immunocompetent adult → TOPICAL BROAD-SPECTRUM (fluoroquinolone) + contagious precautions.
URGENT REFERRAL in bacterialImmunocompromised · CONTACT LENS WEARER · recent eye surgery · foreign body · corneal opacity or suspected keratitis · NO IMPROVEMENT IN 24 HOURS.
GONOCOCCAL — the exceptionSEVERE purulent discharge WITH a PALPABLE PREAURICULAR NODE. NEWBORN = EMERGENCY: hospitalize, SYSTEMIC CEFTRIAXONE, cultures + Gram stain, test for chlamydia and dissemination. Untreated → CORNEAL PERFORATION.
CHLAMYDIAL — adultSerotypes D–K. CHRONIC (a month+), stringy mucoid, FOLLICLES, UNRESPONSIVE TO TOPICALS. Confirm: conjunctival NAAT or DFA. DOXYCYCLINE 100 mg BD × 7 DAYS. Avoid sun, full glass of water, stay upright, separate from antacids/iron/calcium/magnesium. EVALUATE FOR OTHER STIs, NOTIFY PARTNERS.
CHLAMYDIAL — neonateERYTHROMYCIN 50 mg/kg/day divided QID × 14 DAYS. MONITOR UNDER 6 WEEKS FOR INFANTILE HYPERTROPHIC PYLORIC STENOSIS — erythromycin is a MOTILIN RECEPTOR AGONIST. Often admitted because of concomitant PNEUMONIA.
TRACHOMASerotypes A, B, C. ***LEADING INFECTIOUS CAUSE OF BLINDNESS WORLDWIDE. Most active cases ASYMPTOMATIC. MDA: AZITHROMYCIN 1 g PO SINGLE DOSE where prevalence ≥5%. CHAIN: inflammation → LID SCARRING → ENTROPION → TRICHIASIS → blindness. TRICHIASIS NEEDS SURGERY.
AUTOIMMUNERecurrent/chronic hyperemia, MINIMAL PAIN, NO DISCHARGE, systemic complaints. Pemphigoid, Stevens–Johnson, Sjögren, GVHD. ROUTINE ophtho referral.

Episcleritis vs Scleritis

TermWhat you need to know
EPISCLERITISOften IDIOPATHIC. MILD acute pain, FOCAL/SECTORAL redness, NO discharge, NO photophobia. Vessels CAN be moved with a cotton tip.
THE TEST2.5% PHENYLEPHRINE, WAIT 15 MINUTES → EPISCLERAL VESSELS BLANCH.
Episcleritis treatmentArtificial tears + ORAL NSAID TAKEN WITH FOOD. No response in 2 DAYS → refer. Usually self-limited; may recur in either eye.
SCLERITISOften SYSTEMIC AUTOIMMUNE. SEVERE BORING PAIN, WORSE AT NIGHT, radiating to face. VIOLACEOUS HUE = choroid through THINNED sclera. Vessels CANNOT be moved. Pain WITH EYE MOVEMENT.
Scleritis managementURGENT REFERRAL — SCLERA AT RISK OF PERFORATION, may need a surgical patch. Slit lamp + fundoscopy, work up the systemic cause.
THE FIRST SIGN OF RESPONSEDECREASED PAIN — even if the inflammation looks unchanged.
The hedgesNon-infectious ANTERIOR scleritis commonly BEGINS with systemic NSAIDs; steroids/immunomodulators for severe, NECROTISING, posterior or refractory disease. PERFORATION RISK IS GREATEST IN NECROTISING DISEASE, not uniformly.

Cornea

TermWhat you need to know
CILIARY FLUSHRing of red vessels from the LIMBUS around the cornea (anterior ciliary arteries). Means inflammation of CORNEA, IRIS or CILIARY BODY. Seen in: CORNEAL INFLAMMATION (ulcer, keratitis) · ANTERIOR UVEITIS · ACUTE GLAUCOMA. It RULES OUT simple conjunctivitis.
KERATITISRisks: corneal trauma, DRY EYES, CONTACT LENS OVERWEAR, topical ocular STEROIDS. Signs: corneal OPACIFICATION, “BROKEN UP” corneal light reflection, CILIARY FLUSH. URGENT REFERRAL WITHIN 24h for slit lamp + fluorescein.
The ring infiltrateACANTHAMOEBA — contact lens wearers with POOR HYGIENE, e.g. RINSING LENSES IN TAP WATER.
Undertreated keratitisCORNEAL SCARRING or PERFORATION → ENDOPHTHALMITIS → POSSIBLE REMOVAL OF THE EYE. Bacterial prognosis: good for small–moderate, POOR for severe, WORSE INSIDE THE VISUAL AXIS.
HSV vs HZV keratitisSIMPLEX: TRUE DENDRITE — tree-branching, ELEVATED EDGES, TERMINAL END BULBS. PATHOGNOMONIC. Younger. Skin NOT dermatomal, may cross midline. ZOSTER: PSEUDODENDRITE — lacks all three. Older. DERMATOMAL, usually V1, RESPECTS THE MIDLINE, often spares lower lid.
HUTCHINSON SIGNVesicle on the TIP OF THE NOSE = NASOCILIARY branch = HIGHER RISK OF OCULAR INVOLVEMENT.
Herpetic treatmentORAL ANTIVIRALS (aciclovir/valaciclovir/famciclovir) ×10 DAYS, ideally within 72h of rash onset. IV aciclovir for severe, disseminated, orbital, retinal, CNS or significantly immunocompromised. NO TOPICAL GLUCOCORTICOIDS BY THE PCP IN ACTIVE HSV EPITHELIAL DISEASE.
CORNEAL ULCERCONTACT LENS USE = MAJOR RISK. Patient RESISTS OPENING THE EYE. Ciliary flush + corneal defect. EMERGENT REFERRAL — a step above keratitis. Swab central/large ulcers. Start BROAD-SPECTRUM TOPICAL (4th-gen fluoroquinolone). STEROIDS CAN WORSEN INFECTION IF STARTED TOO EARLY, especially FUNGAL or HERPETIC — leave to ophtho. NEXT-DAY follow-up; most heal 2–3 WEEKS.
The contact lens caseREMOVE LENSES, DO NOT PATCH · NO take-home ANESTHETIC (delays healing, masks progression) · NO empiric STEROID · SAME-DAY ophthalmology · PRESERVE LENSES AND CASE for culture. Do NOT delay treatment solely to obtain a culture.

Uveitis

TermWhat you need to know
ANTERIOR (iritis/iridocyclitis)PAIN, photophobia, redness AT THE CORNEAL EDGE, VISION OFTEN PRESERVED. CELLS IN THE ANTERIOR CHAMBER, CONSENSUAL PHOTOPHOBIA, CILIARY FLUSH, variable IOP, IRREGULAR PUPIL stuck to lens/cornea, KERATIC PRECIPITATES (WBC on the corneal endothelium).
Anterior managementURGENT REFERRAL WITHIN 24h for slit lamp + dilated fundoscopy — DELAY MAY COST VISION. Infectious → treat organism. Non-infectious → TOPICAL CORTICOSTEROIDS. Recurrent or systemic features → THOROUGH SYSTEMIC EVALUATION.
POSTERIOR (choroiditis/retinitis)Blurred vision, FLOATERS, SCOTOMAS, METAMORPHOPSIA — and NO PAIN if isolated. CELLS IN THE POSTERIOR VITREOUS, vitreous haze. Idiopathic, autoimmune, INFECTIOUS: TOXOPLASMOSIS, CMV.
Posterior management — THE DIFFERENCEDOES NOT RESPOND TO TOPICAL TREATMENT — may need an INTRAOCULAR CORTICOSTEROID INJECTION. Fluorescein angiography helps separate ACTIVE from INACTIVE lesions. Develops far more slowly, may last YEARS. INFECTION MUST BE EXCLUDED BEFORE IMMUNOSUPPRESSION.

Cellulitis & Diagnostics

TermWhat you need to know
Both formsDIRECT EXTENSION from bacterial SINUS, SKIN or DENTAL infection. In DIABETIC/ELDERLY/IMMUNOCOMPROMISED consider FUNGUS — ASPERGILLOSIS, MUCORMYCOSIS.
THE GIVEAWAYPRE-SEPTAL: THE EYE ITSELF IS WHITE, movements FULL and PAINLESS, vision normal. POST-SEPTAL: eye RED, PROPTOSIS, PAINFUL RESTRICTED MOVEMENT, DIPLOPIA, reduced vision, possible AFFERENT PUPILLARY DEFECT.
WorkupCT ORBITS + PARANASAL SINUSES WITH CONTRAST · complete ocular exam with fundoscopy · Gram stain and culture of drainage · CBC with differential · BLOOD CULTURES.
ManagementMILD PRE-SEPTAL → outpatient ORAL abx 10–14 DAYS vs STAPH (±MRSA) and STREP. ADMIT + IV 48–72h then oral ≥1 week if: moderate-severe/toxic, poor compliance, CHILD ≤5 YEARS, no improvement on orals — AND ALL POST-SEPTAL.
UntreatedINTRACRANIAL SPREAD → MENINGITIS or CAVERNOUS SINUS THROMBOSIS. Expect improvement 24–48h. May need ENT, OMFS, and/or ID consults.
The hedgeMILD, CLEARLY PRE-SEPTAL disease with normal vision, pupils and painless full movements may be managed CLINICALLY WITHOUT ROUTINE CT.
The four modalitiesSLIT LAMP: anterior — lids, cornea, conjunctiva, sclera, iris. OPHTHALMOSCOPY: direct / indirect / SLIT-LAMP (most common). FLUORESCEIN EXAM: dye INSTILLED, Wood's lamp — abrasions, ulcers, foreign bodies. FLUORESCEIN ANGIOGRAPHY: dye INJECTED, reaches eye in 10–15 SEC, blue flash, NO IODINE — retina and choroid blood flow.

★ THE RULE SHE SAID TWICE

TermWhat you need to know
SUDDEN VISION LOSSIS A STROKE UNTIL PROVEN OTHERWISE. You can have a stroke with NO other symptom. EVERYONE GETS AN MRA (magnetic resonance angiography).
The four questionsONE EYE OR BOTH? · SUDDEN OR GRADUAL? · CENTRAL OR PERIPHERAL? · PAINFUL OR PAINLESS? These four decide the diagnosis, not the fundus.
PAINFULACUTE ANGLE-CLOSURE GLAUCOMA (severe, at rest) · OPTIC NEURITIS (on eye MOVEMENT). Everything else here is PAINLESS.
BOTH EYESPAPILLEDEMA, or a lesion at/behind the CHIASM. Everything else is MONOCULAR.
“CURTAIN” = TWO DIAGNOSESAMAUROSIS FUGAX — curtain LIFTS in seconds to minutes. RETINAL DETACHMENT — curtain STAYS and advances over days. DURATION separates them.
Refer emergentlyANY patient OVER 50 with SUDDEN VISUAL LOSS.

Amaurosis Fugax

TermWhat you need to know
WhatTRANSIENT MONOCULAR vision loss. “FLEETING BLINDNESS.” SECONDS TO MINUTES. PAINLESS.
IF IT LASTED HOURSIT IS NOT A TIA (transient ischemic attack). Duration is the first filter.
CauseRetinal emboli, CAROTID or CARDIAC. Most commonly a TIA (transient ischemic attack). Also RETINAL VASCULAR SPASM.
RisksOlder age, DM (diabetes mellitus), HTN (hypertension), ATHEROSCLEROSIS, cardiac VALVE disease, IVDU (intravenous drug use), SICKLE CELL, coagulation disorders, RAYNAUD’S.
WorkupCAROTID DOPPLER if carotid suspected · ECHO (echocardiogram) if cardiac · MRA for everyone.
TreatmentTREAT THE UNDERLYING CAUSE. Stroke risk → ASA (aspirin) + CLOPIDOGREL. Carotid emboli → ENDARTERECTOMY. Raynaud’s/spasm → CALCIUM CHANNEL BLOCKERS.
Prognosis~85% FULL RECOVERY. The rest PROGRESS TO CRAO (central retinal artery occlusion).

Glaucoma — Acute vs Chronic

TermWhat you need to know
ACUTE = CLOSED ANGLEIRIS BLOCKS THE DRAINAGE CIRCUIT. SEVERE SUDDEN EYE PAIN, HEADACHE, NAUSEA/VOMITING, COLORED HALOS, decreased vision. HAZY CORNEA, pupillary dilation, narrow/occluded angle.
THE PRESSURE40–80 mmHg on TONOMETRY or GONIOSCOPY.
Acute treatmentTOPICAL PILOCARPINE (alpha-blocker) or TIMOLOL (beta-blocker) · IV ACETAZOLAMIDE then MANNITOL or ISOSORBIDE. DEFINITIVE = LASER PERIPHERAL IRIDOTOMY, 1–2 DAYS AFTER ONSET.
Acute RISK FACTORSSYSTEMIC ANTICHOLINERGICS (atropine) · NEBULIZED BRONCHODILATORS · prior ANTERIOR UVEITIS · lens dislocation · AFRICAN AMERICAN RACE. Obstruction from TUMOR or SCARRING.
CHRONIC = OPEN ANGLETRABECULAR MESHWORK abnormality by the CANAL OF SCHLEMM, from AGING. MUCH MORE COMMON. ASYMPTOMATIC in most. PAINLESS.
Chronic field lossPERIPHERAL FIRST → patients say “TUNNEL VISION” → then blindness.
THE CLASSIC SIGNOPTIC NERVE CUPPING — increased CUP-TO-DISC RATIO. Also RIM PITTING, BAYONETING (vessels with narrow angulations), SPLINTER HEMORRHAGES, rim thinning.
Chronic pressureMAY BE NORMAL OR ELEVATED — nerve damage occurs either way.
Chronic risksAFRICAN AMERICAN race, HISPANIC, ADULTS OVER 40, DM, age, FAMILY HISTORY, HTN, MYOPIA.
Chronic treatmentFIRST-LINE: LATANOPROST · TAFLUPROST · TIMOLOL drops. Refractory/advanced → LASER TRABECULOPLASTY. SURGERY IS DEFINITIVE FOR BOTH FORMS.
The missed caseAn INTRACTABLE HEADACHE LOCALIZED BEHIND THE EYE with a RED EYE. Glaucoma is a LEADING CAUSE OF BLINDNESS WORLDWIDE.

Optic Neuritis

TermWhat you need to know
Who18–45 YEARS OLD, 75% FEMALE. A much YOUNGER group than everything else here.
CauseMULTIPLE SCLEROSIS, autoimmune, POSTVIRAL, or idiopathic.
SymptomsUNILATERAL loss over HOURS TO SEVERAL DAYS · PAINFUL EYE MOVEMENT · central vision loss · LOSS OF COLOR VISION.
SignsOften a NORMAL-APPEARING DISC. RELATIVE AFFERENT PUPILLARY DEFECT (MARCUS GUNN).
WorkupREFER TO OPHTHALMOLOGY. Slit lamp, dilated fundoscopy, COLOR VISION + neuro exam. MRI (magnetic resonance imaging) BRAIN AND ORBITS, WITH AND WITHOUT CONTRAST.
THE THRESHOLD≥2 CHARACTERISTIC DEMYELINATING LESIONS → treat and refer to NEUROLOGY / NEURO-OPHTHALMOLOGY.
Treatment & prognosisCORTICOSTEROIDS if demyelinating. SPONTANEOUS RECOVERY IS THE RULE — improves within WEEKS, usually NORMAL WITHIN A YEAR.
EducationRECURRENCE = GREATER RISK OF MS (multiple sclerosis). Find the cause; do not just treat the episode.

Retinal Detachment

TermWhat you need to know
WhatTraction detachment, commonly AFTER A RETINAL TEAR OR HOLE. Types: RHEGMATOGENOUS, TRACTION, SEROUS/EXUDATIVE.
WhoMOST COMMON AFTER AGE 50 — the vitreous SHRINKS with age.
RisksMYOPIA, TRAUMA, CATARACT EXTRACTION, DM, tumor, CONNECTIVE TISSUE DISEASE, family history.
FLASHES & FLOATERSREPRESENT THE TEAR, not the detachment.
ThenGRAY OR BLACK SHADOWS peripherally, may cover the WHOLE EYE WITHIN DAYS. “CURTAIN or DARK CLOUD.” PAINLESS.
MACULA INVOLVED→ SUDDEN LOSS OF VISION in that eye.
Odd but usefulVISION CHANGES WITH HEAD POSITION — the retina is floating loose.
FundusELEVATED GRAY retina WITH FOLDS · PIGMENTED WELL-DEMARCATED area · TEARS ARE ORANGE AND CRESCENT SHAPED. ULTRASOUND IS MORE SENSITIVE THAN FUNDOSCOPY and types it.
TreatmentEMERGENCY — REFER IMMEDIATELY. Surgery urgently or within a week by type: LASER PHOTOCOAGULATION · CRYOTHERAPY · PNEUMATIC RETINOPEXY · VITRECTOMY · SCLERAL BUCKLE.

The Four Vascular Occlusions

TermWhat you need to know
CRAO — CENTRAL RETINAL ARTERY OCCLUSIONEMBOLUS. A STROKE IN THE EYE. IRREVERSIBLE DAMAGE AFTER 90 MINUTES.
CRAO presentationPAINLESS PROFOUND LOSS OVER SECONDS. Acuity COUNTING FINGERS TO LIGHT PERCEPTION. “ISLAND” OF VISION IN THE TEMPORAL FIELD.
CRAO PUPIL — the clueSLOW TO DIRECT LIGHT, BUT BRISK WHEN THE OTHER EYE IS ILLUMINATED.
CRAO fundusPALE SWELLING of the posterior segment + CHERRY-RED SPOT AT THE FOVEA. Emboli in the central artery.
CRAO treatmentHIGH-CONCENTRATION INHALED O₂ + DIGITAL MASSAGE OVER THE EYELID · IV ACETAZOLAMIDE · ANTERIOR CHAMBER PARACENTESIS · THROMBOLYTIC INTO THE OPHTHALMIC ARTERY WITHIN 8 HOURS.
CRAO systemicSTROKE RISK RISES AT ONSET — if plaque reached a tiny retinal artery, there is far more in that carotid.
CRVO — CENTRAL RETINAL VEIN OCCLUSIONTHROMBUS. MORE COMMON THAN CRAO. SUDDEN PAINLESS loss; sometimes GRADUAL OVER DAYS TO WEEKS.
CRVO fundus“BLOOD AND THUNDER” — DISC SWELLING, VENOUS DILATION, COTTON WOOL SPOTS, RETINAL HEMORRHAGES.
CRVO treatmentURGENT OPHTHALMOLOGY REFERRAL TO RESTORE BLOOD FLOW. Evaluate and treat the underlying disorders.
Shared risksHTN · DM · HLD (hyperlipidemia) · RAYNAUD’S · AGE >50 · HYPERCOAGULABLE · GIANT CELL ARTERITIS · ENDOCARDITIS · ATRIAL MYXOMA · OBESITY. CRAO adds ATRIAL FIBRILLATION.
Shared laterNEOVASCULARIZATION WEEKS TO MONTHS AFTER the occlusion, in both.
Shared confirmatoryCOLOR FUNDUS PHOTOGRAPHY + FLUORESCEIN ANGIOGRAPHY.
BRAO and BRVO — the BRANCH formsSAME DISEASE, SMALLER VESSEL. A BRANCH is blocked, not the trunk → ONLY PART OF THE RETINA affected, PARTIAL field loss. Everything else identical.

Papilledema

TermWhat you need to know
THE DISTINCTIONINTRACRANIAL pressure, NOT INTRAOCULAR. Every other condition here is pressure inside the GLOBE.
CausesTUMOR · TRAUMA · INTRACRANIAL INFECTION (meningitis) · HEMORRHAGE · VITAMIN A TOXICITY.
Visual symptomsNON-SPECIFIC: FLICKERING, BLURRY, DOUBLE VISION.
Systemic symptomsSigns of raised ICP (intracranial pressure): NAUSEA, VOMITING, HEADACHE.
FundusENGORGED RETINAL VEINS · SWOLLEN OPTIC DISC · ± retinal hemorrhages. BILATERAL.
PhasesACUTE may have HEMORRHAGES and COTTON WOOL SPOTS. CHRONIC = elevation + blurred margins, NO hemorrhage or cotton wool spots. ATROPHIC = the AXONS HAVE DIED.
WorkupMRI and/or CT (computed tomography) HEAD to rule out a MASS, then LUMBAR PUNCTURE — INCREASED OPENING PRESSURE CONFIRMS. TREAT THE UNDERLYING DISORDER.
vs GLAUCOMAPAPILLEDEMA PUSHES THE DISC OUT. GLAUCOMA CUPS IT IN.

Anterior Ischemic Optic Neuropathy

TermWhat you need to know
Both formsSUDDEN PAINLESS loss of SIDE OR CENTRAL vision · SWELLING AND PALENESS of the optic nerve head · ONE EYE FIRST, SECOND EYE AT RISK.
NAION — NON-arteritic90–95% OF CASES. AGE 40–60. Linked to a SMALL STRUCTURAL OPTIC DISC = “DISC AT RISK.” HTN, DM, HIGH CHOLESTEROL, SLEEP APNEA.
NAION workupA DIAGNOSIS OF EXCLUSION. WORKUP IS IDENTICAL TO ARTERITIC — make sure there is no GCA. Then evaluate HTN, DM, ANEMIA; neuroimaging if unclear.
NAION managementOBSERVATION + CARDIOVASCULAR RISK MODIFICATION. Consider AVOIDING ANTIHYPERTENSIVES AT BEDTIME — NOCTURNAL HYPOTENSION worsens it.
AAION — ARTERITICCaused by GIANT CELL (TEMPORAL) ARTERITIS. AGE 55+. Usually ELDERLY, CAUCASIAN WOMEN. A MEDICAL EMERGENCY.
AAION systemicMALAISE, WEIGHT LOSS, FEVER · HEADACHE in the TEMPORAL or OCCIPITAL region · SCALP TENDERNESS on combing the hair · JAW CLAUDICATION on chewing. NO prior headache history → new temporal headache = the warning sign.
AAION workupESR (erythrocyte sedimentation rate) + CRP (C-reactive protein) rule GCA in or out. TEMPORAL ARTERY BIOPSY IS THE GOLD STANDARD — but DO NOT WAIT FOR IT.
AAION treatmentIV METHYLPREDNISOLONE ×3 DAYS, then SLOW ORAL TAPER to the lowest suppressive dose — TYPICALLY 6 TO 12 MONTHS. Add FAMOTIDINE for GI ULCER PROPHYLAXIS.
AAION prognosisDepends on DURATION and WHEN STEROIDS STARTED. Untreated → BLINDNESS.
Her boundaryShe will NOT test GCA as a disease in its own right — learn it as THE CAUSE OF ARTERITIC AION.

Neuro-Ophthalmology — The Pupils

TermWhat you need to know
The principleThe efferent limb is BILATERAL, so both pupils get the same command. UNEQUAL means an EFFERENT PATHWAY IS BROKEN.
WORSE IN THE DARKThe SMALL pupil is abnormal — it is failing to DILATE. HORNER, opioids, Argyll Robertson.
WORSE IN THE LIGHTThe LARGE pupil is abnormal — it is failing to CONSTRICT. CN III PALSY, ADIE, pharmacologic mydriasis.
EQUAL IN BOTHPHYSIOLOGIC ANISOCORIA — the MOST COMMON cause, usually UNDER 0.4 mm.
Pupil size ruleSet by the AVERAGE ILLUMINATION DETECTED BY EACH EYE. Cover one eye and the other DILATES.
MARCUS GUNN (RAPD)AFFERENT defect at the RETINA or OPTIC NERVE. Swing the light to the affected eye and BOTH PUPILS DILATE.
HORNER SYNDROMEPTOSIS + MIOSIS + ANHIDROSIS (anhidrosis may be ABSENT by lesion level). TEST = DILUTE APRACLONIDINE — no effect on a normal pupil, DILATES the Horner pupil.
HORNER HALLMARKDILATION LAG. Anisocoria most evident in the FIRST 4–5 SECONDS after dimming. After 10–15 s it dilates a little — that is PASSIVE, not sympathetic recovery.
HORNER LOCALIZATION1st ORDER: brainstem stroke/tumor, cord lesion ABOVE T1. 2nd ORDER: PANCOAST TUMOR, thyroid cancer. 3rd ORDER: CAROTID DISSECTION, cavernous sinus. OFTEN IDIOPATHIC.
ARGYLL ROBERTSONBILATERAL MIOSIS. NO light reaction, BRISK near reaction — LIGHT-NEAR DISSOCIATION. TERTIARY SYPHILIS, with TABES DORSALIS. Lesion in the DORSAL MIDBRAIN.
ADIE TONIC PUPILMYDRIASIS with POOR light response, SLOW TONIC near response. Ciliary ganglion damage then ABERRANT REINNERVATION. WOMEN IN THEIR 30s, often UNILATERAL. SECTOR PARALYSIS on slit lamp, ABSENT ACHILLES/PATELLAR REFLEXES.

Neuro-Ophthalmology — Nerves, Ptosis, Fields

TermWhat you need to know
CN (cranial nerve) IIISUPERIOR division: LEVATOR + SUPERIOR RECTUS. INFERIOR division: INFERIOR + MEDIAL RECTUS, INFERIOR OBLIQUE, and PARASYMPATHETICS.
CN III causesMOST COMMON: MICROVASCULAR (DM, HTN). MOST DREADED: COMPRESSION BY AN ENLARGING ANEURYSM, usually POSTERIOR COMMUNICATING ARTERY — RUPTURE WITHIN HOURS TO DAYS.
THE CN III DECISIONPUPIL INVOLVED → STAT CTA (computed tomography angiography) HEAD / MRA BRAIN. PUPIL SPARED → reassurance and imaging, but NOT STAT.
CN IVSUPERIOR OBLIQUE — INTORTS and DEPRESSES. The ONLY nerve from the DORSAL brainstem, and it CROSSES. VERTICAL BINOCULAR DIPLOPIA; patient TILTS THE HEAD AWAY from the bad eye. Isolated = usually CONGENITAL, even in adults.
CN VILATERAL RECTUS — ABDUCTS. HORIZONTAL BINOCULAR DIPLOPIA. CHILDREN: INTRACRANIAL TUMORS. ADULTS: MICROVASCULAR, or major trauma/skull base fracture.
CN IV / VI workupIsolated atraumatic → MRI BRAIN WITH AND WITHOUT CONTRAST + HbA1C (hemoglobin A1C) if at risk. TRAUMATIC → OBSERVE ~6 MONTHS, PATCH ONE EYE meanwhile.
PTOSIS — three musclesLEVATOR PALPEBRAE = CN III. MÜLLER’S = SYMPATHETIC, worth 1–2 mm. ORBICULARIS OCULI = CN VII, CLOSES the lid.
PTOSIS — tell them apartCN III PALSY: REDUCED levator + MYDRIASIS. HORNER: NORMAL levator + MIOSIS. MYASTHENIA: REDUCED levator, uni- OR bilateral, VARIABLE THROUGH THE DAY.
The one-linerPTOSIS + SMALL PUPIL = HORNER. PTOSIS + LARGE PUPIL = CN III PALSY.
NYSTAGMUSINVOLUNTARY, BIPHASIC, RHYTHMIC oscillation. Congenital or acquired. SYMPTOMATIC UNLESS ACQUIRED BEFORE AGE 8. VERTIGO is often the primary symptom; also OSCILLOPSIA, blurring, compensatory head position.
JERK NYSTAGMUSNamed for the FAST beat. INCREASES WITH GAZE TOWARD THE FAST PHASE. HORIZONTAL IS THE MOST COMMON FORM.
FIELD DEFECTSMONOCULAR total loss = OPTIC NERVE = PRE-CHIASM. BITEMPORAL = CHIASM. HOMONYMOUS = POST-CHIASM: tract → homonymous hemianopsia; radiation → SUPERIOR QUADRANTANOPIA; STRIATE CORTEX → homonymous hemianopsia WITH MACULAR SPARING.

★ THE “MOST COMMON” LIST SHE KEPT REPEATING

TermWhat you need to know
Vision loss in CHILDRENAMBLYOPIA. 3–5% of kids.
EYE CANCER in ADULTSUVEAL MELANOMA — melanocytes of CHOROID, CILIARY BODY or IRIS.
Form of GLAUCOMAPRIMARY OPEN-ANGLE.
PEDIATRIC cataract typeZONULAR.
Metastatic site for OCULAR MELANOMATHE LIVER.
Treatment for uveal melanomaRADIATION THERAPY — enucleation is now less common.
AMD split80% DRY · 20% WET.

CATARACT — TELL THE TYPES APART

TermWhat you need to know
NUCLEARBROWN central lens. Distance worse than near — a MYOPIC SHIFT, so they may read without glasses again.
CORTICALSPOKE-like opacities from the PERIPHERY. Silent until central, then GLARE is the commonest complaint.
POSTERIOR SUBCAPSULARPlate-like, BEHIND the lens. Faster onset, classically UNDER 50, on CORTICOSTEROIDS or DIABETIC. Symptoms BETTER after dilation.
PEDIATRIC — ZONULARCOMMONEST pediatric type. White opacity round the nucleus.
PEDIATRIC — POLARLess common but CENTRAL, so caught earlier.
The ruleA CATARACT ALONE NEVER CAUSES A RELATIVE AFFERENT PUPILLARY DEFECT. If there is one, something else is wrong.
Advanced signLOSS OF RED REFLEX · leukocoria · pupil looks gray or white.
TreatmentSURGERY ONLY. Deferred until it interferes with daily life — EXCEPT a NEONATE, operated early to prevent AMBLYOPIA.
Clouds again years laterPOSTERIOR CAPSULE OPACIFICATION. Treated with YAG LASER. The lens cannot regrow.

MACULAR DEGENERATION

TermWhat you need to know
Where the vision goesCENTRAL, with DISTORTION. Glaucoma takes the PERIPHERY — that is the split.
DRY (non-exudative)80%. DRUSEN, pigmentary change, atrophy.
WET (exudative)20%. CHOROIDAL NEOVASCULARIZATION bleeds into retina → DISCIFORM SCAR.
Home monitoringAMSLER GRID.
Confirming wetFLUORESCEIN ANGIOGRAPHY · OPTICAL COHERENCE TOMOGRAPHY.
Dry treatmentSTOP SMOKING. AREDS2: vitamins C and E, zinc, copper, lutein, zeaxanthin.
Why not beta caroteneOriginal AREDS used it; dropped because it RAISED LUNG CANCER RISK IN SMOKERS.
Wet treatmentINTRAVITREAL ANTI-VEGF · laser · photodynamic therapy.
PrognosisSLOWS progression. Does NOT reverse loss.

AMBLYOPIA & STRABISMUS

TermWhat you need to know
Amblyopia in one lineBrain FAVORS one eye; the other never develops.
Three routes inSTRABISMUS · ANISOMETROPIA (unequal refraction) · DEPRIVATION (cataract, ptosis, corneal opacity).
Occlusion objection testChild OBJECTS when the GOOD eye is covered. Calm when the BAD eye is covered.
Numeric definitionTWO LINES or more difference on best corrected acuity.
ScreeningALL children UNDER 5.
TreatmentPATCH or ATROPINISE THE GOOD EYE. Never the weak one.
TimingGood before 7, BETTER BEFORE 5.
Treated lateAcuity can recover; STEREO VISION DOES NOT. They struggle with 3D and judging distance.
Strabismus giveawayBINOCULAR diplopia — GONE when either eye is covered.
TestCOVER TEST · displaced CORNEAL LIGHT REFLEX in larger deviations.

★ OCULAR TUMORS

TermWhat you need to know
RETINOBLASTOMA giveawayLEUKOCORIA — white pupil, classically noticed in a PHOTOGRAPH.
WhoYoung children, almost exclusively. Genetic mutation, often RECESSIVE so family history misleads.
NO BIOPSYRisks SEEDING the tumor. Diagnosis is EXAM + IMAGING.
Primary care jobRED REFLEX at every well-child check.
Family historySeen by an experienced ophthalmologist WITHIN THE FIRST 8 WEEKS OF LIFE.
PrognosisUNTREATED close to 100% FATAL. TREATED >95% five-year survival. NO RECURRENCE AT 5 YEARS = CURED.
UVEAL MELANOMACommonest ADULT eye cancer. Choroid, ciliary body or iris. Usually found INCIDENTALLY.
Melanoma vs freckleFEEDER VESSEL. A cancer builds its own blood supply; a freckle has none. Plus >3 mm base, >1 mm deep, GROWING.
Fine needle aspirationFor MOLECULAR PROGNOSTIC TESTING, not to make the diagnosis.
SpreadLIVER. Ten-year mortality ~32% overall; IRIS melanoma only 4–10% because it is VISIBLE and found early.
IRIS NEVUSFLAT, under 3 mm, AVASCULAR, inferior iris, stable. Low transformation risk but still monitored.
LISCH NODULESTan, bilateral, multifocal — NEUROFIBROMATOSIS TYPE 1.
CONJUNCTIVAL MELANOMARAISED and VASCULAR. A conjunctival NEVUS is FLAT with CLEAR CYSTS.

IDIOPATHIC INTRACRANIAL HYPERTENSION

TermWhat you need to know
WhoOVERWEIGHT WOMAN OF CHILDBEARING AGE.
SymptomsIntractable HEADACHE · PULSATILE TINNITUS · TRANSIENT visual obscuration · pain behind the eyes.
SignsPAPILLEDEMA · visual field loss · CN6 (ABDUCENS) PALSY.
Order firstMRI BRAIN + MR VENOGRAPHY — exclude a mass AND a venous sinus thrombosis.
ThenLUMBAR PUNCTURE: ELEVATED OPENING PRESSURE. That is the confirmation.
Not the same asSYSTEMIC hypertension. Blood pressure may be normal.
TreatmentACETAZOLAMIDE promptly + WEIGHT REDUCTION program.
The durable fixWEIGHT LOSS. Everything else buys time.
Last resortCSF diversion — optic nerve sheath fenestration or shunt.

REFRACTIVE ERRORS & THE BLURRY-VISION DIFFERENTIAL

TermWhat you need to know
MYOPIALONG eyeball. Focus IN FRONT of retina. CONCAVE (negative) lens.
HYPEROPIASHORT eyeball. Focus BEHIND retina. CONVEX (positive) lens.
ASTIGMATISMUNEVEN curvature → MULTIPLE focal points. TORIC lens.
Who to refer toIsolated refractive error → OPTOMETRY. Medical eye disease → OPHTHALMOLOGY.
Corneal opacity vs cataractOPACITY is on the CORNEA; CATARACT is the LENS.
Refractive vs everything elseRefractive blur CORRECTS FULLY WITH LENSES. Nothing else here does.
The color clueOPTIC NEUROPATHY is the one that takes COLOR VISION. Think of it first if colors look washed out.
Functional visual lossNORMAL exam, NORMAL pressure, CLEAR lens, symptoms that do not fit anatomy.

★ THE FOUR DO-NOTs — BREAK ONE AND YOU MAKE IT WORSE

TermWhat you need to know
DO NOT remove a penetrating objectIt may be TAMPONADING the wound. Removal can extrude intraocular contents.
DO NOT order MRICT ORBIT. A magnet moves a METALLIC fragment through the eye.
DO NOT dilate the eyeNEVER, when ocular trauma is suspected. It costs you the pupil exam.
DO NOT send home topical anestheticDelays healing, MASKS worsening symptoms, can cause a CORNEAL ULCER.
ALWAYSABCs FIRST. Then tetanus status for any metal or organic penetration.
Automatic CT without contrastLoss of consciousness, alcohol, confusion, TACHYPNEA, apneic breathing, ANTICOAGULANTS, or eye penetration.
EpidemiologyLeading cause of MONOCULAR BLINDNESS in YOUNG ADULT MEN in the US. Usually arrives with MAJOR BRAIN TRAUMA.

★ OPEN GLOBE

TermWhat you need to know
DefinitionFULL-THICKNESS defect in cornea and/or sclera. Compartments open to the outside.
THE SIGNSPUPIL DISTORTED TOWARD THE WOUND · FLAT anterior chamber · uveal tissue protruding · massive hemorrhagic CHEMOSIS · SOFT EYE · deep lid laceration · hyphema or vitreous hemorrhage.
Two formsFULL-THICKNESS EYE WALL LACERATION (sharp / high velocity) vs GLOBE RUPTURE (blunt).
Globe rupture — whereAt a WEAK POINT: posterior to the EOM insertions (esp SUPERONASAL), OLD SURGICAL INCISIONS, LAMINA CRIBROSA.
Globe rupture — suspect whenBlunt trauma + MASSIVE HEMORRHAGIC CHEMOSIS or a SOFT EYE.
THE MOMENT you suspect itRIGID SHIELD taped over the eye + OPHTHO IMMEDIATELY + ANTIEMETIC + analgesia + tetanus. Then SURGICAL REPAIR.
Cut lens capsuleLens becomes HYDRATED, EDEMATOUS, OPAQUE. LENSECTOMY required but often DEFERRED.
Posterior segment foreign bodyLEAVE IT ALONE at initial evaluation — going after it does more damage.

CORNEAL ABRASION & FOREIGN BODY

TermWhat you need to know
Corneal abrasion — historyFINGERNAIL or CONTACT LENS handling. One of the COMMONEST ocular injuries.
Corneal abrasion — symptomsSEVERE foreign body sensation, tearing, photophobia, blurred vision.
Corneal abrasion — diagnosisSLIT LAMP with FLUORESCEIN — stains the exposed BASEMENT MEMBRANE.
Corneal abrasion — treatmentTOPICAL BROAD-SPECTRUM ANTIBACTERIAL. NO PATCH (slide says it may ease pain; it does not). Re-examine.
Foreign body — historyGRINDING or STRIKING METAL.
THE LOCALIZING SIGNLINEAR VERTICAL corneal defects = object in the TARSAL CONJUNCTIVA of the UPPER LID. EVERT THE LID.
Foreign body — removalTopical anesthetic → slit lamp → STERILE 27-GAUGE NEEDLE. RUST RING (iron/copper) → battery BURR.
When to referAny concern the object passed THROUGH the cornea — that is an OPEN GLOBE.

★ HYPHEMA

TermWhat you need to know
WhatBlood in the ANTERIOR CHAMBER from injured vessels. Blunt or penetrating. CAN BE A SIGN OF OPEN GLOBE.
SymptomsBlurred vision, eye pain, photophobia.
Measure the pressureYES — UNLESS penetrating globe injury is suspected.
Whole goal of managementPREVENT A REBLEED.
ManagementBED REST head elevated · ANTIEMETICS · ocular hypotensives · topical or oral CORTICOSTEROIDS · CYCLOPLEGIC drops (atropine, homatropine, scopolamine) · ORAL AMINOCAPROIC ACID (antifibrinolytic, slows clot breakdown).
THE TIMING FACTMOST REBLEEDING IS IN THE FIRST 72 HOURS. Secondary hemorrhage is what causes PERMANENT visual loss.
AvoidASPIRIN and ANTIPLATELETS. Increased risk in SICKLE CELL DISEASE.
Raised pressure treated withBeta blockers, PILOCARPINE, ACETAZOLAMIDE, osmotic agents if needed.

LIDS, CONTUSION & PERIORBITAL HEMATOMA

TermWhat you need to know
Lid laceration — CONSULT OPHTHO IFLID MARGIN · within 6–8 mm of the MEDIAL CANTHUS · LACRIMAL duct or sac · INNER lid surface · associated PTOSIS · TARSAL PLATE or LEVATOR.
Full-thickness lid lacerationComes with a corneal laceration or GLOBE RUPTURE in about TWO THIRDS of cases.
Partial-thicknessRepair in the ED, ophtho follow-up in 2–3 days.
Medial third lacerationMay transect the CANALICULAR system → CHRONIC TEARING FOR LIFE if not repaired properly.
Facial lacerationsMay be left OPEN 24 HOURS before closure — the face is highly vascular.
ORBITAL CONTUSIONSwelling WITHOUT hemorrhage. Held IN FRONT of the septum by the tarsal plate and septal margin → PRESEPTAL ecchymosis. Supportive to surgery. RULE OUT BRAIN TRAUMA.
PERIORBITAL HEMATOMABleeding WITHIN the orbit. NOT ALWAYS TRAUMATIC — eye surgery, peribulbar injections, orbital VARICES, lymphangiomas/AVM, ANTICOAGULANTS, SICKLE CELL, orbital pseudotumour, idiopathic.
Periorbital hematoma — treatmentCANTHOTOMY with CANTHOLYSIS — expose the lateral canthal tendon, cut its INFERIOR branch, let the blood out.

RETINAL & VITREOUS DETACHMENT — THE THREE TYPES

TermWhat you need to know
Presentation (all)CURTAIN or shadow descending · cloudy/smoky vision · FLOATERS · momentary FLASHES · monocular field defect · acuity drops when the MACULA goes.
Diagnosis & timingHistory + DILATED EYE EXAM. Must be seen by ophtho WITHIN 24 HOURS.
RHEGMATOGENOUSMOST COMMON. FULL-THICKNESS BREAKS + vitreous traction + liquefied vitreous into the subretinal space. Preceded by POSTERIOR VITREOUS DETACHMENT. → SURGICAL.
Rhegmatogenous — brought forward byMYOPIA, CATARACT SURGERY, OCULAR TRAUMA.
TRACTIONMost commonly PROLIFERATIVE DIABETIC RETINOPATHY. More LOCALIZED and CONCAVE. → SURGICAL.
EXUDATIVE (serous)NO break, NO traction. Systemic vascular/inflammatory disease or INTRAOCULAR TUMOR. → TREAT THE UNDERLYING CONDITION.
Acute managementOphtho STAT, pain control, antiemetics, HEAD OF BED 30–40 DEGREES.

★ ORBITAL FLOOR (BLOWOUT) FRACTURE

TermWhat you need to know
Mechanism 1 — true blowoutBlunt object raises ORBITAL PRESSURE, blowing out the FLOOR (most often) or MEDIAL WALL. Fist or ball.
Mechanism 2Force to the INFRAORBITAL RIM buckles the floor.
THE GAZE RULEDIPLOPIA ON UPWARD GAZE = INFERIOR RECTUS entrapment. DIPLOPIA ON LATERAL GAZE = MEDIAL RECTUS.
Other findingsPeriorbital ecchymosis, lid edema, chemosis, subconjunctival hemorrhage, INFRAORBITAL NUMBNESS (infraorbital nerve), subcutaneous EMPHYSEMA, enophthalmos, proptosis.
Entrapment also givesSEVERE PAIN + AUTONOMIC disturbance: BRADYCARDIA and VOMITING on attempted eye movement.
THE PEDIATRIC TRAP“WHITE-EYED BLOWOUT” — entrapment with NO orbital soft tissue signs at all. A quiet-looking eye does not exclude it.
DiagnosisCT of ORBITS and MIDFACE.
Management ladderNo injury/entrapment → ICE + analgesia, review 2–3 days. Blood in MAXILLARY SINUS → ANTIBIOTICS. True blowout → OPHTHO (30% have a significant globe injury). ENTRAPMENT → FACIAL TRAUMA SURGEON STAT (muscle NECROSIS).
WHY antibiotics for blood in the sinusPROPHYLACTIC, not treatment. The eye is STERILE; blood in the sinus means the sinus is DISRUPTED and now has a PORTAL OF ENTRY.
WHY the CT includes the MIDFACETo catch ADDITIONAL FRACTURES. Finding the orbital floor is not the same as excluding everything else.
Surgical timingOften DELAYED 1–2 WEEKS to let swelling settle. Already-damaged optic nerve is unlikely to improve and surgery may worsen it.

★ BASILAR SKULL FRACTURE

TermWhat you need to know
WhatLINEAR fracture of the skull base: CRIBRIFORM PLATE of ethmoid, orbital plate of FRONTAL, PETROUS/SQUAMOUS TEMPORAL, SPHENOID, OCCIPITAL.
The catchTrauma there often has NO SYMPTOMS of its own — you find it on INDIRECT SIGNS.
INDIRECT SIGNSRACCOON EYES · BATTLE SIGN · HEMOTYMPANUM · bleeding into middle ear or sphenoid sinus · CSF LEAK with CLEAR or PINK RHINORRHEA.
TWO BEDSIDE TESTS FOR CSFDEXTROSE STICK may be positive. Fluid on FILTER PAPER or the BEDSHEET shows a HALO / DOUBLE RING SIGN — INNER ring of BLOOD, OUTER ring of CSF.
HOW to do the halo testHold a BEDSHEET, paper or tissue under the nostril, let the drip fall, and watch it DRY. Two rings appear. She called this “very classic” and a sign NOT TO MISS.
DiagnosisCT ORBITS — but the fracture is NOT ALWAYS EVIDENT.
ManagementCSF present → NEUROSURGERY CONSULT and ADMISSION. Otherwise admission depends on clinical condition, associated injuries, brain injury on CT.
Antibiotics for a CSF leakCONTROVERSIAL — risk of selecting RESISTANT organisms.

THE EYE IN THREE LAYERS

TermWhat you need to know
FIBROUS (outer)CORNEA — most of the FOCUSING POWER. SCLERA — shape + muscle attachment.
VASCULAR / UVEA (middle)IRIS — controls pupil size. CILIARY BODY — makes AQUEOUS + accommodation. CHOROID — NOURISHES THE RETINA.
NEURAL (inner)RETINA — rods and cones. MACULA — central vision. FOVEA — highest acuity. OPTIC DISC — blind spot.
Why the layer mattersUVEITIS is MIDDLE-layer, which is why it takes iris + ciliary body + choroid together. Scleritis/episcleritis OUTER. Occlusions and detachments INNER.

★ NYSTAGMUS — THE TWO GROUPS

TermWhat you need to know
JERKSLOW phase + FAST phase. Named for the FAST beat. INCREASES with gaze TOWARD the fast phase.
Most common jerk formHORIZONTAL — slow drift one way, quick snap back.
Horizontal jerk SUBTYPESNormal PHYSIOLOGIC GAZE-EVOKED · INFANTILE · SPASMUS NUTANS · LATENT.
PENDULARBOTH phases EQUAL velocity and amplitude — NO fast phase. Most often HORIZONTAL.
Pendular contextCONGENITAL, or after PROLONGED BILATERAL BLINDNESS beginning in CHILDHOOD.
UPBEAT — the alarmALWAYS ABNORMAL. CEREBELLAR or MEDULLARY lesion; less commonly DRUG INTOXICATION. Present only on UPWARD gaze.

★ THE MIMIC LISTS

TermWhat you need to know
MACULAR DYSTROPHIES mimicking AMDSTARGARDT (yellow-white FLECKS) · SORSBY (AUTOSOMAL DOMINANT, CNV like wet AMD) · NORTH CAROLINA (congenital, NON-progressive) · BEST / VITELLIFORM (LIPOFUSCIN mimics drusen).
The tell for all fourINHERITED, and they present YOUNGER than age-related degeneration.
LEUKOCORIA besides retinoblastomaCOATS' (retinal TELANGIECTASIA with exudation) · PERSISTENT FETAL VASCULATURE · TOXOCARIASIS (granulomatous) · RETINAL ASTROCYTOMA (glial, TUBEROUS SCLEROSIS) · MEDULLOEPITHELIOMA (nonpigmented ciliary epithelium) · CONGENITAL CATARACT · OCULAR TOXOPLASMOSIS.
UVEAL MELANOMA by siteIRIS (melanotic OR partly AMELANOTIC) · CILIARY BODY · CHOROID.
Two ciliary body signsSENTINEL VESSEL (dilated episcleral vessel over the tumor) and EXTRASCLERAL EXTENSION.
IRIS NEVUSINFERIOR half · does NOT typically grow · FLAT / under 1 mm · not vascular · may cause CORECTOPIA. Apparent around PUBERTY, ASYMPTOMATIC.
PIGMENTED IRIS differentialFRECKLE (flat, no stromal involvement) · LISCH NODULES (NF1) · MELANOCYTOMA (granular; secondary glaucoma from PIGMENT DISPERSION) · MELANOCYTOSIS (congenital, RAISES melanoma risk) · COGAN-REESE / ICE (corneal ENDOTHELIAL abnormality) · IRIS MELANOMA · METASTATIC CARCINOMA.
Pushes an iris lesion toward MELANOMAINFERIOR location · DIFFUSE configuration · BLOOD in the anterior chamber.
NON-PIGMENTED CONJUNCTIVAL lesionsSQUAMOUS CELL CARCINOMA (gelatinous/LEUKOPLAKIC; mistaken for AMELANOTIC melanoma) · LYMPHOMA (SALMON-PINK, painless, fornix) · KAPOSI SARCOMA (reddish-purple, HIV/AIDS) · PYOGENIC GRANULOMA (rapidly growing red, after TRAUMA or SURGERY).