Background (JAMA 2004;291:1487)
40% of vision loss is preventable; careful hx/PE can establish dx and distinguish between urgent and routine ophtho referrals
Definitions: Legal blindness: Corrected VA ≤20/200 or visual field
<20° diameter in better eye; Visual impairment: Corrected VA worse than 20/40 in better eye
Screening (See AAO PPP Guidelines 2015; aao.org/ppp)
If no RF, comprehensive eye exam: Age 40–54 q2–4y, 55–64 q1–3y, & ≥65 q1–2y If glaucoma RF (see “Vision Loss”): Age 40–54 q1– 3y, 55–64 q1–2y, & ≥65 q1–2y If DM: Dilated exam at time of diagnosis (DM2) or 5 y s/p dx (DM1), then yearly
Basic Eye Anatomy
Anterior segment contents
Cornea: Dome-shaped transparent outermost layer of front of eye Limbus: Circular ring of transition between cornea & sclera Sclerae: White (opaque) outermost layer of the rest of the eye; continuous w/cornea Conjunctiva: Covers the sclerae (bulbar portion) and inner aspect of eyelids (palpebral portion), does not cover cornea Anterior chamber: Fluid (aqueous humor)-filled space between lens and cornea Iris/Ciliary body: Iris is anterior extension of ciliary body, which holds the lens and adjusts it for near/far distances (accommodation); pupil is the opening at center of iris
Posterior segment contents
Retina: Inner lining of eye, vascular, contains photoreceptor cells (rods/cones) Macula: Pigmented area near center of retina; contains fovea (highest concentration of cones) Choroid: Pigmented layer between retina & sclerae, vascular (supplies macula) Optic nerve: Axons from retinal ganglion cells in retina;
transmits images → brain Vitreous cavity: viscous fluid (vitreous humor)-filled space behind lens
History
Complete history below; may be narrowed based on nature of complaint
Age: Relevant in narrowing Ddx (e.g., GCA unlikely if <50 yo) Ocular history: Hx trauma, eye surgery, contact lens use (incl sleeping in lens, failure to change regularly), eye drop use, family ocular hx Symptoms: Gradual vs. sudden onset, monocular vs. binocular, duration, quality, similar prior episodes, painful vs. painless vision
change, irritation, pruritus, FB sensation, discharge (severity & quality), photophobia Associated systemic Sx: HA, fever, rash, arthralgia, GI sx, environmental allergies
| Ocular Side Effects of Systemic Medications | ||
| Medication/Class | Ocular Side Effects & Toxicities | Notes & Mgmt Guidelines |
| Amiodarone | Glare, colored halos, dry eye; possible optic neuropathy | Refer for eye exam if ⊕ sx, D/c if possible |
| Bisphosphonates | Red eye or ocular discomfort due to dryness; uveitis, scleritis | Refer urgently (<1 wk) if acute, painful, or ↓ vision; may need to d/c |
| Corticosteroids | Cataract, glaucoma, central serous retinopathy (→ blurred vision) | Annual eye exam if long- term use, refer more urgently (1–2 wk) if acute or subacute vision δ |
| Hydroxychloroquine/Chloroquine | Ocular irritation, contact lens intolerance (drug crystals in tear film may aggravate ocular surface); can → irreversible central vision loss due to retinal (macular) toxicity | At dose of 5.0 mg/kg, risk of toxicity is <1% at 5 y,
<2% at 10 y; almost 20% after 20 y Baseline eye exam to r/o pre-existing maculopathy Annual screening after 5 y in pts on <5 mg/kg & w/o other RF (CKD, concurrent tamoxifen, Stargardt’s disease) |
| Ethambutol | Bilateral optic neuropathy causing irreversible central VA loss, ↓ color VA, & central scotomas | Onset w/in 2–5 mo of starting tx 1% risk with daily dose ≤15 mg/kg, 5– 6% at 25 mg/kg, 50% at
100 mg/kg Baseline ophthal exam then q1mo for high doses or RF (DM, CKD, EtOH, old age, other eye d/o, neuropathy) |
| Fluoroquinolones | Probable: Diplopia (EOM tendonitis), myasthenia exacerbations, ?uveitis | Sx resolve with drug withdrawal |
| Isoniazid | Optic neuritis (blurred vision, pain w/ EOM) | Refer if suspicion, d/c Rx if able |
| Niacin | Blurred or ↓ vision due to cystoid macular edema | Refer for eye evaluation if suspicion |
| Rifabutin | Uni-or bilateral ocular pain, redness, photophobia due to uveitis | Urgent referral (<1 wk); most cases resolve w/in 1–2 mo of d/c’ing agent |
| Scopolamine (incl patch) | ↓ near vision due to accommodative impairment, pupil dilation | Dose-and proximity-related; may last several days after drug discontinuation |
| Sildenafil and other PDE5 inhibitors | Δ in color perception, blurred vision, conjunctival hyperemia, ocular pain, photophobia Common, dose- dependent, appears to be fully reversible | 3% risk at doses of 50 mg, 10% at 100 mg, 40–50%
at 200 mg; s/e start 15– 30 min after ingestion, peak at 60 min; Avoid use if prior hx of nonarteritic anterior ischemic optic neuropathy (NAION) |
| Statins | Probable: diplopia, ptosis, ↓ EOM 2/2 to localized myositis | Reversible upon d/c, similar to known statin-induced myopathy |
| Sulfa- (incl. thiazide diuretics, acetazolamide, topiramate) | Acute angle closure glaucoma, choroidal effusions, acute or subacute transient blurred vision due to myopia | Urgent referral to ophthalmology
Usually reversed if d/c agent Patients with primary open- angle glaucoma are not at ↑ risk |
| Tamoxifen | ↓ vision due to crystalline retinopathy, cystoid macular edema, retinal hemorrhages, ?cataracts | Baseline eye exam then q4–6mo; d/c’ing drug may halt further ↓ VA but reversal is rare; raloxifene ↓ likely to cause SE |
| Tamsulosin and other alpha- adrenergic antagonists | Intraoperative floppy iris syndrome (IFIS) may complicate cataract surgery (highest risk w/ tamsulosin) | Alpha-1A blocking affects iris dilator muscle → atrophy from disuse; risk of IFIS persists yrs beyond d/c of drug |
| Vit A & derivatives (retinoids, Accutane) | ↓ vision, transient obscurations assoc. w papilledema, ↑ ICP (vs. night blindness, dry eye if vit A deficient) | Risk occurs at ↑ doses |
Drugs 2007; eyedrugregistry.com/aao-syllabus.html; aao.org
Exam
Visual acuity (VA): Measure each eye separately w/ glasses if worn; standard Snellen chart at 20′ distance preferred; near card held at 14″ also OK; if VA worse than 20/40, re-measure w/ pinhole (refractive error typically improves); if unable to read chart, document as follows: CF (can count fingers at x feet) > HM (hand motion) > LP (light perception) > NLP (no light perception); SC: without correction, CC: with correction
Color perception: Unilateral “red desaturation” (red object appears “washed out”) suggestive of optic nerve disease
Confrontational visual field: Assess all 4 peripheral quadrants in each eye separately; field loss can suggest optic nerve pathology (often bitemporal), retinal detachment (RD; unilateral), advanced glaucoma, or neurological disease (e.g., homonymous hemianopsia)
Pupils: Symmetry of size & reactivity; test for RAPD w/ “swinging flashlight test”: Hold penlight on 1st eye for 2–3 s then rapidly switch to the 2nd; pupil of 2nd eye should stay stable or constrict; dilation indicates afferent defect of 2nd eye (“perceives” less light); previous ocular surgery or topical eye gtts can affect pupil exam
Extraocular movements: Should be full & conjugate
Anterior segment exam: Eval w/ penlight for lid changes, conjunctival hyperemia or hemorrhage, corneal opacity or epithelial defect (+ fluorescein staining with Wood lamp, see Figure in “Vision Loss”), anterior chamber (hypopyon, hyphema), iris (irregular shape, obvious defects), lens (visible opacity)
Direct ophthalmoscopy: Allows provider to assess vitreous clarity (e.g., able to visualize nerve?) & evaluate for optic nerve edema, cotton wool spots, peripapillary/retinal hemorrhage; dilated exam provides for
↑ field of view and views of ↑ areas of retina
Overview (cdc.gov/visionhealth)
Visual deficits affect >40 million adults in US; 16% of adults >40 y have cataracts, and 2% have glaucoma; visual loss affects 23.5% of US adults w/diabetes >50 y; only half of the 61 million adults at risk for vision loss have visited an eye specialist in the past year
Important to recognize common causes of vision loss and those that require urgent referral; differential should be guided by acuity and absence/presence of pain
Acute Painless Vision Loss
General approach: Requires same-day ophthalmology evaluation;
usually unilateral
DDx: GCA/temporal arteritis (suspect if >50 y w/ new HA or diplopia;
⊕ systemic sx): amaurosis fugax, diplopia, jaw claudication, scalp tenderness, PMR; check ESR/CRP/PLT
Nonarteritic ischemic optic neuropathy (Mean age 60, ↑ in vasculopath, PDE5 use): painless ↓ vision, ⊕ RAPD, “altitudinal” (in horizontal plane) visual field defect, sectoral optic disc edema Central retinal artery occlusion (Vasculopath, postcardiac
surgery, 5–10% assoc w/ GCA)—presents w/ sudden profound ↓ VA, ⊕ RAPD, ± amaurosis fugax → ED for stroke w/u Central retinal vein occlusion (hx HTN, DM, hypercoagulability, hyperviscosity, glaucoma, OCPs): variably ↓ VA, ± RAPD, + diffuse intraretinal hemorrhages Vitreous hemorrhage: Commonly due to DM or RD/retinal tear; VA variable Retinal detachment: Photopsias (flashes of light), floaters, variable ↓ VA/visual field; ± abnl red reflex Pseudosudden vision loss: Gradual monocular vision loss may be perceived as “sudden” due to inadvertent occlusion of other eye; obtain careful hx
Acute Painful Vision Loss
General approach: See “Painful Red Eye” in “Eye Compllaints” for further discussion
Optic neuritis: Typically unilateral w/ age <50 y; ♀ > ♂; Etiologies include MS, idiopathic, infectious (e.g., postviral, Lyme), & granulomatous (e.g., sarcoidosis); Sx: Blurred vision, pain w/ EOM; photopsia, scotoma Exam: Variably ↓ VA, red desaturation, + RAPD, ± optic disc edema; Refer w/in 24 h
Gradual Painless Decreased Vision
General approach: Determine if uni-or bilateral; routine referral appropriate if slow progressive loss over mo–y
DDx: Refractive error (improves w/ pinhole or glasses): Myopia, hyperopia, astigmatism; presbyopia (farsightedness 2/2 ↓lens flexibility) if >40 y
Cataract: Age-related (most common), metabolic, traumatic, congenital; Sx: ↑ glare, halos, difficulty w/ night driving, difficulty reading in low light, frequent change in glasses
Open-angle glaucoma: Asx peripheral vision loss often w/ ↑ IOP & ↑ cup:disc ratio; RF include: ↑ Age, African or Hispanic ethnicity, ⊕ FHx; Screening: Refer if age >40 & 1st-degree relative w/ glaucoma; progression can be slowed/halted w/ proper tx (incl. laser trabeculoplasty, topical gtts, surgery if severe); Compliance w/ gtt important
Diabetic retinopathy: Initially asx → leading cause of legal blindness among working-age Americans; Nonproliferative (NPDR, early stage) vs. Proliferative (PDR, late stage, neovascular); Common
reasons for ↓ VA in DM: Diabetic macular edema (DME), vitreous hemorrhage, macular ischemia, tractional RD; RF: ↑ HbA1C, ↑ disease duration, HTN, ↑ lipids; Tx: Strict BP/glucose control; peripheral retinal laser (PRP) & intravitreal anti-VEGF if high risk for PDR; anti-VEGF (e.g., ranibizumab, aflibercept, off-label bevacizumab), intravitreal steroids, or macular laser for DME
Age-related macular degeneration (AMD): ↓ central vision; most common cause of blindness in US; “dry” = slowly progressive disease, “wet” = neovascular w/ risk for sudden ↓ central vision due to hemorrhage; RF: tobacco, poor diet/nutrition,↑ age, ⊕ FHx, genetic polymorphisms; Tx: Monitor w Amsler grid (new metamorphopsia suggests progression), AREDS2 vitamins if moderate stage “dry,” & intravitreal anti-VEGF as often as q1–2mo if “wet,” sustained release drugs in pipeline
Medications: See Table “Ocular Side Effects of Systemic Medications” in “Ophtho Eval”
Idiopathic intracranial hypertension (pseudotumor cerebri): RF: ♀ gender, obesity, steroid use & cessation, high-dose vit A, tetracyclines, OCPs; Sx: Transient visual obscuration, diplopia, positional HA worse when supine, pulsatile tinnitus “whooshing sound,” N/V; Findings: Variably ↓ VA, ± CN VI palsy, b/l optic nerve edema, MRI w/o mass/thrombi, ↑ICP; Tx: Referral w/in 24 h; see Neurology section, “HA” for more details
Amblyopia: Unilateral chronic ↓ VA due to asymmetric childhood cortical visual input; normal ocular findings, if mild, may not be detected until adulthood; Tx: Routine referral
Patient Information Driving guidelines:
www.mdsupport.org/library/drivingrequirements.html
Patient education: www.aao.org/eyesmart, for diabetic retinopathy: aao.org/eye-health/diseases/what-is-diabetic-retinopathy
General Approach
Initial management by PCP often appropriate; routine referral → ophtho if sx >3–4 wk
Red flags for vision-threatening etiologies: Severe pain & photophobia, significantly ↓ vision relative to baseline or worse than 20/200, recent eye surgery or trauma, abnl pupil exam, corneal opacities, acute sx onset in a contact lens-wearer
Urgent referral for red flags & vision-threatening etiologies (below); also consider for severe sx, diagnostic uncertainty, & recurrent disease Avoid topical NSAIDs & steroids w/o ophthalmology guidance due to potential s/e
Avoid topical aminoglycosides due to corneal toxicity Symptom-based approach to differential helpful (below):
| Differential of Eye Complaints, by Presentation | |
| Painless red eye | Subconjunctival hemorrhage, episcleritis, dry eye syndrome (DES), blepharitis/meibomian gland dysfunction (MGD); see below |
| Painful red eye | Inflamed pingueculum or pterygium, acute conjunctivitis, keratitis, tear deficiency, iritis/uveitis, scleritis, endophthalmitis, acute angle closure glaucoma; see below |
| Photophobia | Iritis/uveitis, corneal abrasion, keratitis, DES, postconjunctivitis, retinal macular diseases (chronic), physiologic |
| Eye itching/burning | Infectious or allergic conjunctivitis, blepharitis, DES, pterygium |
| Foreign-body sensation | Corneal or upper lid foreign body, DES, trichiasis (misdirected eyelashes), conjunctivitis |
| Swollen eyelid | Hordeolum/“stye” (chronic → chalazion), atopic dermatitis, contact dermatitis, preseptal cellulitis, orbital cellulitis |
| Drooping eyelid | Ptosis, dermatochalasis (excess upper eyelid skin) |
| Other | “Bubble on the white part”: conjunctivochalasis (redundant conjunctiva), conjunctival cyst, pingueculum → all nonurgent referral “Dot on the clear part”: corneal foreign body, corneal ulcer |
PAINLESS RED EYE
Painless Red Eye
Subconjunctival hemorrhage: Etiologies: Valsalva, eye rubbing, HTN, bleeding dyscrasia, anticoagulant use, idiopathic; Findings: Unilateral, no vision change; well-demarcated plane of heme obscuring sclera; Rx: urgent referral if bullous or follows significant trauma, otherwise benign—artificial tears PRN discomfort, check BP, check PLT, & coags if recurrent
Episcleritis: Idiopathic, self-limited unilateral, painless focal erythema w/out d/c or vision change; Findings: Mild hyperemia of superficial vessels, possibly sectoral; Rx: Artificial tears, referral if persistent or recurrent
Dry eye syndrome: S/sx: Bilateral burning, FB sensation, ↑ by wind/cold & prolonged eye use (e.g., computer, tablet, reading), ± reflex tearing; mild diffuse hyperemia, sx severity disproportionate to exam findings, often coexistent with blepharitis; may have diffuse punctate staining on fluorescein exam (see “Findings in Common Eye Disorders”). Etiologies: ↓ tear production or ↑ evaporation from altered composition; idiopathic, autoimmune, rosacea, or 2/2 meds. Rx: Artificial tears QID, artificial tear gel QHS, omega-3 supplementation (e.g., Fish Oil 1000 mg PO BID), cyclosporine (Restasis) or lifitegrast (Xiidra) by ophthalmologist
Blepharitis/Meibomian gland dysfunction: Chronic b/l lid margin inflammation → burning, itching, mild AM lid crusting, minimal d/c, sx worse in AM, dandruff-like flakes on lashes, mild diffuse hyperemia Rx: Warm compresses BID, gentle lid scrubs (commercially available), artificial tears PRN, erythromycin or bacitracin ophthalmic ointment BID if severe
PAINFUL RED EYE
Inflamed pingueculum or pterygium: ± hx UV/sun exposure; irritation, foreign body sensation; Findings: Wing of hyperemic thickened tissue from conjunctiva (often nasal) → cornea; Rx: UV protection, artificial tears PRN, referral if persistent
Keratitis (corneal inflammation) S/sx: pain & photophobia, tearing, ±
↓ vision, diffuse hyperemia ± mild lid edema; pain relieved w/ proparacaine gtts
Corneal ulcer (usually bacterial): White corneal opacity often visible w/ penlight, ± mucopurulent d/c, ± hypopyon, often hx contact lens use; same-day referral
Herpetic: Vesicles in V1 dermatome on affected side (VZV), ± lid vesicles or hx oral lesions (HSV), corneal dendrites w/ fluorescein & Wood lamp (see “Findings in Common Eye Disorders”) → start systemic tx (e.g., valacyclovir 1 g PO TID), see “HSV”; same-day referral
For management of UV or chemical-associated keratitis, as well as corneal abrasion, see “Eye Injury”
Severe tear deficiency (e.g., Sjogren’s, ocular GVHD): Diffuse punctate staining may be visualized on fluorescein exam (see “Findings in Common Eye Disorders”); Preservative-free artificial tears q1h while awake, gel lubricants qhs, refer w/in 1 wk, sooner if severe pain or ↓ VA
Iritis/Uveitis: Autoimmune disease (assoc w/ HLA-B27), post-trauma, idiopathic; S/sx: Often unilateral, severe photophobia, tearing, ↓ vision, conjunctival & limbal hyperemia, sluggish pupillary rxn → Refer w/in 24 h, defer steroids until after ophtho exam
Scleritis: vasculitis, 50% assoc w/ autoimmune dz (e.g., RA). S/sx: “Boring” HA-like pain, sectoral or diffuse boggy red/pink sclera, exquisitely tender globe, pain w/ EOM, wakes pt from sleep, vision change rare. Rx: Oral NSAIDs (e.g., naproxen 250–500 mg BID), refer w/in 24 h
Endophthalmitis: Assoc w/ hx recent eye surgery or intravitreal injection, IDU, trauma, immunosuppression, systemic bacteremia or fungemia; S/sx: Severe pain, floaters, ↓ vision, variable degrees of conjunctival injection, + hypopyon → same-day referral
Acute angle closure glaucoma. S/sx: Sev unilateral eye pain & HA, halos around lights, N/V, ↓ vision, fixed & mid-dilated pupil, ± cloudy cornea, noticeable difference in firmness of globes to gentle palpation through lids → same-day referral
ACUTE CONJUNCTIVITIS (JAMA 2013;310:1721)
Evaluation
Background: Viral > bacterial, although difficult to distinguish clinically; culture not needed for routine cases; consider if severe purulence, recurrent disease, or if no improvement either after 7–10 d or after course of topical abx; POC adenoviral swab commercially available may help with diagnosis/risk stratification
Viral: Microbiology: Frequently adenovirus, highly contagious; Hx: ± sick contact, URI sx, watery discharge, gritty sensation, mild photophobia, itching, crusty eyelids, unilateral can → bilateral; Exam: Diffuse hyperemia, ± periocular swelling, seromucoid discharge, preauricular LAD common, epidemic keratoconjunctivitis (EKC) may → sequelae, refer if ↓ vision, severe photophobia
Bacterial: Microbiology: Typically S. pneumoniae, S. aureus, or H. influenzae, contagious; may also be chlamydia (1–5% of all cases) or gonorrheal, often if concurrent genital infection; Exam: Thick/purulent d/c; copious crusting, intense hyperemia, LAD rare
Hyperacute: Severe, sudden variant of above, typically N. gonorrhoeae; referral w/in 24 h as ↑ risk of corneal perforation; Chronic: Duration weeks-months, usually C. trachomatis, suspect if no improvement w/ ocular abx • Allergic: Commonly occurs w/ allergic rhinitis; Precipitants: Ragweed, grass pollen common; hx: chronic or seasonal pattern, hx atopy, “watery” discharge, severe ocular pruritus; Exam: b/l, mild hyperemia, serous/stringly discharge
Treatment
Counseling: No contact lens wear while sx present; if infectious, good hand hygiene to ↓ risk of transmission (including unaffected eye if unilateral)
Viral or mild bacterial: Mostly self-limiting; cool compresses & artificial tears PRN; may consider 0.5% erythromycin ointment QID × 7 d Mod–severe bacterial: Broad-spectrum topical abx offer slight improvement in time to remission (e.g., Ofloxacin 0.3% 1 gtt QID × 7 d or Polytrim 1 gtt QID × 7 d) (Cochrane Database Syst Rev 2012;9:CD001211)
Additional indications for broad-spectrum topical abx: Consider if persistent sx >1 wk, immunocompromised, health care worker, or tx prerequisite to return to work/school; also tx if chlamydial or gonorrheal
Allergic: Avoidance of allergens when possible, artificial tears PRN; OTC topical antihistamines gtt & mast-cell stabilizers (e.g., ketotifen 1 gtt OU BID until sx resolve), artificial tears PRN (see “Allergic Rhinitis” for systemic tx)
Recurrent or chronic: refer to r/o insidious or chronic infectious/inflamm etiology
EYELID COMPLAINTS (AFP 2015;92:106)
Swollen Lid
Hordeolum (“stye”): Acute lid inflammation due to occluded meibomian gland; S/sx: Lid erythema, typically focal palpable and/or visible tender nodule; ± conjunctival hyperemia, drainage, cellulitis; Rx: Warm compresses QID, erythromycin oint BID, oral abx if cellulitis present (see “Skin and Soft Tissue Infections”)
Chalazion: Chronic granulomatous lesion resulting from obstructed gland; S/sx: typically painless, rubbery nodule; Rx: warm compresses; referral to ophthalmology if persistent
Contact dermatitis (see “Dermatitis”): Use caution with steroid ointments around eyes; recommend low-potency (e.g., loteprednol, fluorometholone if possible, otherwise Dex/Neo/Poly ophthalmic ointment); need Ophthalmology f/u if long-term use of periocular steroid Preseptal cellulitis: Superficial periocular skin infection, may be assoc w/ hordeolum, hx eyebrow tweezing, no visual s/sx, eyes white and quiet; tx with antibiotics (e.g., amox/clav, cefpodoxime); see “Skin and Soft Tissue Infections”
Orbital cellulitis: RF: Hx sinusitis, orbital trauma, facial surgery, diabetes/DKA; S/sx: Severe lid edema & erythema, chemosis, ↓ VA, proptosis, ↓ EOM ± diplopia, pain w/ EOM, HA, ± nasal congestion, ± fever; Rx: orbital or maxillofacial CT w/ contrast, CBC, same-day referral w/ hospital admission for IV abx, close monitoring Idiopathic orbital inflammation/orbital pseudotumor: S/sx: Can mimic orbital cellulitis (must r/o infectious etiology first); same-day referral as above
Droopy Lid
Ptosis: congenital, age-related (levator muscle dehiscence), postsurgical (eyelid speculum can hasten dehiscence) Dermatochalasis; redundant upper eyelid skin, benign
Lid Skin Lesion or Rash
Differential includes SCC or BCC; see “Skin Cancer”; consider atopic dermatitis, contact dermatitis, HSV, or rosacea (see respective chapters)
General Approach (AFP 2015;92:106)
Detailed hx re: mechanism & general ophthalmic screening exam critical
Urgent referral if ↓ vision, or ambiguity re: mechanism of trauma or full extent of injuries
Do not prescribe topical anesthetics (e.g., proparacaine); overuse → severe corneal damage; Rx topical corticosteroids & eye patch only in conjunction w/ specialist
Prevention: Remind pts of importance of eye protection (e.g., polycarbonate safety goggles/glasses w/ yard & household chores; appropriate occupational eyewear)
Cornea and Conjunctiva
Chemical (acid/alkali) exposure: Alkali exposure (e.g., plaster, cement, lye) far more damaging than acid, rapid neutralization of pH critical; S/sx: Pain, ↓ vision, diffuse conjunctival hyperemia & chemosis; Mgmt: Immediate testing of pH prior to any other eval, litmus paper placed under lower lid (nl 6.8–7.2); followed by proparacaine drop & irrigation w/ Ringer’s or saline for 30 min; recheck after 10 min & continue cycle until pH neutralized; ensure fornices adequately flushed as retained particulates may prevent neutralization. Tx: Refer w/in 24 h in all cases w/ erythromycin or bacitracin ophth oint QID in interim; immediate referral if unable to neutralize pH or ⊕ limbal ischemia (vessels at boundary btw cornea & conjunctiva replaced by marbled whitening) or corneal haze
UV/thermal exposure: Follows unprotected exposure to welder’s arc, tanning bed, high-altitude “snow blindness,” electric sparks; sx often begin hrs post-exposure; Findings: punctate or confluent fluorescein staining on cornea; Rx: Artificial tears q1h PRN, erythromycin oint QID
× 5 d; refer if severe or not improved w/in 24 h
Corneal abrasion: (AFP 2013;87:114) Often hx mild identifiable trauma; Sx: Pain, FB sensation, photophobia, tearing; Findings: ± ↓ VA if within visual axis, pain relieved w/ topical proparacaine, focal fluorescein staining w/ Wood lamp (see “Findings in Common Eye Disorder”), possible FB w/ eversion of upper lid; Tx: No contact lenses until healed; patching not routinely done; do not send home w/ topical anesthetics; artificial tears & cool compresses PRN; Peripheral abrasion: 0.5% erythromycin oint QID × 5 d for small (e.g., 1–2 mm diameter); if larger or from contaminated object (e.g., fingernail, organic material) add FQ (e.g., 0.3% ofloxacin 1gtt QID × 5 d); Refer w/in 24 h if central (involving visual axis, or concern for corneal laceration); Refer if not improved w/in 48 h
Cyanoacrylate adhesive (“Super glue”): Tx: Warm compress to separate lids/lashes; glue usually flakes off over days; do not cut lashes w/o ophtho involvement; tx as corneal abrasion
Corneal or conjunctival foreign body: Corneal more common, often occupational assoc (e.g., mechanic w/ metallic corneal FB); Sx: Pain, FB sensation, photophobia, tearing, ± ↓ vision; Findings: ± ↓ VA, FB visible on cornea, conjunctiva, or w/ upper lid eversion; fluorescein staining (see “Findings in Common Eye Disorder”); Tx: Conjunctival: If provider comfortable, may remove conjunctival FB w/ cotton swab & tx w/ 0.5% erythromycin or bacitracin ophthalmic ointment QID × 5 d; corneal: Refer w/in 24 h
Anterior Chamber
Hyphema: Typically follows blunt orbital trauma (e.g., soccer ball or fist) but maintain suspicion for penetrating injury; Sx: Dull pain, ± ↓ vision; Findings: ± ↓ VA, clot or layered blood in the anterior chamber visible w/ penlight; may have ↑ IOP; Tx: Same-day referral: Bed rest, protective shield over eye, avoid NSAIDs & anticoagulants
Retina and Optic Nerve
Vitreoretinal pathology: Typically follows blunt trauma; may include
vitreous hemorrhage, retinal tear or detachment; Sx: ↓ Vision, flashing lights, floaters, sensation of veil coming down over vision; Findings: ± ↓ VA, ± altered fundus visualization (impaired if significant vitreous hemorrhage or nl if peripheral retinal pathology); Tx: Same-day referral
Orbit, Adnexa, and Globe
Orbital fracture: Follows blunt trauma (e.g., MVC, fist, fall); Findings: Periorbital ecchymosis, point tenderness ± palpable orbital rim deformities, V1/V2 hypesthesia, painful or ↓ EOMs; Tx: ED/Same-day referral for imaging & DFE
Lid lacerations: Superficial-appearing injuries may mask more significant injury to surrounding tissues and globe; Tx: Tetanus update, cool gauze to injury, same-day referral for repair
Ruptured globe: Full-thickness disruption of eye wall; can follow penetrating or blunt injury; have ↑ suspicion in elderly w/ facial trauma after fall (esp. w/ hx prior eye surgery); Findings: ↓ VA (mild to NLP), subconjunctival hemorrhage (↑ suspicion if circumferential & bullous), irregular or peaked pupil, shallow anterior chamber w/ penlight, leaking intraocular fluid visualized w/ fluorescein & Wood lamp; Tx: Emergent referral for suspected rupture as repair w/in 24 h å risk of endophthalmitis, NPO, update tetanus, place hard protective shield over the eye
ALLERGIC RHINITIS
Background (Lancet 2011;378:2112)
Definition: Inflammation of the nasal membranes in response to known or unknown allergen(s); also known as “hay fever” → rhinorrhea, sneezing, nasal congestion/pruritus
Pathophysiology: 1st exposure → production of allergen-specific IgE
→ IgE binds receptors on mast cells & basophils; subsequent exposures → allergen crosslinks IgE on cell surface → cellular activation (i.e., mast cell degranulation)
Epidemiology: Prevalence is increasing; highest in children and teens; currently affects >8% of US adults; accounts for >13 million US health care visits annually (cdc.gov/nchs)
Risk factors: Include ⊕ FHx of allergic disease (possibly mediated by
genetics [multiple loci]), ↑ exposure to pollutants, dust mites, and early exposure to cigarette smoke (JACI 2011;128:816)
Complications: Nasal inflammation sx can affect QoL & productivity; additionally, ↑ incidence/severity of URIs (2/2 mucosal inflammation) & bacterial sinusitis (2/2 sinus obstruction) (Otolaryngol Head Neck Surg 2007;137:S1)
Comorbidities: 40% of pts w/ AR also have asthma; tx of AR → improved asthma sx & ↓ hospitalizations (JACI 2002;109:57); ocular sx occur in 50–70% of pts w/ AR (see “Eye Complaints”); also strongly assoc w/ AD (“atopic march”)
Evaluation (Clin Exp Allergy 2000;30:1314;1417)
General approach: Establish sx severity & potential triggers, consider DDx & assess for comorbidities (OSA, asthma, atopy)
History: Assess sx, including functional (impaired sleep & work)
Meds: Important to r/o rhinitis medicamentosa as cause of sx (see below); include OTC decongestants & nasal sprays, OCPs, ASA, NSAIDs, anti-HTN
PMHx/Soc hx: Hx atopy (asthma, AD), OSA, environmental or food allergies, occupational hx, risk factors (above), current pregnancy, cocaine use
| Allergic Rhinitis Triggers | |
| Seasonal | Tree pollen (spring), grasses (summer), weeds (fall) |
| Perennial | Animal hair (cat, dog, etc.), dust mites, cockroaches (urban |
| areas), mold | |
| Occupational | Agricultural workers, animal lab workers, food services |
Exam: HEENT + skin (atopic dermatitis) & lung (asthma) exam
Eyes: Bilateral conjunctival hyperemia ± clear d/c (allergic conjunctivitis), infraorbital “shiners” (↑ venous stasis 2/2 nasal congestion) Ears: Serous otitis media (Eustachian tube dysfunction)
Nose: Saddle-nose deformity (granulomatosis w/polyangiitis, or GPA) or septal deviation (trauma) or perforation (cocaine), pallor of mucosa, pallor/edema of turbinates; “allergic salute” (rubbing nasal tip upward w/ palm → supratip crease); polyps (chronic sinusitis, ASA Se)
Differential diagnosis: Up to 30% of rhinitis nonallergic
Infectious: Acute viral rhinosinusitis, chronic rhinosinusitis (consider immunodeficiency) Medication-induced: S/e of ASA/NSAID, ACEI, PDE5, HCTZ, β-blockers; and OCPs (JACI 2006;16:148) rhinitis medicamentosa (“rebound” 2/2 chronic use of topical nasal decongestants, e.g., oxymetazoline; also seen w/ cocaine) Autoimmune: Churg–Strauss, GPA, sarcoid
Idiopathic: Vasomotor rhinitis (nonallergic, noninfectious)
Structural: Nasal polyps, deviated septum, adenoid hypertrophy Other: Pregnancy, assoc w/ menstrual cycle (2/2 ↑ circulating estrogen/progesterone)
WHO classification (JACI 2001;108:S147)
Frequency: Intermittent (<4 d/wk or <4 wk) vs. persistent (>4 d/wk or
>4 wk) Severity: Mod–severe (≥1 of the following: sleep disturbance, impaired school/work performance, impaired daily activities, troublesome sx) vs. mild (no significant sx)
Management (JACI 2008;122:S1; Lancet 2011;378:2112)
Allergen avoidance: Identify/avoid triggers when possible
Dust mite: Humidity control, dust mite covers for bedding, HEPA vacuuming of carpeting Pollen: Avoid outdoors during AM (when pollen counts highest), use air conditioners when possible, don’t hang clothes out to dry For further allergen avoidance suggestions, see “Asthma”
Nasal irrigation: Beneficial for chronic rhinorrhea; may be used alone or as adjuvant; Neti pot superior to saline mist (advise pts to use sterile saline, risk of N. fowleri); may also be done w/ low-pressure irrigation squeeze bottle (AFP 2010;81:1440)
Pharmacotherapy: Multiple tx options; intranasal corticosteroids most effective for mod–severe disease; oral antihistamines reasonable for intermittent or milder disease; avoid topical nasal decongestants b/c of risk of rebound congestion & rhinitis medicamentosa
Intranasal therapy technique: Direct spray superiorly/laterally (“toward ipsilateral ear”)
| Pharmacotherapy | |
| Class | Example Rx & Notes |
| Intranasal corticosteroids (1st line for mod–severe disease) | Fluticasone (50 μg/spray): 2 sprays/nostril QD or 1 spray/nostril BID
Can ↓ to 1 spray/nostril QD for maintenance; onset ~12 h, should be used consistently for ↑ efficacy Also effective in mixed rhinitis (e.g., irritant) S/e: Nasal irritation, epistaxis, bitter taste; systemic s/e rare No difference in efficacy w/in class (J Laryngol Otol 2003;117:843) |
| Oral antihistamines | Fexofenadine (OTC): 60 mg BID or 180 mg once daily Cetirizine 10 mg QD
2nd-generation preferred (↓ sedation, ↓ anticholinergic effects, although may be ↓ effective rhinorrhea tx) Faster onset, less effective than ICS for severe disease or nasal congestion; can be used PRN but more effective if used regularly Fexofenadine/loratadine/desloratadine less sedating, cetirizine more sedating Cetirizine and loratadine are category B for pregnancy |
| Nasal antihistamines | Azelastine 1–2 sprays/nostril BID or olopatadine 2 sprays/nostril BID
Equal or superior efficacy to oral Rx for nasal sx; less effective than intranasal corticosteroids S/e: Bitter taste, somnolence May be given in combination with glucocorticoid sprays and oral antihistamines |
| Intranasal anticholinergics | Ipratropium (0.03%): 2 sprays/nostril BID–TID Good for ↓ rhinorrhea; not effective at ↓ congestion |
| Leukotriene receptor antagonists | Montelukast 10 mg PO QD; also effective in asthma |
Other:
Mast cell stabilizer (intranasal cromolyn): Can be used as ppx (take just before exposure → 4–8 h protection) or maintenance (best if started prior to exposure); less effective than intranasal corticosteroids Acupuncture: Nonpharmacologic therapy; may ↑ QoL and ↓ symptoms (Ann Allergy Asthma Immunol 2015:115:4) Oral decongestants: Pseudoephedrine: IR: 60 mg q4–6h; Extended release: 120 mg q12h or 240 mg QD (max 240 mg/24 h); unclear efficacy—may be no better than placebo; use only short term (5–7 d) (JACI In Practice 2015;3:5); S/e: HTN, insomnia, palpitations, urinary retention
When to Refer
Allergy/immunology: For severe/refractory/recurrent sx; for allergen- specific IgE skin/serum testing; if dx uncertain; for treatment with sublingual immunotherapy (ragweed or grass pollen) or subQ immunotherapy (desensitization, “allergy shots,” often requires 3–5 y of tx) to alter immune response
Otolaryngology: If suspect structural etiology (e.g., deviated septum, nasal obstruction)
Background (Ann Intern Med 2009;151:ITC-5-1; NEJM 2003;348:1256; 2009;360:2245)
“The Common Cold”; adults have 2–3 viral upper respiratory infections each y → 25 mil PCP visits/y in US (AFP 2012;86:817); rhinovirus most common, also adeno, metapneumo, RSV, influenza
Differential diagnosis: Bacterial pharyngitis, bacterial sinusitis, infectious mononucleosis, pertussis, PNA, bronchitis, otitis media, & allergic rhinitis (see “Pharyngitis,” “Allergic Rhinitis,” “Rhinosinusitis,” “Otitis,” “Pneumonia,” and “Influenza”)
Sinus inflammation occurs in majority of cases, but only ~2% of cases complicated by bacterial rhinosinusitis (see “Rhinosinusitis”)
Evaluation
History: Typically, onset of symptoms 24–72 h after exposure, including rhinorrhea, low-grade fever, conjunctivitis, nonproductive cough, coryza, sneezing, pharyngitis, HA, & malaise; symptoms may last up to 2 weeks; consider bronchitis (cough >5 d), mononucleosis (adenopathy, splenomegaly), pertussis (paroxysmal cough, ask re: TDaP); see “Sinusitis” & “Pharyngitis”; high fever + sudden onset + profound fatigue should prompt consideration of influenza (see “Influenza”)
Exam: HEENT: Nasal discharge, middle ear effusion, sinus tenderness, tonsillar exudates; Lymph nodes: Cervical, periauricular; Pulmonary: Consolidation, wheezing
Diagnostics: None needed in simple URI, if influenza suspected, see below
Treatment
Supportive care (AFP 2012;86:153; 2016;94:1016)
Decongestants: Intranasal oxymetazoline (limit to 3 d to avoid rebound congestion), phenylephrine, pseudoephedrine; caution in pts w/ arrhythmias, HTN
Antihistamines: Diphenhydramine, chlorpheniramine effective if combined w/ decongestant; monotherapy no more effective than placebo; s/e include altered mental status in the elderly, exacerbation of BPH/glaucoma, & drowsiness; nonsedating antihistamines unlikely to be beneficial Analgesics: ASA, APAP, ibuprofen, naproxen Ipratropium: Inhaler (to control cough) or intranasal (to control rhinorrhea) Cough suppressants: Dextromethorphan (avoid in pts on MAOIs), benzonatate Other: Mentholatum, intranasal cromolyn, ice chips for sore throat, lozenges, hydration, humidifiers, guaifenesin Zinc: Controversial; some trials suggest ↓ in duration of illness; s/e include nausea, abnl taste; avoid intranasal zinc due to risk of permanent anosmia
Patient education: (1) Validate concerns; (2) Acknowledge discomfort;
- Recommend specific sx relief (consider Rx of sx relief agent above);
- Advise f/u if sx do not improve
Abx misuse: Risks include disruption of nl flora, C. diff, resistance, & allergic reactions; abx do not alter the course of viral diseases (JAMA 2003;289:2750) Combination OTC remedies: May
interact w/ other medications, inadvertent overuse Prevention: Wash hands, cover cough, avoid immunocompromised pts, stay home
Background (Otolaryngol Head Neck Surg 2015;152:S1)
Rhinosinusitis (term preferred to “sinusitis,” as nasal cavity inflammation almost always accompanies sinusitis) symptomatic inflammation of the nasal cavity & paranasal sinuses, characterized by purulent nasal discharge, accompanied by sx of nasal obstruction (congestion, ↓ airflow), and/or facial pain
Etiology: Viral rhinosinusitis (VRS) accounts for >98% of acute rhinosinusitis; only 1–2% go on to develop secondary acute bacterial infection (acute bacterial rhinosinusitis, or ABRS)
Pathogens: Viral: Rhinovirus, parainfluenza, influenza; Acute bacterial:
- flu (75%), S. pneumoniae, M. catarrhalis; Chronic: Bacterial often involved (although may not be primary cause): S. aureus, anaerobes; Fungal: Mucor, rhizopus, aspergillus
Epidemiology: >12% of US adults have received sinusitis dx in the past year; accounts for >11 million health care visits annually (Vital Health Stat 2012;10:256)
Prescription antibiotic overuse: More than half of US pts presenting to PCP w/ uncomplicated acute rhinosinusitis receive antibiotic Rx; acute rhinosinusitis is associated w/more outpt abx Rx than any other diagnosis; abx overuse → abx resistance (Laryngoscope 2016;126:2439, Otolaryngol Head Neck Surg 2015;137:152)
Complications of ABRS are rare (1/10,000 cases); most common are orbital (orbital cellulitis or abscess) & CNS (meningitis or epidural abscess)
Risk factors: VRS: Upper respiratory infection (87% assoc w/sinus inflammation)
ABRS: Allergies, mechanical obstruction of the nose, swimming, odontogenic infection, intranasal cocaine, impaired mucociliary
clearance (CF, cilial dysfunction, smoking) Chronic: Allergy, immunosuppression or immunodeficiency (CVID, IgA deficiency), ciliary dyskinesia (incl CF), Aspirin-Exacerbated Respiratory Disease (AERD, formerly Samter’s Triad), nasal polyps Invasive fungal: Immunosuppression, DM
Evaluation (Ann Allergy Asthma Immunol 2014;113:347; NEJM 2004;351:902)
General approach: Dx of CRS and distinction between VRS & ABRS are clinical; consider fungal on DDx for all pts w/chronic sinusitis or those w/ DM or immunocompromise; ask about red flags (below) and obtain further imaging/eval if ⊕
History: Nasal congestion, purulent nasal discharge, facial
pain/pressure, hyposmia/anosmia, tooth discomfort (ABRS Se/Sp 66%/49%), cough, HA, fever, malaise, halitosis, ear pressure/fullness Exam: Purulence of nasal cavity/posterior pharynx (ABRS Se/Sp 35%/78%), nasal turbinate edema, ↑ pain w/ leaning forward (ABRS Se/Sp 75%/77%)
Red flags: Dark, necrotic turbinates (suspect fungal = surgical emergency), Systemically ill: High fevers (>102°F), Orbital complaints: Eyelid edema/erythema, proptosis, visual Δ, diplopia, ophthalmoplegia, CNS complaints: Severe HA, ΔMS, stiff neck → ED; persistent unilateral sx should ↑ concern for neoplasm
Labs: None typically needed (may be helpful in the acutely ill); pts with CRS or recurrent acute rhinosinusitis (RARS) should be tested for specific IgE antibodies to airborne allergens (by allergist/immunologist) Imaging: Sinus CT w/ contrast indicated in complicated ARS, tx- resistant or CRS, or if concern for neoplasm or other noninfectious cause of facial pain
| Sinusitis Diagnostic Criteria | |
| Acute bacterial rhinosinusitis (ABRS) | ≤4 wk of s/sx that are:
Persistent: >10 d w/o improvement and Severe: Temp >102°F, severe facial pain/purulent discharge and Worsening: “Double-sickening”: 5–6 d of typical URI, initially improving → new onset of fever, HA, ↑ nasal d/c |
| Recurrent acute rhinosinusitis (RARS) | ABRS occurring ≥3–4 (guidelines vary) times/y w/o s/sx of rhinosinusitis btw episodes; each episode must meet ABRS diagnostic criteria |
| Chronic rhinosinusitis | ≥12 wk of inflammation documented by imaging and/or rhinoscopic exam (edema, polyps, purulent mucus) and ≥2 of the following: (1) Mucopurulent drainage (anterior, posterior, or both) (2) Nasal congestion
(3) Facial pain/pressure/fullness (4) Hyposmia (↓ sense of smell [hyposmia]) |
DDx: Acute: URI, noninfectious rhinitis (see “Allergic Rhinitis”), HA (migraine, tension, cluster), odontogenic pain (see “Dentofacial Pain”)
Chronic: AR, nonallergic rhinitis, septal deviation, nonrhinogenic facial pain; neoplasm
Treatment (Otolaryngol Head and Neck Surg 2015;152:S1)
General approach: All pts should be offered sx treatment; those w/coexisting asthma or other comorbidities should have lower threshold
for abx tx, but for most patients antibiotics not indicated
Symptomatic: Recommended in all acute rhinosinusitis
Oral analgesics/antipyretic: APAP, NSAIDs
Oral decongestants: Pseudoephedrine, phenylephrine
Saline rinses: Neti pot, nasal irrigation; → ↓ need for pain medication & ↑ comfort Topical decongestants: Oxymetazoline, neosynephrine; limit to 3 d to avoid rebound
Antihistamines (i.e., loratadine, fexofenadine, cetirizine) if underlying allergy present; showed to ↓ rhinorrhea & nasal obstruction (Allergy 1997;52:650), no efficacy studies for acute rhinosinusitis Intranasal steroids: Moderate benefit in acute setting, meta-analysis found sx benefit w/ NNT = 15 (Cochrane Database Syst Rev 2009;CD005149)
Antibiotics: Ineffective & risk for harm if pts w/ VRS; for ABRS, data mixed re: effectiveness (likely in part 2/2 inclusion of VRS in trials → ↓ est of tx effect); however, can ↓ risk of serious complications, particularly in immunocompromised (cdc/gov/getsmart)
Mild illness or dx uncertain: Reasonable to prescribe watchful waiting; initiate abx if no improvement after 3–7 d and can ensure f/u (consider “Wait and see” Rx – see “Otitis”) Mod illness or mild illness in immunocompromised/ill: Empiric tx (table) Severe illness: Referral (below), esp in immunocompromised
| Antibiotic Therapy for Acute Bacterial Rhinosinusitis (Clin Infect Dis 2012;54:e72) | |
| Antibiotic | Comments |
| Amoxicillin/Clavulanate
875/125 mg BID × 5–7 d |
1st line (rather than amoxicillin) based on ↑ H. flu resistance to amox; evidence primarily in children; ↑ cost & ↑ risk of diarrhea |
| High-dose amoxicillin/clavulanate
2 gm BID × 7–10 d |
1st line for pts from regions (≥10%) of invasive PCN-resistant S. pneumo, those w/ severe infection (e.g., e/o systemic toxicity w/ T ≥102°F, threat of suppurative complications), age >65 y, recent hospitalization, abx use w/in the past mo, or immunocompromised |
| Doxycycline | 1st line in true PCN allergy
100 mg Q12h d 1, then 50 mg Q12h, 5–7 d |
| FQs: Levofloxacin 500 mg QD × 5–7 d, Moxifloxacin 400 mg QD × 7–10 d | 2nd line in true PCN allergy; no evidence for ↑ efficacy over β- lactam; ↑ s/e |
| Other (TMP–SMX, | Avoid empiric use given ↑ resistance to S. pneumo (&, for TMP– |
| macrolide, 2nd/3rd-gen
cephalosporin) |
SMX, to H. flu) |
Chronic sinusitis treatment: (Once confirmed) intranasal corticosteroids, nasal irrigations, allergen control & reduction (antihistamines, allergen immunotherapy, avoidance measures), consider surgical tx in refractory disease
When to Refer (Clin Infect Dis 2012;54: e72)
Emergency department: If red flags (above) → ED for urgent CT w/contrast, initiation of abx, & ENT eval, ophthalmology, possible neurosurgery consultation
Infectious disease (ID): Immunocompromised, multiple limited tx options or h/o unusual organisms
Otolaryngology or allergy/immunology: Referral indicated if
CRS: All pts with w/ confirmed/suspected CRS (ideally w/ CT prior to visit) RARS: Concern for immunodeficiency or anatomic abnormality; pts w/allergic component may be candidates for immunotherapy (see “Allergic Rhinitis”)
Treatment failure: If pt worsens or fails to improve w/ initial mgmt at 5 d after initial eval, reassess & exclude other causes of illness, detect complications → ENT referral (if dx uncertain/cultures desired), allergy (if allergy suspected), or ID (if resistance suspected, immunocompromised host)
Background (AFP 2011;83:26; Infect Dis Clin North Am 2007;21:449; NEJM 2001;344:205)
Epidemiology: Pharyngitis (sore throat, hoarse voice) results in ~2M outpatient visits in US annually (Vital Health Stat 2011;13:169).
Commonly results in inappropriate antibiotic rx; 50–70% tx w/antibiotics despite GAS prevalence of 20–30%; significant contributor to population-level abx resistance
Etiology: 25–45% viral, 20% bacterial, (co-infection w/ group A Streptococcus [GAS] + viral may occur), 30% no pathogen isolated (Mandell, 2011;815:821); STIs, GAS, EBV, Arcanobacterium
haemolyticum, Fusobacterium necrophorum more likely in younger pts Complications: Rare, but can include peritonsillar or retropharyngeal abscess, suppurative jugular thrombophlebitis (Lemierre syndrome 2/2
- necrophorum); spread to parapharyngeal space (carotid sheath) or sublingual space (Ludwig angina)
Evaluation (Ann Intern Med 2009;151:812; NEJM 1999;340:969; 2011;364:648)
History: Inquire about coryza-like sx (URI, influenza), profound fatigue, wt loss (EBV), fever (GAS, EBV, influenza), new sexual partners and oral sex (gonorrhea, HIV, HSV), rash (GAS, A. haemolyticum)
Exam: OP erythema, soft palate petechiae, swollen uvula (GAS) tonsillar exudate, cervical LAD (GAS, EBV), generalized LAD, splenomegaly, hepatomegaly, or jaundice, rash (EBV, acute HIV), oral ulcers (HSV 1/2), scarlatiniform rash (GAS, A. haemolyticum),
Other etiologies: HSV (5–10% pharyngitis in college students; minority assoc w/ anterior mouth or lip lesion see “HSV”); Mycoplasma & Chlamydophila pneumoniae (assoc w/ acute bronchitis); influenza (assoc w/ cough, coryza see “Influenza”); gonorrhea (assoc w/ urethritis see “STI”); thrush (DM, recent steroids, immunosuppressed)
Red flags: Systemic toxicity/respiratory sx; severe unilateral pain, inability to swallow, drooling, hoarse voice, trismus, worsening sx after several days (peritonsillar or retropharyngeal abscess), pseudomembrane, ↑↑ tonsillar swelling (diphtheria)
General approach: No need for testing if suspect viral etiology; consider throat culture if suspect F. necrophorum or A. haemolyticum; GAS testing as below
If EBV is suspected: Epstein–Barr virus: Heterophile Ab: (Se/Sp 85/100%), 25% false ⊖ in 1st wk; CBC: Lymphocytosis w/ >10% atypical lymphocytes, mild ↓ PLTs, ↑ LFTs; also consider CMV & HIV (~1% of those tested for mono actually have acute HIV)
Treatment (Ann Intern Med 2001;134:506; CID 2002;2:113)
Sx management: Antipyretics, NSAIDs, warm salt water gargles, lozenges, humidifier
Non–GAS infection: Group G or C β-hemolytic strep: not assoc w/ rheumatic fever, but abx may result in earlier sx relief (BMJ 2000;320:150); in young adults w/o associated viral sx, F. necrophorum causes similar proportion of pharyngitis to GAS; consider
empiric tx (B-lactam, clindamycin, or flagyl, not macrolide)
- gonorrhoeae: Treat as per genital infection (see “Sexually Transmitted Infections”); more difficult to clear from oropharynx than from GU tract
Red flags: Refer to ED for persistent fever, trismus, odynophagia, muffled voice, dysphonia, otalgia, unilateral deviation of uvula, swelling of mandible, bulging of pharyngeal wall, stiff neck
GROUP A STREP (CID 2012;55:1279)
Prevalence: Causes 5–15% of acute pharyngitis in adults; ↑ risk in those w/ contact w/ school age children (parents, teachers)
Natural history: Usually self-resolves w/o complications; tx advised to reduce symptoms: Sore throat & fever ↓ by 0.5–3 d, prevent suppurative complications: sinusitis, parapharyngeal abscess; prevent rheumatic fever (extremely rare in adults) & ↓ community spread of infection; tx does not ↓ risk of PSGN (Cochrane Database Syst Rev 2006;4:CD000023)
General approach: Test if mod pretest probability, treat if rapid test ⊕ otherwise wait for culture; if high pretest probability: Treat empirically w/o testing; empiric tx can lead to unnecessary abx use (59% appropriate, 32% unnecessary, 9% underuse)
Testing: Rapid Ag-detection test: (Se 86%; Sp 95%) (Cochrane Database Syst Rev 2016;7:CD010502); recommended if ↑ suspicion (>2 criteria, below); throat culture can be obtained if other causes suspected or to ↑ Se; Throat cx: (Se 90%, Sp 95–99%) ⊕ in acute infection & asx carriers; not needed in adults due to very low incidence of GAS pharyngitis and rheumatic fever; Anti-strep Abs: Used in dx of post-strep complications; not helpful in acute setting (JAMA 2004;291:1587)
Treatment: PCN V 500 mg PO BID or TID ë 10 d or benzathine PCN G 1.2 million units IM × 1; alternatively amoxicillin 500 mg BID × 10 d; if pen-allergic (not anaphylaxis), cephalexin 500 mg BID × 10 d or clindamycin 300 mg TID × 10 d; often macrolide resistant; avoid unless confirmed sensitivity; NSAIDs helpful but adjunctive tx with steroids not recommended
Follow-up: Advise pts to seek care if no sx improvement 3–4 d after abx; failure to improve → reconsider dx or complication; if repeat tx necessary, repeat w/ amoxicillin–clavulanate or 1st-gen cephalosporin
| Centor Clinical Scoring Criteria (JGIM 1986;1:1; NEJM 2004;344:205) | ||
| Tonsillar exudates | 1 pt | |
| Tender anterior cervical LAD | 1 pt | |
| Absence of cough | 1 pt | |
| Fever by hx | 1 pt | |
| Age ≥45 | –1 pt | |
| Treatment Algorithm | ||
| Points | Risk of GAS | Treatment |
| -1, 0 | 1–2.5% |
No tx or testing |
| 1 | 5–10% | |
| 2 | 11–17% | Test, treat pts w/ a ⊕ rapid test or cx |
| 3 | 28–35% | Option 1: Test, treat pts w/ a ⊕ rapid test or cx Option 2: Treat empirically |
| 4 | 51–53% | Treat empirically |
Background (JAMA 2009;302:1954; Otolaryngol Head Neck Surg 2009;141:S1)
Definition: Hoarseness (dysphonia) is a change in voice quality, pitch, amplitude, or vocal effort that impairs communication or reduces voice- related QoL
Physiology: Phonation requires harmonic function of the cartilaginous skeleton, mucosa (incl vocal folds), muscles (intrinsic & extrinsic), & nerves (vagus, recurrent, & superior laryngeal); airway obstruction → hoarseness can occur at any level and in multiple anatomic structures (oral cavity, pharynx, larynx, or trachea)
Epidemiology: ♀:♂, 3:2; lifetime prevalence 30%, point prevalence
~7%; ↑ in at-risk populations (usually occupational, e.g., telemarketers, aerobic instructors, teachers, singers) (Laryngoscope 2005;115:1988)
Figure 10-1. Larynx (Coronal View)
Figure 10-2. The Upper Aerodigestive Tract (Sagittal View)
Modified from Oatis CA. Kinesiology: The Mechanics and Pathomechanics of Human Movement. 3rd ed. Philadelphia, PA: Wolters Kluwer, 2016.
Evaluation
History: Characteristics: Chronicity, onset, fatigability, “running out of air,” voice “cracking”
Assoc sx: URI, dysphagia, odynophagia, globus, throat clearing, allergies, aspiration, cough, acid reflux, constitutional, hemoptysis, dyspnea, otalgia PMHx: Intubation, trauma, neck/chest surgery,
XRT, DM, parkinsonism, MG, MS, ALS, allergies, CA, hypothyroidism, GERD
Meds: ACEI, antihistamines, antipsychotics, inh corticosteroids,
anticoagulants Soc hx: Tob, EtOH, occupation, exposures, vocal abuse
Exam: HEENT (assess for oronasopharyngeal lesions, cervical LAD, thyromegaly); Pulm (consolidation or focal wheezing); Neuro (tremor, weakness, bulbar signs)
Vocal quality: Coarse: irregular vocal cord (e.g., laryngitis/mass), breathy; incomplete glottic closure (e.g., vocal fold paresis); wet/gurgling; pooling of secretions (e.g., supraglottic infection); tremulous (parkinsonism)
Diagnosis: Most acute cases can be diagnosed clinically; laryngoscopy necessary if ↑ risk of serious condition, if sx are persistent or concern for airway obstruction
Management (Rubin et al. Diagnosis and Treatment of Voice Disorders, 2006)
General approach: Specific etiologies below; most cases self- limited/benign; refer for full ENT exam and laryngoscopy if dysphonia persists >2 wk in absence of acute URI, esp. if ⊕ tob or heavy EtOH use (↑ risk laryngeal CA) or other concern for CA; imaging not indicated prior to laryngoscopy
Acute infectious laryngitis: Acute inflammation/edema of entire larynx; may be 2/2 phonotrauma (voice misuse, protracted coughing → hemorrhage of true vocal cord); viral (rhinovirus > VZV, coronavirus), or rarely bacterial (dramatic, more commonly epiglottis) or fungal; S/sx: loss of voice +/– fever, cough, throat pain, difficulty swallowing; may occur w/hemorrhage—abrupt onset during ↑ vocal cord effort (see “Hemoptysis”); Tx: Phonotrauma or viral; supportive/rest; no role for abx or steroids
Chronic infectious laryngitis: Similar process to acute but longer time course; more likely to be 2/2 bacterial (incl TB) or fungal infection; refer and tx underlying process
Laryngeal irritation: Multiple etiologies: Smoking, EtOH, GERD, inhaled fumes/smoke, vocal strain, post-nasal drip; Tx: Withdraw/treat irritants or treat underlying d/o, refer if refractory/persistent; more details on specific etiologies below
Laryngopharyngeal reflux: Damage to supraglottic and glottic mucosa by reflux contents (controversy re: role of acid in damage); presents w/ throat clearing, persistent cough, dyspepsia, & globus present in >95% (Curr Opin Otolaryngol Head Neck Surg 2006;14:143); Tx: Consider trial of acid suppression/PPI; no evidence to initiate w/o other GERD sx
Neurologic: Incomplete closure of vocal cords; presents w/ breathy voice
Unilateral true cord paralysis: 2/2 nerve injury, compression, neuropathy; Tx: laryngoscopic tx/VF injections or surgery Bilateral paresis: Consider MG, ALS (25% p/w dysphonia); Tx: Refer for swallow eval Parkinsonism: Hypophonia, tremor, breathiness, monotone: Tx: See “Parkinson’s”
Essential tremor: (25% have laryngeal tremor); Tx: see “Tremor” Functional: Dx of exclusion, cannot be made w/o laryngoscopy; often occupational; paradoxical true vocal cord motion (dysphonia w/ stridor),
conversion d/o (see “Somatic Symptoms”); Tx: Voice therapy
(Otolaryngol Head Neck Surg 2008;138:557)
Other:
Benign vocal fold lesions: Polyps, nodules, or polypoid corditis affecting true vocal cords; presents w/coarse, irregular voice, chronic hoarseness: generally 2/2 chronic irritation Systemic inflammation: Deposition of inflammatory cells in larynx (sarcoidosis → supraglottic, amyloidosis → glottis) Autoimmune disease: Epithelial loss & inflammation triggered by auto- antibodies; can affect entire larynx
Background
Pain may be 2/2 pathology of nerves (CN V), joints (temporomandibular joint, or TMJ), bones (maxilla/mandible), teeth, salivary glands, soft tissue (gums, oral mucosa)
Evaluation (NEJM 2008;359:2693)
History: Onset & duration of sx; assess for facial/alveolar
erythema/swelling (dental or salivary infection), cold/hot sensitivity (pulpitis), pain/swelling w/ food (sialadenitis), dysphagia/dyspnea (deep neck space infection), trismus (TMJ d/o or muscular inflammation); shooting facial pain or numbness (neuralgia); h/o XRT or bisphosphonate exposure (osteonecrosis), tobacco & EtOH use d/o (↑ risk of oral cavity malignancy)
Physical exam: Full head and neck exam
Dental exam: Inspect teeth & palpate → tenderness (caries/periapical infection) TMJ exam: Nl jaw opening is 35–55 mm; eval for tenderness over joint (capsulitis), limited range of opening (ankylosis), tenderness of muscles of mastication (myofascial pain) Oral cavity exam: Oral tongue, floor of mouth firmness (sialadenitis, Ludwig angina) nonhealing ulcers of tongue or oral mucosa (malignancy) CN exam: Dysesthesias of CN V branches (neuralgia)
Diagnostic studies: Dental pathology → panoramic radiograph of jaw; TMJ dysfunction → MRI of joint (assess articular disk & soft tissues); salivary gland infection, deep neck space infection → CT w/ contrast of neck; oral cavity or oropharyngeal ulcer/mass → referral to specialist prior to imaging; salivary gland mass, cranial neuropathy → MRI w/ contrast to assess for tumor/lesion
Epidemiology and Management (Oral Maxillofac Surg Clin North Am 2009;21:293)
TMJ d/o: Most common among people ages 20–50 y, ♂:♀ >3:1
Etiology: Myofascial pain (most common), intra-articular disc d/o, OA, & RA Sx: Unilateral pain localized to jaw, TMJ, muscles of mastication but can radiate → ears, posterior neck; sx ↑ in AM esp in pts who clench/grind teeth at night; +limited or asymmetric opening/closing of jaw & TMJ sounds (e.g., clicking) Tx: NSAIDs, jaw rest (soft diet, prevention of wide opening), hot compresses, physical therapy, muscle relaxants, trigger point injections; consider TCAs (NEJM 2008;359:2693)
Salivary gland dysfunction: Submandibular > parotid; ↑ incidence in
⊕ tob, diuretic use, HCV, Sjögren/sicca syndrome
Etiology: Sialolith (can → sialadenitis); rarely: Sarcoid, Sjögren, HIV, malignancy Sx: Unilateral tenderness/pain under mandible (submandibular) or preauricular/maxillary buccal mucosa (parotid);
sialolith may be palpable/visible Tx: Initially conservative; massage, warm compress, sialogogues (e.g., lemon drop candy), hydration, NSAIDs, abx if evidence of 2° infection (purulence from duct, erythema, fever) (Otolaryngol Head Neck Surg 2011;145:935)
Odontogenic disorders (cdc.gov/oralhealth/): Advanced periodontal disease affects 4–12% of US adults; ↑ prevalence of poor oral health in racial/ethnic minorities, poor; ↑ risk in smokers, sicca/Sjögren, eating d/o, meth use, chemo, antipsychotic meds
Etiology: Gingivitis (inflammation of the gums), periodontitis (inflammation → loose teeth), pulpitis/pulp necrosis (dental caries), dental abscess Sx: Tooth/jaw pain, heat/cold sensitivity
Tx: Analgesics; abx if e/o acute infection (purulence, erythema, fevers/chills)
Trigeminal neuralgia: Onset typically >50 y, ♀ > ♂; ↑ risk w/ HTN or ⊕
FHx;
Etiology: Vascular compression or idiopathic
Sx: Typically unilateral (R > L), sharp/stabbing pain lasting <2 min
Rx: 1st r/o malignancy or MS w/ imaging (MRI)
Tx: Carbamazepine > baclofen, lamotrigine; surgical tx if refractory (decompression, rhizotomy) (Neurology 2008;71:1183)
When to Refer
TMJ d/o: Severe, consideration of injections/interventions → OMFS Sialolithiasis or sialadenitis: If unresolved w/ conservative tx → specialist; if marked swelling (acute infection w/ abscess), CN VII involvement (w/ parotitis) → ED
Neuralgia/paresthesia: If severe, not responsive to initial tx → Neuro or NSG
Oral cavity/oropharyngeal ulcer/mass: Referral to specialist (OMFS or ENT) for endoscopy/biopsy
Caries or tooth pain: Dentist; severe dental infection: E.g., facial swelling, trismus; (suggestive of deep neck space infection, can develop acute airway compromise) → ED for ENT/OMFS eval (Emerg Med Clin North Am 2000;18:481)
OTITIS EXTERNA
Background (Otolaryngol Head Neck Surg 2014;150:S1)
Definition: Inflammation of the external ear canal, often w/ infection, that may be acute (AOE <6 wk), subacute (6–12 wk), or chronic (>3 mo)
Microbiology: Primarily bacterial (98% in North America) in origin (P. aeruginosa, S. aureus), fungal “otomycosis” (aspergillus, candida); viral (VZV, HSV)
Epidemiology: Lifetime incidence 10%; often after local trauma or swimming; ↑ in summer
Risk factors: Eczema of auditory canal, swimmers, humidity, poor production or removal of ear wax, narrow auditory canals, hearing-aids, mechanical trauma (including scratching/instrumentation of ear canal w/ cotton swab)
Risk factors for complicated otitis externa: DM, cranial radiation, immunocompromise (incl HIV), hx cranial XRT
Complications (rare): Osteitis, abscess, middle ear disease, or recurrent infection
Evaluation (AFP 2012;86:1055; Otolaryngol Head Neck Surg 2014;134:S4)
History: Otalgia (70%), itching (60%), fullness (20%), ± hearing loss, ± jaw pain, ± vertigo; assess for risk factors (above); acute otitis externa typically rapid onset (<48 h)
Exam: Tenderness of tragus/pinna, ear canal edema or erythema, ± otorrhea, ± regional LAD, ± TM erythema or cellulitis of the pinna; verify TM intact if possible
Red flags: Pain/HA out of proportion to exam, fever, granulation tissue at bony-cartilaginous junction (floor of EAC) all concerning for necrotizing infection
DDx: Otitis media w/ perforation (see below); otomycosis, varicella zoster oticus, atopic or contact dermatitis, psoriasis, seborrheic dermatitis, acne, SLE (rare); assess for other skin conditions
Treatment (Cochrane Database Syst Rev 2010:CD004740)
General approach: Pts w/uncomplicated OE should have gentle cleaning and otic gtt; avoid cleaning in pts w/ DM or immunocompromise, use FQ gtt in pts w/known or suspected TM perforation; no role for oral abx unless extension beyond ear canal or specific host consideration, as no e/o benefit over topical and ⊕ evidence of harm, incl ↑ s/e and ↑ disease persistence/recurrence (Int J Antimicrob Agents 2005;25:282; J Infect 1991;22:233)
Ear canal cleaning: For healthy patients w/intact TM, in-office gentle cleaning w/warmed 3% H2O2
Symptom management: PO analgesia as needed; avoid topical anesthetic as can mask sx of progression
Topical otic agents: Steroids, antiseptic, antibacterial, antifungal, & combination available; no difference shown between agents for empiric Rx;
Pts w/intact TM: 2% acetic acid typically effective; apply TID–QID × 7–14 d Pts w/known or suspected TM perforation: Rx may pass through middle ear → inner ear; avoid aminoglycosides, neomycin, or EtOH-containing drops; FQ safe (ofloxacin 0.3% 10 gtt QD x 7d) Gtt admin instructions: Lie down w/affected ear toward ceiling; instill 3–4 drops (have someone else administer drops if possible), light tragal massage w/ 3–5 min of head tilt (set a timer)
Pt counseling: Keep ear dry for 7 d, including no swimming, if water cannot be avoided, recommend cotton in ear coated on outside w/ petroleum jelly to keep canal dry; avoid cleaning ear canal at home (to avoid injury); may take 1–2 wk to resolve; f/u (call vs. visit) if not improving w/in 3 d → ENT referral; avoid ear candling (proven harm, no proven benefit)
Necrotizing (malignant) otitis externa: Osteitis of temporal bone, can be life-threatening; almost always Pseudomonas; ↑ risk in immunosuppressed pts; Hx/PE: See “Red Flags” above; Mgmt: ✓ CBC, ESR, Glu, Cr, culture canal, & CT of temporal bone, urgent referral → ED for abx ± surgical debridement (Lancet Infect Dis 2004;4:34)
When to refer: For known or suspected complicated OE, failure to improve w/in 48–72 h or failure to resolve w/in 2 wk, suspected
malignant otitis externa
OTITIS MEDIA
Background (Nat Rev Dis Primers 2016;2:16063, NEJM 2002;347:1169)
Definitions: Acute otitis media (AOM): Is clinical dx, defined by acute onset of sx, e/o effusion & inflammation of middle ear; Otitis media with effusion (OME): Fluid without e/o infection, 2/2 URI ± Eustachian tube dysfunction; Chronic Suppurative Otitis Media (CSOM): Infection & inflammation of middle ear >3 wk; can be assoc w/ TM perforation or cholesteatoma; often multiple bacteria w/ combo aerobes/anaerobes Microbiology: Viral > bacteria, in AOM (S. pneumo > H. influenzae, M. catarrhalis)
Pathophysiology: Viral infection of nasopharynx → Eustachian tube dysfunction → ↓ clearance of viruses & bacteria that reach middle ear
→ bacterial replication
Epidemiology/risk factors: Incidence ↓↓ ↓ w/ age, ↑ risk if: H/o previous AOM, recent viral URI or sinus infection, hx Eustachian tube dysfunction, AR, anatomical ear abnormalities (i.e., Down syndrome), immunosuppression, presence of OM w/ effusion
Evaluation (JAMA 2010;304:2161)
History: Duration, pain, fever, recent URI sx, presence of risk factors (above)
Exam: For AOM, pneumatic otoscopy must show e/o fluid in middle ear (bulging TM, ↓ or absent mobility, abnl TM opacity, air–fluid level) & inflammation of TM (erythematous patches or streaks, ↑ vascularity); for OME: fluid (usually serous) without inflammation
Red flags: Pain/swelling over mastoid, bloody otorrhea, facial weakness, vertigo, nystagmus, HA, neck pain, photophobia
Treatment (Cochrane Database Syst Rev 2013:CD000219)
General approach: No large RCTs/guidelines for AOM in adults; abx can → significant clinical improvement by 3 d in children; APAP, NSAIDs for analgesia (NEJM 2011;364:116)
Antibiotics: Amoxicillin 500 mg PO TID × 7–10 d (1st line) or other S.
pneumo-active Rx
In pts in whom dx uncertain, afebrile, mild–mod disease, may consider “wait & see Rx”: Give pt Rx, only to be filled if no improvement after 48– 72 h (JAMA 2006;296:1235)
OME: Neither abx nor decongestants shown to be helpful; >70% resolve in 4 wk; if persistent >3 mo → ENT referral (Cochrane Database Syst Rev 2012;9:CD009163)
When to Refer
Recurrent AOM (>2 episodes/6 mo), OME lasting >3 mo, unilateral persistent OME or otalgia (ENT exam to r/o nasopharyngeal tumor), CSOM, or AOM complications (TM perforation, mastoiditis, labyrinthitis, facial palsy, meningitis)
Patient Information
Otitis externa: www.nlm.nih.gov/medlineplus/ency/article/000622.htm; www.aafp.org/afp/2001/0301/p941.html
Background (NEJM 2008;359:833; Otolaryngol Head Neck Surg 2012;146:S1)
Hearing loss is underdiagnosed & undertreated, despite affecting >25% of those over 65; assoc w/ social isolation, functional decline, poor QoL, depressive sx, & cognitive deficits
Risk Factors: ↑ Age; ♂ > ♀, Caucasian, HTN, DM, CKD, immunosuppressed
Screening: Required in Medicare annual wellness visit; ask “Would you say you have any difficulty hearing?”; ask family members when feasible
Conductive hearing loss (CHL): A mechanical problem; hearing loss 2/2 abnormalities in the structures that “conduct” sound waves to the cochlea: Auricle, external auditory canal, tympanic membranes, middle ear airspace or ossicles
Sensorineural hearing loss (SNHL): A neurologic problem; hearing loss 2/2 abnormalities in the structures that transmit neural impulses to the auditory cortex: cochlea, auditory nerve
Mixed hearing loss: Hearing loss w/ conductive & sensorineural components
Severity/Classification: Mild: 20–40 dB loss, Mod: 40–70 dB, Severe:
70–90 dB, Profound: >90 dB
Hearing physiology: Sound waves enter the ear canal → vibrate TM and ossicular chain → stimulus to cochlea, where sensory cells convert sound energy to electrical stimuli → brain via the auditory nerve
Evaluation (AFP 2012;85:1150; JAMA 2012;307:1185)
History: Auditory sx: Duration, sidedness & symmetry, pain, otorrhea, head/ear trauma, acoustic trauma (duration & sound intensity); Assoc sx: Tinnitus, vertigo; Medical: Occupational noise exposure; ototoxic meds (salicylates, NSAIDs, APAP, aminoglycosides, cisplatin, diuretics, quinine), hx infection (Lyme, syphilis, meningitis), hx ear infections,
tympanostomy tubes, FHx hearing loss
Exam: Inspect auricle, mastoid, canal, TM, pneumatic otoscopy for drum mobility
Whisper test → stand each side at 2 ft from ear (⊕ test indicated by
failure to repeat at least 3 of 6 letter/number combinations)
Tuning fork tests (NEJM 2008;359:833)
When to Refer
Sudden hearing loss → emergent ENT referral (NEJM 2008;359:833); gradual SNHL → ENT, audiologist; gradual CHL—depends on etiology; see CHL, below
CONDUCTIVE HEARING LOSS
General Approach (Cummings Otolaryngology 2015;143)
Diagnosis: Usually apparent on exam of auricle, canal, & tympanic membrane; most common causes in adults are cerumen impaction > otosclerosis & otitis media
Cerumen impaction: Often 2/2 cotton swab use → medial packing of cerumen over time. Tx: Irrigation w/ warm water → limited curettage under direct visualization; if ineffective, then cerumenolytic (e.g., H2O2)
× 5 d, then repeat; if ineffective → ENT referral for otomicroscopy & removal; pts w/ TM perforation, prior ear surgery, otitis externa, vertigo or abnormal canal should be managed directly by ENT (AFP 2007;75:1523)
| Common Causes and Treatment of Conductive Hearing Loss | ||
| Etiology | Diagnosis | Treatment |
| Cerumen impaction | Visualized on otoscopy | |
| Otitis externa or eczema | Pain, itchiness, edema | See “Otitis” |
| Exostosis (external canal osteoma) | Otoscopy ± temporal bone CT | Observe if nonobstructing + asx, otherwise ENT referral |
| Acute otitis media, OM w/ effusion | Pneumatic otoscopy, tuning fork exam, tympanometry | See “Otitis” |
| TM perforation | Otoscopy, tympanometry | H2O precautions, ENT referral for repair if persistent |
| Cholesteatoma (cyst in middle ear) | Otoscopy, audiometry, CT scan of temporal bone | ENT referral, possible tympanoplasty/ mastoidectomy |
| Ossicular fixation (e.g., otosclerosis) | Audiometry, otoacoustic emissions, possible CT of temporal bones | ENT referral for middle ear exploration, ossiculoplasty (stapedectomy) |
(Nadol JB. Surgery of the Ear and Temporal Bone 2004)
SENSORINEURAL HEARING LOSS
General Approach (Cummings Otolaryngology 2015;150:2319–2335.e6)
Most common cause of hearing loss in older adults; presbycusis leading cause of SNHL in elderly; pts often c/o difficulty “filtering out” background noise
Assess degree of loss, laterality, chronicity
Causes (Otolaryngol Clin N Am 2012;45:941)
Presbycusis: Age-related hearing loss (90% of SNHL in elderly)—a gradual, symmetric loss of hearing, starting in high frequencies & progressing to mid frequencies (necessary for speech recognition) Noise-induced hearing loss: Symmetric SNHL 2/2 occupational exposure, industrial equipment, firearms—preventable w/ regular use of hearing protection
Ménière disease: Fluctuating, progressive asymmetric hearing loss, aural fullness, tinnitus & peripheral vertigo attacks lasting 2–3 d—tx w/ dietary Na restriction, ENT referral for possible diuretic Rx (Otolaryngol Clin N Am 2010;43:1011)
Sudden sensorineural hearing loss: A sudden asymmetric loss of hearing/deafness in one ear, new-onset tinnitus → an otologic emergency—pt needs rapid eval & high-dose steroid tx (Otolaryngol Head Neck Surg 2012;146:S1)
Trauma: External trauma to temporal bone may involve the cochlea resulting in profound, permanent SNHL; barotrauma from scuba diving or sudden pressure changes may result in hearing loss, tinnitus, or vertigo
Neoplastic disease: Tumors at the CPA can present w/ progressive or sudden onset unilateral hearing loss, vestibular schwannoma most common, but metastatic disease to CPA can also result in hearing loss
→ refer to ENT for eval/MRI
Other: Ototoxicity: NSAIDs, cisplatin, aminoglycosides, loop diuretics (high frequency); Infection: Bacterial meningitis, recurrent AOM, toxoplasmosis, syphilis; Congenital: Anatomic or genetic d/o, in utero infections (CMV, VZV, syphilis) or exposure (EtOH, isotretinoin, cisplatin ↑ bili), anatomic abnormalities
Management (JAMA 2012;307:1185)
Listening strategies: Lip reading, directly facing the pt, speaking slowly and clearly
Amplification: Improve outcomes of speech perception, understanding & hearing-related QoL, but are expensive & infrequently covered by insurance; Personal Sound Amplification Products (PSAPs or “pocket talkers”) are less costly alternative to hearing aids, but less-targeted sound amplification (e.g., all noises louder) & not regulated by FDA
Pt education: Key for managing expectations; hearing aids help but cannot erase deficit, take multiple adjustments to be set properly & can take a few months to be helpful
Cochlear implantation (NEJM 2010;363:1438): Considered in setting of severe/profound SNHL in adults or congenital deafness→ significant gain in hearing clarity and sensitivity
TINNITUS
Background (Otolaryngol Head Neck Surg 2014;151:S1; JAMA 2016;315:2221)
Definition: The false perception of sound in the absence of an acoustic stimulus; it is a symptom rather than single disease process, and etiology not well understood; thought to be often due to abnormal neural activity in response to hearing loss
Many people experience occasional or nonbothersome tinnitus; others have significantly ↓ QoL (affects hearing, sleep, concentration) Epidemiology and risk factors: prevalence ↑ w/age, affecting 9% of 60–69 y in US, assoc w/hearing loss, noise exposure; more common in
♂, whites, pts w/ HTN, DM, HLD, obesity, depression, and/or anxiety Natural hx: Persistent bothersome tinnitus may resolve spontaneously, 20–50% over several years
Classification: Management determined by bothersome or not bothersome, persistent (≥6 mo) or not persistent (<6 mo); can be primary (idiopathic, often assoc w/SNHL) or secondary to other process (cerumen impaction, Eustachian tube dysfunction, Ménière’s, vascular anomalies, vestibular schwannoma, intracranial HTN)
Evaluation
General approach: Targeted Hx/PE to identify conditions that may be causing/contributing to tinnitus, presence of red flags
History: Quality of sound: may be buzzing, rushing, whooshing, or clicking, usually worse in quiet room, may seem to derive from internal/external source; onset, unilateral (focal anatomic lesion), pulsatile (vascular lesion)
Hearing: Sudden hearing loss, unilateral or bilateral
Medications: Salicylates, ototoxic meds, NSAIDs, loop diuretics, quinine Comorbid d/o: SNHL, anxiety, depression, dementia
Bothersome vs. not: affecting QoL? Bothersome enough to desire tx?
Red flags: persistent pulsatile tinnitus (vascular lesion), unilateral tinnitus w/hearing loss (anatomic/focal lesion—r/o cerumen impaction), sudden onset hearing loss, vertigo/balance problem, objective tinnitus, head/neck mass, focal neurologic signs
Exam: VS: BP; Head/Neck: Auscultate over the ear/mastoid to differentiate subjective (no noise, usually benign) from objective tinnitus (rare, heard by clinician, can suggest ICA/vertebral artery aneurysm), LN exam, Otoscopy: Evidence of otitis externa/AOM, cerumen impaction, other EAC pathology); CV: If concern for vascular d/o; Neuro: Attention to CN and vestibular exam
Audiology referral: For all pts w/ unilateral, persistent, or assoc w/hearing loss; consider for others w/persistent, bothersome tinnitus Imaging: Generally not indicated; however, for pts w/pulsatile tinnitus that corresponds to cardiac cycle, focal neurologic abnormalities, concomitant asymmetric hearing loss or concern for vascular cause, obtain CTA or MRA/MRV of neck/skull base to r/o vascular abnormality
Treatment
General approach: For those in whom evaluation has not determined reversible cause, pt education on prognosis and tx options key; no need to tx if not bothersome
Pt education: Tinnitus is a symptom, not dangerous in and of itself; may remit or persist; no obvious cure but mgmt strategies exist; counsel pts on hearing protection, self-help (CBT) books may ↓ depression and ↑QoL by managing pt response to sx; sound therapy Other therapies: Some evidence for CBT, sound therapy (use of “white noise”) to cancel out tinnitus, tinnitus retraining therapy (by
specialist) may ↑ QoL (Cochrane Database Syst Rev
2010;CD007330); acupuncture of unclear benefit
Anxiolytics, antidepressants, anticonvulsants, ginkgo biloba, melatonin, zinc, other supplements not shown to have benefit and not recommended
Patient Information
Hearing loss: asha.org/public/hearing/Hearing-Loss Tinnitus: asha.org/public/hearing/Tinnitus, ata.org/resources, entnet.org/content/tinnitus