Primary Care Medicine

Primary Care Medicine

Section 1: Ears

Auricle Hematoma

Introduction (Definitions/Classification): A collection of blood or tissue under the perichondrium of the external ear separates the cartilage of the ear from the nutrient-rich perichondrial layer. Fibrosis from cartilage necrosis, incomplete evacuation of clotted blood, or infection leads to a deformity resembling a cauliflower; hence the common term “cauliflower ear.” Auricle hematoma is commonly encountered in participants of contact sports such as boxing, rugby, martial arts, and wrestling; usually a consequence of a traumatic blow to the auricle.

History and Physical Examination:

  • History: Blunt trauma to the auricle.

  • Physical examination:

    • Soft, fluctuant swelling of the auricle.

    • Pain, swelling, and discoloration.

    • Left untreated, the ear becomes deformed with areas of fibrous swelling.


  • Signs/symptoms on physical examination.


  • Acute phase (hematoma).

    • Drainage is recommended to release pressure and prevent cartilage death and deformity.

      • Incision and drainage under local anesthesia.

      • A bulky pressure bolster is placed to prevent reaccumulation of blood/tissue fluid.

    • Other emerging techniques include securing the skin flap with mattress sutures, leaving the incision sites open to drain and heal with antibiotic ointment; no bulky dressing required for this technique.

    • Oral antibiotics recommended because the auricle is prone to infection.

  • Chronic phase (fibrosis).

    • Marked by irreversible changes.

    • Plastic surgery consultation.

Other Considerations:

  • “Cauliflower ear” may also develop as a complication from infection following “ear piercing” of the upper ear cartilage.

  • “Cauliflower ear” is often considered a “badge” of experience or toughness in participants; thus, the individual might defer treatment.

  • For prevention, wear protective headgear, such as a scrum cap.

Return to Play Criteria:

  • No restrictions unless athlete is febrile and the auricle is infected.

Recommended Readings

Prasad K, Karthik S, Prasad S. A comprehensive study on lesions of the pinna. Am J Otolaryngol. 2005;26(1):1-6.

Roy S, Smith L. A novel technique for treating auricular hematomas in mixed martial artists (ultimate fighters). Am J Otolaryngol. 2010;31(1):21-24.

Vuyk H, Bakkers E. Absorbable mattress sutures in the management of auricular hematoma. Laryngoscope. 1991;101:1124-1126.

Bacterial External Otitis

Introduction (Definitions/Classification): Bacterial infection of the external auditory canal is the most common form of external otitis. Common pathogens include Pseudomonas aeruginosa and Staphylococcus aureus. Predisposing factors include the following.

  • Excess wetness—alters protective skin-cerumen barrier and increased pH of the ear canal that favors bacterial growth.

  • Aggressive cleaning of the external ear canal—reduces amount of protective cerumen and induces abrasions, which allows bacteria to ingress into deeper tissues.

History and Physical Examination: Individuals typically have a history of recurrent external otitis, and may present with a history of either tympanic membrane perforation or ear surgery. Common symptoms include discharge, earache, pruritus, and change in hearing acuity. Tinnitus or vertigo may be present in more severe cases. Physical examination typically reveals the following.

  • Erythematous external canal impacted to varying degrees (depending on severity) with discolored debris that varies in color (white, gray, or brown).

  • Tympanic membrane maybe erythematous and “boggy,” yet should be intact and mobile.

  • Increased pain with superior distraction of the auricle.

  • Fever, periauricular lymphadenopathy, or periauricular erythema in more severe cases.


  • Signs/symptoms on physical examination.

  • Cultures are typically unnecessary. Consider cultures, complete blood count (CBC) with differential, erythrocyte sedimentation rate (ESR), and imaging (CT or MRI) in individuals with increased ear discharge, fever, periauricular lymphadenopathy, periauricular erythema, or earache out of proportion to clinical examination findings to rule out necrotizing otitis externa.


  • Examine all patients before commencing treatment.

  • Remove debris with gentle irrigation using 3% hydrogen peroxide only if tympanic membrane is visible and intact.

  • Topical preparations containing acetic acid reduce pH and inhibit growth of common pathogens.

  • Topical preparations that contain corticosteroids and either acetic acid or antibiotics have a higher cure rate.

  • Compared to topical preparations, there is no difference in clinical response with systemic antibiotics.

  • Various combinations of topical antibiotics polymyxin and neomycin are available and effective.

  • Neomycin can be ototoxic if the tympanic membrane is perforated and is a common cause of contact dermatitis following treatment for bacterial external otitis.

  • Topical fluoroquinolones (FQs), including ciprofloxacin and ofloxacin used once to twice daily may improve compliance because of reduced dosing; as compared to topical preparations containing polymyxin and neomycin that need to be used at least three times daily.

  • Duration of treatment is typically from 2 to 7 days and varies with disease severity and individual compliance and response to therapy.

  • Patient education to prevent recurrence should include “dry ear” precautions, regular use of acidifying ear drops, the avoidance of ear phones and hearing aids, and the use of ear plugs for swimming practice.

Other Considerations:

  • Consider fungal (candida) infections in individuals who frequently use hearing aids and headphones, and those who do not respond to antibiotic therapy.

  • Refer to otolaryngology if the tympanic membrane is not intact.

  • Refer all individuals to otolaryngology who have severe ear discharge, fever, periauricular lymphadenopathy, periauricular erythema, or earache out of proportion to clinical examination findings to rule out necrotizing otitis externa—a potential life-threatening complication of bacterial external otitis.

Return to Play Criteria:

  • Improving symptoms and normal hearing acuity.

  • Absence of fever, severe ear discharge, fever, periauricular lymphadenopathy, periauricular erythema, or earache out of proportion to clinical examination findings.

Recommended Readings

Clark WB, Brook I, Bianki D, Thompson DH. Microbiology of otitis externa. Otolaryngol Head Neck Surg. 1997;116:23-25.

Cohen D, Friedman P. The diagnostic criteria of malignant external otitis. J Laryngol Otol. 1987;101:216-221.

Goffin FB. pH as a factor in external otitis. N Engl J Med. 1963;268:287-289.

Kaushik V, Malik T, Saeed SR. Interventions for acute otitis externa. Cochrane Database Syst Rev. 2010;(1):CD004740.

Rosenfeld RM, Brown L, Cannon CR, et al. Clinical practice guideline: acute otitis externa. Otolaryngol Head Neck Surg. 2006;134:S4-S23.

RussellJD, Donnelly M, McShane DP, Alun-Jones T, Walsh M. What causes acute otitis externa? J Laryngol Otol. 1993;107:898-901.

van Balen FA, Smit WM, Zuithoff NP, Verheij TJ. Clinical efficacy of three common treatments in acute otitis externa in primary care: Randomised controlled trial. BMJ. 2003;327:1201-1205.

Van Ginkel CJ, Bruintjes TD, Huizing EH. Allergy due to topical medications in chronic otitis externa and chronic otitis media. Clin Otolaryngol. 1995;20:326-328.

Yelland MJ. The efficacy of oral cotrimoxazole in the treatment of otitis externa in general practice. Med J Aust. 1993;158:697-699.

Otitis Media

Introduction (Definitions/Classification): Mucosal infection or inflammation of the middle ear. Eustachian tube obstruction or dysfunction leads to accumulation of fluid in the middle ear which is a precursor for infection or inflammation. Streptococcus pneumoniae is the most common bacteria implicated in adults. Several viruses may induce otitis media in children. Various pathologic variants include the following.

  • Acute otitis media with or without effusion.

    • “With effusion.”

      • Usually associated with allergies or barotraumas.

      • Associated with conductive hearing loss.

  • Chronic otitis media.

    • Serous.

    • Purulent.

History and Physical Examination: Individuals typically have a history of seasonal allergies or an upper respiratory infection preceding the following symptoms and signs.

  • Otalgia.

  • Otorrhea—serous or purulent associated with tympanic membrane perforation.

  • Conductive hearing loss.

  • Tympanic membrane fluid level.

  • Fever is usually absent.


  • Signs/symptoms on physical examination.

  • Otoscopic examination of tympanic membrane may reveal bulging, erythema, blisters (bullous myringitis), opacities, or decreased mobility.

  • Lack of inflammation, an immobile tympanic membrane with retraction, or an air-fluid level usually signifies otitis media with effusion.

  • Either serous or purulent fluid in the external ear canal signifies tympanic membrane perforation.

  • Weber tuning fork test lateralizes to affected ear secondary to conductive hearing loss.

  • Rinne tuning fork test (512 Hz) may reveal bone conduction greater than air conduction secondary to conductive hearing loss.


  • Treat all adults with antibiotics.

  • Intact tympanic membrane.

    • First-line antibiotic—amoxicillin for 7 to 10 days.

    • Individuals with penicillin allergy—macrolide (azithromycin or clarithromycin).

    • Failure to respond to first-line antibiotics—amoxicillin-clavulanate or second-generation cephalosporin (PO cefdinir or IM ceftriaxone).

  • Ruptured tympanic membrane.

    • Topical ofloxacin otic drops.

    • Avoid acidic, antiseptic, and otic drops containing neomycin that can be ototoxic if used in the presence of a perforated tympanic membrane.

    • Patient education to prevent recurrence should include “dry ear” precautions.

  • Supportive care with antihistamines, decongestants, or nasal steroids may be beneficial in otitis media with effusion.

Other Considerations:

  • Consider mastoiditis in individuals with swelling or pain behind the auricle.

  • Refer all individuals to otolaryngology who have the following.

    • Swelling or pain behind the auricle.

    • Hearing loss that persists after resolution of infection.

    • Persistent or recurrent tympanic membrane perforation.

    • Fever.

    • Persistent, painful effusion.

    • Forthcoming airline travel (for consideration of myringotomy and placement of pressure equalization tubes).

Return to Play Criteria:

  • Improving symptoms and intact tympanic membrane without hearing loss.

  • No fever or symptoms or signs concerning for mastoiditis.

Recommended Readings

Chole RA, Cook GB. The Rinne test for conductive deafness. A critical reappraisal. Arch Otolaryngol Head Neck Surg. 1988;114:399-403.

Chonmaitree T, Revai K, Grady JJ, et al. Viral upper respiratory tract infection and otitis media complication in young children. Clin Infect Dis. 2008;46:815-823.

Ginsburg CM, Rudoy R, Nelson JD. Acute mastoiditis in infants and children. Clin Pediatr. 1980;19:549-553.

Gray BM, Converse GM 3rd, Dillon HC Jr. Serotypes of Streptococcus pneumoniae causing disease. J Infect Dis. 1979;140:979-983.

Luxford WM, Sheehy JL. Myringotomy and ventilation tubes: A report of 1,568 ears. Laryngoscope. 1982;92:1293-1297.


Introduction (Definitions/Classification): A type of dizziness, with a sense of “spinning,” “swaying,” or “tilting” “movement” while stationary. It is not a disease but a symptom of numerous underlying disorders that affect vestibular function (balance and equilibrium). It is two to three times more common in women. Common causes in “otherwise healthy individuals” include the following.

  • Benign paroxysmal positional vertigo (BPPV)—most common cause, secondary to canalithiasis.

  • Ménière disease—idiopathic, endolymphatic hydrops (excessive fluid in inner ear).

  • Vestibular neuritis—viral-induced inflammation of vestibular nerve.

  • Labyrinthitis—inflammation of the inner ear labyrinth induced by either infection, stress, trauma, medications, or autoimmune diseases.

  • Other causes—posttraumatic, motion sickness, otitis media, acoustic neuroma, multiple sclerosis, vertebrobasilar stroke.

History and Physical Examination: All except BPPV, usually associated with nausea and vomiting.

  • BPPV—RECURRENT and BRIEF (<1 minute) with change in position.

  • Ménière disease—THERE (Tinnitus, Hearing loss, Episodic vertigo, Recurrent, Ear fullness) that lasts several hours to days, progressive, usually UNILATERAL.

  • Vestibular neuritis—SAW (Single or Sudden, Acute vertigo, Without hearing loss) that last days to weeks.

  • Labyrinthitis—US (Unilateral, Sudden) hearing loss and vestibular function.


  • In addition to history and physical evaluation:

    • BPPV—Dix-Hallpike maneuver.

    • Ménière disease—Weber test (sound localizes to normal ear).

    • Vestibular neuritis—check hearing acuity (usually normal).

    • Labyrinthitis—consider temporal bone CT or MRI in selected cases.


  • Examples of common medications used to suppress vestibular symptoms include antihistamines (diphenhydramine, meclizine), antiemetics (promethazine, ondansetron), and benzodiazepines (diazepam).

  • BPPV.

    • Epley maneuver (canalith repositioning).

    • Vestibular rehabilitation (recommend early).

  • Ménière disease.

    • Low sodium diet.

    • Intratympanic dexamethasone or gentamicin.

  • Vestibular neuritis.

    • Steroids may be superior than antivirals (valacyclovir).

  • Labyrinthitis.

    • First-line management—bed rest and hydration.

    • Short course of steroids in refractory cases.

    • No clear role for antivirals.

Other Considerations:

  • If associated with vertigo, consider brain MRI/MRA.

    • Acoustic neuroma—ipsilateral sensorineural loss, deafness, and/or tinnitus.

    • Multiple sclerosis—episodic neurologic symptoms.

    • Vertebrobasilar stroke—diplopia, dysphagia, dysarthria, and/or weakness.

  • Refer athletes to ENT or neurologist if common measures fail to resolve symptoms.

  • Caution with medications includes the following.

    • Use medications for the shortest duration possible.

    • Promethazine can potentially prolong QT interval and induce fatal arrhythmia.

    • Drugs used to treat vertigo can have undesirable side effects including dry mouth and urinary retention.

Return to Play Criteria:

  • Normal balance, hearing, vision with sport-specific tasks.

  • No nausea or vomiting.

Recommended Readings

Furman JM, Barton J. Approach to the patient with vertigo. UpToDate, Accessed September 1, 2010.

Herraiz C, Plaza G, Aparicio JM, Gallego I, Marcos S, Ruiz C. Transtympanic steroids for Ménière’s disease. Otol Neurotol. 2010;31(1): 162-167.

Mark AS, Seltzer S, Nelson-Drake J, Chapman JC, Fitzgerald DC, Gulya AJ. Labyrinthine enhancement on gadolinium-enhanced magnetic resonance imaging in sudden deafness and vertigo: Correlation with audiologic and electronystagmographic studies. Ann Otol Rhinol Laryngol. 1992;101(6):459-464.

Neuhauser HK, Lempert T. Vertigo: Epidemiologic aspects. Semin Neurol. 2009;29(5):473-481.

Schuknecht HF, Kitamura K. Second Louis H. Clerf Lecture. Vestibular neuritis. Ann Otol Rhinol Laryngol Suppl. 1981;90(1 Pt 2):1-19.

Strupp M, Zingler VC, Arbusow V, et al. Methylprednisolone, valacyclovir, or the combination for vestibular neuritis. N Engl J/Med. 2004;351(4):354-361.

Figure 117. Ears

Section 2: Eyes


Introduction (Definitions/Classification): Commonly known as “pink or red eye;” caused by inflammation of the “conjunctiva,” which covers the eyeball and lines the inner portion of eyelids. Etiologic factors include the following.

  • Noninfectious—allergic, chemical exposure, mechanical.

  • Infectious—viruses (more common) and bacteria.

History and Physical Examination: Chemosis (conjunctival edema), erythema, discharge, morning “eyes stuck,” and “lid crusting” are typical features, yet not useful in distinguishing different types of conjunctivitis. Other differentiating features may include the following.

  • Bilateral itching and watery discharge with a history of seasonal or environmental allergies—allergic.

  • Unilateral or bilateral pain and thick purulent discharge—especially at the lid margins—bacterial.

  • Unilateral, bilateral involvement over 2 days, “sandy, gritty, or burning” feeling, or watery discharge with mucus during an ongoing upper respiratory infection—viral.


  • Signs/symptoms on physical examination.

  • Cultures are usually unnecessary.

  • Consider gram stain of discharge to rule out gonococcal conjunctivitis.

  • Consider rapid 10-minute test (RPS Adeno Detector) for adenovirus.

    • Can save costs and reduce bacterial resistance by eliminating need for empiric topical antibiotic therapy.

  • Visual acuity testing as needed on an individual basis.


  • Examine all patients before commencing treatment.

  • Allergic and viral conjunctivitis are usually self-limited.

    • Over-the-counter antihistamine and decongestant eye drops provide symptomatic relief but do not treat disease.

    • Extended use of drops can be toxic and irritating.

    • Preservative-free eye drops are effective for refractory symptoms and may reduce toxicity and irritation noted with prolonged use of antihistamine and decongestant eye drops.

  • Various drops and ointments for bacterial conjunctivitis.

    • Sulfacetamide, azithromycin, or FQ drops—latter highly effective against pseudomonas.

    • Bacitracin, polymyxin-bacitracin, or sulfacetamide ointment.

    • Counsel individuals regarding blurring of vision following the application of ointments.

  • Discontinue contact lens use.

  • No role for glucocorticoids for conjunctivitis. Can be extremely toxic and may cause various complications.

  • Educate on contagiosity. Avoid sharing linens, towels, cups, and silverware.

  • Obtain ophthalmology consult for all individuals with failure to respond to antibiotic therapy, change in visual acuity, inability to keep the eye open, persistent and severe foreign body sensation, nausea, headache, refractory photophobia, pupil dysfunction, or corneal opacities.

Other Considerations:

  • Consider gonococcal conjunctivitis in individual with a purulent discharge that develops hyperacutely within 12 hours, eyelid swelling, marked chemosis, with or without preauricular lymphadenopathy and concomitant urethritis. Gonococcal conjunctivitis is severe and can cause blindness if treatment is delayed.

  • Consider keratoconjunctivitis (adenovirus) in individuals with “foreign body” sensation, acute vision changes, and corneal infiltrates that may not be readily visible on penlight corneal examination. May be severe and cause blindness if treatment is delayed.

  • Consider chlamydia-induced inclusion conjunctivitis in individuals with chronic symptoms refractory to topical antibiotic therapy.

  • Consider keratitis (corneal inflammation) in individuals who use contact lenses. Empiric treatment of conjunctivitis without ruling out keratitis can potentially cause eye perforation.

  • Consider “pterygium” in individuals with a localized, triangular area of conjunctival thickening or redness extending from the inner canthus to the medial corneal margin.

Return to Play Criteria:

  • Improving symptoms and normal visual acuity.

  • At least 24 hours on antibiotics for bacterial conjunctivitis.

  • Address vision needs for individuals who use contact lenses and are unable to use during recovery from conjunctivitis.

Recommended Readings

Cheng KH, Leung SL, Hoekman HW, et al. Incidence of contact-lens-associated microbial keratitis and its related morbidity. Lancet. 1999;354:181-185.

Jernigan JA, Lowry BS, Hayden FG, et al. Adenovirus type 8 epidemic keratoconjunctivitis in an eye clinic: Risk factors and control. J Infect Dis. 1993;167:1307-1313.

Rietveld RP, ter Riet G, Bindels PJ, Sloos JH, van Weert HC. Predicting bacterial cause in infectious conjunctivitis: Cohort study on informativeness of combinations of signs and symptoms. BMJ. 2004;329:206-210.

Udeh BL, Schneider JE, Ohsfeldt RL. Cost effectiveness of a point-of-care test for adenoviral conjunctivitis. Am J Med Sci. 2008;336:254-264.

Ullman S, Roussel TJ, Culbertson WW, et al. Neisseria gonorrhoeae keratoconjunctivitis. Ophthalmology. 1987;94:525-531.

Wan WL, Farkas GC, May WN, Robin JB. The clinical characteristics and course of adult gonococcal conjunctivitis. Am J Ophthalmol. 1986;102:575-583.

Eyelid Diseases

Introduction (Definitions/Classification): Common eyelid diseases encountered in athletes include the following.

  • Hordeolum.

    • External—commonly known as a “stye.” Caused by bacterial infection of the eyelid sebaceous (Zeis) or sweat glands. S. aureus is the most common bacteria. May be associated with eyelid (periorbital, preseptal) cellulitis.

    • Internal—inflammation of meibomian glands.

  • Chalazion.

    • Chronic noninfectious, inflammatory lesion following obstruction of either the Zeis sebaceous glands or meibomian glands.

History and Physical Examination:

  • Eyelid pain with foreign body sensation in eyelid.

  • Increased tearing (epiphora).

  • Blurring of vision.

  • Stye—focal swelling noted on inner lid, best noted following eversion of lid.

  • Chalazion—focal pustule or papule at lid margin (external or internal).

  • Medial, lower eyelid swelling—concerning for infection of either lacrimal sac (dacryocystitis) or lacrimal gland (dacryoadenitis).

  • In individuals with preseptal cellulitis look for

    • diffuse eyelid erythema and edema.

    • lack of pustule or papule at lid margin.

    • preauricular, submandibular, or cervical lymphadenopathy.

  • Impaired eyeball motility, change in vision, bulging eyeballs (proptosis), altered pupillary reflexes, or optic nerve swelling and retinal vein engorgement on fundus examination—concerning for orbital cellulitis.


  • Signs/symptoms on physical examination.

  • Cultures of tissue fluid for styes that fail to respond to common therapies.

  • CBC with differential in selected cases.

  • CT scan of orbit for all individuals with symptoms or signs concerning for

    • dacryocystitis.

    • dacryoadenitis.

    • orbital cellulitis.


  • Examine all patients before commencing treatment.

  • Warm compresses for 10 to 15 minutes, up to four times per day.

  • For stye and chalazion, gentle massage for 5 minutes, up to four times per day. NO massage for diffuse eyelid erythema or edema.

  • Topical antibiotic ophthalmic drops containing bacitracin or erythromycin.

  • Consider oral antibiotics for concomitant periorbital cellulitis.

    • First-line antibiotic—amoxicillin-clavulanate or first-generation cephalosporin.

    • Failure to respond to first-line antibiotics—IM ceftriaxone or oxacillin.

    • Consider IV antibiotics (oxacillin or nafcillin) if symptoms fail to improve in 48 to 72 hours.

  • Consider clindamycin or Bactrim for methicillin-resistant S. aureus (MRSA) as directed by cultures.

  • Counsel treated individuals on eyelid hygiene—to keep eyelid margins clean by regular, gentle washing with a few drops of baby shampoo.

Other Considerations:

  • When to refer to ophthalmologist?

    • Refractory or recurrent chalazion for biopsy to rule out malignancy, and treatment with either corticosteroid injection and/or curettage.

    • Individuals being considered for IV antibiotics.

    • To rule out orbital cellulitis—individuals with impaired eyeball motility, change in vision, proptosis, altered papillary reflexes, or optic nerve swelling and retinal vein engorgement on fundus examination.

  • Consider infection with MRSA in individuals who fail to respond to common therapeutic interventions.

Return to Play Criteria:

  • Improving symptoms and normal vision.

  • No fever or symptoms or signs concerning for orbital cellulitis.

Recommended Readings

Goawalla A, Lee V. A prospective randomized treatment study comparing three treatment options for chalazia: Triamcinolone acetonide injections, incision and curettage and treatment with hot compresses. Clin Experiment Ophthalmol. 2007;35:706-712.

Mueller JB, McStay CM. Ocular infection and inflammation. Emerg Med Clin North Am. 2008;26:57-72.

Wald ER. Periorbital and orbital infections. Pediatr Rev. 2004;25:312-320.

Corneal Abrasion

Introduction (Definitions/Classification): Defect of the corneal epithelium. Common causes in athletes include the following.

  • Trauma.

  • Prolonged use of contact lenses.

  • Foreign body.

History and Physical Examination:

  • Severe eye pain.

  • Foreign body sensation.

  • Inability to open eyelids that precludes activities of daily living.

  • Increased tearing (epiphora), blurring of vision, corneal edema (grayish appearance).

  • Recurrent corneal abrasions induce “nocturnal” and “early morning” pain.

  • Perform thorough eye examination to rule out penetrating trauma.

    • Check for foreign body with penlight examination.

    • Check for discharge, opacities, or infiltrate—corneal abrasions induce only tearing.

    • Check pupils.

      • Small (corneal abrasion).

      • Large and nonreactive (consider penetrating trauma).

    • Check eyelids for foreign bodies.

    • Check anterior chamber for blood or pus.

    • Visual acuity may be completely normal.

    • Funduscopic examination to confirm red reflex (absent in retinal detachment).


  • Signs/symptoms on physical examination.

  • Fluorescein examination should be performed only to confirm diagnosis after physical examination has been completed (presumptive diagnosis). Visualization of cornea under cobalt blue light reveals green discoloration of the affected area.

  • Stained abrasion appears yellow to the naked eye.


  • As needed, remove foreign body using gentle irrigation with saline.

  • May benefit from eye lubrication with hourly application of “over-the-counter lubricant” (e.g., preservative-free artificial tears).

  • Pain relief with systemic narcotics or nonsteroidal anti-inflammatory medications.

  • Choice of topical antibiotics (sulfacetamide, erythromycin, ciprofloxacin, ofloxacin, polymyxin/trimethoprim).

    • Optimal dosing—QID for 3 to 5 days.

    • Ointment facilitates lubrication of cornea and is preferred.

  • Eye patch for 24 hours may help healing of corneal epithelium and relief of symptoms.

    • No data to prove that patching reduces symptoms or improves healing.

    • Noninfected corneal abrasions, those secondary to trauma (with the exception of abrasions induced by contact lens), and abrasions following removal of foreign bodies can be treated without an eye patch.

    • Properly placed eye patch will prevent athlete from blinking.

    • Contraindicated, if abrasion induced by contact lenses. Using an eye patch for corneal abrasions induced by contact lenses can lead to “sight-threatening infections.”

  • Avoid topical steroids or anesthetics (delays corneal healing).

Other Considerations:

  • When to refer to ophthalmologist?

    • Corneal abrasions >3 mm.

    • Lack of improvement within 24 hours following use of common therapies, even if the abrasion is <3 mm in size.

    • Clinical features of penetrating trauma (large, nonreactive pupil; blood in anterior chamber [hyphema]; pus in anterior chamber [hypopyon]; extrusion of ocular contents).

    • Change in acuity and/or questionable corneal infection (altered color and infiltrate of cornea), especially following prolonged use of contact lenses while sleeping.

      • Contact lenses can induce infectious pseudomonas keratitis complicated by corneal perforation.

    • With foreign body that cannot be removed by gentle irrigation with saline.

  • Consider a short course of cycloplegic eye drops that can alleviate pain induced by pupil miosis.

    • Cyclopentolate or homatropine.

    • Avoid use before consulting with an ophthalmologist.

  • Consider tetanus prophylaxis for penetrating eye injuries.

  • Educate athletes to avoid driving with an eye patch secondary to “altered depth perception.”

Return to Play Criteria:

  • Improving symptoms and normal vision.

  • Off narcotics for pain relief.

Recommended Readings

Benson WH, Snyder IS, Granus V, Odom JV, Macsai MS. Tetanus prophylaxis following ocular injuries. J Emerg Med. 1993;11:677-683.

Clemons CS, Cohen EJ, Arentsen JJ, Donnenfeld ED, Laibson PR. Pseudomonas ulcers following patching of corneal abrasions associated with contact lens wear. CLAO J. 1987;13:161-164.

Jacobs DS. Corneal abrasions and corneal foreign bodies. UpToDate. Accessed October 10, 2010 and October 27, 2012.

Kaiser PK. A comparison of pressure patching versus no patching for corneal abrasions due to trauma or foreign body removal. Corneal abrasion patching study group. Ophthalmology. 1995;102:1936-1942. Accessed October 27, 2012.


Introduction (Definitions/Classification): Wing or triangular shaped, proliferation of conjunctival tissue of unclear etiology. Pathogenic factors include genetic predisposition, viral (human papilloma virus), ultraviolet light (UV), and immunologic alterations. Commonly in athletes exposed to sun and wind for prolonged durations.

History and Physical Examination:

  • Growth (over months to years) arises from limbus and progresses to cornea.

    • As opposed to “pinguecula“—arise from and stay confined to the conjunctiva.

  • Most common symptoms are irritation and redness.

  • If growth extends to cornea:

    • Mild to moderate—can cause blurring of vision (induced by astigmatism).

    • Severe—can reduce visual acuity.


  • Clinical, based on characteristic appearance.


  • Symptomatic measures:

    • Sunglasses with good UV protection.

    • Avoid excess sun and wind exposure, when possible.

    • Topical over the counter decongestants, nonsteroidal anti-inflammatory drugs (NSAIDs), and steroids may be effective.

      • Only ophthalmologists should prescribe steroids (which can raise intraocular tension).

      • All may induce side effects when used on a chronic basis, especially “rebound.”

      • No data to show that any of these treatments can either arrest growth or cure.

  • Routine, scheduled checks to document growth or stability of lesion.

  • Surgical excision of large, refractory, problematic pterygia are associated with the following.

    • Astigmatism.

    • Changes in visual acuity.

Other Considerations:

  • Educate—“prevention better than cure.”

    • Encourage prophylactic use of sunglasses in athletes exposed to elements (wind and sun).

    • UV protection after development of pterygium, does not guarantee growth limitation.

  • Usually benign, yet can be problematic and cause vision changes if growth extends to corneal visual axis.

  • Refer to ophthalmologist/optometrist for

    • rapid growth.

    • untreatable irritation.

    • restricted eye movement.

    • blurring of vision—to rule out astigmatism.

    • change in visual acuity.

    • cosmetic reasons.

  • Educate athletes regarding

    • high recurrence rate after surgery.

    • decreased risk of recurrence after surgery with advancing age. Therefore, the best is to delay surgical excision.

Return to Play Criteria:

  • Corrected astigmatism.

  • Normal visual acuity.

  • Postsurgical cases—off narcotics for pain relief.

Recommended Readings

Bradley JC, Yang W, Bradley RH, Reid TW, Schwab IR. The science of pterygia. Br J Ophthalmol. 2010;94:815-820. Accessed October 10, 2010 and October 27, 2012.

Hirst LW. The treatment of pterygium. Surv Ophthalmol. 2003;48:145-180.

Jacobs DS. Pterygium. UpToDate. Accessed October 10, 2010 and October 27, 2012.

Threlfall TJ, English DR. Sun exposure and pterygium of the eye: A dose-response curve. Am J Ophthalmol. 1999;128:280-287.

Traumatic Hyphema

Introduction (Definitions/Classification): Blood in the anterior chamber of the eyeball induced by trauma.

History and Physical Examination:

  • History of blunt trauma to orbit or head.

  • First evaluate for open globe.

    • BEET: Blood + Eccentric pupil + Extrusion of ocular contents + Tenting of sclera, with

  • PEA: Photophobia secondary to miosis (pupillary constriction; direct and consensual) to bright light, Eye pain, Decreased Visual Acuity, with

  • Blood in anterior chamber, which may be

    • visible, or

    • invisible (seen only on slit examination; microhyphema).

  • Other symptoms and signs.

    • Worsening vision while lying flat.

    • Pupil dilation (mydriasis).

  • Check for other complications.

    • Tearing of iris at its root (iridodialysis).

    • Lens subluxation or dislocation.

    • Retinal tear.

  • Physical examination of orbit.

    • “Step-off”—infraorbital ridge.

    • Crepitus.

    • Decreased and painful extraocular movements.

    • Orbital swelling.

    • Check for foreign body.


  • Signs/symptoms on physical examination (characteristic appearance).

  • Other blood tests.

    • Sickle cell solubility (screening test for sickle cell trait).

    • Hemoglobin electrophoresis (confirmatory test for sickle cell trait; especially in athletes for higher risk—based on ethnicity).

    • CBC, PT, PTT, INR—to evaluate for bleeding disorders.

  • Fine-cut (1- to 2-mm cuts) CT without contrast to rule out

    • intraocular foreign body.

    • ruptured globe.

    • facial (orbital) fractures.

  • Defer fluorescein examination (if corneal abrasion is suspected) until an open (ruptured) globe has been excluded.

  • Funduscopy may be limited secondary to miosis.


  • Refer to ophthalmologist earty! Early recognition and expeditious referral is pivotal for preservation of vision (even if blood is not readily visible and high index of clinical suspicion).

  • All decisions regarding activity modification and treatment should be made by ophthalmologist.

  • Activity limitation is of pivotal importance.

  • Bed rest and elevation of the head of the bed to 30 degrees not shown to be advantageous over infrequent movement.

  • Consider sedation and hospitalization for highly active, young athletes.

  • Restrict reading.

  • On-field management.

    • Place an eye shield without compressing underlying globe.

    • Avoid eye patches.

    • Pain relief with Tylenol and/or opioids.

    • Do not administer NSAIDs—to prevent further bleeding.

    • Do not instill any eye drops.

    • Control nausea and vomiting with ondansetron expeditiously—to prevent rise in intraocular pressure.

Other Considerations:

  • Prognosis based on grading of hyphema.

    • Microhyphema and grade I (<33%) have a 90% prognosis for 20/50 vision or better.

    • Grade II (33% to 50%) hyphema has a 70% prognosis for 20/50 vision or better.

    • Grade III (>50%) and grade IV (100%) hyphemas have a 50% prognosis for 20/50 vision or better.

  • Consider “orbital hemorrhage” or “orbital compartment syndrome” in athletes with proptosis following blunt force orbital trauma.

    • These conditions can cause permanent blindness very rapidly.

  • Test for “sickle cell trait,” “bleeding disorders,” or diabetes mellitus in athletes with spontaneous hyphema.

  • Hospitalization for the following.

    • Grade III and IV hyphemas.

    • Bleeding disorders and sickle hemoglobinopathy.

Return to Play Criteria:

  • After full clearance by ophthalmologist.

  • Normal visual acuity.

  • Postsurgical cases—off narcotics for pain relief.

Recommended Readings

Andreoli CM, Gardiner MF. Traumatic hyphema: Clinical features and management. UpToDate, Accessed September 1, 2010 and October 27, 2012.

Brandt MT, Haug RH. Traumatic hyphema: A comprehensive review. J Oral Maxillofac Surg. 2001;59:1462-1470.

Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. 2002;47:297-334.

Wright KW, Sunalp M, Urrea P. Bed rest versus activity ad lib in the treatment of small hyphemas. Ann Ophthalmol. 1988;20:143-145.

Retinal Detachment

Introduction (Definitions/Classification): Parting of the retinal pigment epithelium and choroid from the neurosensory retinal layer with resultant ischemia of the retina, progressive degeneration of photoreceptors, and loss of vision. Caused by either

  • a tear or a hole in the retina which allows vitreous fluid to leak into the subretinal space that causes detachment.

    • Spontaneous: More common; 1 in 10,000 individuals per year.

    • Traumatic: Less common.

  • traction of vitreous on retina.

    • In athletes with sickle cell or diabetic retinopathy.

    • Following previous “eyeball perforation” injuries.

History and Physical Examination:

  • Symptoms may develop suddenly and progress from hours to days to weeks.

    • Change in vision, including “change in peripheral vision in one eye.”

    • Loss of vision.

  • Commonly described symptoms:

    • “Floaters” described as either “cobwebs” or “housefly.”

    • “Progressive” loss of peripheral vision of affected eye.

    • Fleeting (<1 second), “light flashes” with eye movement of the affected eye.

    • A “shower of black spots.”

    • “A curtain coming across my eye.”


  • Signs/symptoms on physical examination.

  • Check visual acuity to assess.

    • Change in vision (compare with baseline vision during preparticipation evaluation).

    • Loss of vision (highly suggestive of retinal tear).

  • Evaluate visual fields.

  • Funduscopy may reveal either a “wrinkled” appearance or a “tear” of the retina.

  • Key point—examine both eyes.


  • Rapid recognition and referral to ophthalmologist are critical for preservation of vision.

  • Refer all athletes with any of the following.

    • Loss of vision.

    • Change in vision.

    • Visual field loss.

  • Athletes with symptomatic tears or holes in the retina (without detachment) may benefit from prophylactic retinopexy (laser or cryo).

Other Considerations:

  • Risk for untreated symptomatic, full-thickness holes to progress to retinal detachment is 30% versus 1 % following retinopexy.

Return to Play Criteria:

  • Normal visual acuity.

  • Normal visual field testing.

  • Clearance from ophthalmology.

Recommended Readings

Arroyo JG. Retinal detachment. UpToDate. Accessed October 11, 2010 and October 27, 2012.

Byer NE. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment Ophthalmology. 1994;101:1503-1513.

Hollands H, Johnson D, Brox AC, Almeida D, Simel DL, Sharma S. Acute-onset floaters and flashes: Is this patient at risk for retinal detachment? JAMA. 2009;302:2243-2249.

Wilkes SR, Beard CM, Kurland LT, Robertson DM, O’Fallon WM. The incidence of retinal detachment in Rochester, Minnesota, 1970-1978. Am J Ophthalmol. 1982;94:670-673.

Figure 118. Eyes

Section 3: Nose

Acute Sinusitis

Introduction (Definitions/Classification): Inflammation of the paranasal sinuses and nasal mucosa of less than 4 weeks duration. Thus, more appropriately termed “acute rhinosinusitis.” Classified as:

  • Viral—more common.

  • Bacterial—only 0.5% to 2% of cases and develops typically secondary to viral inflammation of paranasal sinuses.

  • Common pathogens include S. pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

History and Physical Examination:

  • Most predictive symptoms in acute viral and bacterial sinusitis include the following.

    • Purulent rhinorrhea either with sinus or ear pressure/pain and nasal congestion.

  • Other clinical features may include the following.

    • F’s—facial pain (unilateral tooth and maxillary tenderness; especially while leaning forward), fever, fatigue.

    • H’s—headache (worse under water), halitosis, hyposomnia (dulled sense of smell).

  • Important to distinguish between viral and bacterial etiologies. Bacterial more likely, if

    • persistent symptoms >10 days.

    • fever >102°F, facial pain, and/or purulent nasal discharge at the beginning of an illness.

    • Worsening signs and symptoms following improvement of a viral infection.

  • Alarm signs and symptoms: Persistent or severe headache despite treatment, high fever, vision changes (diplopia, change in acuity), periorbital edema, or mental status changes may suggest complications:

    • Periorbital/orbital cellulitis.

    • Brain abscess.

    • Meningitis.


  • Signs/symptoms on physical examination.

  • Cultures are usually unnecessary except for individuals with recurrent sinusitis, unresponsive to antibiotics.

  • Otoscopic examination of nasal passages may reveal turbinate thickening, mucosal edema, or purulent discharge.

  • Transillumination of frontal or maxillary sinuses not helpful to distinguish viral from bacterial sinusitis.

  • Consider CT scanning (to rule out potential complications) for individuals with

    • alarm signs and symptoms (noted above).

    • recurrent signs and symptoms (despite therapy).


  • Sinusitis is usually a self-limited illness, yet, 85% to 95% are treated with antibiotics.

  • Supportive care in mild cases for first 7 to 10 days.

    • Pain control.

    • Irrigation with hypertonic, buffered saline.

    • Topical oxymetazoline restricted to 3 days.

    • Three to five days of oral decongestants may benefit selected individuals.

  • Antibiotics for persistent symptoms beyond 7 to 10 days.

    • Amoxicillin/clavulanate for 5 to 7 days.

    • For penicillin-allergic individuals—doxycycline or FQ (levofloxacin or moxifloxacin).

    • Avoid trimethoprim/sulfamethoxazole, macrolides, or cephalosporins (high-resistance patterns).

  • Intranasal corticosteroids are likely to be effective in individuals with allergic rhinitis.

  • No research data to support routine use of systemic glucocorticoids. Can cause various complications.

  • Educate.

    • Avoidance of nose blowing that can push viruses from nasal mucosa to paranasal sinuses and facilitate development of bacterial sinusitis.

    • Use of oxymetazoline for >3 days can induce rebound congestion (rhinitis medicamentosa).

    • Restrict the use of oral decongestants in hot weather, and with other medications (including yet not limited to)—stimulant medications for ADHD, thyroid replacement, bronchodilators.

    • Antihistamines can dry mucosa and prolong discomfort.

    • Zinc use linked to anosmia (loss of smell).

Other Considerations:

  • Obtain otolaryngology consult for all individuals with aforementioned “alarm signs and symptoms.”

  • Consider differential diagnoses (secondary to overlapping clinical features) including

    • allergic rhinitis.

    • neuralgias.

    • various etiologies for headaches (migraine, tension, cluster).

    • temporomandibular joint syndrome.

    • dental pathologies.

Return to Play Criteria:

  • Improving symptoms and signs.

  • May need to modify activity for swimming and diving athletes for a few days.

Recommended Readings

Ah-See KW, Evans AS. Sinusitis and its management BMJ. 2007;334:358-361.

Chow AW, Benninger MS, Brook I, et al. IDSA clinical practice guideline for acute bacterial rhinosinusitis in children and adults. Clin Infect Dis. 2012;54:e72-e112.

Hwang PH, Getz A. Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis. UpToDate. Accessed August 9, 2010 and October 27, 2012.

Meltzer EO, Hamilos DL, Hadley JA, et al. Rhinosinusitis: Establishing definitions for clinical research and patient care. Otolaryngol Head Neck Surg. 2004;131:S1-S62.

Osguthorpe JD, Hadley JA. Rhinosinusitis. Current concepts in evaluation and management. Med Clin North Am. 1999;83:27-41.

Rosenfeld RM, Andes D, Bhattacharyya N, et al. Clinical practice guideline: Adult sinusitis. Otolaryngol Head Neck Surg. 2007;137: S1-S31.

Allergic Rhinitis

Introduction (Definitions/Classification): Inflammation of the nasal mucosa marked by paroxysms of sneezing, rhinitis, and itchy eyes.

  • Common triggers include environmental allergens, pet dander, molds, and dust mites.

  • Prevalence varies between 9% and 42%.

History and Physical Examination:

  • History:

    • Time course (perennial vs. seasonal vs. episodic/occupational).

      • Perennial—symptoms for >2 hours daily for >9 months/year.

      • Seasonal—symptoms predictable annually.

        • Rose fever: Grass, tree pollen exposure in spring.

        • Hay fever: Ragweed exposure in fall.

      • Episodic/occupational—acute response to known trigger (animals, coffee beans, tobacco).

    • Family history of allergies, asthma.

    • Exposure to possible triggers.

  • Presenting symptoms: Inquire about duration, severity, exposures, and treatments.

    • Rhinorrhea.

    • Sneezing.

    • Pruritus of eyes, nose, throat, palate.

    • Postnasal drip.

    • Fatigue, irritability.

    • Cough.

  • Physical examination:

    • General: Mouth breathing.

    • Nose: Bluish discoloration of mucosa, swollen turbinates, polyps, clear discharge, transverse nasal crease.

    • Pharynx: Cobblestoning.

    • Eyes: Conjunctivitis, periorbital edema/darkening (allergic shiners).

    • Ears: Air-fluid levels.

    • Additional findings: Eczema and asthma suggests “atopy.”


  • Clinical:

    • Signs/symptoms on physical examination.

    • History (personal and family history).

  • Allergen testing:

    • Percutaneous skin test—introducing controlled amounts of allergen into skin and observing for reaction (acute, delayed, none).

    • Allergen-specific IgE (radioallergosorbent testing [RAST])—blood test looking for presence of IgE to precise allergen.

  • Miscellaneous:

    • Nasolaryngoscopy/nasal cytology in addition to percutaneous skin testing.


  • Avoidance of allergens.

  • Medications (most commonly used):

    • Intranasal glucocorticoids.

      • Most effective maintenance therapy.

      • Use with caution during concurrent use of topical or inhaled glucocorticoids for asthma or dermatitis.

      • Superior to other medications.

    • Antihistamines.

      • Variety of oral and topical (sprays) available.

      • Combination (intranasal glucocorticoid + antihistamine) is effective for refractory cases.

      • First generation (diphenhydramine, chlorpheniramine, hydroxyzine)—not advised secondary to sedative effects.

      • Second generation (cetirizine, loratadine) and third generation (fexofenadine) effective.

      • Third generation thought to have, yet unproven, fewer central nervous system side effects.

      • Superior to cromolyn.

    • Mast cell stabilizers (cromolyn sodium).

      • Available over-the-counter (OTC), safe, yet requires frequent dosing.

      • Choice for individuals unresponsive to antihistamines.

    • Leukotriene modifiers (montelukast).

      • May have equal efficacy to antihistamines and superior efficacy when combined with an antihistamine.

      • May be beneficial in those with nasal polyps and coexistent asthma.

    • Refractory cases:

      • Referral to allergist for allergen testing and consideration of immunotherapy.

      • Consider evaluation for asthma.

Other Considerations:

  • Educate—intranasal glucocorticoids.

    • To direct spray away from nasal septum.

    • Can potentially cause epistaxis and nasal perforation; yet, have been generally shown to be extremely safe following long-term use.

    • May be effective within hours, yet may take days to weeks to be fully effective in athletes with chronic symptoms.

  • Educate—side effects.

    • Have athletes consult with medical staff before using OTCs.

    • OTC or prescription medicines containing pseudoephedrine (PSE) can induce insomnia, irritability, and hypertension, and thus should be avoided in athletes (author opinion).

    • Antihistamines can cause sedation, flushing, fever, and electrolyte imbalance.

    • Leukotriene modifiers can induce anaphylaxis and aggressive behaviors.

  • Swimmers may find benefit from nasal clips to prevent nasal mucosa contact and irritation with chlorinated water.

  • Educate athletes on national teams.

    • Systemic glucocorticoids and PSEs are banned “in-competition.”

    • Inhaled corticosteroids require a “Declaration of Use,” both on the website of United States Anti-doping Agency (USADA) and on the Doping Control Official Record (DCOR), at the time of drug testing.

Return to Play Criteria:

  • If athlete feels well and has no difficulty breathing.

  • Adequate treatment and control of concurrent respiratory illness or conditions (asthma).

Recommended Readings

Carr W, Bernstein J, Lieberman P, et al. A novel intranasal therapy of azelastine with fluticasone for the treatment of allergic rhinitis. J Allergy Clin Immunol. 2012;129:1282-1289.

Cingi C, Ozlugedik S. Effects of montelukast on quality of life in patients with persistent allergic rhinitis. Otolaryngol Head Neck Surg. 2010;142:654-658.

deShazo RD, Kemp SF. Allergic rhinitis: Clinical manifestations, epidemiology, and diagnosis. UpToDate. Accessed October 28, 2012.

Dykewicz MS, Fineman S, Skoner DP, et al. diagnosis and management of rhinitis: Complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. American Academy of Allergy, Asthma, and Immunology. Ann Allergy Asthma Immunol. 1998;81(5 pt 2):478-518.

Gelardi M, Ventura MT, Fiorella R, et al. Allergic and non-allergic rhinitis in swimmers: Clinical and cytological aspects. Br J Sports Med. 2012;46:54-58.

Nayak A, Langdon RB. Montelukast in the treatment of allergic rhinitis: An evidence-based review. Drugs. 2007;67:887-901.

Patel D, Garadi R, Brubaker M, et al. Onset and duration of action of nasal sprays in seasonal allergic rhinitis patients: Olopatadine hydrochloride versus mometasone furoate monohydrate. Allergy Asthma Proc. 2007;28:592-599.

Salib RJ, Howarth PH. Safety and tolerability profiles of intranasal antihistamines and intranasal corticosteroids in the treatment of allergic rhinitis. Drug Saf. 2003;26:863-893.

Settipane RA, Charnock DR. Epidemiology of rhinitis: Allergic and nonallergic. Clin Allergy Immunol. 2007;19:23-34.

van Bavel J, Findlay SR, Hampel FC Jr, Martin BG, Ratner P, Field E. Intranasal fluticasone propionate is more effective than terfenadine tablets for seasonal allergic rhinitis. Arch Intern Med. 1994;154:2699-2704.

Nasal Trauma

Introduction (Definitions/Classification): The nose is the most commonly injured area of the face. Logically, nasal trauma is more common during participations in contact sports. Injuries include the following.

  • Nose bleeding (epistaxis).

  • Nasal fracture.

  • Nasal septum deviation.


History and Physical Examination:

  • History:

    • Mechanism: Usually posttraumatic, sustained during play.

    • Recurrent and difficult to control: Hereditary hemorrhagic telangiectasia, thrombocytopenia, platelet dysfunction, or coagulopathy.

    • Medications and drugs: Warfarin, aspirin, intranasal glucocorticoids (fluticasone), alcohol, and cocaine abuse.

    • Miscellaneous: Cold and dry environments, sinusitis, allergic rhinitis, septal deviation, “nose picking,” and remote history of head and neck surgery.

  • Physical examination:

    • Source of the bleed should be identified by direct visualization using good light source, nasal speculum, or bayonet forceps; suction may help.

    • Approximately 90% of nosebleeds occur from the anterior blood vessels involving the Kiesselbach plexus; 10% are posterior bleeds.

    • Yet, may be difficult to pinpoint location; persistent bleeding despite thorough anterior nasal packing suggests posterior bleed.


  • First rule out fracture!

  • General measures:

    • Nose blowing will help clear existing clots, which otherwise can lengthen duration of bleeding.

    • Have patient sit with head elevated (to prevent swallowing blood).

    • Squeeze nose with constant pressure for 10 minutes, while leaning forward at the waist.

    • Two sprays of intranasal oxymetazoline.

    • Cold compress.

  • Specific measures:

    • Cautery.

    • Administer local anesthetic (lidocaine with epinephrine) or oxymetazoline, and/or oral anxiolytic (lorazepam) prior to procedure.

    • First-line management for anterior bleeds.

    • Chemical (silver nitrate) or electrical—equally effective, yet thorough hemostasis prior to cautery is essential for success.

  • Nasal packing.

    • Synthetic nasal (Merocel) tampons coated with antibiotic ointment not vaseline (to reduce risk for toxicshock syndrome [TSS]).

    • Compared to traditional gauze packing, use of Merocel tampons may decrease risk for infection with S. aureus.

    • Hemostatic agents such as oxidized cellulose or gelatin foam. Can use for 2 to 3 days.

  • Refractory bleeding.

    • Consider etiology to be a posterior bleed.

    • Refer emergently to otolaryngologist for posterior packing (balloon or Foley catheters), embolization, or surgery.

  • Miscellaneous treatment information.

    • Foams and gels for thrombogenesis—under development.

Other Considerations:

  • Routine use of NSAIDs is not associated with increased risk for epistaxis.

  • Counsel that use of oxymetazoline in small doses does not enhance risk for elevated blood pressure (BP).

  • Posterior epistaxis can result in significant hemorrhage and it is important to rule out nasopharyngeal cancer for posterior epistaxis, especially in individuals from China and Southeast Asia.

  • Routine testing for coagulopathy is unnecessary for occasional epistaxis.

  • Be vigilant for the development of TSS (fever, hypotension, skin lesions) in athletes who have been treated with nasal packing.

  • In healthy athletes, routine use of antibiotics to prevent TSS not studied and has no benefit in preventing secondary bacterial sinusitis.

  • Hematomas can form between cartilage and overlying mucous membrane. Refer to otolaryngologist expeditiously for surgical consultation, to prevent complications including cartilage avascular necrosis, septal perforations, or irreversible nasal damage.

Return to Play Criteria:

  • Bleeding controlled.

  • Hemodynamically stable.

  • No recurrent epistaxis with sport-specific exertion.

Nasal Fracture

  • Common in athletes. The anatomy of the nose (prominence off the facial surface) increases vulnerability to injury or fracture.

History and Physical Examination:

  • History:

    • Blunt facial injury.

    • Inquire regarding the mechanism of injury from available witnesses.

  • Physical examination:

    • Begins with a thorough examination!

      • Complete head, eyes, ears, nose, mouth (including teeth), and throat.

      • Complete neurologic examination.

    • Dislocation, swelling, or crepitus highly suggestive of fracture.

    • During examination, remember that nasal fractures can be associated with other facial fractures.

    • Key examination points (needing immediate specialist referral).

      • Open fracture or septal hematoma.

      • Significantly depressed nasal dorsum, widening of palpebral fissures, and intercanthal distance—suggestive of a naso-orbito-ethmoid fracture.

      • Halo test: Clear nasal or ear discharge (that forms a halo surrounding blood on gauze)—suggestive of cerebrospinal fluid (CSF) leak. Test maybe positive with other body fluids including saliva.

      • Decreased facial sensation—suggestive of fifth cranial nerve injury.

      • Facial paralysis—suggestive of seventh cranial nerve injury.

      • Dysphonia—suggestive of a significant hematoma surrounding the airway or an associated fracture of the maxilla or mandible.

      • Postauricular ecchymosis (Battle sign)—suggestive of a basilar skull fracture. May not develop for 2 days post injury.


  • Signs/symptoms on physical examination.

  • Imaging:

    • Radiographs.

      • Unnecessary if individual can breathe comfortably, and there is no significant curvature, or septal hematoma.

      • Do not change initial management, if not needed.

    • CT scanning.

      • CT scans with three-dimensional (3D) reconstructions for concerns regarding associated facial fractures.


  • In the acute setting:

    • Remove from activity and apply a cold pack to minimize swelling and associated bleeding.

    • If concern for CSF leak and individual is stable:

      • Elevate the head 40 to 50 degrees to decrease intracranial pressure.

      • Refer expeditiously to otolaryngologist to rule out associated fractures and consider reduction.

    • If closed fracture and no CSF leak:

      • Consider referral to otolaryngologist within 3 to 6 hours post injury.

      • After 3 to 6 hours, edema precludes adequate reduction. Thus, need to wait 5 days for reduction.

      • Most nasal fractures are responsive to elective reduction in the first 10 days following injury.

Other Considerations:

  • Cover any associated lacerations with clean dressings.

  • A septal hematoma can separate the nasal cartilage from the overlying perichondrium leading to pressure-induced avascular necrosis, septal perforation, or infection. It is a significant complication and should be promptly identified followed by immediate referral to otolaryngology.

  • Consider tetanus prophylaxis for any contaminated wounds.

  • Consider antibiotic prophylaxis for fractures complicated by exposed nasal cartilage.

Return to Play Criteria:

  • Varies and should be individualized in consultation with otolaryngologist.

  • Many otolaryngologists recommend customized face masks for prolonged periods following return to activity.

Nasal Septal Deviation

  • May be a congenital variant, yet commonly a result of trauma from a sports injury or other facial trauma. A deviated septum may result in nasal obstruction and difficulty breathing.

History and Physical Examination:

  • History: Few individuals have an entirely straight septum. Degree of deviation determines symptom severity and characteristics. Inquire regarding the following.

    • Presence of difficulty with nasal breathing.

    • Unilateral (obstruction) or bilateral (mucosal congestion) symptoms.

    • Facial pain.

    • Difficulty smelling common odors.

    • Preceding history of sinus infections or trauma.

    • Possible irritants.

      • Drug use.

      • Smoke exposure.

      • Known allergens.

  • Physical examination:

    • Careful inspection of the nose and oropharynx with a light source looking for

      • structural abnormalities.

      • to rule out the presence of masses, polyps, or swellings.

    • Observe the individual’s breathing pattern—noisy, open mouth?


  • Signs/symptoms on physical examination.


  • If symptoms are pronounced, refer to otolaryngology for possible surgical intervention.

  • Septoplasty can reduce symptoms ˜90%.

Other Considerations:

  • Alteration of the septum can lead to changes in the natural air turbulence with nose breathing and lead to a sensation of “chronic sinus congestion.”

  • Age-related alteration of nasal cartilage morphology may potentiate septal deviation.

  • Concomitant rhinitis or rhinosinusitis may worsen nasal obstruction, thus imperative to adequately treat comorbid conditions.

Return to Play Criteria:

  • No restrictions if symptoms well controlled and no signs or symptoms of respiratory distress.

Recommended Readings

Alter H. Approach to the adult with epistaxis. UpToDate. Accessed October 28, 2012.

Bhattacharyya N. Clinical presentation, diagnosis, and treatment of nasal obstruction. UpToDate. Accessed October 29, 2012.

Biswas D, Mal RK. Are systemic prophylactic antibiotics indicated with anterior nasal packing for spontaneous epistaxis? Acta Otolaryngol. 2009;129:179-181.

Breda SD, Jacobs JB, Lebowitz AS, Tierno PM Jr. Toxic shock syndrome in nasal surgery: A physiochemical and microbiologic evaluation of Merocel and NuGauze nasal packing. Laryngoscope. 1987;97:1388-1391.

Fractures and dislocations—midface. Marx: Rosen’s Emergency Medicine. 7th ed. Elsevier; 2009. Retrieved from Accessed January 15, 2011.

Gandomi B, Bayat A, Kazemei T. Outcomes of septoplasty in young adults: The Nasal Obstruction Septoplasty Effectiveness study. Am J Otolaryngol. 2010;31:189-192.

Krempl GA, Noorily AD. Use of oxymetazoline in the management of epistaxis. Ann Otol Rhinol Laryngol. 1995;104:704-706.

Kucik CJ, Clenney T Management of epistaxis. Am Fam Physician. 2005;71:305-311.

McKay MP, Mayersak RJ. Facial trauma in adults. UpToDate. Accessed October 28, 2012.

Nasal obstruction. Essential Evidence Plus. Retrieved from Accessed January 6, 2011.

Ruhl, Terry S. Epistaxis and nosebleeds. Essential Evidence Plus. Retrieved from Accessed January 6, 2011.

Tay HL, Evans JM, McMahon AD, MacDonald TM. Aspirin, nonsteroidal anti-inflammatory drugs, and epistaxis. A regional record linkage case control study. Ann Otol Rhinol Laryngol. 1998;107:671-674.

Wilson SW, Milward TM, Delayed diagnosis of septal haematoma and consequent nasal deformity. Injury. 1994;25(10):685-686.

Figure 119. Nose

Section 4: Mouth

Common Dental Injuries

Introduction (Definitions/Classification): Contact sports increase risk for orofacial injuries including fracture, tooth avulsion, luxation, with subsequent complications such as abscess formation. Time is of the essence in treating dental injuries.

History and Physical Examination:

  • History:

    • Inquire about the mechanism of injury and time course for associated signs and symptoms.

    • Rule out loss of consciousness, concussion, or prior facial injury.

    • Perform thorough review of systems including the nervous system; head, eyes, ears, nose, and throat; neck, respiratory system.

    • Obtain prior cardiac history of congenital or acquired heart disease, including valve or septal defects.

  • Physical examination: Prior to examination, ensure airway safety and no additional facial/skull fractures.

    • Evaluate gingiva for laceration, ecchymosis, and implanted foreign bodies (chipped teeth).

    • Evaluate for pulpal exposure or inflammation; assess sensitivity to air as well as hot and cold liquids.

    • Appraise teeth for fractures (change in bit), chips, and other deformities.

    • Have the individual bite down on a tongue depressor to assess for any tooth displacement.

    • Percuss individual teeth with tongue depressor to evaluate sensitivity (in an otherwise normal tooth, this may indicate damage to the neurovascular bundle which may lead to subsequent pulp degeneration).

    • Palpate for tooth mobility (periodontal ligament damage), any swelling, or fluctuations in the soft tissues.


  • Classification system for dental fractures:

    • Class I: Fracture involves only the enamel (usually nonpainful).

    • Class II: Fracture involves enamel and dentin (yellow in color; may be painful).

    • Class III: Dental pulp exposed (red line or dot; exquisitely painful).

  • Avulsion, luxation, and abscess: Diagnosed clinically.

  • Consider obtaining blood cultures and an echocardiogram if systemic symptoms such as fever, chills, sweats, and vomiting are present (to rule out systemic spread of the infection).


  • Fractures: Management depends upon severity.

    • Class I and II: Dental care is nonurgent. Consider covering with a clean dressing (calcium hydroxide) and aluminum foil.

    • Class III: Early evaluation by dentist or specialist.

  • Abscess: Seek medical evaluation to rule out need for surgical drainage or root canal.

    • Culture pocket, if possible (anaerobic bacteria, S. pyogenes, or S. aureus).

    • Antibiotics (usually oral).

    • Warm water gargles.

    • Analgesics—OTC or prescription.

    • Avoid placing aspirin over the area as this increases mucosal irritation.

  • Avulsion: The sooner the tooth is replaced, the greater the success and healing rate. Reimplantation of completely avulsed tooth:

    • Only reimplant if secondary (permanent) tooth is affected.

    • Minimize disturbance to the socket.

    • Rinse (do not wipe) tooth gently.

    • Replace into socket (“snaps” into place). If deferring until other evaluation, store in culture media or room-temperature milk.

    • If milk is unavailable, saliva works well; have individual spit into a cup to store tooth.

    • Stabilize tooth until evaluated by specialist; pending evaluation by specialist, have individual bite on a moist gauze pad.

    • It may take weeks to see if the tooth is successfully reincorporated into the gingiva and may require follow-up radiographs.

  • Partial tooth avulsion or luxation: Do not remove and attempt repositioning. Expeditious referral to specialist; primary goal is to maintain vitality of the periodontal ligament.

Other Considerations:

  • If a partially avulsed tooth is noted in a backboarded individual, consider complete removal of the tooth as an aspiration precaution. Store tooth in saline at room temperature.

  • If the tooth is missing, consider obtaining a chest radiograph for localization:

    • In bronchus or esophagus: Requires removal.

    • Below the diaphragm: Does not require removal.

  • Mouthguards reduce the percent of oral injuries. In high school, basketball players who did not wear mouthguards, incidence of orofacial injury is 31% and less than 1% in players who wore mouthguards.

  • Custom-fitted mouthguards do not significantly decrease the incidence of oral soft tissue injuries, but has been shown to significantly reduce the morbidity and expense resulting from dental injuries in men’s Division I college basketball.

  • Educate staff and trainers regarding the benefits of mouthguards.

  • Consider antibiotic prophylaxis on an individual basis as necessary for concurrent, significant cardiac history.

  • Consider tetanus prophylaxis on an individual basis.

  • When to refer?

    • Soft tissue injury.

    • Altered bite or teeth occlusion.

    • Teeth sensitivity to temperature.

    • Either anterior or posterior teeth fracture.

    • Pulp exposure.

    • Moveable, malpositioned, or missing teeth.

Return to Play Criteria:

  • If the individual is medically stable, without excessive pain, discomfort, or need for expeditious referral, they may continue activity.

  • If there is a class III fracture, partial avulsion or reimplantation discontinues physical activity until evaluated and cleared by a specialist.

  • Following treatment for abscess, athlete must be afebrile without added systemic signs of infection.

Recommended Readings

Cohenca N, Roges R, Roges R. The incidence and severity of dental trauma in intercollegiate athletes. J Am Dent Assoc. 2007;138;1121-1126.

Fractures and dislocations—dental and alveolar trauma. Marx: Rosen’s Emergency Medicine. 7th ed. Elsevier. 2009. Retrieved from Accessed January 15, 2011.

Labelle C, Smith B, Sigurdsson A. Effect of mouthguards on dental injuries and concussions in college basketball. Med Sci Sports Exerc. 2002;34(1):41-44.

Maestrello-deMoya MG, Primosch RE. Orofacial trauma and mouth-protector wear among high school varsity basketball players. ASDC J Dent Child. 1989;56(1):36-39.

McTigue DJ. Evaluation and management of dental injuries in children. UpToDate. Accessed October 16, 2012.

Schatz J, Hasher C, Joho J. A retrospective clinical and radiologic study of teeth re-implanted following traumatic avulsion. Endod Dent Traumatol. 1995;11:235-239.

Aphthous Ulcers

Introduction (Definitions/Classification): “Recurrent aphthous stomatitis” or “canker sores” is a common finding in the second to fourth decades of life, and can cause significant discomfort. They are not contagious or sexually transmitted. They typically resolve spontaneously within 2 weeks.

History and Physical Examination:

  • History: There is no clear etiology for these ulcers, although associations exist.

    • Stress (including physical stress).

    • Trauma.

    • Bowel pathology: Celiac disease, Crohn disease.

    • Drugs: NSAID and methotrexate use.

    • Deficiencies in folic acid, iron, vitamin B-12.

    • Menstrual cycle hormonal fluctuations.

    • Auto-inflammatory syndromes (Behçet disease).

    • Immunodeficiencies.

    • Food allergies.

    • Smoking cessation.

    • Genetics.

  • Physical examination: Lesions are limited to the oral cavity and present as the following:

    • Small (2- to 4-mm diameter) yellow or grayish circular ulcerations.

    • Circumscribed borders.

    • Surrounding erythema and edema.

    • Located mainly on the nonkeratinized tissue (labia/buccal mucosa, floor of the mouth, and lateral or undersurface of tongue).

Diagnosis: Made by clinical examination.

  • In the athlete, consider basic laboratories to rule out some of the known associations listed below:

    • CBC with differential.

    • Hemoglobin.

    • Iron studies.

    • Vitamin B-12 levels.

    • Anti-endomysium antibody and transglutaminase assay to rule out celiac disease.

Treatment: Little evidence exists for medicines used to decrease rate of recurrence.

  • For symptomatic treatment:

    • Topical agents:

      • Corticosteroids (hydrocortisone hemisuccinate pellets).

      • Triamcinolone acetonide in paste form.

      • Topical tetracycline.

    • Rinses:

      • Betamethasone sodium phosphate elixir rinse.

      • Chlorhexidine gluconate rinses.

  • If an association exists, correct the deficiency or avoid causal agent.

  • Education on avoidance of sodium sulfate (toothpaste detergent) which prolongs ulcer-healing time.

Other Considerations:

  • Rule out Behçet disease, a neutrophilic inflammatory disorder that presents with recurrent oral and genital ulcerations.

  • Herpes simplex virus (HSV) and aphthous ulcers have similar morphologic characteristics; differentiation is important for adequate treatment.

  • Use topical corticosteroids only after excluding HSV.

  • Adequate pain control necessary, especially in sports that mandate the use of mouthguards.

Return to Play Criteria:

  • No restrictions.

Recommended Readings

Aphthous ulcers. In: Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition, 8th ed. Saunders; 2009. Retrieved from Accessed January 5, 2011.

Goldstein B, Goldstein A. Oral lesions. UpToDate. Accessed on January 13, 2011 and October 16, 2012.

Scully C. Aphthous ulcers. Retrieved from Accessed January 5, 2011.

Tilliss T, McDowell J. Differential diagnosis: Is it herpes or aphthous? J Contemp Dent Pract. 2002;(3)1:1-15.

Streptococcal Pharyngitis/Tonsillitis

Introduction (Definitions/Classification): Otherwise known as “strep throat (ST),” inflammation of the pharynx and tonsils caused by primarily group A beta-hemolytic streptococcus (GAS). Less common etiologies include group C and group G streptococci. Duration of illness is 2 to 5 days in untreated patients.

History and Physical Examination: Patients will present with an array of symptoms so it is important to discern if there exists a concern for streptococcal etiology. Have a high suspicion for GAS if two or more of the following are present (think FEAT).

  • Fever >38°C in past 24 hours.

  • Enlarged tonsils or erythematous oropharynx; Exudate.

  • Absence of cough.

  • Tender anterior cervical lymph nodes.

Overlapping signs and symptoms that are suggestive of a viral etiology include the following.

  • Cough.

  • Diarrhea.

  • Conjunctival injection.

  • Coryza.

  • Hoarse voice.

Complications include the following.

  • Acute rheumatic fever: Results from persistence of GAS organisms in respiratory tract leading to increased risk of acute rheumatic fever (particularly in children). Antibiotics beneficial in prevention, if initiated within the first 9 days of symptoms. Symptoms may include arthritis, carditis, chorea, subcutaneous nodules, erythema marginatum.

  • Poststreptococcal glomerulonephritis: Inflammation of glomeruli vasculature can cause hematuria, proteinuria, and hypertension. No clear benefit with antibiotic therapy.

  • PANDAS (“Pediatric Autoimmune Neuropsychiatric Disorders Associated with group A Streptococci”): Symptoms may include exacerbation of tic or obsessive compulsive disorder. Consider group A Streptococcus testing for abrupt onset of tic disorder. No good evidence for efficacy of antibiotic treatment.

  • Scarlet fever: A desquamating, diffuse, papular, “sandpaper-like” rash accompanied by circumoral pallor and a strawberry tongue.

  • Streptococcal TSS: Widespread infection leads to shock and organ failure.

  • Tonsillopharyngeal cellulitis or abscess: Occurs in <1% of acute pharyngitis infections.

  • Other potential complications: Sinusitis, otitis media, necrotizing fasciitis.


  • Rapid antigen detection test for high clinical level of suspicion for GAS tonsillopharyngitis; if positive, treat.

  • If negative, obtain a confirmatory throat culture for verification.

  • Consider testing for infectious mononucleosis (IM).


  • For high level of suspicion, initiate antibiotic therapy while awaiting laboratory confirmation.

  • Discontinue treatment if cultures are negative.

  • Antibiotics have been shown to shorten duration of symptoms by approximately 1 day and also decrease rate of infectivity.

  • Antibiotic regimens for GAS include the following.

    • No penicillin (PEN) allergy: Penicillin is first-line.

    • PEN allergy but not anaphylactic-type reaction: narrow-spectrum cephalosporin (cephalexin, cefadroxil).

    • True PEN allergy: Macrolide (erythromycin, clarithromycin).

  • Avoid sulfonamides, FQs, and tetracyclines because of high failure rate and increasing resistance.

  • Treat for 10 days.

  • Supportive therapy.

    • Fever, sore throat: NSAIDs and acetaminophen (use with caution in concomitant mononucleosis because of possible, mononucleosis-induced thrombocytopenia and infective hepatitis).

    • Sore throat: Consider liquids and soft foods for sore throat.

    • Miscellaneous: Hydration and rest.

  • Educate.

    • Contagiosity—rate of transmission with close contacts is ˜35%. Antibiotic use will lessen the rate, yet reinforce good hand hygiene, and avoidance of sharing toothbrushes, linens, and utensils.

  • Currently, no vaccine available.

  • Prophylaxis is only indicated in the setting of previous rheumatic fever.

Other Considerations:

  • If duration of pharyngitis lasts longer than 5 days, consider alternative etiologies (viral—Epstein-Bar virus (EBV), CMV; bacterial—mycoplasma, chlamydia; fungal).

  • Tests for cure (e.g., repeat rapid antigen tests or cultures) after treatment are unnecessary unless

    • personal history of rheumatic fever.

    • acute pharyngitis presents during an outbreak of poststreptococcal glomerulonephritis or acute rheumatic fever.

  • Group C and G streptococcal infections warrant a course of antibiotics for only 5 days, as rheumatic fever is not a complication of these strains.

Return to Play Criteria:

  • Minimum of 24 hours on antibiotics.

  • Improvement of symptoms—afebrile for at least 24 hours without antipyretic.

  • No concerning respiratory symptoms.

Recommended Readings

Bisno A, Lichtenberger P. Evaluation of acute pharyngitis in adults. UpToDate. Accessed October 16, 2012.

Bisno AL, Gerber MA, Gwaltney JM Jr, Kaplan EL, Schwartz RH. Practice guidelines for the diagnosis and management of group a streptococcal pharyngitis. Clin Infect Dis. 2002;35:113-125.

Catanzaro FJ, Stetson CA, Morris AJ, et al. The role of the streptococcus in the pathogenesis of rheumatic fever. Am J Med. 1954;17: 749-756.

Del Mar CB, Glasziou PP, Spinks AB. Antibiotics for sore throat. Cochrane Database Syst Rev. 2000;(4):CD000023.

Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute Streptococcal pharyngitis: A scientific statement from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young, the Interdisciplinary Council on Functional Genomics and Translational Biology, and the Interdisciplinary Council on Quality of Care and Outcomes Research: endorsed by the American Academy of Pediatrics. Circulation. 2009;119(11):1541-1551.

Gerber MA. Treatment failures and carriers: Perception or problems?. Pediatr Infect Dis J. 1994;13:576-579.

Micromedex. Accessed February, 2011.

Webb KH, Needham CA, Kurtz SR. Use of a high-sensitivity rapid strep test without culture confirmation of negative results: 2 Years’ experience. J Fam Pract. 2000;49:34-38.

Infectious Mononucleosis

Introduction (Definition/Classification): Known as “mono” or “the kissing disease,” IM is a widespread illness spread by saliva. The most common etiology is the EBV. Peak incidence is 10 to 24 years of age. Complications may include involvement of any organ, yet more common problems include the following.

  • Spleen—enlargement/rupture.

  • Hematologic—neutropenia, thrombocytopenia, and rarely aplastic anemia, disseminated intravascular coagulation, or hemolytic uremic syndrome.

  • Neurologic—Guillain-Barré syndrome, neuritis, meningitis.

  • Cardiac—myocarditis, risk for sudden cardiac death (SCD).

  • Respiratory—airway compromise.

History and Physical Examination:

  • Fatigue, malaise, changes in appetite, and chills are common presenting symptoms that appear between 4 and 6 weeks’ postexposure. These symptoms usually last a few days prior to the onset of the characteristic triad (that can be observed in “ST” as well).

    • Fever between 102°F and 104°F.

    • Cervical lymphadenopathy.

    • Tonsillitis/pharyngitis—erythema with or without an exudate.

    • Other features may include the following.

      • Fatigue.

      • Splenomegaly in 50% to 60%; only 20% to 50% palpable on examination.

      • Hepatomegaly—less common.

      • Rash—petechial or maculopapular rash; before or after the administration of antibiotics.

      • Palatal petechiae (with cervical lymphadenopathy and splenomegaly, is highly suggestive of IM).

Diagnosis: Established by a combination of clinical and laboratory data.

  • Signs/symptoms on physical examination, with the following.

    • Positive “monospot” or “heterophile antibody (Paul Bunnell)” tests.

      • Sensitivity ˜85%; specificity ˜100%.

      • If positive with clinical features of IM, no further testing necessary.

      • Not as sensitive or specific in younger athletes.

    • EBV-specific antibody testing—in selected cases, to establish diagnosis and detect past illness or reactivation of EBV. Summary:

      • EBV VCA (viral capsid antigen) IgM—suggests acute infection.

      • EBV VCA IgG—suggests previous infection/immunity.

      • EBNA (Epstein-Barr nuclear antigen)—typically appears 6 weeks after onset of illness, suggests previous infection.

    • Miscellaneous:

      • Leukocytosis or leukopenia.

      • Lymphocytosis >50% on differential count.

      • Increased atypical lymphocytes >10%.

      • Mild, self-limited neutropenia and thrombocytopenia.

      • Liver Function Tests (LFTs).

        • Highly suggestive of mononucleosis in individuals with pharyngitis.

        • Recheck weekly if high on initial assessment (author opinion).

  • Peripheral smear evaluation—confirm viral characteristics in those with clinical or laboratory features concerning for occult hematologic pathology.


  • Discontinuation from all activities for a minimum of 3 weeks.

  • Supportive therapy for symptoms.

    • Fever, malaise, sore throat—NSAIDs at the lowest effective dose.

    • Avoid acetaminophen to minimize liver dysfunction, especially in those with elevated LFTs.

    • Appropriate diet—avoidance of fatty foods.

  • No effective antiviral drugs or vaccines available.

  • Conflicting data on the role of steroids.

    • May be warranted in individuals with either airway compromise from impending obstruction or fulminant organ failure (liver). Yet, used more often than conventionally recommended.

    • May decrease overall duration and severity of disease.

    • Often used for symptom relief. However, may need more than a single dose for symptom relief.

    • Thus, need to consider potential for systemic immunosuppression during EBV infection known to be linked to malignancies.

  • Educate.

    • Contagiosity.

      • Avoid intimate contact, and sharing of toothbrushes, linens, and utensils.

      • EBV is often found in the saliva of healthy people who spread the virus intermittently throughout their lives, thus transmission is almost impossible to prevent.

      • EBV transmission does not normally occur through air or blood.

      • EBV spreads from those with active disease to healthy individuals may last several weeks after clinical resolution.

    • Steroid side effects—avoidance of alcohol and NSAIDs is recommended during treatment with steroids, to reduce the possibility of gastritis.

Other Considerations:

  • Approximately 10% of cases that present with features of IM are not induced by EBV (mono-like illness). Other pathogens that can induce a mono-like illness include cytomegalovirus, adenovirus, and toxoplasmosis.

  • Splenic rupture:

    • How common—rare, 0.1% of all cases.

    • When—most common, 2 to 21 days after symptom onset; no reports of spleen rupture (in medical literature) after 7 weeks of symptom onset.

    • Is there a difference between traumatic and spontaneous rupture?—no

    • Is there a correlation between severity of illness and likelihood of spleen rupture?—no

    • Can the spleen rupture in a “mono-like illness”?—yes.

    • Should all athletes with IM get an ultrasound examination during illness or prior to “return to play”?—no. Recommendation based on:

      • limited clinical value of obtaining only one ultrasound.

      • “high cost” for serial ultrasounds. Routine ultrasound evaluation of all individuals with IM would, cost ˜1 million dollars to prevent one rupture.

      • study that showed no difference in spleen size >30 days between IM and controls.

    • Yet, consider splenic ultrasound in selected cases to establish reduction in size—particularly, individuals involved in contact sports with prolonged splenic enlargement beyond 8 weeks.

    • CT or MRI is the study of choice to diagnose splenic rupture.

  • IM and ST have several overlapping features. Establishing the correct diagnosis is critical to prompt treatment, prevention of complications, and reducing “lost time from practice and competition.” Both illnesses can occur concurrently. Clinical and laboratory features highly suggestive of IM include the following.

    • Unusual fatigue.

    • Posterior cervical lymphadenopathy.

    • Hepatosplenomegaly.

    • IM-specific tests (noted above), elevated LFTs, lymphocytosis (total and atypical), neutropenia, thrombocytopenia.

  • EBV establishes a lifelong dormant infection in some cells of the body and may reactivate under certain circumstances.

  • Several features of HIV acute retroviral syndrome can mimic mononucleosis. Recommend HIV testing for athletes who

    • have mucocutaneous lesions; or

    • develop rash within 72 hours following the onset of fever (in the absence of concurrent use of antibiotics in an illness with clinical features suggestive for IM); and

    • have negative heterophile antibody test.

Return to Play Criteria:

  • May gradually reintegrate into “light,” “noncontact” activity at 4 weeks if laboratory studies and clinical examination are “entirely normal,” fluid and caloric intake are optimal, and there are no complicating features.

  • Reassess weekly following reintegration to light activity.

  • Typically, individuals can return to full activity in 6 to 8 weeks.

Recommended Readings

Aronson MD, Auwaerter PG. Infectious mononucleosis in adults and adolescents. UpToDate. Accessed October 29, 2012.

Asgari MM, Begos DG. Spontaneous splenic rupture in infectious mononucleosis: A review. Yale J Biol Med. 1997;70:175-182.

Burroughs KE. Athletes resuming activity after infectious mononucleosis. Arch Fam Med. 2000;9:1122-1123.

Candy B, Hotopf M. Steroids for symptom control in infectious mononucleosis. Cochrane Database Syst Rev. 2006;(3):CD004402.

Dommerby H, Stangerup SE, Stangerup M, Hancke S. Hepatosplenomegaly in infectious mononucleosis assessed by ultrasonic scanning. J Laryngol Otol. 1986;100:573-579.

Ebell MH. Epstein-Barr virus infectious mononucleosis. Am Fam Physician. 2004;70:1279-1287.

Epstein- Barr Virus and Infectious Mononucleosis. Retrieved from Accessed August 14, 2010.

Evans AS, Niederman JC, Cenabre LC, West B, Richards VA. A prospective evaluation of heterophile and Epstein-Barr virus-specific IgM antibody tests in clinical and subclinical infectious mononucleosis: Specificity and sensitivity of the tests and persistence of antibody. J Infect Dis. 1975;132:546-554.

Haines J Jr. When to resume sports after infectious mononucleosis. How soon is safe? Postgrad Med. 1987;81:331-333.

Hosey RG, Mattacola CG, Kriss V, Armsey T, Quarles JD, Jagger J. Ultrasound assessment of spleen size in collegiate athletes. Br J Sports Med. 2006;40:251-254.

Kinderknecht JJ. Infectious mononucleosis and the spleen. Curr Sports Med Rep. 2002;1:116-120.

Luzuriaga K, Sullivan JL. Infectious mononucleosis. N Engl J Med. 2010;362:1993-2000.

Maki D, Reich R. Infectious mononucleosis in the athlete. diagnosis , complications, and management. Am J Sports Med. 1982;10(3): 162-173.

Niu MT, Stein DS, Schnittman SM. Primary human immunodeficiency virus type 1 infection: Review of pathogenesis and early treatment intervention in humans and animal retrovirus infections. J Infect Dis. 1993;168:1490-1501.

Roy M, Bailey B, Amre DK, Girodias JB, Bussières JF, Gaudreault P. Dexamethasone for the treatment of sore throat in children with suspected infectious mononucleosis: A randomized, double-blind, placebo-controlled, clinical trial. 2004;158:250-254.

Peritonsillar Cellulitis/Abscess

Introduction (Definitions/Classification): A peritonsillar abscess (PTA or “quinsy”) is the most common infection of the head and neck in adults. An acute pharyngitis causes local inflammation or cellulitis which compresses nearby salivary ducts. Complete obstruction leads to an abscess. The etiology is polymicrobial with a predominance of GAS although Fusobacterium necrophorum is much more widespread than previously thought in adolescents and young adults.

History and Physical Examination: History of recent pharyngitis or tonsillitis is common. Inquire about recurrent infections, previous abscesses, and symptoms concerning for airway compromise.

Presenting signs and symptoms:

  • Sore throat, usually unilateral.

  • Muffled or “hot potato” voice.

  • Trismus.

  • Fever.

  • Dysphagia/odynophagia.

  • Otalgia (ipsilateral).

  • Drooling/salivary collections.

  • Contralateral uvular deviation.

Complications include the following.

  • Airway constriction/obstruction.

  • Aspiration pneumonitis or pulmonary abscess, if abscess ruptures.

  • Bacteremia.

  • Vascular complications—internal jugular thrombosis, erosion of carotid sheath, and hemorrhage.

  • Poststreptococcal complications—rheumatic fever, TSS, glomerulonephritis.

  • F. necrophorum causes Lemmiere syndrome (an anaerobic septicemia with higher morbidity and mortality than rheumatic fever).

  • Mediastinitis.

  • Necrotizing fasciitis.

Diagnosis: Consider imaging for epiglottitis, retropharyngeal abscess, or airway compromise, which assists in diagnosing cellulitis versus an abscess in setting of limited physical examination.

  • Imaging:

    • Plain radiographs—lateral view to rule out epiglottitis.

    • Ultrasound—transcutaneous or intraoral.

    • CT with IV contrast (preferred)—distinguishes cellulitis from PTA, quantifies spread of infection.

    • MRI—superior to CT if complications suspected (thrombus or erosion into vasculature); disadvantageous for patients with respiratory compromise.

  • Laboratory tests:

    • Leukocytosis with a left shift (polymorphonuclear predominance).

    • Electrolyte disarray if decreased oral intake secondary to dysphagia.

    • Throat culture for GAS.

    • Gram stain, aerobic and anaerobic cultures with sensitivities of any aspirate.

If individual is stable without signs of airway compromise, a 24-hour trial of antibiotics may distinguish cellulitis (improvement) from PTA (no improvement).


  • Prompt treatment is imperative to avoid serious complications.

  • Antibiotics—14-day course.

    • Parenteral antibiotics.

      • Ampicillin-sulbactam.

      • Clindamycin.

        (Add vancomycin to either regimen if rapid improvement is not noted).

    • Transition to oral regimen when clinically improved and afebrile.

      • Amoxicillin-clavulanate.

      • Clindamycin.

        (Linezolid may be added if vancomycin was required).

  • F. necrophorum—aggressive treatment with antibiotics. Avoid macrolides.

  • Supportive care.

    • Maintain hydration.

    • Pain control—acetaminophen.

  • For confirmed PTA:

    • Needle aspiration.

    • Incision and drainage.

    • Quinsy tonsillectomy—less common.

  • Evidence for use of steroids to shorten duration of infection is inconclusive.

Other Considerations:

  • Rule out epiglottitis, retropharyngeal and parapharyngeal abscess/cellulitis, and severe tonsillopharyngitis.

  • Despite drainage, recurrence is 10% to 15%.

  • The presence of a PTA in children or young adults pose greater risk of airway compromise given the more compact nature of their oropharynx. Consider hospitalization.

Return to Play:

  • Reintegration into activity after clinically asymptomatic, afebrile, and on a suitable oral antibiotic regimen.

  • Monitor closely for airway symptoms including resolution of neck swelling, presence of new airway hyperresponsiveness or cough, which may indicate incomplete resolution or recurrence.

Recommended Readings

Brodsky L, Sobie SR, Korwin D, Stanievish JF. A clinical prospective study of peritonsillar abscess in children. Laryngoscope. 1988;98: 780-783.

Centor R. Expand the pharyngitis paradigm for adolescents and young adults. Ann Intern Med. 2009;151(11):812-815.

Galioto NJ. Peritonsillar abscess. Am Fam Physician. 2008;77(2):199-202.

Goldenberg D, Golz A, Joachims HZ. Retropharyngeal abscess: A clinical review. J Laryngol Otol. 1997;111(6):546-550.

Johnson RF, Stewart MG, Wright CC. An evidence-based review of the treatment of peritonsillar abscess. Otolaryngol Head Neck Surg. 2003;128(3):332-343.

Ozbek C, Aygenc E, Tuna EU, Selcuk A, Ozdem C. Use of steroids in the treatment of peritonsillar abscess. J Laryngol Otol. 2004; 118(6):439-442.

Page C, Biet A, Zaatar R, Strunski V. Parapharyngeal abscess: diagnosis and treatment. Eur Arch Otorhinolaryngol. 2008;265(6):681-686.

Steyer TE. Peritonsillar abscess diagnosis and treatment. Am Fam Physician. 2002;65(1):93-96.

Wald ER. Peritonsillar cellulitis and abscess. UpToDate. Accessed October 16, 2012.

Yellon RF. Head and neck space infections. In: Bluestone CD, Casselbrant ML, Stool SE, et al. eds. Pediatric Otolaryngology. 4th ed. Philadelphia, PA: Saunders; 2003:1681-1701.

Figure 120. Mouth

Section 5: Cardiopulmonary

Exertional Dyspnea

Introduction (Definitions/Classification):

  • Breathing discomfort or difficulty with increased activity that varies in intensity.

  • A common symptom that can be influenced by psychological, physiologic, environmental, and social factors.

  • May be secondary to dysfunction of cardiovascular, respiratory, gastrointestinal, musculoskeletal, and/or metabolic systems.

  • Two common causes of exertional dyspnea in athletes include the following:

    • Exercise-induced bronchoconstriction (EIB).

      • Airway constriction with or without underlying asthma.

      • Exercise is a trigger for EIB in those with underlying asthma.

      • More common in elite athletes participating in endurance sports, especially in winter sports (cross-country skiing, figure skaters, or ice hockey).

    • Paradoxical vocal cord motion (PVCM) or vocal cord dysfunction (VCD).

      • Inappropriate movement (paradoxical adduction) of vocal cords during inspiration or expiration resulting in airway obstruction.

      • Most frequently noted in females between 20 and 40 years old.

  • Clinical distinction of these two etiologies (which may have similar clinical features) is critical for adequate management (see figure for summary).

  • Differentiation of these two etiologies from occult, congenital, or acquired cardiac disease is critical for prevention of SCD in athletes.

Exercise-induced Bronchoconstriction

History and Physical Examination:

  • History:

    • Past medical history:

      • EIB, asthma, allergic rhinitis, atopy, gastroesophageal reflux disease (GERD), smoking, second-hand smoke, irritant inhalation.

        • Athletes most affected have persistent, unidentified, or inadequately controlled asthma.

        • About 40% to 50% of athletes with allergic rhinitis also have EIB.

        • EIB can occur in 10% without a history of asthma or atopy.

    • Family history:

      • Inquire about congenital heart disease, pulmonary diseases, and SCD in relatives <50 years of age.

    • Symptoms:

      • Clinical manifestations are highly variable ranging from little impairment to severe bronchospasm.

      • Cough, chest tightness, shortness of breath, wheezing, activity avoidance, and diminished exercise tolerance.

      • Timing:

        • Symptoms typically commence ˜3 to 8 minutes after the start of exercise, peak at 10 to 15 minutes after exercise cessation, and can last approximately 30 minutes (“locker room” cough).

      • “Refractory period”:

        • For ˜4 hours after exercise during which symptoms are diminished or completely absent.

  • Physical examination:

    • Heart: Tachycardia.

    • Lungs: Tachypnea and expiratory wheezing, but often unremarkable at rest.

    • HEENT: Boggy and edematous nasal mucosa, especially in athletes with atopy.


  • Predictive value of history and physical evaluation is poor.

    • Sixty-one percent of EIB-positive athletes and 45% of athletes with normal testing report symptoms.

    • Thus, pulmonary function tests (PFTs) for clinical suspicion of EIB is highly recommended.

  • Exercise challenge (6 minutes on treadmill at 80% to 85% maximum HR).

    • FEV1 >15% drop from baseline indicative of EIB.

    • Spirometry before and after beta-agonist therapy.

    • False-negatives common with environmental stress and inadequate exercise intensity.

  • Bronchoprovocation challenge tests (for athletes with symptoms of asthma, normal PFTs and poor response to bronchodilator therapy):

    • Pharmacologic.

      • Mannitol inhalation challenge.

      • Methacholine inhalation challenge.

    • Eucapnic voluntary hyperpnea (EVH).

      • In athletes with negative pharmacologic tests.

      • Recommended by the International Olympic Committee-Medical Commission (IOC-MC).

  • Differential diagnosis pearls:

    • In the absence of an established diagnosis of EIB, exertional dyspnea may be induced by cardiovascular, pulmonary, or gastroenterologic etiologies remote from asthma.

    • Occult cardiac diseases can induce SCD (arrhythmias, cardiac shunts, and cardiomyopathy).

    • Other common mimickers include PVCM, allergic rhinitis, GERD, laryngeal dysfunction (tracheomalacia, laryngomalacia), psychological etiologies, and seeking behaviors for performance enhancement drugs (PEDs).

    • Association of EIB and GERD is debated and probably nonexistent.


  • Nonpharmacologic.

    • Avoidance of triggers: Dry and cold air exposure, chlorine (swimming pool), pollen, animal dander, molds, house dust mites, cigarette smoke, and airborne pollutants/chemicals.

    • Breathing through a mask or loose-fitting scar in cold and dry environments.

    • Adequate warm-up prior to exercise.

    • Educate on nasal breathing and correct use of inhalers to maximize pharmacologic efficacy.

    • Diets rich in omega-3 fatty acids may have protective anti-inflammatory effects in asthmatics with EIB.

  • Pharmacologic.

    • Beta-agonists.

      • Intermittent, prophylactic beta-agonists are most effective for EIB.

      • Rapid-acting beta-agonists (albuterol/formoterol) 10 minutes before exercise is effective for prophylaxis.

      • Consider long-acting beta-agonists (salmeterol/formoterol) in those who exercise on an intermittent basis daily.

        • Monotherapy may be ineffective with chronic use.

        • Thus, combine with inhaled glucocorticoid, cromolyn sodium, or anti-leukotrienes.

    • Inhaled glucocorticoids.

      • Effective for refractory EIB.

      • Do not improve EIB acutely, yet offer favorable control of EIB following several weeks to months of compliant therapy.

    • Mast cell stabilizers (cromoglycates).

      • Effective when combined with beta-agonists in high-performance athletes exercising in extreme conditions.

      • Do not independently relieve bronchoconstriction.

    • Leukotriene antagonists.

      • Once daily dose provides protection from EIB for ˜12 hours.

      • Protects against EIB within 2 hours of administration.

      • Enhances postexercise recovery.

      • Superior to long-acting beta-agonists.

Other Considerations:

  • Miscellaneous “key” facts:

    • EIB may lead to a severe asthma exacerbation and respiratory compromise requiring emergent care.

    • Health professionals should be prepared and equipped for intervention. Devices that monitor pulmonary function, rescue inhalers, and nebulizers should be available for emergent use.

    • Rapid breathing without wheezing may be a presenting sign of exertional sickling collapse or underlying cardiac disease. Thus, not safe to assume that all rapid breathing is EIB.

    • Drug interactions:

      • Beware of potential additive effects of sympathomimetic drugs.

      • Beta-agonists + stimulant medications for attention deficit hyperactivity disorder (e.g., amphetamines) + over-the-counter decongestants (e.g., PSE) can potentially induce arrhythmias.

  • Doping considerations:

    • Be aware of USADA and World Anti-doping Agency (WADA) guidelines. Monitor websites for changes annually.

    • Recommend carrying “USADA Wallet Card” in medical kit for quick reference.

    • When in doubt, USADA resources include the following:

    • Current pharmacologic guidelines summary:

      • Beta-agonists.

        • Most prohibited in- and out-of-competition.

        • Albuterol (<1600 mcg per 24 hours), formoterol (<54 mcg per 24 hours), and salmeterol are permitted in- and out-of-competition.

      • Glucocorticoids.

        • Inhaled: Permitted in- and out-of-competition.

        • Oral: Prohibited in- and out-of-competition.

      • Mast cell stabilizers (cromoglycates).

        • Permitted in- and out-of-competition.

      • Leukotriene antagonists.

        • Permitted in- and out-of-competition.

Return to Play:

  • Established diagnosis and stable-management protocol.

  • Able to exercise without breathing difficulty or discomfort.

  • Modify activity until peak expiratory flow is at least 80% of personal best.

  • Recommend reporting medications to USADA and WADA to obtain therapeutic exemption (TUE), as needed, prior to competition.

Paradoxical Vocal Cord Motion or Vocal Cord Dysfunction

History and Physical Examination:

  • History:

    • Past medical history:

      • Studies have shown that PVCM is associated with underlying psychosocial disorders including anxiety, childhood sexual abuse, posttraumatic stress disorder, depression, and/or personality disorders).

      • Other potential associations include GERD (LPR variant), inhalation of irritants (smoke, dust, cleaning chemicals), recent trauma, and/or surgery (postoperative phase).

      • Exercise itself, without any other underlying etiology, may be the sole precipitant of PVCM.

    • Symptoms:

      • Often normal at rest.

      • Cough (most common), choking, dyspnea, dysphagia, throat tightness, anxiety, perioral cyanosis, dysphonia, inspiratory or expiratory stridor (as opposed to expiratory wheezing in EIB).

    • Timing and duration varies.

      • Symptoms begin and peak during exercise.

      • Resolution of symptoms typically occurs within a few minutes after cessation of exercise.

  • Physical examination:

    • Heart: Tachycardia.

    • Lungs: Tachypnea and inspiratory stridor above the cricoid cartilage which decrease over the lung fields.

    • Skin: Possible perioral cyanosis during episode.


  • “Gold standard” test is fiberoptic laryngoscopy, yet typically difficult to perform during episode (secondary to logistics).

    • Vocal cord adduction is commonly seen only during acute episodes.

    • Yet, may be induced by asking athlete to “mimic” an attack of PVCM.

    • Methacholine challenge in conjunction with laryngoscopy:

    • To verify that inadequate airflow is secondary to PVCM.

  • PFTs.

    • Normal spirometry in most individuals.

    • Flow-volume curve assessment:

      • Typically normal between episodes of PVCM.

      • May show flattening of inspiratory loop.

      • Increased proportion of forced expiratory flow to forced inspiratory flow at half the athlete’s vital capacity.

  • Arterial blood gas, chest x-rays (CXRs), and lung volumes are typically normal.

  • Differential diagnosis pearls:

    • Asthma.

      • Typically responds to beta-agonist therapy.

    • Angioedema of the larynx induced by anaphylaxis.

      • Monitor for associated symptoms/signs of anaphylaxis.

    • Vocal cord paralysis.

      • Herpes simplex infection induced polycranial neuropathy.

      • Vagal or recurrent laryngeal nerve injury.


  • Nonpharmacologic.

    • Reassurance and supportive care are usually sufficient.

    • “Panting” may help abort an active episode.

    • Continuous positive airway pressure (CPAP) and intermittent positive pressure ventilation (IPPV) may be helpful.

    • Prevention better than cure.

      • Speech language pathology (SLP) therapy has a 90% response rate.

        • Relaxing and breathing exercises.

      • Psychological counseling (as indicated).

  • Pharmacologic.

    • Inadequate data.

    • Heliox (helium oxygen) inhalation may be beneficial.

    • Buspar may be beneficial in athletes with a psychosocial history (anecdotal evidence).

    • Prophylactic anticholinergic (ipratropium) may be beneficial (limited data).

    • Severe cases of PVCM may be amenable to intralaryngeal injection of botulinum toxin type A.

Other Considerations:

  • Rarely, athletes may have respiratory distress substantial enough to require endotracheal intubation.

  • PVCM can co-occur with asthma.

  • A facemask that provides resistance during inspiration may be helpful in reducing inspiratory stridor and may therefore provide both physiologic and psychological benefits.

Return to Play:

  • Established diagnosis and stable-management protocol.

  • Cardiac etiologies that may induce SCD are excluded.

  • Athlete is able to exercise without breathing difficulty or discomfort.

Recommended Readings

Anderson SD, Argyros GJ, Magnussen H, Hozer K. Provocation by eucapnic voluntary hyperpnoea to identify exercise induced bronchoconstriction. Br J Sports Med. 2001;35(5):344-347.

Archer GJ, Hoyle JL, Cluskey AM. Inspiratory vocal cord dysfunction, a new approach in treatment. Eur Respir J. 2000;15:617-618.

Corren J, Newman KB. Vocal cord dysfunction mimicking bronchial asthma. Postgrad Med. 1992;92:153-156.

Doshi DR, Weinberger MM. Long-term outcome of vocal cord dysfunction. Ann Allergy Asthma Immunol. 2006;96:794-799.

Edelman JM, Turpin JA, Bronsky EA, et al. Oral montelukast compared with inhaled salmeterol to prevent exercise-induced bronchoconstriction. A randomized, double-blind trial. Exercise Study Group. Ann Intern Med. 2000;132:97-104.

Gavin LA, Wamboldt M, Brugman S, Roesler TA, Wamboldt F. Psychological and family characteristics of adolescents with vocal cord dysfunction. J Asthma. 1998;35:409-417.

Inman MD, O’Byrne PM. The effect of regular inhaled albuterol on exercise-induced bronchoconstriction. Am J Respir Crit Care Med. 1996;153:65-69.

Irwin CG. Bronchoprovocation testing. UpToDate. Accessed March 2, 2013.

Maillard I, Schweizer V, Broccard A, Duscher A, Liaudet L, Schaller M. Use of botulinum toxin type to avoid tracheal intubation or tracheostomy in severe paradoxical vocal cord movement. Chest. 2000;118(3):874-876.

Mickleborough TD, Lindley MR, Ionescu AA, Fly AD. Protective effect of fish oil supplementation on exercise-induced bronchoconstriction in asthma. Chest 2006;129:39-49.

National Asthma Education and Prevention Program: Expert panel report III: Guidelines for the diagnosis and management of asthma. Bethesda, MD: National Heart, Lung, and Blood Institute, 2007. NIH publication no. 08-4051. Accessed on September 10, 2012.

O’Byrne PM. Exercise-induced bronchoconstriction. UpToDate. Accessed March 2, 2013.

Pitchenik AE. Functional laryngeal obstruction relieved by panting. Chest. 1991;100:1465-1467.

Powell SA, Nguyen CT, Gaziano J, Lewis V, Lockey RF, Padhya TA. Mass psychogenic illness presenting as acute stridor in an adolescent female cohort. Ann Otol Rhinol Laryngol. 2007;116:525-531.

Saxon KG, Shapiro J. Paradoxical vocal cord motion. UpToDate. Accessed March 2, 2013.

Sullivan MD, Heywood BM, Beukelman DR. A treatment for vocal cord dysfunction in female athletes: An outcome study. Laryngoscope. 2001;111:1751-1755.

United States Anti-doping Agency Accessed March 2, 2013.

Weir M. Vocal cord dysfunction mimics asthma and may respond to heliox. Clin Pediatr (Phila). 2002;41:37-41.

World Anti-doping Agency Accessed March 2, 2013.


Introduction (Definitions/Classification): An acute, typically “self-limited” viral illness caused by either Influenza A or B.

History and Physical Examination:

  • Can present with either or both, upper and lower respiratory tract symptoms and signs.

  • Incubation period is 1 to 4 days.

  • Abrupt onset of symptoms including fever (>100°F), headache, malaise, myalgias (usually back and neck), sore throat, and cough (with or without sputum).

  • Aside from fever, physical examination is usually benign in uncomplicated influenza. Physical findings may include pharyngeal erythema and/or shotty cervical lymphadenopathy.

  • Symptoms after 5 to 7 days including persistent fever, cough with sputum, tachypnea, tachycardia, cyanosis, and constitutional symptoms signify either “secondary” viral (severe) or bacterial pneumonia.

    • Consider secondary methicillin-resistant S. aureus (CA-MRSA) in individuals who initially improve and then relapse with high fever, purulent sputum, and infiltrates on CXR.


  • Signs/symptoms on physical examination (during the flu season).

  • Laboratory testing:

    • Rapid influenza diagnostic tests (RIDTs).

      • Sensitivity = 40% to 70%; specificity = 90% to 95%; thus, false-negative rates common.

      • During the flu season, rapid tests for influenza have the same sensitivity as clinical diagnosis and are usually unnecessary in otherwise, “low-risk,” healthy individuals.

  • More tests:

    • Reverse transcription polymerase chain reaction (RT-PCR), viral culture, and immunofluorescence are accurate, yet take long to complete.

  • Obtain CXR in all individuals with fever >100°F, respiratory rate >24, and pulse >100 who first improve and relapse.

  • Sputum cultures are usually unnecessary except for individuals with secondary pneumonia diagnosed with a CXR.


  • By prevention—immunize athletes (if desired by individuals).

  • Most cases improve with symptomatic treatment including Tylenol, NSAIDs, cough suppressants, and decongestants.

  • Antiviral therapy pearls.

    • Do not wait for laboratory confirmation to initiate treatment.

    • Most effective when used within first 24 to 30 hours of symptoms, especially in those with fever.

    • May reduce complications and mortality.

    • Either oseltamivir (75 mg twice daily) or zanamivir (10 mg; two inhalations twice daily) for 5 days in “high-risk” groups.

    • Zanamivir not recommended in individuals with underlying asthma.

    • Due to resistance patterns, amantadine and rimantadine should not be used in the United States.

  • When necessary, guided by sputum gram stain and culture, antibiotics for secondary bacterial pneumonia.

    • Options for “non-CA-MRSA” outpatient:

      • Azithromycin or clarithromycin: No recent antibiotic use, local resistance patterns, or risk for QT-interval prolongation.

      • Moxifloxacin or levofloxacin (monotherapy) or combination (beta-lactam + doxycycline): If nonpregnant, recent antibiotic use, local resistance patterns, or risk for QT-interval prolongation.

    • For “CA-MRSA” pneumonia—vancomycin.

  • Educate.

    • Information regarding flu can be obtained at

    • Medical providers to access weekly CDC updates on influenza activity during flu—

    • Treatment with either oseltamivir or zanamivir “does not cure,” yet “shortens duration of symptoms” by 1 to 3 days.

    • Information on pre- and postexposure chemoprophylaxis can be obtained at Regimens include either oseltamivir (75 mg daily) or zanamivir (10 mg; two inhalations daily).

    • Oseltamivir can induce transient neuropsychiatric symptoms including delirium and self-injury.

    • “Peak” viral shedding occurs during the first 2 days of illness.

    • Infection is transmitted by droplet contact, therefore, imperative to cover the mouth during coughing.

    • Encourage individuals to stay home until symptoms have improved and to wear a face mask for 5 days after onset of illness.

    • Avoid aspirin in children <17 years of age to prevent potential Reye syndrome.

    • Restrict use of oral decongestants in hot weather, and with other medications, including yet not limited to, stimulant medications for attention deficit-hyperactivity disorder, thyroid replacement, or bronchodilators.

Other Considerations:

  • Secondary viral and bacterial (CA-MRSA) pneumonia can be life threatening even in adolescents. Yet, secondary bacterial pneumonia can be induced by non-MRSA pathogens (S. pneumoniae most common).

  • Use CURB-65 score for decision to admit for pneumonia (0 to 1—low severity, outpatient; 2—moderate severity, consider admission; 3 to 5—high severity, admit).

    • Confusion (new disorientation to person, place, or time; or based on specific mental tests).

    • Urea (blood urea nitrogen in the United States) >20 mg/dL.

    • Respiratory rate >30 breaths/minute.

    • BP (systolic <90 mm Hg or diastolic <60 mm Hg).

    • Age >65 years.

  • Consider myositis in younger individuals with muscular tenderness, swelling, decreased strength, and elevated creatine kinase. Obtain urinalysis for myoglobin and basic metabolic panel to assess renal function.

  • Influenza can also induce complications of other systems.

    • Central nervous—aseptic meningitis, encephalitis, Guillain-Barré syndrome.

    • Cardiovascular—pericarditis, myocarditis.

    • TSS.

Return to Play Criteria:

  • Improving symptoms and signs.

  • No cough, fever, tachycardia, or tachypnea.

  • Normal musculoskeletal examination.

Recommended Readings

Centers for Disease Control and Prevention (CDC). Severe methicillin-resistant Staphylococcus aureus community-acquired pneumonia associated with influenza—Louisiana and Georgia, December 2006-January 2007. MMWR Morb Mortal Wkly Rep. 2007;56: 325-329.

Dolin R. Clinical manifestations of seasonal influenza in adults. UpToDate. Accessed November 4, 2012.

File TM Jr. Treatment of community-acquired pneumonia in adults in the outpatient setting. UpToDate. Accessed August 30, 2010 and November 4, 2012.

Fiore AE, Fry A, Shay D, et al. Antiviral agents for the treatment and chemoprophylaxis of influenza—recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2011;60:1-24.

Fiore AE, Shay DK, Broder K, et al. Prevention and control of influenza: Recommendations of the Advisory Committee on Immunization Practices (ACIP), 2008. MMWR Recomm Rep. 2008;57:1-60.

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Jul 9, 2020 | Posted by in SPORT MEDICINE | Comments Off on Primary Care Medicine
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