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Summary Table

Category	Details
Risk Factors	Children < 2 years old, recurrent acute otitis media (AOM), incomplete or inadequate antibiotic therapy for AOM, immunocompromised states, cholesteatoma
Etiology	Bacterial spread from middle ear to mastoid air cells; most common organisms are Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, and Pseudomonas aeruginosa (especially in chronic cases)
Patient Presentation	Fever, ear pain, and otorrhea that persist or worsen despite treatment for AOM; irritability in infants
Classic Physical Exam	Postauricular erythema, swelling, and tenderness with outward and downward displacement of the auricle; loss of the postauricular crease; bulging and erythematous tympanic membrane
Key Diagnostic Results	CT temporal bone with contrast showing coalescence or opacification of mastoid air cells with bony erosion; elevated WBC count and inflammatory markers (CRP, ESR)
Management	IV antibiotics (vancomycin + ceftriaxone or cefepime for empiric coverage); myringotomy with tube placement; mastoidectomy if complications arise or no clinical improvement
Keywords	"Postauricular swelling," "protruding ear," "displaced pinna," "recent otitis media," "failed antibiotic therapy"

1. Pathophysiology

Mastoiditis is fundamentally a complication of acute otitis media and represents the most common intracranial complication of middle ear infection. The mastoid bone, located posterior to the ear, contains a network of air cells that communicate directly with the middle ear cavity through the aditus ad antrum. This anatomical connection is the reason middle ear infections can extend posteriorly into the mastoid.

When AOM is inadequately treated or particularly virulent, bacteria migrate from the middle ear into the mastoid air cells, producing acute mastoiditis. In the early phase, there is mucosal inflammation and accumulation of purulent material within the air cells. If the infection progresses, the thin bony septae between the mastoid air cells begin to demineralize and erode under the pressure of pus and the osteoclastic activity driven by inflammatory mediators. This stage is called coalescent mastoiditis and marks the transition from a mucosal process to an osteitic one.

This bony destruction explains why patients develop postauricular swelling and tenderness: the infection erodes through the lateral cortex of the mastoid bone, forming a subperiosteal abscess that pushes the auricle outward and downward. The loss of the postauricular crease is a direct consequence of this swelling.

Because the mastoid is anatomically close to several critical structures, untreated mastoiditis can lead to dangerous complications. Erosion medially can reach the sigmoid sinus, causing septic thrombosis. Extension superiorly through the tegmen tympani can cause an epidural abscess or meningitis. Tracking of infection along the medial aspect of the mastoid tip into the digastric groove can lead to a deep neck abscess known as a Bezold abscess, which presents as a neck mass along the sternocleidomastoid muscle.

2. Classification and Clinical Manifestation

Stage	Pathology	Clinical Features
Acute Mastoiditis (without coalescence)	Mucosal inflammation and fluid in mastoid air cells; no bony destruction	Persistent AOM symptoms (otalgia, fever, otorrhea) beyond 2 weeks despite antibiotics; mild postauricular tenderness; TM appears erythematous and bulging
Acute Coalescent Mastoiditis	Destruction of bony septae between mastoid air cells; empyema formation	Postauricular erythema, swelling, and fluctuance; auricle displaced outward and downward; high fever; toxic appearance
Subperiosteal Abscess	Pus erodes through lateral mastoid cortex, collecting beneath the periosteum	Visible fluctuant mass behind the ear; marked auricular protrusion; severe tenderness
Chronic Mastoiditis	Low-grade persistent infection, often associated with cholesteatoma; granulation tissue replaces normal mucosa	Chronic foul-smelling otorrhea, progressive conductive hearing loss, intermittent otalgia; often associated with cholesteatoma on exam
Masked (Latent) Mastoiditis	Partially treated infection; bony changes present but acute signs suppressed by antibiotics	Subtle or absent postauricular signs; vague deep ear pain; diagnosis often delayed; CT reveals coalescence despite mild clinical findings

Complications by Anatomical Spread

Complication	Mechanism
Bezold abscess	Pus tracks through mastoid tip into digastric muscle/SCM; presents as neck mass
Sigmoid sinus thrombosis	Infection erodes into posterior fossa dura; presents with headache, high spiking fevers ("picket fence" pattern), papilledema
Epidural/subdural abscess	Superior extension through tegmen tympani
Meningitis	Hematogenous or direct spread to meninges
Facial nerve palsy	Inflammation or compression of CN VII within the fallopian canal
Labyrinthitis	Spread to inner ear; vertigo, sensorineural hearing loss, nystagmus

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination	Initial assessment	Postauricular swelling, displaced pinna, bulging TM
CT temporal bone with contrast	Best initial imaging and confirmatory test	Opacification of mastoid air cells, erosion of bony septae (coalescence), subperiosteal abscess, rim enhancement
MRI brain with contrast	Evaluate intracranial complications	Epidural/subdural abscess, sigmoid sinus thrombosis, meningeal enhancement
MR venography	When sigmoid sinus thrombosis is suspected	Filling defect or absent flow in sigmoid sinus
CBC, CRP, ESR	Supportive	Leukocytosis with left shift; elevated inflammatory markers
Blood cultures	Rule out bacteremia	May identify the causative organism, especially if febrile and toxic
Tympanocentesis / myringotomy culture	Identify pathogen and guide antibiotic therapy	Culture and sensitivity of middle ear fluid

The diagnosis of mastoiditis is primarily clinical, based on the combination of recent or ongoing AOM with the characteristic postauricular findings. However, imaging is essential to confirm the diagnosis and assess the extent of disease.

CT of the temporal bone with IV contrast is the imaging study of choice and should be obtained promptly when mastoiditis is suspected. The hallmark finding is coalescence of mastoid air cells with destruction of the bony septae. Simple opacification of the air cells alone is not diagnostic, as this can be seen with uncomplicated AOM. What distinguishes mastoiditis on CT is the loss of the normal bony architecture combined with abscess formation. If a subperiosteal abscess is present, CT will show a rim-enhancing fluid collection between the mastoid cortex and the overlying periosteum.

If there is clinical concern for intracranial extension (altered mental status, focal neurological deficits, high spiking fevers, papilledema), MRI with contrast should be added. MRI is superior to CT for detecting epidural or subdural collections and for evaluating sigmoid sinus thrombosis. MR venography or CT venography can confirm sinus thrombosis when suspected.

Laboratory studies serve a supportive role. Leukocytosis and elevated CRP help gauge the severity of the infection and monitor treatment response. Blood cultures should be drawn before starting IV antibiotics, particularly in patients who appear septic. Tympanocentesis or culture from myringotomy provides the most reliable specimen for identifying the causative organism and is especially valuable when empiric therapy fails.

4. Management and Treatment

Clinical Scenario	Management
Acute mastoiditis without abscess	IV antibiotics; myringotomy with tympanostomy tube placement
Subperiosteal abscess	IV antibiotics + cortical (simple) mastoidectomy with abscess drainage
Coalescent mastoiditis with no improvement after 48-72 hours of IV antibiotics	Cortical mastoidectomy
Intracranial complications (epidural abscess, sigmoid sinus thrombosis, meningitis)	IV antibiotics + urgent neurosurgical or otologic intervention; anticoagulation considered for sinus thrombosis
Chronic mastoiditis / cholesteatoma-associated	Canal wall up or canal wall down mastoidectomy with cholesteatoma excision

Acute Stabilization

All patients with mastoiditis require hospital admission and intravenous antibiotics. Empiric regimens must cover the common pathogens including resistant pneumococcus and staphylococcal species. A standard approach is:

Vancomycin (15 mg/kg IV every 6 hours in children; 15-20 mg/kg IV every 8-12 hours in adults, targeting trough levels of 15-20 mcg/mL) plus ceftriaxone (50-100 mg/kg/day IV divided every 12-24 hours in children; 2 g IV every 12-24 hours in adults). If Pseudomonas is a concern (chronic otitis media, immunocompromised host), cefepime (50 mg/kg IV every 8 hours in children) or piperacillin-tazobactam should replace ceftriaxone.

Antibiotic therapy is then narrowed based on culture results. Total antibiotic duration is typically 3-4 weeks, with a transition to oral therapy once there is clear clinical improvement (resolution of fever, decreasing swelling, improving labs), usually after at least 7-10 days of IV therapy.

Myringotomy with tympanostomy tube insertion is performed early to drain the middle ear, obtain culture material, and decompress the system. This is considered part of the initial management in nearly all cases.

Surgical Management

If there is a subperiosteal abscess, surgical drainage with cortical mastoidectomy is indicated and should not be delayed. Cortical mastoidectomy involves removing the diseased mastoid air cells while preserving the ear canal wall and the ossicular chain. This procedure both drains the infection and removes necrotic bone that perpetuates it.

If a patient fails to improve clinically after 48-72 hours of appropriate IV antibiotics and myringotomy, mastoidectomy should be pursued even in the absence of a clear abscess on imaging. Persistent fever, worsening postauricular swelling, or rising inflammatory markers all signal inadequate source control.

For intracranial complications, management is multidisciplinary. Sigmoid sinus thrombosis may warrant anticoagulation with heparin, though this remains somewhat controversial and is decided case by case. Epidural or subdural abscesses require neurosurgical drainage.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Severe acute otitis media	Fever, ear pain, bulging TM, sometimes postauricular tenderness in young children	AOM alone does not cause postauricular swelling, erythema, or auricular displacement; CT will show intact bony septae
Postauricular lymphadenitis	Swelling behind the ear in a child with fever	Swelling is discrete and nodular, not diffuse; the auricle is not displaced; no TM abnormality; associated with scalp infections or dermatitis
Otitis externa (malignant/necrotizing)	Ear pain, otorrhea, fever; can involve bone	Malignant otitis externa occurs in diabetic or immunocompromised elderly patients, involves the external ear canal (not the middle ear), and is caused by Pseudomonas; granulation tissue visible at the bony-cartilaginous junction of the EAC
Cholesteatoma	Chronic ear drainage, conductive hearing loss, can erode mastoid bone	Cholesteatoma presents with chronic painless foul-smelling otorrhea and a pearly white mass or retraction pocket on otoscopy; it is not typically acute or febrile
Parotitis	Swelling near the ear, fever in a child	Parotid swelling is preauricular and along the angle of the mandible, not postauricular; TM is normal; pain worsens with eating
Periauricular cellulitis	Erythema and swelling around the ear	Usually follows trauma, insect bite, or skin infection; no middle ear findings; TM is normal; no auricular displacement
Langerhans cell histiocytosis	Can cause lytic lesions of the temporal bone with ear discharge in a child	Chronic course, often multifocal bone lesions, may have skin rash (seborrheic dermatitis-like) and diabetes insipidus; biopsy shows Birbeck granules

6. Traps and High-Yield Pearls

The single most common way students lose points on mastoiditis questions is by confusing simple AOM with mastoiditis. A vignette describing a child with fever and ear pain after recent AOM is intentionally designed to test whether you recognize the transition from otitis media to mastoiditis. The discriminating feature is always the postauricular findings: swelling, erythema, tenderness, and displacement of the pinna outward and downward. If these signs are absent, the answer is not mastoiditis regardless of how sick the child appears.

Another frequent trap involves the imaging interpretation. Students see "opacified mastoid air cells" on CT and immediately select mastoiditis. However, simple fluid in the mastoid air cells is an expected finding in uncomplicated AOM. The CT finding that confirms coalescent mastoiditis is destruction of the bony septae, not merely opacification. Always look for this distinction in the question stem.

On management questions, the test often presents a child with mastoiditis who is already on IV antibiotics but not improving after 48-72 hours. The "next best step" in this scenario is mastoidectomy, not switching antibiotics. Students who reflexively choose broader antibiotic coverage will be penalized. Source control is the priority when medical therapy fails.

Finally, be alert for complication-recognition questions. A patient with mastoiditis who develops a swelling along the SCM muscle points to Bezold abscess. A patient with mastoiditis who develops spiking fevers, headache, and papilledema points to sigmoid sinus thrombosis. These complications are tested because they require the student to connect the anatomical relationships of the mastoid bone to surrounding structures, which is the core competency being evaluated.

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