Eduovisual
Special Senses & Otolaryngology
Keratitis: bacterial, viral, contact-lens-related
— Microbial keratitis is the leading infectious cause of monocular blindness in working-age US adults.
— Contact lens (CL) wear accounts for the majority of bacterial cases; HSV is the leading infectious cause of corneal blindness in developed countries.
— Misdiagnosis as "pink eye" with delayed referral is a recurring malpractice and patient-safety theme.
— Pain (not just irritation), photophobia, decreased visual acuity, foreign-body sensation.
— Focal corneal opacity, infiltrate, or ulcer on penlight exam.
— Unilateral red eye in a contact lens wearer, particularly with overnight wear, swimming/showering in lenses, or tap-water rinsing.
— Recent HSV cold sore, immunosuppression, or recent corneal trauma/foreign body (think bacterial or fungal after vegetative injury).
— CL-related: extended wear, poor hygiene, water exposure → Pseudomonas, Acanthamoeba.
— Trauma: vegetative matter → fungal (Fusarium, Aspergillus); soil/metal → bacterial.
— Ocular surface disease: dry eye, blepharitis, prior HSV, neurotrophic cornea (post-LASIK, diabetes, CN V lesions).
— Immunosuppression / topical steroid misuse → atypical, fungal, HSV reactivation.
Board pearl: The triad "pain, photophobia, decreased acuity" plus a corneal infiltrate flips the diagnosis from conjunctivitis to keratitis and changes disposition from reassurance to emergent referral.
— Rapid onset (hours to 1–2 days) of unilateral pain, redness, photophobia, mucopurulent discharge, lid swelling, blurred vision.
— Almost always a risk factor: soft contact lens overnight wear, trauma, ocular surface disease, post-surgical.
— Pseudomonas aeruginosa is the classic CL pathogen — aggressive, can perforate within 48–72 hours.
— Recurrent unilateral episodes; pain may be less than expected because of corneal hypoesthesia.
— Prior cold sores, prior episode of "red eye," tingling/dysesthesia prodrome.
— Triggers: UV light, stress, fever, immunosuppression, topical steroids.
— VZV (herpes zoster ophthalmicus): vesicular V1 dermatomal rash, Hutchinson sign (nasal tip lesion) predicts ocular involvement.
— Bilateral (often starts unilateral), watery discharge, preauricular lymphadenopathy, recent URI or sick contact, follicular conjunctivitis, then subepithelial infiltrates at 1–2 weeks causing glare and decreased vision.
— Sleeping in lenses (most common modifiable risk), extended-wear lenses, swimming/showering/hot tub in lenses, topping off solution, expired lenses, tap-water rinsing → Acanthamoeba (pain out of proportion to exam, ring infiltrate late).
— History of vegetative trauma (tree branch, lawn mower debris), agricultural workers, chronic topical steroids; indolent course over days–weeks; feathery infiltrate with satellite lesions.
— Contact lens type, wear schedule, sleeping in lenses, water exposure, cleaning routine.
— Trauma, vegetative matter, welding, foreign body.
— Prior episodes, HSV/VZV history, immunosuppression, recent steroid drops.
— Glasses-only patient with vegetative trauma → think fungal, not bacterial first.
Key distinction: Pain out of proportion to slit-lamp findings in a CL wearer with water exposure → Acanthamoeba until proven otherwise; this exam-stem cue is nearly pathognomonic.
— Visual acuity first — always; medicolegal anchor.
— External lids/lashes for vesicles (HSV/VZV), preauricular node (viral).
— Pupils, EOM, confrontation fields.
— Penlight + fluorescein under cobalt blue (Wood's lamp acceptable in clinic).
— Slit lamp if available; otherwise refer.
— Focal white/gray stromal infiltrate with overlying epithelial defect that stains with fluorescein.
— Hypopyon (layered WBCs in anterior chamber) suggests virulent organism (Pseudomonas, Streptococcus).
— Mucopurulent discharge, ciliary flush (perilimbal injection), lid edema.
— Dendritic ulcer with terminal bulbs that stains brightly with fluorescein; rose bengal stains the devitalized edges.
— Decreased corneal sensation (touch wisp of cotton before instilling anesthetic) — a high-yield bedside test.
— Stromal/disciform keratitis: deeper stromal edema, immune ring, may have keratic precipitates.
— V1 dermatomal vesicles, Hutchinson sign, pseudodendrites (lack true terminal bulbs, stain poorly), uveitis, elevated IOP.
— Diffuse follicular conjunctivitis, watery discharge, tender preauricular node, subepithelial infiltrates after epithelial phase.
— Early: pseudodendrites, punctate epitheliopathy, perineural infiltrates (radial keratoneuritis — pathognomonic).
— Late: ring-shaped stromal infiltrate, severe pain.
— Gray-white infiltrate with feathery edges, satellite lesions, endothelial plaque, hypopyon.
— Hypopyon, infiltrate >1 mm, central location, perforation risk (Seidel-positive), severe vision loss, unresponsive to 24–48 h of therapy.
Board pearl: Always check corneal sensation before instilling topical anesthetic — reduced sensation supports HSV/VZV or neurotrophic keratitis and changes both diagnosis and prognosis.
— Snellen acuity, penlight, fluorescein strips, cobalt blue / Wood's lamp, topical anesthetic (proparacaine — diagnostic only, never dispense), Schirmer if dry eye suspected.
— Cotton wisp for corneal sensation testing.
— Tonometry if available and no obvious epithelial defect risk for perforation.
— Dendrite with terminal bulbs → HSV epithelial keratitis.
— Pseudodendrite (no terminal bulbs, stains poorly) → VZV or healing epithelium.
— Round/oval ulcer with stromal infiltrate → bacterial.
— Punctate epithelial erosions, perineural infiltrates → early Acanthamoeba.
— Feathery-edged infiltrate, satellites → fungal.
— Seidel test positive (stream of dye from cornea) → perforation → emergency.
— Infiltrate ≥1–2 mm, central or paracentral location, sight-threatening location, atypical features, immunocompromised host, contact lens wearer with severe disease, failure to improve in 48 hours on empiric therapy.
— Scrapings sent for Gram stain, KOH/calcofluor white (fungi, Acanthamoeba), bacterial/fungal cultures on blood, chocolate, Sabouraud, and non-nutrient agar with E. coli overlay (Acanthamoeba).
— Save and culture the contact lens, case, and solution — often higher yield than the cornea itself.
— Usually clinical diagnosis; PCR of corneal scraping is most sensitive when needed.
— Serology is generally not useful (high background seroprevalence).
— Routine bloodwork not indicated for isolated keratitis.
— Consider HIV testing if recurrent/atypical HSV-VZV or fungal keratitis in unexpected hosts.
— Confocal microscopy (specialty) can detect Acanthamoeba cysts and fungal hyphae non-invasively.
Step 3 management: In the office, document visual acuity, fluorescein pattern, corneal sensation, and CL history, then call ophthalmology the same day for any suspected microbial keratitis — do not "trial" topical antibiotics and recheck in a week.
— Corneal scraping with Kimura spatula or blade at infiltrate edge before initiating fortified antibiotics when possible; if already started, hold drops briefly per ophthalmology.
— Specimens plated directly: blood agar (most bacteria), chocolate agar (Haemophilus, Neisseria, Moraxella), Sabouraud and brain-heart infusion (fungi), non-nutrient agar with E. coli lawn (Acanthamoeba), thioglycollate broth (anaerobes).
— Stains: Gram, Giemsa (Acanthamoeba trophozoites/cysts, inclusion bodies), KOH/calcofluor white (fungi, Acanthamoeba cysts under fluorescence).
— PCR of corneal scraping for HSV, VZV, adenovirus, Acanthamoeba — useful when cultures negative or patient already on therapy.
— In vivo confocal microscopy: Detects Acanthamoeba cysts (double-walled, highly reflective) and fungal hyphae in real time — sensitivity ~80–90%.
— Anterior segment OCT: Measures infiltrate depth, epithelial defect size, residual stromal thickness — guides surgical decisions.
— Recurrent or bilateral HSV/VZV in young or atypical hosts → HIV testing; consider immunodeficiency workup.
— Refractory peripheral ulcerative keratitis → screen for rheumatoid arthritis, ANCA-associated vasculitis (GPA), relapsing polychondritis with RF, anti-CCP, ANA, ANCA.
— Recurrent fungal keratitis → assess for diabetes, chronic topical steroid exposure.
— HSV vs Acanthamoeba early: both can show pseudodendrites; HSV responds to antivirals within days; Acanthamoeba does not and causes escalating pain.
— Fungal vs bacterial in trauma cases: indolent course, feathery edges, satellite lesions, endothelial plaque favor fungal.
Board pearl: A CL wearer not improving on appropriate fortified antibiotics by 48–72 hours mandates re-culture and broadened workup for Acanthamoeba and fungal disease — do not simply switch antibiotics empirically.
— Mild: small (<1 mm) peripheral infiltrate, no significant AC reaction, vision near baseline, reliable patient → outpatient with fluoroquinolone monotherapy and 24-hour follow-up.
— Moderate–severe: infiltrate ≥1–2 mm, central/paracentral, hypopyon, vision <20/40, scleral involvement, perforation risk, immunocompromise, monocular patient → fortified topical antibiotics, hourly dosing including overnight, consider admission.
— ≥1 mm infiltrate, within 2 mm of visual axis, ≥3 mm AC cell/hypopyon → high risk → admit/fortified drops.
— CL wearer → cover Pseudomonas (fluoroquinolone ± fortified tobramycin).
— Trauma with vegetative matter → cover fungi; obtain cultures before empiric antifungals.
— Prior HSV, dendrite, decreased sensation → oral or topical antiviral, avoid steroids initially.
— Pain out of proportion + water exposure → presume Acanthamoeba and refer for biguanides.
— Any suspected microbial keratitis → same-day ophthalmology. If unavailable, ED referral.
— Adenoviral conjunctivitis with subepithelial infiltrates and decreased vision → ophthalmology within 24–48 hours; supportive care otherwise.
— Recurrent HSV without active dendrite → routine ophthalmology follow-up and chronic suppression discussion.
— No topical steroids without ophthalmology involvement — can devastate untreated bacterial/fungal/Acanthamoeba/HSV epithelial disease.
— No eye patching of infected ulcers — promotes pathogen growth, especially Pseudomonas.
— Never dispense topical anesthetic — causes epithelial toxicity and masks worsening disease.
Step 3 management: When the stem offers "add topical prednisolone" as an answer for an undiagnosed corneal ulcer in primary care, it is wrong — defer steroids to ophthalmology after pathogen control.
— Small, peripheral, non-vision-threatening: topical moxifloxacin 0.5% or gatifloxacin 0.5% or besifloxacin 0.6% — 1 drop every 1 hour while awake for 24–48 h, then taper.
— Sight-threatening / central / large / hypopyon: fortified tobramycin 14 mg/mL + fortified cefazolin 50 mg/mL (or vancomycin 25–50 mg/mL if MRSA/Strep concern) — alternating every 30–60 minutes, including overnight, after loading dose every 5 min × 5 doses.
— Cycloplegic (cyclopentolate 1% or homatropine 5%) for comfort and synechiae prevention.
— Oral analgesia; no topical NSAIDs (risk of corneal melt).
— Topical: ganciclovir 0.15% gel 5×/day or trifluridine 1% 9×/day until healed, then taper.
— Oral (equally effective, often preferred): acyclovir 400 mg PO 5×/day × 7–10 days, or valacyclovir 500 mg TID, or famciclovir 250 mg TID.
— Avoid topical steroids during active epithelial disease.
— Stromal/disciform HSV keratitis: oral antiviral plus topical steroid under ophthalmology supervision (HEDS trial basis).
— Oral valacyclovir 1 g TID × 7–10 days (or acyclovir 800 mg 5×/day) — start within 72 hours of rash for best outcomes; still give if active eye disease beyond 72 h.
— Ophthalmology co-management; topical steroids only for stromal/uveitic disease.
— Supportive: cold compresses, artificial tears, strict hand hygiene (highly contagious 10–14 days). No antibiotics. Topical steroids only by ophthalmology for visually significant subepithelial infiltrates.
— Biguanides (PHMB 0.02% or chlorhexidine 0.02%) ± diamidines (propamidine, hexamidine) — months of therapy.
— Natamycin 5% topical (filamentous, e.g., Fusarium — MUTT trial); voriconazole topical/oral adjunct for yeast/refractory cases.
Board pearl: Oral acyclovir/valacyclovir is first-line for HSV epithelial keratitis in modern US practice — it avoids topical toxicity and prevents recurrence when continued as suppression.
— Cycloplegics (cyclopentolate 1% TID, homatropine 5% BID) — reduce ciliary spasm pain, prevent posterior synechiae in associated iritis.
— Oral analgesia — acetaminophen, short-course oxycodone for Acanthamoeba pain.
— Preservative-free artificial tears between medicated drops for ocular surface support.
— Bandage contact lens — only by ophthalmology, only after pathogen control, for persistent epithelial defects.
— HSV stromal keratitis (HEDS-confirmed benefit when on antiviral coverage).
— Adenoviral subepithelial infiltrates causing visual loss.
— After 48 h of confirmed bacterial response, to limit scarring (controversial; SCUT trial showed modest benefit, no harm overall, possible benefit in central/severe ulcers).
— Never in undiagnosed ulcer, fungal, or Acanthamoeba without intensive antimicrobial control.
— Corneal scraping/debridement — diagnostic + therapeutic (HSV dendrites, fungal debulking).
— Intrastromal antifungal injection (voriconazole) for deep fungal infiltrates not responding to topical therapy.
— Corneal collagen cross-linking (PACK-CXL) — emerging adjunct for refractory bacterial/fungal keratitis.
— Amniotic membrane transplant — persistent epithelial defects, neurotrophic ulcers.
— Tissue adhesive (cyanoacrylate glue) — descemetocele or small perforation as a temporizing measure.
— Therapeutic penetrating keratoplasty (PKP) — frank perforation, impending perforation, uncontrolled infection.
— Optical PKP / DALK — definitive visual rehabilitation after scarring (months later).
— Long-term oral acyclovir 400 mg BID or valacyclovir 500 mg daily indefinitely after a single stromal episode or ≥2 epithelial recurrences — HEDS showed ~50% reduction.
CCS pearl: For a hospitalized severe bacterial keratitis case, your standing orders should include hourly fortified drops with explicit overnight dosing, daily slit-lamp exam by ophthalmology, pain control, cycloplegic, eye shield (not patch), and culture results check at 48 hours with antibiotic narrowing.
— Higher prevalence of dry eye, blepharitis, neurotrophic cornea (post-stroke, diabetes, prior HZO) → predispose to bacterial superinfection and delayed healing.
— HZO is far more common >50; vaccination history (recombinant zoster vaccine, RZV/Shingrix at age ≥50) should be reviewed and updated.
— Polypharmacy: anticholinergics, antihistamines worsen ocular surface; review and minimize.
— Falls risk in monocular patients — counsel on home safety, driving restrictions.
— Acyclovir/valacyclovir/famciclovir are renally cleared — reduce dose when CrCl <50.
— Acyclovir 400 mg 5×/day → reduce frequency to BID–TID for CrCl <25.
— Valacyclovir 1 g TID for HZO → 1 g BID (CrCl 30–49), 1 g daily (CrCl 10–29), 500 mg daily (<10).
— Inadequate dose reduction → acyclovir neurotoxicity (confusion, hallucinations, myoclonus, AKI from crystal nephropathy) — ensure hydration with IV/oral fluids especially in elderly.
— Topical fluoroquinolones have negligible systemic absorption — no renal adjustment.
— Voriconazole (used for fungal keratitis) — hepatic metabolism, monitor LFTs; reduce maintenance dose 50% in Child-Pugh A/B; avoid or specialty-dose in C.
— Itraconazole, ketoconazole — significant hepatotoxicity risk; avoid in advanced liver disease.
— Neurotrophic corneas, delayed epithelial healing, higher fungal and bacterial risk.
— Glycemic optimization aids healing; consider HbA1c check during workup of recurrent/refractory keratitis.
— Atypical organisms (fungal, mycobacterial, microsporidial), bilateral disease, recurrent HSV/VZV.
— Lower threshold for cultures, broader empirics, longer antiviral courses, lifelong HSV suppression.
Step 3 management: Before prescribing valacyclovir 1 g TID for HZO in an 82-year-old, check creatinine and CrCl — failure to renally dose is a common boards-flagged error leading to delirium and AKI.
— Topical fluoroquinolones, erythromycin, polymyxin/trimethoprim — minimal systemic absorption, considered acceptable.
— Acyclovir and valacyclovir — Category B historically; extensive safety data, used for HSV/VZV in pregnancy including third-trimester suppression.
— Avoid topical aminoglycosides chronically if alternatives exist; avoid tetracyclines (used sometimes for blepharitis/MMP-9 modulation) — teratogenic, dental staining.
— Avoid oral fluconazole/voriconazole in first trimester for fungal keratitis when possible; topical natamycin preferred.
— Neonatal keratoconjunctivitis — N. gonorrhoeae (hyperacute, 2–5 days, sight-threatening, IM ceftriaxone + saline irrigation + admission) and C. trachomatis (5–14 days, oral erythromycin or azithromycin — note pyloric stenosis risk with erythromycin in <1 month).
— HSV neonatal keratitis — part of disseminated/CNS HSV; IV acyclovir, infectious disease consult, mandatory.
— Pediatric CL keratitis — orthokeratology and cosmetic lens use in teens; same Pseudomonas/Acanthamoeba risks; counsel against shower/swim/sleep in lenses.
— Vernal keratoconjunctivitis — shield ulcer (sterile epithelial defect from giant papillae) — treat allergy, not infection.
— Post-LASIK → flap interface keratitis (DLK or microbial), neurotrophic cornea, dry eye.
— Post-PRK → bacterial keratitis risk during epithelial healing window with bandage CL.
— Welders — UV photokeratitis (sterile, bilateral, severe pain 6–12 h post-exposure, punctate staining) — treat with cycloplegic, lubrication, analgesia; resolves 24–72 h.
— Farmers/landscapers — fungal keratitis predominates after vegetative trauma.
— Swimmers/hot tub users in CL — Acanthamoeba.
— RZV (Shingrix) at ≥50, and ≥19 if immunocompromised — prevents HZO and post-herpetic neuralgia.
Board pearl: Hyperacute purulent conjunctivitis/keratitis in a neonate at days 2–5 = gonococcal until proven otherwise — admit, IM/IV ceftriaxone, saline irrigation, and treat mother and partners.
— Corneal perforation — risk highest with Pseudomonas, Streptococcus, fungal, and steroid-treated undiagnosed ulcers; signs include shallow AC, Seidel-positive fluorescein, sudden pain relief with vision drop.
— Descemetocele — herniation of Descemet membrane through stromal melt, imminent perforation.
— Endophthalmitis — intraocular spread; severe pain, hypopyon, vitritis, profound vision loss → vitreous tap + intravitreal antibiotics, often vitrectomy.
— Scleritis or scleral abscess — limbal extension of infection.
— Corneal scarring (leukoma, nebula, macula) — visual axis involvement causes permanent vision loss; leading sequel of healed bacterial/HSV keratitis.
— Irregular astigmatism, ectasia — distorted vision even after healing; may require rigid CL or keratoplasty.
— Neovascularization and lipid keratopathy — chronic inflammation, especially HSV stromal disease.
— Band keratopathy, persistent epithelial defects, neurotrophic ulcer — particularly post-HSV/HZO.
— Recurrent stromal keratitis → progressive scarring (leading infectious cause of corneal blindness in developed countries).
— HZO sequelae: chronic uveitis, glaucoma, neurotrophic keratopathy, post-herpetic neuralgia, acute retinal necrosis (rare but devastating).
— Topical aminoglycoside toxicity — punctate keratopathy, delayed epithelial healing.
— Topical anesthetic abuse — ring infiltrate, melts, perforation.
— Steroid misuse — accelerates fungal, HSV, and Acanthamoeba disease; causes steroid-induced glaucoma and cataract.
— Acyclovir-induced AKI/neurotoxicity when underdosed for renal function.
— Monocular vision loss → driving restrictions (most US states require ≥20/40 in better eye), occupational impact, depression risk.
— Cosmetic disfigurement from leukoma; chronic pain syndromes.
Key distinction: Sudden decrease in pain with worsening vision in a corneal ulcer is not clinical improvement — it suggests perforation with decompression of intraocular pressure. Emergent ophthalmology.
— Any corneal infiltrate or ulcer on fluorescein exam.
— Contact lens wearer with red eye, pain, and decreased vision.
— Suspected HSV dendrite or HZO with eye involvement (Hutchinson sign, conjunctivitis, decreased vision).
— Hypopyon, severe photophobia, vision <20/40 in affected eye, monocular patient with any red eye.
— Trauma with corneal involvement, suspected foreign body, suspected perforation.
— Severe infiltrate ≥6 mm or threatening perforation.
— Inability to administer hourly fortified drops at home (poor adherence, no caregiver, cognitive impairment, homeless, monocular patient).
— Pediatric patients requiring frequent dosing or exam under anesthesia.
— Suspected or confirmed endophthalmitis → urgent vitreous tap and intravitreal antibiotics.
— Severe pain requiring parenteral analgesia (Acanthamoeba).
— Systemic illness requiring IV therapy (disseminated HZO, neonatal HSV, gonococcal ophthalmia neonatorum).
— Rare for isolated keratitis; consider for neonatal disseminated HSV, severe HZO with CNS involvement (encephalitis, stroke from VZV vasculopathy), endophthalmitis with sepsis, or immunocompromised hosts with systemic instability.
— Ophthalmology — always.
— Infectious disease — atypical organisms, immunocompromised hosts, neonatal HSV/gonococcal disease.
— Rheumatology — peripheral ulcerative keratitis / scleritis with systemic vasculitis features.
— Social work / case management — adherence support, CL practices counseling, home health for fortified drop administration.
— Community hospital without ophthalmology coverage → transfer to tertiary center; do not delay if perforation or endophthalmitis suspected.
CCS pearl: In a CCS case of severe bacterial keratitis, your first 10 orders should include: visual acuity, ophthalmology consult STAT, fluorescein exam, corneal cultures, fortified vancomycin + tobramycin every hour, cycloplegic drops, eye shield, analgesia, antiemetic if needed, and admit to ophthalmology service.
— Bacterial: mucopurulent, lids stuck shut, bilateral often, no decreased vision, no significant photophobia — treat with topical erythromycin/polymyxin-trimethoprim; CL wearers cover Pseudomonas (fluoroquinolone) and discontinue lenses.
— Viral (adenoviral): watery, follicular, preauricular node, recent URI — supportive.
— Allergic: itching predominant, bilateral, chemosis, papillae — antihistamine/mast-cell stabilizer.
— Pain, photophobia, decreased vision, ciliary flush, AC cell and flare, miotic pupil — no corneal infiltrate.
— Associated with HLA-B27 disease, sarcoid, IBD, syphilis, TB, JIA; treat with topical steroids + cycloplegic by ophthalmology.
— Episcleritis — sectoral redness, mild, blanches with phenylephrine, benign.
— Scleritis — deep boring pain, violaceous hue, does not blanch, often autoimmune (RA, GPA) — systemic immunosuppression.
— Acute trauma, fluorescein uptake without infiltrate, rapid improvement; treat with prophylactic topical antibiotic (CL wearer → Pseudomonas coverage), no patch.
— History of prior abrasion (often fingernail, paper), morning pain on lid opening, punctate or epithelial defect without infiltrate; treat lubrication, hypertonic saline ointment, possible epithelial debridement.
— Focal redness without true keratitis.
— Inferior punctate staining, no infiltrate, foreign body sensation, worse evening; treat lubrication, lid hygiene, address exposure (Bell's, proptosis, nocturnal lagophthalmos).
— Peripheral sterile infiltrate with clear zone to limbus, associated with blepharitis; treat with lid hygiene + low-dose topical steroid (ophthalmology).
Key distinction: Painful red eye with infiltrate + epithelial defect = microbial keratitis until proven otherwise; painful red eye with cell/flare but no infiltrate = uveitis. Both photophobic, both decreased vision — the slit-lamp finding differentiates.
— Severe pain, headache, nausea/vomiting, halos around lights, mid-dilated fixed pupil, hazy cornea (microcystic edema, not infiltrate), IOP often >40 mmHg.
— Older, hyperopic, dim-light precipitant. Emergent — topical timolol, brimonidine, dorzolamide, pilocarpine after IOP lowering, oral/IV acetazolamide, definitive laser peripheral iridotomy.
— Post-operative (recent cataract surgery, intravitreal injection), endogenous (sepsis, IV drug use, Candida), or extension from keratitis. Hypopyon, vitritis, severe vision loss → emergent vitreous tap and intravitreal antibiotics.
— Lid swelling, fever; orbital: proptosis, painful EOM, decreased vision, RAPD, sinusitis history — IV antibiotics, CT orbits, ENT/ophthalmology.
— Painless, blood-red, vision normal — reassure; check BP, anticoagulation, Valsalva history.
— Alkali > acid in severity; irrigate immediately with Morgan lens or copious saline before exam; check pH; ophthalmology emergent.
— Open globe (Seidel-positive, irregular pupil, decreased acuity, history of high-velocity injury) — shield, NPO, IV antibiotics, anti-emetics, tetanus, OR.
— Hyphema — blood in AC; rest, head elevation, shield, sickle cell screening, IOP monitoring.
— Cluster headache, trigeminal neuralgia, giant cell arteritis (>50, jaw claudication, ESR/CRP, temporal tenderness — start steroids before biopsy if AION suspected).
— Migraine with ocular aura.
— Bilateral chemosis, proptosis, multiple CN palsies (III, IV, V1, V2, VI), fever — emergent MRI/MRV and anticoagulation/antibiotics.
Board pearl: Pain + nausea/vomiting + halos + mid-dilated pupil is angle closure, not keratitis — and conversely, pain + photophobia + fluorescein infiltrate is keratitis, not migraine. The slit-lamp/fluorescein step is what differentiates these high-stakes look-alikes.
— No sleeping in lenses (even FDA-approved "extended wear" increases infection risk 5–10×).
— No water exposure — no showering, swimming, or hot tub use in lenses; no rinsing lenses or cases with tap water.
— Replace lens case every 3 months; air-dry upside down; never "top off" solution.
— Adhere to replacement schedule (daily, biweekly, monthly).
— Hand washing before insertion/removal; daily lens cleaning by rubbing-and-rinsing even with multipurpose solutions.
— Carry backup glasses; remove lenses immediately if eye is red or painful ("when in doubt, take them out").
— Chronic oral suppression: acyclovir 400 mg BID or valacyclovir 500 mg daily for ≥12 months after stromal keratitis or ≥2 epithelial recurrences (HEDS).
— Avoid known triggers; sunglasses for UV protection.
— Patient education on prodromal symptoms; early presentation for recurrences.
— Lifelong ophthalmology follow-up — late uveitis, glaucoma, neurotrophic keratopathy can present years later.
— Address post-herpetic neuralgia (gabapentin, pregabalin, TCAs, topical lidocaine, capsaicin).
— RZV vaccination for unvaccinated household contacts and the patient (if not previously immunized — can be given after HZO).
— Tapered topical antibiotic over 1–2 weeks per ophthalmology.
— Preservative-free artificial tears for ongoing ocular surface support.
— Address modifiable risk factors: blepharitis (warm compresses, lid hygiene), dry eye (cyclosporine 0.05%, lifitegrast), CL practices.
— Vision insurance counseling, low-vision rehabilitation referral if significant scarring.
— Drivers with monocular vision — state-specific reporting and vision testing.
Step 3 management: A patient discharged after Pseudomonas keratitis from CL overuse needs three durable interventions: (1) CL hygiene counseling documented, (2) glasses-only period until cornea fully heals, and (3) ophthalmology follow-up to assess scarring and refit lenses only after clearance.
— Initial: 24-hour recheck by ophthalmology after starting therapy — assess infiltrate size, epithelial defect, AC reaction, pain.
— Improving (smaller infiltrate, less pain, healing defect) → continue regimen, taper drops over 1–2 weeks.
— Not improving at 48–72 h → re-culture, broaden coverage, consider atypical organisms (fungal, Acanthamoeba, mycobacterial).
— After resolution: visual acuity at 4–6 weeks; refract for residual astigmatism; address scarring.
— Epithelial: weekly until healed (typically 7–14 days), then transition to suppression discussion.
— Stromal/disciform: every 1–2 weeks during steroid taper; monitor for recurrence, IOP rise on steroids.
— Document corneal sensation at each visit (neurotrophic risk).
— Weekly during acute phase, monthly for 3 months, then every 3–6 months for at least a year — late complications common.
— IOP monitoring during topical steroid therapy.
— No lens wear until cornea fully re-epithelialized and ophthalmology clears; usually weeks.
— Refit with daily-disposable lenses preferred; review case and solution practices.
— Visual acuity (each eye, with correction).
— Pain score.
— Infiltrate size (length × width in mm), location relative to visual axis.
— Epithelial defect size, Seidel test.
— AC reaction (cells, flare, hypopyon height).
— IOP (especially on steroids).
— Medication adherence and side effects.
— Adherence to hourly drops — set alarms; involve caregivers.
— Symptoms warranting return (worsening pain, vision drop, sudden pain relief — perforation).
— Driving restrictions during monocular phase.
— Mental health screen — chronic ocular pain (especially Acanthamoeba, HZO) is depressogenic.
Board pearl: A bacterial corneal ulcer that is not improving in 48–72 hours on appropriate empiric therapy is the single most important re-evaluation timepoint — re-culture and re-think the organism rather than blindly switching antibiotics.
— In the US, decorative lenses (Halloween, "circle lenses") are FDA-regulated medical devices requiring a prescription. Sale without prescription is illegal under the Contact Lens Rule (FCLCA, 2005).
— Patients buying lenses online without exams, sharing lenses, or using novelty lenses are at high keratitis risk — document counseling on this at every opportunity, especially in adolescents.
— For long-term HSV suppression or HZO antiviral therapy, discuss risks (renal dosing, drug interactions), benefits (recurrence reduction), and alternatives.
— For therapeutic keratoplasty, document discussion of graft rejection, lifelong steroid use, recurrence of infection in graft, and refractive outcomes.
— Patient discharged from ED with "conjunctivitis" but undiagnosed bacterial keratitis → missed diagnosis is a leading ophthalmology malpractice claim. Mitigate with: documented visual acuity, fluorescein exam, explicit return precautions, 24-hour follow-up with ophthalmology arranged before discharge, and warm handoff.
— Communicate with the receiving clinician — closed-loop referral, shared EHR notes, telephone confirmation for high-risk cases.
— Neonatal gonococcal/chlamydial conjunctivitis — reportable in most US jurisdictions; partner notification and treatment required.
— Suspected child abuse — retinal hemorrhages with corneal findings in infants (abusive head trauma) trigger mandatory reporting.
— Never dispense topical anesthetics for home use — abuse causes severe keratopathy and perforation; document in the chart that proparacaine was used only for exam.
— Counsel against borrowing/sharing eye drops or contact lens solutions.
— Hourly drops for 48–72 h require caregiver support; if absent → admission is the ethical choice, not blaming the patient for "noncompliance."
— Monocular patients must meet state visual requirements; document counseling.
Step 3 management: When the stem features a teen who bought "Halloween contacts" at a gas station and now has a corneal ulcer, your answers should include same-day ophthalmology, culture, fortified antibiotics, and explicit counseling/documentation that decorative lenses are FDA-regulated devices requiring a prescription.
— Pseudomonas aeruginosa ↔ soft CL overnight wear, ICU patients (exposure keratopathy).
— Staphylococcus aureus / Streptococcus pneumoniae ↔ trauma, blepharitis, post-surgical.
— Moraxella ↔ alcoholic, debilitated patients — indolent ulcer.
— Neisseria gonorrhoeae ↔ hyperacute purulent conjunctivitis/keratitis (can penetrate intact epithelium) — neonate or sexually active adult.
— Acanthamoeba ↔ CL + tap water/shower/hot tub; perineural infiltrates; ring infiltrate; pain out of proportion.
— Fusarium / Aspergillus ↔ vegetative trauma, agricultural exposure, contaminated CL solution (historic ReNu MoistureLoc outbreak).
— HSV-1 ↔ dendrite with terminal bulbs, decreased corneal sensation, prior cold sores, recurrent unilateral.
— VZV ↔ V1 dermatomal rash, Hutchinson sign, pseudodendrites.
— Adenovirus ↔ EKC outbreaks (schools, eye clinics), preauricular node, subepithelial infiltrates at 1–2 weeks.
— Dendrite with terminal bulbs → HSV.
— Pseudodendrite without terminal bulbs → VZV or healing epithelium.
— Ring infiltrate in CL wearer with severe pain → Acanthamoeba.
— Feathery infiltrate with satellites → fungal.
— Hypopyon with central ulcer in CL wearer → Pseudomonas.
— HEDS — oral acyclovir suppression reduces HSV stromal recurrence ~50%.
— SCUT (Steroids for Corneal Ulcers Trial) — topical steroids after 48 h of antibiotics may benefit central/severe bacterial ulcers; safe overall.
— MUTT (Mycotic Ulcer Treatment Trial) — topical natamycin superior to voriconazole for filamentous fungal keratitis, especially Fusarium.
Board pearl: Pseudomonas keratitis can perforate within 48–72 hours in a CL wearer — that compressed timeline is why ophthalmology referral is same-day, not next-week.
— "22-year-old soft CL wearer who sleeps in lenses presents with 1 day of severe pain, photophobia, mucopurulent discharge, vision 20/200, central infiltrate with hypopyon."
— Answer: Same-day ophthalmology, corneal scraping/culture, fortified tobramycin + vancomycin or topical moxifloxacin hourly; discontinue lenses; no patch; no steroids initially.
— "35-year-old with prior cold sores has unilateral red eye, foreign body sensation, decreased corneal sensation, fluorescein reveals branching lesion with terminal bulbs."
— Answer: Oral valacyclovir 500 mg TID × 7–10 days (or topical ganciclovir gel); no topical steroid; discuss suppression if recurrent.
— "Young CL wearer who swims and showers in lenses, pain out of proportion to exam, perineural infiltrates, later ring infiltrate."
— Answer: Ophthalmology, confocal microscopy, culture on non-nutrient agar with E. coli, biguanides (PHMB or chlorhexidine).
— "Farmer struck in the eye by a tree branch a week ago, now feathery white infiltrate with satellite lesions and endothelial plaque."
— Answer: Cultures (Sabouraud), topical natamycin 5%, hold any steroids.
— "70-year-old with V1 vesicular rash and lesion at nasal tip (Hutchinson sign), now red painful eye."
— Answer: Oral valacyclovir 1 g TID × 7–10 days (renally dose), same-day ophthalmology, monitor for uveitis/glaucoma; counsel on PHN; ensure RZV vaccination plan.
— Hyperacute purulent conjunctivitis day 3 of life → gonococcal — admit, IM/IV ceftriaxone, saline irrigation, treat mother and partners; report.
— Topical steroids in undiagnosed ulcer → wrong.
— Eye patching of CL ulcer → wrong.
— Dispensing proparacaine → wrong.
— Continuing CL during treatment → wrong.
— Annual visit with CL wearer who sleeps in lenses → counsel on CL hygiene, switch to daily disposables, document.
Key distinction: Stems hinge on one decisive cue — water exposure (Acanthamoeba), vegetative trauma (fungal), prior cold sores + reduced sensation (HSV), Hutchinson sign (HZO), sleeping in lenses + hypopyon (Pseudomonas). Identify the cue first, then pick therapy.
One-line recap: Any painful red eye with photophobia, decreased visual acuity, and a fluorescein-staining corneal infiltrate is microbial keratitis until proven otherwise — requiring same-day ophthalmology, etiology-targeted therapy, and durable counseling on the underlying risk factor (especially contact lens hygiene), because delay or topical steroid misuse causes permanent blindness.
Board pearl: When a Step 3 stem features a contact lens wearer with a painful red eye, the highest-yield single best next step is almost always same-day ophthalmology referral with corneal cultures and empiric topical fluoroquinolone, plus documented CL hygiene counseling — that combination wins both the management question and the preventive-medicine follow-up.