Infections of the Temporal Bone





Chondritis, Perichondritis, and Cellulitis of the Auricle



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  • Spectrum of disease from mild superficial skin infection to chondritis.



  • Cellulitis is an infection of the skin of the auricle.



  • Perichondritis and chondritis are infections of the auricular perichondrium and cartilage, respectively.



  • Bacterial infections typically result from blunt or penetrating trauma, or extension of infectious otitis externa (OE).



  • Superficial infections commonly related to Staphylococcus and Streptococcus.



  • Deeper infections often involve Pseudomonas.




Etiology





  • Trauma—most common cause



  • Blunt trauma (assault, wrestling) resulting in hematoma and secondary infection



  • Penetrating trauma—bites, knives, foreign, body, firearms



  • Ear piercing—transcartilagenous piercings



  • Iatrogenic—otologic surgery



  • Extension of OE



  • Extension of subperiosteal abscess



  • Rule out:




    1. Relapsing perichondritis—autoimmune condition that involves the cartilage and spares the lobule from inflammation



    2. Cutaneous lymphoma



    3. Gouty tophus




Physical Examination





  • Pain and erythema common in cellulitis, perichondritis, and chondritis.



  • Induration and edema typical for chondritis and perichondritis.



  • Induration usually not seen with cellulitis.



  • Hematoma with or without abscess formation—fluctuation present with abscess.



  • Cartilage deformity (“cauliflower ear”) in chronic or recurrent infections and in advanced or untreated cases.



  • Fever, chills, and elevated white blood cell count can be seen.




Diagnosis and Pathogens





  • Diagnosis made on clinical grounds



  • Cellulitis of the auricle typically due to Staphylococcus spp



  • Pseudomonas spp most common cause of perichondritis and chondritis




    1. Most commonly cultured organism from auricular abscess



  • Incision and drainage with culture when possible



  • Other rare bacteria—Escherichia coli and Proteus spp



  • Erysipelas caused by beta-hemolytic Streptococcus




    1. Auricle typically erythematous, indurated, and painful



    2. Infection typically follows a well-demarcated border




Treatment





  • Mild infections




    1. Oral anti-staphylococcal and anti-streptococcal antibiotics



  • Severe infection or immunocompromised patient




    1. IV anti-staphylococcal, anti-streptococcal, and anti-pseudomonal antibiotics



  • Perichondritis or chondritis




    1. Involvement of cartilage with inflammation or abscess can result in cosmetic deformity (cauliflower ear)



    2. Goal of treatment: rapid diagnosis and initiation of therapy, maximize aesthetic outcome



    3. No abscess—oral antibiotics with anti-pseudomonal coverage (fluoroquinolone)



    4. Abscess—incision and drainage with cartilage debridement as needed



    5. Antibiotic therapy for 2 to 4 weeks



    6. Placement of bolsters as needed





Viral Processes of the Auricle



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Herpes Zoster



Etiology





  • Thought to occur following viral reactivation within ganglion nerve cells



  • Can result following insult due to direct trauma, dental work, or upper respiratory infection (URI)



  • Most commonly seen in the elderly and immunocompromised




Signs and Symptoms





  • Often includes prodrome of otalgia which precedes vesicular eruption.



  • Vesicles in the external auditory canal (EAC) and conchal bowl.



  • May included tinnitus, hearing loss, vertigo, decreased lacrimation (associated ganglion).



  • Facial paralysis with Herpes Zoster Oticus is known as Ramsay Hunt Syndrome.



  • Other cranial neuropathies (V, IX, X, XI, XII) can be seen.




Diagnosis and Pathogens





  • Tzanck smear to look for multinucleated giant cells at the base of ruptured vesicle




    1. Differential diagnosis includes: herpes zoster, herpes simplex, cytomegalovirus (CMV), and pemphigus vulgaris



  • Viral antibody titers



  • Assess for evidence of herpetic keratitis with eye complaints




Treatment





  • Prognosis for facial nerve paralysis in Ramsay Hunt Syndrome is worse than Bell palsy (only 60% regain normal function).



  • High-dose steroids (1 mg/kg/d for 14 days) in cases of facial nerve paralysis and/or sensorineural hearing loss (SNHL).



  • Antiviral (valacyclovir 1000 mg every 8 hours × 7 days).



  • Surgical decompression not advocated as neural degeneration widespread rather than localized to geniculate ganglion and labyrinthine segment as in Bell palsy.



  • Gabapentin can be used for post-herpetic neuralgia.





Fungal Infections of the Auricle



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Etiology





  • Can be primary or secondary (manifestation of disseminated fungal infection)



  • Geographic location, particular hobbies (rose handling, etc.) may aid in diagnosis



  • More common in immunocompromised patients




Signs and Symptoms





  • Often difficult to distinguish from bacterial cellulitis



  • Pruritus



  • Hearing loss



  • Otalgia (often dull and mild)



  • Erythematous and edematous skin similar to bacterial cellulitis



  • Multisystem disease present in disseminated disease




Diagnosis





  • High index of suspicion—consider if cellulitis unresponsive to antibiotics



  • Fungal smear and culture—may require tissue biopsy to identify organism



  • Fungal serologic titers and chest X-ray if systemic disease suspected




Pathogens





  • Most common are Aspergillus and Candida species



  • Histoplasma



  • Mucormyces



  • Coccidiomyces



  • Blastomyces



  • Dermatophyses



  • Sporothrix species




Treatment





  • Topical antifungals for mild infection



  • IV therapy for severe or disseminated disease



  • Consider infectious disease consultation





Rare Pinna Infections



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Parasites





  • Cutaneous leishmaniasis



  • Scabies




Mycobacterium





  • Leprosy (Mycobacterium leprae)



  • Cutaneous tuberculosis





External Auditory Canal



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Bacterial



Acute Otitis Externa (AOE) (Swimmer’s ear, tropical ear)





  • Furuncle is a localized abscess of the apopilosebaceous unit.



  • Rupture of furuncle may result in more diffuse cellulitis and AOE.




Etiology




  • Associated with warm, humid climates.



  • Common in swimmers.



  • Most common in children 5 to 10 years old.



  • Maceration of EAC skin allows invasion of skin commensal bacteria to the apopilosebaceous unit.




    1. Trauma to skin from cotton tip applicators or other instrumentation.



    2. Chronic skin conditions (eczema, psoriasis, seborrhea dermatitis).



    3. Devices that occlude EAC (hearing aids, earbuds)




Risk Factors




  • Immunosuppression



  • Congenitally narrow EAC with poor self-cleaning ability



  • Obstructive exostoses



  • Lack of cerumen




    1. Antibacterial properties (acidic, lysozymes, antibodies)



    2. Hydrophobic—repels water



    3. Traps debris



  • History of external beam radiation




Signs and Symptoms




  • Rapid onset (< 48 hours)



  • Generally unilateral



  • Pain—often severe, extreme tenderness to manipulation



  • “Tragal sign”—pressure on the tragus induces extreme pain



  • Pruritus



  • Otorrhea—often purulent



  • Fever is rare unless significant periauricular cellulitis




Physical examination




  • Erythema



  • Edema—may result in near complete occlusion of EAC



  • Tympanic membrane (TM) mobility normal (vs suppurative otitis media)



  • Lymphadenopathy of the preauricular or cervical lymph nodes




Pathogens




  • Bacterial infections account for 90% of AOE (see later for fungal AOE)



  • Most commonly Pseudomonas aeruginosa



  • Also Staphylococcus aureus, Staphylococcus epidermidis, and other gram-negative rods




Treatment




  • Goals include pain control, aural toilet, and topical therapy.



  • Debridement of EAC allows penetration of ototopical therapy.



  • Otowick may be necessary in cases with obstructive edema.




    1. Allows ototopical drops to penetrate to medial EAC tissue



    2. Replaced every 3 to 5 days to avoid toxic shock syndrome



  • Maintain dry ear precautions with bathing.



  • Ototopical treatments:




    1. Mild disease—irrigation with acidifying agent (dilute vinegar, acetic acid) may be sufficient.



    2. Moderate to severe disease—topical antibiotics with or without steroid.




      • Provides high concentration of medication without systemic absorption.



      • Examples include neomycin, ciprofloxacin, ofloxacin, and tobramycin.



      • Frequently effective in treatment of periauricular cellulitis.



      • Neomycin can cause dermatitis in some patients—consider switching agents with lack of response.



  • Oral antibiotics




    1. Not effective in uncomplicated AOE.



    2. May be considered for severe periauricular cellulitis or immunocompromised patients.



  • Incision and drainage




    1. Used for furuncles or carbuncles.



    2. Treat similar to AOE after I&D.




Myringitis Uncommon infection of the TM



Acute Bullous Myringitis




  • Inflammation involving lateral surface of TM and medial portion of EAC wall



  • Typically associated with upper respiratory infections



  • More common in winter months



  • Can occur alone (primary) or with serous otitis media (secondary) in 30% to 40%




SIGNS AND SYMPTOMS




  • Severe pain lasting 3 to 4 days, then subsiding



  • Hallmark finding—bullae over the TM and medial canal filled with serous or serosanguinous fluid



  • Rupture of bullae can cause serosanguinous discharge



  • 60% can demonstrate mixed or SNHL that typically resolves




PATHOGENS




  • Mycoplasma pneumoniae used to be considered offending agent—not proven



  • Others—Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis




TREATMENT




  • Analgesics



  • Dry ear precautions



  • Lancing bullae for pain relief



  • Topical antibiotic/steroid drops to prevent bacterial superinfection



  • If associated with acute otitis media (AOM), treat accordingly




Chronic (Granular) Myringitis




  • Uncommon, prolonged, infection of the squamous surface of TM.



  • Characterized by loss of epithelium of TM and replacement with granulation tissue.



  • Relapsing and recurring symptoms are common.



  • Difficult to treat.




ETIOLOGY




  • Unclear, no predisposing factors identified




SIGNS AND SYMPTOMS




  • Painless, usually foul smelling otorrhea



  • Aural fullness



  • Pruritus



  • Conductive hearing loss due to thickening and blunting of the TM



  • Many patients can be asymptomatic




PHYSICAL EXAMINATION




  • Replacement of epithelium with granulation tissue (most commonly posterior superior quadrant)



  • Late stages—scarring of anterior EAC angle resulting in blunting or acquired EAC stenosis or obliteration



  • TM perforation common and frequently heals spontaneously



  • Middle ear (ME) normal




DIAGNOSIS




  • Diagnosis based on history and physical examination



  • May require computed tomography (CT) of temporal bone to rule out COM




PATHOGENS




  • Staphylococcus aureus



  • Pseudomonas aeruginosa



  • Proteus mirabilis




TREATMENT




  • Numerous treatment options have been described




    1. Ototopical antibiotics



    2. Drying agents (desiccation)



    3. Chemical cautery (silver nitrate or trichloroacetic acid)



    4. Laser ablation (CO2)



    5. Acidification with dilute vinegar irrigation



    6. Surgical removal of granulation tissue



  • Two most effective treatments: irrigation with dilute vinegar, surgical removal



  • Tympanoplasty with canalplasty reserved for severe obliterative disease



  • High rate of recurrence or exacerbation with surgery




Chronic Otitis Externa (COE)



Etiology




  • Several mechanisms have been proposed




    1. Allergen exposure (allergic reaction to topical agents, contact dermatitis)



    2. Systemic disease (ie, amyloid, sarcoid, psoriasis, Wegener)



    3. Chronic infection



    4. Local factors (seborrheic dermatitis, elevated pH, chronic moisture)



  • Leads to chronic inflammation within dermis and surrounding apocrine glands



  • Results in increased depth of rete pegs and loss of normal sebaceous glands




Signs and Symptoms




  • Pruritus



  • Mild discomfort but usually no otalgia



  • Aural fullness




Physical Examination




  • Thickened skin in cartilaginous canal



  • Mild to moderate erythema with clear, scant drainage



  • Keratosis—adherent skin debris



  • Lichenification



  • Canal obliteration in late stage—medal canal fibrosis




Diagnosis




  • Clinical findings



  • Biopsy chronic granulation tissue to rule out malignancy




Pathogens




  • Gram-negative species (ie, Proteus)



  • Fungus common (see below) (Aspergillus, Candida)




Treatment




  • Focused on reducing inflammation




    1. Dry ear precautions



    2. Avoidance of Q-tips



    3. Frequent, microscopic debridement of debris and dead skin



  • Topical therapy




    1. Acidification of EAC (vinegar and alcohol solution, acetic acid)



    2. Antifungal preparations (see later)



    3. Topical steroids when infection ruled out



    4. Topical immunosuppressant (ie, tacrolimus) described, not widely used



  • Elimination of underlying skin condition



  • Surgery




    1. Canalplasty with skin grafting




Skull Base Osteomyelitis (Malignant Otitis Externa [MOE], Necrotizing Otitis Externa [NOE])





  • Primarily seen in immunocompromised patients (diabetic, HIV, transplant)



  • Infection begins in soft tissues of EAC



  • Spreads via fissures of Santorini and to stylomastoid and jugular foramen via tympanomastoid suture line



  • High morbidity due to typical delay in treatment from symptom onset



  • Must have high index of suspicion



  • Mortality between 5% to 20% even in antibiotic era




Etiology




  • Microangiopathy and increased EAC pH leads to bacterial invasion of vessel walls



  • Causes vascular thrombosis



  • Coagulative necrosis of surrounding tissue




Signs and Symptoms




  • Severe, deep-seated and long-standing aural pain often worse at night



  • Otalgia often “out of proportion to examination findings”



  • Otorrhea



  • Ear canal edema



  • Hallmark—granulation tissue at isthmus of EAC (bony-cartilaginous junction)



  • Occasionally can involve lower cranial nerves (VII-XII)



  • Facial nerve most commonly affected (stylomastoid foramen involvement)



  • Multiple cranial neuropathies imply a worse prognosis



  • Septic thrombophlebitis of sigmoid sinus can occur resulting in “picket fence” pattern of fevers



  • Meningeal signs as infection moves intracranial




Diagnosis




  • Must biopsy granulation tissue to rule out malignancy



  • ESR typically elevated—nonspecific but can be used to follow treatment response and possible recurrence



  • Bacterial and fungal cultures




Imaging




  1. Nuclear medicine




    1. Technetium (Tc-99) scintigraphy imaging of choice to confirm diagnosis




      1. Concentrates in areas of osteoblastic activity



      2. High sensitivity for bone infection



      3. Test positive before CT visibly abnormal



      4. Single-photon emission computed tomography (SPECT) more sensitive than planar imaging



      5. Tc-99 remains in bone long after acute infection resolves—not used to track disease progress



    2. Gallium-67 or Indium-111 labeled leukocyte scan




      1. Shows areas of inflammatory cell activity



      2. Sensitivity increased with Tc-99 scan



      3. Used to follow treatment response as tests return to normal quickly



      4. Scan every 4 weeks during treatment



  2. CT




    1. Findings include bony erosion and soft tissue abnormalities around EAC



    2. Unable to distinguish infection from malignancy



    3. Significant bony erosion must occur before grossly abnormal on imaging



    4. Contrast not necessary unless concern for abscess



    5. Not useful in following response to treatment



  3. MRI




    1. Useful in detecting soft tissue changes and dural involvement




Pathogens




  • Pseudomonas aeruginosa accounts for more than 90% of cases



  • Staphyloccocus aureus, S. epidermidis, Proteus mirabilis, Klebsiella spp. also reported



  • Fluoroquinolone-resistant Pseudomonas increasing in incidence



  • Fungal MOE less common




    1. Associated with HIV+ patients



    2. Usually Aspergillus fumigatus




Treatment




  • Aggressive blood glucose control in diabetic patients.



  • Correct other causes of immunodeficiency if possible.



  • EAC debridement.



  • Surgical intervention warranted only for abscess drainage or debridement of bony sequestrum.



  • More heroic surgical measures necessary with recalcitrant disease.



  • Role of hyperbaric oxygen therapy is unproven for MOE.




ANTIBIOTIC THERAPY




  • Monotherapy with oral fluoroquinolone is first-line therapy.



  • Culture directed therapy when possible.



  • Advanced cases may require primary parenteral therapy.



  • Parenteral antipseudomonal aminopenicillins if unable to take fluoroquinolones.



  • Typical treatment duration of 6 weeks.



  • Treatment should continue until clinical examination normal.




    1. Can treat until Gallium-67 scan normalizes but may result in prolonged treatment




ANTIFUNGAL THERAPY




  • Parenteral antifungal therapy for culture positive disease



  • Amphotericin B commonly used, significant side effects



  • Voriconazole first-line therapy for invasive Aspergillosis




Fungal



Acute Fungal Otitis Externa (Otomycosis)



Etiology




  • 10% of all AOE



  • Warm, wet ear canal (swimmers, surfers, divers, tropical environments)



  • EAC trauma



  • Chronic moisture of ear canal (hearing aid users)



  • Fungal overgrowth in modified radical mastoid cavities



  • Immunocompromised patients




Signs and Symptoms




  • Same as acute bacterial OE.



  • Pruritus is more common than bacterial OE.



  • Fungal hyphae or fungal ball (“wet newspaper”) may be visible.



  • Otalgia and otorrhea may be present.




Diagnosis




  • Cultures not typically helpful



  • Biopsy in immunocompromised patients or atypical presentations




Pathogens




  • Aspergillus most common



  • Candida and Penicillium also seen




Treatment




  • Frequent aural toilet



  • Dry ear precautions



  • Acidifying and drying agents (ie, gentian violet, boric acid)



  • Topical antifungal agents first-line pharmacologic treatment




    1. Clotrimazole



    2. Cresylate otic



    3. Ketoconazole ointment



    4. CSF powder (chloromycetin, amphotericin B [Fungizone], sulfanilamide)



  • Systemic therapy reserved for refractory disease, immunocompromised patients with suspicion of invasive fungal disease




Keratosis Obturans and EAC Cholesteatoma



Keratosis Obturans





  • Abnormal accumulation of keratin in EAC.



  • Primarily seen in adults (30-60 years).



  • Theories for disease include abnormal epithelial migration and excessive production of epithelial cells in the EAC and on the TM.



  • Involves entire circumference of skin of the medial EAC.



  • Dense keratin plug forms in the EAC.



  • Can lead to conductive hearing loss from mechanical obstruction and/or thickening of TM and blunting of the annulus.



  • Severe pain.



  • Often associated with secondary AOE and otorrhea.



  • Most often involves both ears.



  • Disease progression can cause bony widening of the EAC and in severe cases auto-mastoidectomy.



  • Treatment




    1. Frequent aural toilet and debridement



    2. Lifelong cleanings may be necessary




EAC Cholesteatoma





  • Ulceration of EAC skin and necrosis of underlying bone most often at posteroinferior EAC.



  • Physical examination involves focal findings (vs keratosis obturans).



  • Theories for disease include invasion of bone by epithelium and secondary necrosis versus focal bone injury with secondary invasion of epithelium.



  • Physical examination often shows EAC defect filled with desquamated epithelium and surrounding granulation tissue.



  • Treatment




    1. Mechanical removal of keratin



    2. Topical therapy




      • Antibiotic drops



      • Silver nitrate for granulation tissue



    3. Frequent microscopic cleanings



    4. Surgery for refractory cases




      • Removal of necrotic bone with coverage of the cavity (fascia)





Infections of the Middle Ear (ME) and Mastoid



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Acute Otitis Media



Epidemiology




  • Most common reason for pediatrician visit in the United States



  • Risk factors




    1. Environmental




      • Day care attendance



      • Tobacco smoke exposure



      • Pacifier use



      • Presence of siblings



      • Supine bottle feeding



      • Lack of breast-feeding in first 6 months



    2. Anatomic




      • Cleft palate



      • Eustachian tube dysfunction



      • Craniofacial syndromes (ie, Treacher Collins)



    3. Genetic predisposition (Down syndrome)



    4. Indigenous populations (Native American, Inuit, Native Australians)



    5. Low socioeconomic status



    6. Premature birth



    7. Obesity




Etiology




  • Association with upper respiratory infections implicates Eustachian tube (ET).




    1. Inflammation of Gerlach tonsil compromising ET function.



    2. Adenoid pad harbors bacteria that can reflux into the ME.



    3. ET is shorter and more horizontal in children resulting in impaired clearance and drainage.



    4. Recurrent AOM may be due to functional obstruction of ET (ie, adenoid hypertrophy).



  • Combination of poor ME clearance and refluxed bacteria leads to inflammation of ME.




Signs and Symptoms




  • Otalgia (often rapid onset < 48 hours)



  • Irritability



  • Fever



  • Ear pulling



  • Signs and symptoms are not specific to AOM




Physical Examination




  • Bulging and erythematous TM.



  • Limited or absence of movement on pneumatic otoscopy.




    1. Pneumatic otoscopy is the key diagnostic tool and required to make diagnosis.



  • Air-fluid level in ME.



  • Purulent otorrhea if TM ruptured (suppurative otitis media).



  • Tympanometry can be used in equivocal cases.




Pathogens




  • Streptococcus pneumoniae most common organism




    1. Introduction of PCV7 and Prevnar 13 vaccinations have altered prevalence of certain serotypes.



    2. Decreased absolute number of invasive complications.



    3. Serotype 19A is a highly multidrug-resistant strain increasing in prevalence.



    4. Penicillin (PCN) resistance due to alterations of PCN-binding proteins in cell wall.



  • Haemophilus influenzae and M. catarrhalis also common




    1. Haemophilus influenzae strains largely nontypeable since introduction of HIB vaccine.



    2. 50% of H. influenza and 100% of M. catarrhalis are beta-lactamase positive.



  • Viruses




    1. RSV, rhinovirus, coronavirus, parainfluenza virus, enterovirus, adenovirus



    2. Virus isolated in up to 75% of AOM aspirates




Treatment




  • Original guidelines published in 2004 by American Academy of Pediatrics (AAP), American Academy of Family Practice (AAFP), and American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS)



  • Revised guidelines for children 6 months to 12 years published in 2013



  • Guidelines written for children without underlying immunodeficiency, genetic conditions, cochlear implants, recurrent AOM, or AOM with underlying chronic otitis media with effusion (COME)




PAIN CONTROL




  • Cannot be overlooked



  • Oral analgesics/antipyretics




    1. Acetaminophen



    2. Ibuprofen



    3. Narcotics—risk of respiratory depression; use sparingly



  • Topical analgesics




    1. Benzocaine drops—short-lived



  • Myringotomy with or without tympanostomy tube




    1. Relives pressure within ME space



    2. Requires sedation in children



    3. Risk of chronic perforation




OBSERVATION




  • Children more than 2 years, option to observe for 48 to 72 hours without antibiotic intervention.



  • May be advised since natural history of AOM is for resolution of symptoms and effusion over time.



  • Observation feasible if diagnosis uncertain or symptoms mild in children more than 2 years.



  • Pain control should still be initiated.



  • Initiate antibiotic therapy with failure to improve.



  • Requires compliant parents with ready access to health care provider.



  • Observation does not increase rates of complications (ie, mastoiditis).




ANTIBIOTICS




  • Unilateral or bilateral AOM in children at least 6 months old with severe signs or symptoms (moderate to severe otalgia > 48 hours or temperature > 39°C).



  • Nonsevere, bilateral AOM in children 6 to 23 months.



  • Children less than 2 years have prolonged symptoms and higher recurrence rates without treatment.



  • Antibiotic therapy decreases symptomatic infection by 1 day compared to observation.



  • 2010 analysis




    1. 80% with AOM improve within 3 days without antibiotics



    2. 92% more improve within 3 days with antibiotics



    3. 3 out of 10 develop rash, 8 out of 10 develop diarrhea




Guidelines for Healthy Children





  • Amoxicillin 90 mg/kg/d divided tid




    1. Provides tissue concentrations to overcome bacterial resistance in most intermediate-resistant (> 0.1-1 µg/mL minimal inhibitory concentration [MIC]) pneumococcal, H. influenza, and M. catarrhalis strains.



  • Length of treatment controversial




    1. 7-day therapy increases rate of recurrence but lowers side effects.



    2. 10-day therapy lowers rate of recurrence but increases side effects.



    3. Therapy more than 10 days has no advantage in reducing failure rates or duration of middle ear effusion (MEE) vs 10-day course.



    4. Current recommendations




      • Children less than 2 years: 10 days



      • Children 2 to 5 years: 10 days



      • Children less than 6 years: 5 to 7 days



  • Highly resistant Pneumococcal strains (MIC > 2 µg/mL) will not respond.



  • Day care attendees and children with older siblings at risk for resistant strains.



  • Amoxicillin should not be used in patients receiving amoxicillin in the past 30 days, cases of AOM with concurrent purulent conjunctivitis, or PCN allergic patients.



  • Amoxicillin-clavulanic acid (amox-clav)




    1. Recommended for children receiving amoxicillin in past 30 days, concurrent purulent conjunctivitis, or history of recurrent AOM unresponsive to amoxicillin.



    2. Patients with severe illness (fever > 39°C, severe otalgia) or if H. influenzae or M. catarrhalis suspected.



    3. 90 mg/kg/d of amoxicillin and 6.4 mg/kg/d clavulanate



  • PCN-allergic patients




    1. Type 1 hypersensitivity (ie, urticaria and anaphylaxis)




      • Azithromycin 10 mg/kg for 1 day, then 5 mg/kg for 4 days



      • Clarithromycin



      • Erythromycin



      • Trimethoprim-sulfamethoxazole



      • Clindamycin 30 to 40 mg/kg/d divided tid for known resistant Pneumococcus



  • Ceftriaxone IM




    1. Patients unable to take oral medications or with mild-delayed hypersensitivity to amoxicillin



    2. 50 mg/kg IM per day for 1 to 3 days (higher failure rate with 1 day vs 3 days)




AOM Treatment Failure





  • Failure of symptoms to improve within 48 to 72 hours after initiation of treatment




    1. If on amoxicillin, switch to amox-clav



    2. If on amox-clav, initiate 3-day course of ceftriaxone IM



    3. If on erythromycin or trimethoprim-sulfamethoxazole, start parenteral therapy with third-generation cephalosporin for pneumococcal resistance



  • Tympanocentesis with cultures




    1. Considered in patients who fail second-line therapy



  • Treatment failure higher in younger patients, day care attendees, regions with highly resistant bacteria




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Apr 30, 2020 | Posted by in OTOLARYNGOLOGY | Comments Off on Infections of the Temporal Bone

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