em 5.2 - eent

What is preseptal (periorbital) cellulitis?

Infection limited to the eyelid/preseptal tissues; it is not an emergency.

What is orbital cellulitis?

Infection of extraocular muscles around the eye; it is an emergency.

You cannot tell with the pictures alone. need more info/CT.

What 5 findings most strongly favor orbital over preseptal cellulitis?

Proptosis; ophthalmoplegia (may not open the eye); pain with EOMs (so test EOMs), fever, leukocytosis.

Why must you explicitly test EOMs in suspected eyelid cellulitis?

Pain or restriction with eye movement suggests orbital involvement.

Initial antibiotic framework for orbital cellulitis?

Vancomycin for MRSA PLUS either ceftriaxone + metronidazole OR ampicillin-sulbactam.

Why might ampicillin-sulbactam be avoided in orbital cellulitis with suspected CNS involvement?

It penetrates the CNS poorly.

What consultations/disposition are required for orbital cellulitis?

Urgent ophthalmology or ENT consultation; determine need for surgery; IV therapy/admission, with later PO step-down if improving.

First-line outpatient treatment for preseptal cellulitis in the lecture?

Amoxicillin-clavulanate 45 mg/kg/day divided every 12 hours.

Preseptal cellulitis with a nonserious penicillin allergy: lecture alternatives?

Cefpodoxime, cefuroxime, cefdinir, or levofloxacin.

When should outpatient preseptal cellulitis be reassessed, and what if it is not improving?

Reassess in 24-48 hours; if no improvement, consider MRSA coverage.

Which agents does the lecture list for MRSA coverage in preseptal cellulitis?

TMP-SMX or linezolid.

Remember viral and allergic conjunctivitis more common than. bacterial conjunctivitis.

Classic bacterial conjunctivitis presentation?

Eyelash matting, mild-moderate mucopurulent discharge, and conjunctival inflammation.

What dx test should be performed in bacterial conjunctivitis to exclude a corneal abrasion?

Fluorescein staining.

Other than fluorescein exclusion of abrasion, how is routine bacterial conjunctivitis diagnosed?

Clinically.

Lecture treatment for uncomplicated bacterial conjunctivitis?

Topical fluoroquinolone antibiotic for 5-7 days.

Why can topical fluoroquinolones can be used in children for bacterial conjunctivitis?

Not systemically absorped

Red flag: Severe purulent conjunctival discharge with onset in less than 1 day suggests what?

Gonococcal conjunctivitis.

What is the next step for suspected gonococcal conjunctivitis?

Emergent ophthalmology consultation.

Classic viral conjunctivitis presentation?

Watery discharge, chemosis, and conjunctival inflammation.

Viral conjunctivitis diagnosis: when may fluorescein be used?

To rule out a corneal lesion.

Supportive treatment for viral conjunctivitis?

Cool compresses four times daily.

Medication option listed for viral conjunctivitis?

Naphazoline/pheniramine three times daily as a decongestant/antihistamine.

Classic allergic conjunctivitis presentation?

Watery discharge and chemosis in a patient with an allergy history.

When is fluorescein staining needed in allergic conjunctivitis?

Only if needed to rule out another lesion.

Treatment for allergic conjunctivitis?

Remove the inciting allergen and use artificial tears as needed.

One-line discharge comparison: bacterial vs viral/allergic conjunctivitis?

Bacterial is mucopurulent with matting; viral and allergic are usually watery.

What is herpes zoster ophthalmicus (HZO)?

Herpes zoster in a trigeminal distribution with ocular involvement.

What is Hutchinson sign?

Herpes zoster lesions on the tip of the nose.

Why is Hutchinson sign important?

It is a harbinger of ocular involvement/HZO.

What fluorescein pattern is shown with HZO in the lecture images?

A dendritic-appearing (tree-like) pattern.

Image recognition: Vesicular V1 rash including the nose plus a dendritic fluorescein lesion suggests what?

Herpes zoster ophthalmicus.

Lecture-specific oral antiviral options for HZO?

Valacyclovir 1 g PO BID; acyclovir 400 mg TID; or famciclovir 500 mg TID. Verify clinically because these are lecture-specific doses.

What is a corneal ulcer?

Infection of the corneal stroma, most often caused by Pseudomonas in this lecture.

Other infectious causes of corneal ulcer listed in the lecture?

HSV, varicella, and fungi.

Classic corneal ulcer symptoms?

Eye pain, redness, tearing, photophobia, and blurry vision.

2 major risk groups for corneal ulcer?

Contact lens wearers and immunocompromised patients.

Contact lens wearers definitely need

Pseudomonas coverage.

Slit-lamp/fluorescein finding of a corneal ulcer?

A staining corneal defect with a surrounding white, hazy infiltrate.

Treatment for corneal ulcer?

Topical ofloxacin 0.3% or ciprofloxacin 0.3%, 1 drop in the affected eye every hour.

Image recognition: A white corneal spot plus fluorescein uptake in a contact lens wearer suggests what?

(skipped this image)

Corneal ulcer.

Iritis = pathophysiology?

Inflammation of the anterior uveal tract: the iris and ciliary body.

Classic iritis presentation?

Red eye, photophobia, decreased vision, ciliary/limbal injection, and a constricted pupil.

What is consensual photophobia/pain?

Light in the unaffected eye triggers pain in the affected eye; it supports iritis.

Diagnostic slit-lamp exam finding in iritis?

Cells and flare: WBCs/protein in the anterior chamber.

Treatment principle for iritis?

Urgent ophthalmology consultation; topical steroids may be recommended, but only after ophthalmology approval.

Classic acute angle-closure glaucoma patient presentation?

Acute monocular/ONE-sided eye pain, red eye, blurry vision/halos, headache, nausea, and abdominal pain.

What is the pathophysiology of acute angle-closure glaucoma in the lecture?

Aqueous humor outflow obstruction causing markedly elevated intraocular pressure.

Best diagnostic test for acute angle-closure glaucoma?

Tonometry; check both eyes.

What is the normal intraocular pressurer range?

10-21 mmHg.

Some say normal IOP is up too 15 mmHg.

What IOP values should you remember from the slide?

diagnosis is IOP >21; acute attacks are often >40.

First topical beta-blocker treatment listed for acute angle-closure glaucoma?

Timolol 0.5%, 1 drop every 30 minutes for 2 doses in the affected eye only.

Alpha-2 agonist treatment listed for acute angle-closure glaucoma?

Brimonidine 0.1%-0.2%, 1 drop every 30 minutes for 2 doses in the affected eye only.

Systemic carbonic anhydrase inhibitor regimen listed for acute angle-closure glaucoma?

Acetazolamide 500 mg PO/IM/IV, then 250 mg every 6 hours.

When is IV mannitol used in acute angle-closure glaucoma?

If there is no response to the other medications; 1-2 g/kg IV over 30-60 minutes.

Contraindications/cautions for mannitol in acute glaucoma?

Contraindicated in renal failure or pulmonary edema; use caution in CHF.

What consultation is mandatory in acute angle-closure glaucoma?

Emergent ophthalmology consultation.

Call them while they're at the office.

Classic central retinal artery occlusion (CRAO) patient presentation?

Older patient (60+) with sudden, painless, monocular severe vision loss.

Remember for all eye complaints,

Get a visual acuity exam. "Vital sign" of the eye!

Due to the nature of occlusion, patients may present with

other acute embolic

events, including stroke or limb ischemia. so consider these as well.

What is the underlying event in CRAO?

Acute blockage of the central retinal artery, usually from an embolus/clot.

Important etiologies of CRAO listed in the lecture?

Carotid atherosclerosis, cardiogenic embolism, hematologic disease, and inflammatory disease.

Why must CRAO trigger a systemic emergency evaluation?

The patient may have concurrent or impending embolic events such as stroke or limb ischemia.

Typical visual acuity in severe CRAO?

Finger counting or worse.

Key pupillary finding in CRAO?

Relative afferent pupillary defect, also called a Marcus Gunn pupil.

Funduscopic finding in CRAO?

Ischemic retinal whitening.

What labs should be obtained in CRAO to evaluate for GCA?

ESR and CRP.

What complete eye-exam elements should be documented in CRAO?

Visual acuity, EOMs, IOP, pupillary function, and ocular structures/fundus.

Immediate bedside maneuver listed for CRAO, despite questionable efficacy?

Gentle ocular massage with the eye closed.

Reperfusion treatment considered for CRAO?

tPA may be considered.

Essential consultations/workup for CRAO?

Call ophthalmology and perform a stroke/embolic-source evaluation.

Make sure to work them up for potential causes of stroke.

Retinal vein occlusion is the 2nd most common cause of:

Vision loss from retinal vascular disease.

How does retinal vein occlusion commonly present?

Often asymptomatic or with peripheral field defects; central blurred vision occurs if the macula is involved.

Where do branch retinal vein occlusions commonly occur?

At arteriovenous crossings.

Proposed mechanism of central retinal vein occlusion?

Thrombus.

Retinal vein occlusion is the second most common cause of vision loss from retinal vascular disease; what is first?

Diabetic retinopathy.

How is retinal vein occlusion diagnosed and treated in the lecture?

Clinical diagnosis with history and complete eye exam; ophthalmology consult and treatment of the underlying cause.

Artery vs vein occlusion: which classically causes acute, profound, painless monocular loss?

Retinal artery occlusion.

Classic giant cell arteritis (GCA) patient?

Age 60+, unilateral temporal headache, and jaw claudication.

Which rheumatologic condition is associated with GCA?

Polymyalgia rheumatica.

Screening inflammatory markers for GCA?

ESR and CRP.

Confirmatory test listed for GCA?

Temporal artery biopsy.

Lecture treatment for GCA?

High-dose steroids prednisone 40-60 mg daily for 2-4 weeks. I think he said u def have to taper this?

u probbaly wont be able to get back the biopsy today so get the steorids.

Why must GCA be treated immediately rather than waiting for biopsy?

Delay can cause irreversible vision loss; prognosis is poor if not aggressively managed in the first 24 hours.

Vignette: 72-year-old with temporal headache, jaw fatigue while chewing, and transient visual loss. Diagnosis?

Giant cell arteritis.

What feature makes GCA less likely in a younger patient?

GCA is primarily a disease of adults older than 50; the lecture emphasizes 60+.

What does "amaurosis fugax" mean?

"Fleeting darkness": transient loss of vision in one or both eyes.

First 2 history questions in transient visual loss?

Was it monocular or binocular, and how long did it last?

Required eye exam for amaurosis fugax?

Visual acuity, EOMs, pupils, IOP, ocular structures, and fundoscopic exam.

Lecture shortcut differential for transient visual loss?

- Monocular ischemia, carotid disease, other embolic source.

eizure

papilledema.

Monocular ischemia from carotid/embolic disease: typical duration and pattern?

1-10 minutes; rapid-onset monocular, often altitudinal loss.

Findings that may accompany monocular retinal ischemia?

Hollenhorst plaque or hemispheric neurologic symptoms.

Papilledema-related transient visual obscurations: typical duration and associated symptoms?

Seconds; graying/blurring with headache or diplopia.

Idiopathic retinal vasospasm: typical duration and pattern?

5-60 minutes; monocular positive or negative visual symptoms, sometimes headache.

Migraine visual symptoms: typical pattern and duration?

Usually binocular positive symptoms that spread over 10-30 minutes, often followed by migraine headache.

Vertebrobasilar ischemia visual loss pattern?

1-10 minutes of homonymous hemianopia, with or without brainstem deficits.

Ictal visual symptoms: typical duration and associated features?

3-5 minutes; binocular/lateralized positive phenomena with altered consciousness or motor symptoms.

Postictal visual loss: typical pattern and duration?

Binocular field loss lasting about 20 minutes or longer after a seizure.

Classic retinal detachment presentation?

Older patient with progressive, painless, monocular visual loss, often preceded by flashes or floaters.