Ear Infections: Acute Otitis Media, Mastoiditis, and Chronic Otitis Media

I. Acute Otitis Media (AOM)

Definition & Epidemiology

Pathophysiology

1. Viral URI causes Eustachian tube inflammation → mechanical or functional obstruction
2. Negative middle ear pressure develops → fluid accumulates
3. Nasopharyngeal bacteria enter the middle ear cavity → inflammation, pus, increased pressure

• Streptococcus pneumoniae (most virulent; commonest cause)
• Haemophilus influenzae (non-typeable; increasing in frequency post-pneumococcal vaccination)
• Moraxella catarrhalis
• Rarer: S. pyogenes, S. aureus, Mycobacterium tuberculosis, gram-negatives
• In neonates: additionally Group B Streptococcus and gram-negatives

Clinical Features

• Otalgia (most important symptom — unilateral or bilateral)
• Fever, irritability, pulling at ears (non-specific in children)
• Otoscopy: erythematous, bulging tympanic membrane (TM) with decreased mobility (by pneumatic otoscopy) — the hallmark finding
• Bullous myringitis (bullae on TM) may be seen; treatment is the same as standard AOM
• Middle ear effusion present
• Conductive hearing loss

Examination of the TM is essential — no constellation of symptoms alone reliably predicts AOM.

Management

Complications of AOM

• Persistent otitis media with effusion (OME) — leading cause of childhood hearing loss
• Acute mastoiditis (most common suppurative complication)
• TM perforation, ossicular erosion, tympanosclerosis
• Petrous apicitis (Gradenigo's syndrome)
• Facial nerve palsy
• Labyrinthitis
• Intracranial extension (meningitis, brain abscess, lateral sinus thrombosis)

II. Mastoiditis

Definition & Pathogenesis

• Pus accumulates in a closed space
• Infection spreads via venous channels → periosteal inflammation
• Destruction of bony trabeculae → coalescent mastoiditis (acute mastoid osteitis)
• Subperiosteal abscess may form, pushing the auricle anteroinferiorly

• Streptococcus pneumoniae (leading cause)
• Group A Streptococcus
• P. aeruginosa, S. aureus, Fusobacterium necrophorum (particularly after prior antibiotic use)

Clinical Features

• Fever, headache, otalgia, hearing loss
• Postauricular erythema, edema, and tenderness (classic)
• Protrusion (displacement) of the auricle anteroinferiorly — highly characteristic
• Abnormal TM (erythema, bulging) — may be normal in ~10% of cases
• Symptoms of AOM lasting >2 weeks should raise suspicion

Differential Diagnosis

• Severe AOM / otitis externa
• Skull fracture
• Posterior auricular lymphadenitis
• Deep space neck infection (Box 58.4)

Investigations

• Clinical diagnosis is possible with classic findings
• CT scan of temporal bones: indicated when neurologic symptoms suggest intracranial spread, or failure to improve with conservative therapy. Shows opacification of mastoid air cells, bony destruction (coalescence), subperiosteal abscess

CT scan demonstrating acute mastoiditis. — Rosen's Emergency Medicine, Fig. 58.1

Management

• Myringotomy ± tympanostomy tube placement (to drain middle ear)
• Mastoidectomy for coalescent mastoiditis, subperiosteal abscess, or failure of medical therapy

III. Chronic Otitis Media (COM)

A. Mesotympanitis (Tubotympanic Disease / "Safe" COM)

• Central TM perforation (pars tensa), with intact annulus
• Persistent or recurrent mucoid/mucopurulent otorrhea through the perforation
• Conductive hearing loss proportional to perforation size and ossicular involvement
• Mucosa of the middle ear is inflamed (granulation tissue in 97% of operated cases — Cummings, Table 140.3)
• No cholesteatoma (distinguishes it from epitympanitis)

• P. aeruginosa (most common in chronic disease)
• S. aureus
• Gram-negative rods
• Anaerobes in long-standing cases

• Granulation tissue: 97.4%
• Ossicular changes: 90.5%
• Tympanosclerosis: 19.8%
• Cholesterol granuloma: 12.1%
• Cholesteatoma: 4.3%

• Conservative (dry ear): Aural toilet, topical quinolone drops (e.g., ofloxacin — avoids ototoxicity risk of aminoglycosides)
• Systemic antibiotics for acute exacerbations guided by culture
• Surgery (tympanoplasty / myringoplasty): TM repair once ear is dry; ossiculoplasty if ossicular chain is disrupted. Goal: eliminate infection, restore hearing, prevent recurrence

B. Epitympanitis (Atticoantral Disease / "Unsafe" COM)

• Congenital: develops behind an intact TM from embryonic epithelial rests
• Acquired (primary): most common — a retraction pocket in the pars flaccida or posterosuperior pars tensa deepens due to Eustachian tube dysfunction, accumulates keratin, and forms a cyst
• Acquired (secondary): keratinizing epithelium migrates through a pre-existing TM perforation

• Osteoclastic activity driven by inflammatory cytokines, pressure, keratin, bacterial toxins
• The attic communicates with the antrum only through two narrow openings (between the tensor tympani tendon and stapes; and between the short process of incus and stapedial tendon) — blockage by edema/granulation tissue promotes chronic infection and bone erosion

• Attic (marginal/posterosuperior) perforation of TM
• Scanty, foul-smelling otorrhea (keratin debris; typically less profuse than mesotympanitis)
• Conductive hearing loss
• Otoscopy: white pearly debris or crusting in the attic area (Shrapnell's membrane region)
• Aural polyp may protrude through the perforation
• Potential for serious complications due to bone erosion

• Ossicular erosion → conductive hearing loss
• Labyrinthine fistula → sensorineural hearing loss, vertigo
• Facial nerve canal erosion → facial palsy
• Tegmen erosion → meningitis, brain abscess
• Sigmoid sinus erosion → lateral sinus thrombosis
• Petrous apicitis (Gradenigo's syndrome: trigeminal pain, abducens palsy, otorrhea)

• Surgery is mandatory — cholesteatoma cannot be eradicated medically
• Canal wall up (CWU) tympanomastoidectomy: preserves the posterior canal wall; better hearing outcome; requires "second-look" surgery at 12 months to check for residual cholesteatoma
• Canal wall down (CWD) mastoidectomy / modified radical mastoidectomy: removes the posterior canal wall, creating an open mastoid cavity; better visualization and lower recurrence, but creates a permanent "mastoid bowl" requiring lifelong care

Summary Comparison

Middle Ear Infections: Acute Otitis Media, Mastoiditis, and Chronic Otitis Media

I. Acute Otitis Media (AOM)

Definition & Epidemiology

Pathophysiology

Clinical Features

• Otalgia — the cardinal symptom (unilateral or bilateral)
• Fever, irritability, poor feeding, ear-pulling (nonspecific in infants)
• Otoscopy (essential for diagnosis):
  • Bulging, erythematous, opacified tympanic membrane (TM)
  • Obscured bony landmarks
  • Absent or reduced TM mobility on pneumatic otoscopy — the most reliable sign
• Conductive hearing loss
• Severe AOM criteria: otalgia ≥48 hours, temperature >39°C (102.2°F), moderate-to-severe bulging of TM

Management

• Children ≥6 months with mild, unilateral AOM
• Children ≥2 years with nonsevere symptoms

• Age <6 months (all cases)
• Bilateral AOM in children 6–24 months
• AOM with otorrhea (any age >6 months)
• Severe otalgia, fever >39°C, or symptoms >48 hours (any age)
• Adults: treat all with antibiotics

The number needed to treat to prevent one case of mastoiditis is approximately 5,000 — antibiotics provide modest benefit but are warranted in higher-risk patients.

II. Mastoiditis

Definition & Pathogenesis

1. Incipient mastoiditis — fluid fills mastoid cells, no bony destruction yet
2. Coalescent mastoiditis (acute mastoid osteitis) — progressive demineralization and destruction of bony septa between air cells → coalescence into a single cavity
3. Subperiosteal abscess — infection spreads through the mastoid cortex to the subperiosteal space, displacing the auricle

Clinical Features

• Fever, otalgia, hearing loss, headache
• Postauricular erythema, tenderness, and swelling — most consistent finding
• Protrusion of the auricle downward and laterally — due to abscess displacing the upper mastoid → highly characteristic
• TM typically shows AOM changes (bulging, erythema); may be normal in ~10%
• Superoposterior protrusion of the posterior bony canal wall on otoscopy
• Symptoms of AOM persisting >2 weeks should raise suspicion

Fig. 141.4 Postauricular abscess associated with coalescent mastoiditis. Auricle is displaced laterally and inferiorly. — Cummings Otolaryngology

Masked Mastoiditis

Investigations

• Clinical diagnosis is sufficient with classic findings
• CT temporal bones (HRCT): Indicated for neurologic symptoms, failure to improve, or uncertain diagnosis. Shows:
  • Opacification of mastoid air cells
  • Loss/destruction of bony septa (coalescence)
  • Subperiosteal abscess
  • Erosion of tegmen, sigmoid sinus plate, labyrinth
  • Sensitivity 97%, positive predictive value 94% for AOM complications
• MRI with gadolinium: Preferred for intracranial complications (meningitis, brain abscess, sigmoid sinus thrombosis) — better soft tissue detail

Fig. 141.3 CT scan: opacification of middle ear (white arrow) and mastoid (black arrow). — Cummings Otolaryngology

Management

• Myringotomy ± tympanostomy tube: First step — decompresses middle ear, provides culture material
• Mastoidectomy: If no improvement within 48 hours of IV antibiotics, coalescent mastoiditis confirmed on CT, or complications present
• Abscess drainage: Subperiosteal or Bezold's abscess requires direct surgical drainage

Complications (Box 141.1)

III. Chronic Otitis Media (COM)

A. Mesotympanitis (Tubotympanic COM / "Safe" Disease)

• Persistent or intermittent otorrhea — mucoid or mucopurulent, typically odourless or mildly malodorous, often profuse
• Central TM perforation visible on otoscopy
• Conductive hearing loss — proportional to perforation size and ossicular involvement
• Recurrent episodes often triggered by upper respiratory infections (water entering through the perforation)
• Middle ear mucosa appears thickened, edematous, with granulation tissue

• Pseudomonas aeruginosa (most common in chronic disease)
• Staphylococcus aureus
• Mixed gram-negatives, anaerobes
• Biofilms are common and contribute to antibiotic resistance

1. Aural toilet — meticulous cleaning (microsuction) to remove debris and secretions
2. Topical therapy: Fluoroquinolone ear drops (ciprofloxacin/dexamethasone, ofloxacin) — avoid aminoglycosides due to ototoxicity risk through perforated TM; acetic acid/alcohol solutions have antiseptic utility
3. Systemic antibiotics for acute exacerbations guided by culture/sensitivity
4. Surgery (definitive): Tympanoplasty (myringoplasty) once the ear is dry — to close the perforation and restore the sound-conducting mechanism. Ossiculoplasty if the ossicular chain is disrupted. Goal: dry ear, hearing rehabilitation, prevention of recurrence.

B. Epitympanitis (Atticoantral COM / "Unsafe" Disease)

Cholesteatoma

• Congenital: Develops behind an intact TM from embryonic epithelial rests; found in children
• Primary acquired (most common): A retraction pocket in the pars flaccida deepens progressively due to chronic Eustachian tube dysfunction and negative middle ear pressure. Keratin accumulates, and the self-cleaning mechanism of the skin fails, creating an expanding cyst
• Secondary acquired: Keratinizing squamous epithelium migrates through an existing TM perforation (typically in mesotympanitis), invades the middle ear/mastoid, and forms a cholesteatoma

• Osteoclastic activation by inflammatory cytokines (IL-1, TNF-α), localized pressure, keratin, bacterial toxins
• Fibroblasts in the subepithelium with invasive phenotype

• Attic/marginal or posterosuperior perforation on otoscopy — white pearly debris, crust, or granulation in the attic (Shrapnell's membrane area)
• Scanty but foul-smelling (fetid) otorrhea — keratin debris; less voluminous than mesotympanitis
• Conductive hearing loss (progressive with ossicular erosion)
• Aural polyp may prolapse through the perforation
• High risk of serious complications from bone destruction

• Ossicular erosion → conductive hearing loss (incus long process most commonly eroded)
• Labyrinthine fistula (most often horizontal SCC) → sensorineural hearing loss, vertigo; positive fistula test (Hennebert's sign)
• Facial nerve canal erosion → peripheral facial palsy
• Tegmen plate erosion → meningitis, brain abscess, CSF otorrhea
• Sigmoid sinus erosion → lateral sinus thrombosis
• Petrous apicitis → Gradenigo's syndrome (trigeminal pain, abducens palsy, otorrhea)

• High-resolution CT temporal bones: Reveals the extent of cholesteatoma, ossicular chain erosion, tegmen/sigmoid sinus/labyrinthine erosion. Guides surgical planning.
• MRI (non-EPI DWI): Diffusion-weighted MRI is now the gold standard for detecting residual/recurrent cholesteatoma post-surgery without the need for a "second-look" operation.

Summary Comparison

Labyrinthitis and Otogenic Intracranial Complications

Routes of Spread from the Middle Ear to Intracranial Structures

1. Direct extension through bone eroded by cholesteatoma, granulation tissue, or coalescent mastoiditis
2. Venous propagation — thrombophlebitis of diploic veins and mastoid emissary veins carries septic thrombus to adjacent sinuses and intracranial vessels
3. Labyrinthine pathway — through the foramina of the internal auditory canal, the cochlear aqueduct, or labyrinthine windows, connecting the middle ear/mastoid with the CSF
4. Preformed pathways — congenital bony dehiscences, prior surgical defects, tegmen perforations, perilymph fistulas

Critical diagnostic point: The TM and middle ear may appear normal or near-normal even when serious complications are developing in the mastoid — particularly in masked mastoiditis. The mastoid does not necessarily respond in parallel with the middle ear under antibiotic treatment.

I. Labyrinthitis

A. Serous (Toxic) Labyrinthitis

• Bacterial toxins/inflammatory mediators enter the labyrinth via the oval window, round window membrane, or labyrinthine fistula
• Round window membrane permeability is significantly increased during middle ear inflammation
• Labyrinthine dysfunction results from changes in ionic potentials caused by inflammatory mediators rather than neuroepithelial destruction
• Because the neuroepithelium is not destroyed, cochlear/vestibular function can return to normal after the inflammatory state resolves

• Typically unilateral
• Dizziness (not required for diagnosis)
• Hearing loss (mild to severe sensorineural) — typically reversible
• Symptoms resolve over time as inflammation subsides

• Audiogram (SNHL)
• Culture of middle ear effusion when present
• Vestibular testing when necessary
• Imaging only if other complications suspected

• Directed at the infectious source — oral antibiotics typically effective
• Steroids (oral and/or intratympanic) may improve hearing outcomes but evidence is limited
• Myringotomy for unresolved middle ear infection
• Tympanomastoidectomy if cholesteatoma is present

B. Suppurative (Purulent) Labyrinthitis

1. From the subarachnoid space (meningitis) — bacteria enter the scala tympani via the patent cochlear aqueduct or travel up the IAC through perineural/perivascular spaces
2. From the temporal bone (osteomyelitis) — direct erosion
3. From the middle ear (AOM/COM ± cholesteatoma):
   • Through a weakened or dehiscent oval window membrane (especially in Mondini deformity, enlarged vestibular aqueducts, or post-stapes surgery)
   • Through a cholesteatomatous lateral semicircular canal fistula — infected granulation tissue lies directly on the endosteal membrane; bacteria contact underlying perilymph
   • Through foramina of the internal auditory canal

Both directions of spread are possible: suppurative labyrinthitis can cause meningitis, and meningitis can cause suppurative labyrinthitis. This bidirectional relationship is clinically important, particularly in children with congenital labyrinthine anomalies.

• Tinnitus and dizziness → rapidly progressing to whirling vertigo, pallor, diaphoresis, nausea, and vomiting
• Brisk nystagmus directed toward the opposite (unaffected) ear
• Over first several hours: spontaneous vertigo and nystagmus begin to abate
• Over 2–3 weeks: central compensation restores near-normal balance
• Complete, permanent, unilateral sensorineural hearing loss (total cochlear destruction)
• If due to meningitic spread: bilateral profound deafness (10% average; range 2–20%)
• Fever, meningeal signs if associated meningitis; cranial neuropathies if disease spreads beyond the otic capsule

Fig. 141.14 — CT and MRI findings in acute suppurative labyrinthitis. — Cummings Otolaryngology

• Labyrinthitis ossificans — ossification of the cochlea following inflammation; detected by MRI and HRCT; if bilateral SNHL is present, early cochlear implantation is indicated before the cochlear duct is obliterated
• Meningitis (via cochlear aqueduct/IAC spread)

• Parenteral antibiotics with CSF penetration for 10 days (to eradicate infection and prevent meningeal spread)
• Directed at underlying cause (AOM or COM/cholesteatoma)
• Myringotomy ± ventilation tube for non-cholesteatoma otogenic infection
• Tympanomastoidectomy if cholesteatoma present (labyrinthectomy is NOT necessary in cases secondary to AOM)
• Dexamethasone improves hearing outcomes in meningitic labyrinthitis due to H. influenzae and S. pneumoniae
• Serial CT/MRI for labyrinthitis ossificans if SNHL present; early cochlear implant referral for bilateral cases

II. Otogenic Intracranial Complications

Nearly all patients with lateral sinus thrombosis have one or more additional intracranial complications. Multiple simultaneous complications are common in COM.

1. Otogenic Meningitis

• Hematogenous dissemination (most common in children <2 years with AOM)
• Extension through the tegmen tympani (bony plate separating middle ear from middle cranial fossa)
• Via the labyrinthine route — cochlear aqueduct, foramina of the IAC
• Congenital anomalies (Mondini dysplasia, enlarged vestibular aqueduct, CSF fistulas)
• After stapes surgery (perilymph gusher/fistula)
• Traumatic temporal bone fracture with dural laceration

• Severe, generalized headache — earliest and most persistent symptom
• Photophobia, general hyperesthesia, social withdrawal
• High, sustained fever (universal)
• Nuchal rigidity — pain with neck flexion, most consistent meningeal sign
• Brudzinski sign — passive neck flexion causes involuntary bilateral hip and knee flexion
• Kernig sign — with thigh flexed at 90°, passive knee extension meets resistance and pain from hamstring spasm
• Altered level of consciousness (ranges from normal to unresponsive)
• Papilledema on fundoscopy

• CT scan first (before lumbar puncture) — to rule out brain abscess, cerebritis, subdural empyema; assesses safety of LP
• Lumbar puncture: elevated CSF pressure; early: protein ↑ and glucose ↓ vs. serum; bacteria absent until late; cells: neutrophilic pleocytosis
• MRI with gadolinium: shows dural enhancement; superior for detecting labyrinthine route of infection and additional complications

• Parenteral antibiotics with CSF penetration — directed at S. pneumoniae (consider resistance), gram-negatives
• Dexamethasone adjunct — evidence suggests decreased adverse outcomes in community-acquired pneumococcal meningitis; likely beneficial in otogenic cases
• When AOM/suppurative labyrinthitis is source: myringotomy + antibiotics; no surgery on mastoid required
• When COM/mastoiditis is source: mastoidectomy is mandatory as soon as patient is neurologically stable — the infected mastoid must be exenterated to eliminate the source
• If profound ipsilateral SNHL develops: route through labyrinth is confirmed; if SNHL is unchanged from baseline: route was extralabyrinthine

Otogenic meningitis is more lethal when caused by COM/mastoiditis than when it occurs as a hematogenous complication of AOM in infancy.

2. Meningoencephalitis and Arachnoiditis

• Focal neurological deficits
• Altered sensorium progressing to obtundation/coma
• Seizures
• MRI shows parenchymal edema and enhancement adjacent to the infected temporal bone

• CSF outflow obstruction → communicating or non-communicating hydrocephalus
• Cranial nerve entrapment (particularly CN VIII → sensorineural hearing loss; CN VI → diplopia)
• Chronic headaches

3. Epidural (Extradural) Abscess

• Deep mastoid pain — the dominant symptom; may be the only symptom
• No specific signs or symptoms attributable to epidural abscess alone — many are discovered only at surgery
• Signs of underlying otomastoiditis (ear discharge, postauricular swelling)
• If large: can be detected on contrast-enhanced CT/MRI as a fluid collection between temporal bone and enhanced dura

• Surgery is the only recommended treatment
• Type of mastoidectomy appropriate to underlying otitis (canal wall-up or canal wall-down)
• Surgical approach: progressive exenteration from lateral to medial, from less diseased to more diseased regions; careful removal of overlying bone until healthy dura is evident on all margins; granulation tissue scraped from abscess cavity with a blunt elevator

4. Brain Abscess (Temporal Lobe and Cerebellar)

1. Bacteria propagate in and around venous channels from the mastoid into adjacent brain parenchyma → cerebritis (stage 1)
2. Cerebritis spreads to form a necrotic center of liquefied pus surrounded by cerebral edema (stage 2)
3. A fibrous capsule forms from the surrounding gliosis (encapsulation, stage 3)
4. Further spread/rupture (stage 4) — intraventricular rupture is catastrophic (mortality >80%)

• Early (cerebritis phase): Headache, low-grade fever, malaise — often subtle and non-specific
• Established abscess:
  • Increasing headache, high fever, signs of raised ICP (nausea, vomiting, papilledema, altered consciousness)
  • Temporal lobe abscess: Dysphasia (dominant side), contralateral hemiparesis, visual field defects, focal seizures
  • Cerebellar abscess: Ataxia, nystagmus, ipsilateral limb dysmetria (past-pointing), intention tremor, gait disturbance; may mimic labyrinthitis early
• Symptoms evolve over days to weeks (contrast with subdural empyema which can evolve in hours)
• Patients appear severely systemically ill; obtundation may be present

Fig. 141.17 — Left temporal lobe abscess with petrous apicitis and mastoiditis on MRI. — Cummings Otolaryngology

• CT with contrast: Ring-enhancing lesion with central hypodensity; surrounding edema; mass effect; midline shift if large
• MRI with gadolinium: More sensitive; defines extent, multiplicity, and capsule formation; diffusion-weighted imaging (DWI) confirms restricted diffusion in abscess cavity (distinguishes from necrotic tumor)
• CT/MRI of temporal bones: establishes underlying otologic diagnosis

• Neurosurgical drainage of the abscess takes precedence over mastoid surgery if both are present — drain the abscess first, then immediately proceed to mastoidectomy to eliminate the source
• Methods: stereotactic aspiration (for deep/eloquent areas), or craniotomy with excision (for superficial, encapsulated, posterior fossa lesions)
• Intravenous antibiotics covering gram-positives, gram-negatives, and anaerobes for extended duration (6–8 weeks)
• Mastoidectomy (canal wall-up or canal wall-down) to eliminate underlying COM/cholesteatoma
• Dexamethasone may be used to reduce cerebral edema

5. Thrombophlebitis of the Sigmoid (Lateral) Sinus

1. Bone erosion from cholesteatoma, granulation tissue, or coalescent mastoiditis creates a perisinus abscess
2. Pressure on the outer dural wall → necrosis → extension to the intima
3. Fibrin, blood cells, and platelets aggregate → mural thrombus forms
4. Thrombus becomes infected, enlarges, and occludes blood flow
5. Infected clot propagates in either direction:
   • Anteriorly: to the transverse sinus, torcular herophili, superior sagittal sinus, cavernous sinus
   • Inferiorly: to the jugular bulb and internal jugular vein in the neck
6. Infected clot showers bacteria into the bloodstream → septicemia → metastatic abscesses (most commonly pulmonary)

• "Picket fence" fever pattern — diurnal temperature spikes exceeding 39.4°C (103°F), with intervening afebrile periods; characteristic of septicemia from infected thrombus shedding bacteria intermittently
• Severe headache and evidence of raised ICP
• Signs of otomastoiditis (ear pain, discharge, postauricular swelling)

• Neck pain — from sternocleidomastoid inflammation (tenderness to percussion of mastoid tip distinguishes this from meningitis-induced neck stiffness)
• Diplopia — from CN VI palsy with raised ICP (increasingly the presenting sign in the antibiotic era)
• Jugular foramen syndrome (if thrombosis extends to jugular bulb): palsies of CN IX, X, XI → hoarseness, dysphagia, shoulder weakness
• Progressive obtundation, worsening headache → bilateral involvement of venous outflow → cerebral edema → otitic hydrocephalus

In patients previously treated with antibiotics, the classic picket fence fever pattern is less common. Diplopia or other neurological signs may be the first manifestation. History of recent OM symptom resolution following antibiotics followed by new neurological symptoms should trigger investigation.

• MRI/MRV (gold standard): Demonstrates absent flow in sigmoid/transverse sinus; extent of thrombus; associated complications (subdural empyema, cerebritis, cerebellar abscess)
• CT with contrast: The "delta sign" — absence of contrast within the vessel lumen with enhancement of the sinus wall; sensitive but less so than MRI
• Blood cultures (may be positive during septic emboli)
• CT/MRI temporal bones: cholesteatoma or mastoiditis as underlying cause

1. Mastoidectomy — mandatory in all cases to eliminate underlying mastoid disease
2. IV antibiotics — broad spectrum, covering gram-positives, gram-negatives, and anaerobes; prolonged course
3. Anticoagulation — controversial; not routinely indicated given risks vs. unproven benefit in most cases; strongly considered when:
   • Clot extends to transverse sinus or cavernous sinus
   • Septic embolic events are present
4. Clot evacuation from the sinus — considered if the sinus wall appears disrupted during exploration; a needle aspirates the sinus, and if pus is present, a linear incision is made for drainage; recent studies show no significant mortality benefit, but may shorten hospital stay
5. Internal jugular vein ligation in the neck — considered if clot extends into the neck or septic emboli are present; not routinely performed
6. For associated otitic hydrocephalus: urgent neurosurgical/neurological consultation; serial lumbar punctures or lumbar drain to reduce ICP; consider acetazolamide

6. Otitic Hydrocephalus

1. The relative size of the occluded sinus vs. the opposite sinus (right > left in 60%)
2. Adequacy of the collateral venous network (cavernous sinus, opposite inferior petrosal sinus)
3. Whether propagation affects additional venous outflow (superior sagittal sinus)

• Diffuse severe headache and nausea — dominant early symptoms
• With inadequate collateral drainage: dulling of sensorium, decreased visual acuity (retinal vein occlusion), papilledema
• Progression to coma and death possible if untreated
• CN VI palsy (diplopia) from raised ICP stretching the abducens nerve over the petrous tip

Summary: Routes, Complications, and Key Distinguishing Features