Alexis Furze, MD 
Definitions:
Otitis Media (OM): inflammatory condition of the middle ear and mastoid space which can present with or without a middle ear effusion
Acute (AOM): 0-3 weeks in duration
Subacute: 3-12 weeks in duration
Chronic (COM): > 12 weeks in duration, often associated with cholesteatoma
Recurrent OM: 4 or more episodes in 1 year or 3 or more episodes in 6 months
Chronic Suppurative OM: persistent purulent otorrhea through a TM perforation or tympanostomy tube that is unresponsive to medical therapy.
Pathophysiology:
Abnormal eustacian tube (ET) function is commonly caused by URI, anatomic abnormality, allergy, smoke exposure or ciliary dysfunction. ET dysfunction causes negative pressure in the middle ear drawing in bacteria and viruses from the nasopharynx as well as increasing mucosal secretions in the middle ear. Secretions accumulate in the middle ear either in response to infection or secondary to the negative pressure. Bacterial or viral organisms are poorly cleared and proliferate in the middle ear fluid.
Microbiology:
Most common bacterial pathogens in AOM include:
- Streptococcus pnuemoniae
- Haemophilus influenza
- Moraxella Catarrhalis
- group A streptococci.
Most common bacterial pathogens in COM include:
- Proteus Mirabilis
- Pseudomonas Aeruginosa
- Enterococcus
Diagnosis:
History:
Symptoms of acute infection or exacerabation of chronic infection include:
- fever
- irritability
- otalgia
- hearing loss
- anorexia
- nausea/vomiting
- headache
- dizziness
- tinnitus.
Physical:
Otoscopy:
- TM can be bulging, retracted, neutral or full
- Air fluid levels or bubbles may be seen
- Abnormal TM color – opaque, yellow, blue
- Decreased mobility with pneumatic otoscopy
- If perforation present, may have purulent otorrhea
Hearing evaluation will usually demonstrate a conductive hearing loss
Tympanometry can show decreased mobility or increased negative pressure.
Treatment:
- Observation (Acute otitis media has a spontaneous resolution rate of 60% in 24 hours and 80% in 2-3 days.)
- Analgesics
- Antimicrobials
- Tympanostomy tubes
- Adenoidectomy with or without tonsillectomy
Complications of Acute Otitis Media
Definition: spread of infection beyond the pneumatized spaces of the temporal bone and their mucosa.
Most complications are associated with subacute or chronic OM.
The complication rate has decreased from 2.3% to 0.04% since the advent of antibiotics
Mortality rate from complications has decreased from 35% to 5% due to antibiotics
Early signs of a complication include:
- Persistent acute infection > 2 weeks
- Recurrence of infection within 2 weeks
- Acute exacerbation of chronic infection
- Fetid discharge
- Presence of anaerobic organisms or H. influenzae
- Pain
Complications can be divided into intratemporal complications and intracranial complications and are as follows:
Intratemporal Complications
Mastoiditis
Pathophysiology:
Spread of infection and inflammation into the air cells of the mastoid cavity
Signs and symptoms:
- no response to antibiotics within 1 week
- persistent fever
- edema, erythema and tenderness over the mastoid
- posterior-superior canal wall edema.
- Subperiosteal abscess would displace pinna inferolaterally
- Bezold’s abscess occurs when infection spreads through a perforation in the mastoid cortex and tracts into the SCM causing a posterior triangle mass
Diagnosis:
- Myringotomy for culture and sensitivity
- High resolution CT temporal bones
Treatment:
- Myringotomy, antibiotic treatment, close follow up
- If symptoms persist, consider IV antibiotics and mastoidectomy
- Drainage of subperiosteal or Bezold’s abscess if present
Petrositis
Pathophysiology:
Spread of infection around the air cells around the labyrinth and into the petrous apex of the temporal bone
Signs and symptoms:
- no response to antibiotics within 1 week
- persistent fever
- Triad of Gradenigo
o Retroorbital pain
o Ipsilateral acute or chronic otitis media
o Abducens palsy
- Abducens palsy is rare and not necessary to make the diagnosis
Diagnosis:
- Symptom complex
- Evidence of petrous apex bone destruction
Treatment:
- IV Antibiotics
- Drainage of the petrous apex by lateral transmastoid, perilabyrinthine approach
- If infection persists, middle cranial fossa approach may be needed
Labyrinthitis
Pathophysiology:
- Bacterial invasion from the middle ear through the round window, oval window, or bone erosion through the otic capsule
- If chronic disease present, cholesteotoma could contribute to bone erosion
- If meningitis present, bacterial invasion could occur through the cochlear aquaduct
Signs and symptoms:
- Sudden vertigo and hearing loss
- Middle ear infection usually present
- Tinnitus
Diagnosis:
- Clinical history and exam
- Audiogram - SNHL
Treatment:
- Myringotomy
- IV antibiotics
- Vestibular suppressants
- Possible mastoidectomy and petrosectomy
- Repair of labyrinthine fistula if present
- Removal of cholesteotoma if present
Facial Paralysis
Pathophysiology:
- Infection around the facial nerve can either cause edema and compression or destruction of the nerve
- In chronic ear disease cholesteotoma can contribute to facial nerve damage
Signs and symptoms:
- Middle ear infection
- Partial or total weakness of the ipsilateral facial muscles
Diagnosis:
- History and physical
- CT/MRI
- Nerve excitability test/electroneurography/electromyography
Treatment:
- IV antibiotics
- Myringotomy
- If infection is subacute or chronic or if there is evidence of neural degeneration, mastoidectomy is suggested
- Surgery is aimed at clearing middle ear infections and thinning the fallopian canal bone so that the nerve sheath can be inspected through thin bone
- If cholesteatoma or granulation is present, careful removal of this disease is suggested
Intracranial Complications
Epidural abscess or granulation:
Pathophysiology:
- Abscess or accumulation of granulation tissue between the skull and the dura
- Usually direct extension of infection through bone erosion
Signs and symptoms:
- May be asymptomatic
- Headaches
- Low grade fevers
- Malaise
Diagnosis:
- CT/MRI help to identify larger lesions
- Intraoperative inspection – involve inspecting tegmen tympani, tegmen mastoideum, sigmoid sinus, and posterior fossa bone
- May need to remove bone and inspect dura directly
Treatment:
- IV antibiotics
- Debride diseased bone until normal dura is exposed
- Exposure of abnormal dura will adequately drain the abscess
- Careful removal of granulation tissue
Subdural abscess
Pathophysiology:
- Purulent collection forms between the dura and subarachnoid membrane
- Direct extension of infection
Signs and symptoms:
- Focal neurologic deficits
- Seizures
- Delerium
- Rapid loss of consciousness
Diagnosis:
- CT/MRI – crescent shaped enhancement that does not cross midline
Treatment:
- IV antibiotics
- Myringotomy
- Mastoidectomy with inspection of the dura with removal of granulation if present
- Usually requires drainage from separate burr holes or craniotomy – Neurosurgery consult
Sigmoid sinus thrombophlebitis
Pathophysiology:
- Inflammation causes thrombus formation in the sigmoid sinus
- Mural thrombus forms which can propagate distally and begin to seed
Signs and symptoms:
- Intermittently spiking “picket fence” fever
- Septicemia
- Torticollis
- Headache
- Papilledema
- Signs of septic embolization
- Griesinger’s sign – pain over mastoid from occlusion of the mastoid emissary vein
- Retrograde thrombosis of cerebral veins leading to brain abscess or infarction
- Focal neurologic deficits
- Coma
- Death
Diagnosis:
- CT – enhancement within the sinus
- MRI – increased signal intensity
- MRA – may reveal total vs. partial occlusion
- Tobey-Ayer or Queckenstedt’s test – external compression of jugular vein will not rapidly increase CSF pressure as it normally does because of the obstruction within the vein
- Blood cultures
- Lumbar puncture – not if signs of intracranial hypertension
Treatment:
- IV antibiotics
- Myringotomy
- Mastoidectomy – expose diseased dura and remove excess granulation tissue
- In the presence of a septic thrombus, aspirating or carefully opening the sigmoid and evacuating the thrombus may be appropriate
- Possible ligation of the internal jugular vein to avoid further embolization may be needed
- Possible ligation or hemostatic stapling of the sinus may be needed
- Anticoagulation is controversial
Brain abscess
Pathophysiology:
- Direct extension of infection
- Retrograde thrombosis of sigmoid sinus
- Most often manifest in the temporal lobe or cerebellum
Signs and symptoms:
- Clinical stages of brain abscess
1. Invasion (encephalitis) – usually resolves after several days
- Low grade fever
- Drowsiness
- Inability to concentrate
- Headache
- Malaise
- Nuchal rigidity
2. Localization (latent or quiescent abscess) – may last for weeks
- Clinically silent
- Organization of abscess – liquifactive necrosis
3. Enlargement
- Focal neurologic symptoms
o Temporal lobe – nominal aphasia, quadrantic homonymous hemianopia, motor paralysis
o Cerebellum – nystagmus, gait disturbances
- Intracranial hypertension
- Seizures
- Loss of consciousness
4. Termination (rupture of abscess)
- Ruptures into the ventricle or subarachnoid space
- Rapidly progressive neurological deterioration and subsequently death
Diagnosis:
- Imaging – CT/MRI
- Brain abscesses take several weeks to manifest – so repeat imaging in 2-3 weeks should be considered based on clinical suspicion
Treatment:
- IV antibiotics
- Myringotomy
- Surgical exploration through mastoidectomy
- Neurosurgical consultation for drainage of the intracranial portion of the infection
- The patient’s stability may require neurosurgical intervention prior to exploration of the middle ear
- Possible anticonvulsant prophylaxis
Otitic Hydrocephalus
Pathophysiology:
- Increased intracranial pressure secondary to acute or chronic middle ear infection without evidence of meningitis or subdural or brain abscess
- Thought to be the result of sigmoid sinus thrombosis
- Does not cause dilatation of the ventricles
Signs and symptoms:
- Chronic course - weeks
- Headache
- Lethargy
- Papilledema
- Diplopia
- Nausea
- Abducens palsy
Diagnosis:
- MRI reveals sigmoid sinus thrombosis
- Papilledema on optic exam
Treatment:
- IV antibiotics
- Myringotomy
- Mastoidectomy and management similar to that for sigmoid sinus thrombophlebitits
- Neurosurgery consult
- Lower intracranial hypertension
o Acetazolamide
o Prednisone
o Repeated lumbar punctures
o Furosemide
o Mannitol
o High dose barbiturates
o Ventricular or lumboperitoneal shunt
o Venous bypass from lateral sinus to jugular vein – rarely needed
- Visual monitoring - if progressive visual deterioration persists despite the above treatments, fenestration of the optic nerve sheath may be effective
Meningitis
Pathophysiology:
- Hematogenous dissemination of invasive organisms
- Mondini Malformation can lead to rapid onset of meningitis secondary to intracranial bacterial spread through a dilated cochlear aquaduct – patients will have a baseline SNHL with this deformity
- Bacteria can also spread through a communicating meningoencephalocele, dural defect around the geniculate ganglion, or through a patent tympanomeningeal (Hyrtl) fissure
- Bacteria can enter the meninges through the labyrinth if there is a previous labyrinthine fistula
Signs and symptoms:
- Headache
- Lethargy
- Nuchal rigidity
- Irritability
- Fever
- Photophobia
- Seizures
- Kernig’s sign – with hip flexion, pain is elicited with leg extension
- Brudzinski’s sign – flexion at neck causes a reflexive flexion of the legs
Diagnosis:
- Lumbar puncture if no evidence of increased intracranial pressure
- Consider MRI
Treatment:
- IV antibiotics
- IV steroids
- Myringotomy
- Repair of Mondini malformation or meningoencephalocele toward the end of treatment
- In subacute or chronic disease, mastoidectomy is needed to exenterate all middle ear disease and debride any granulation or diseased dura
Concluding Comments
- Although complications of otitis media are relatively rare, it is important to recognize the early signs and symptoms so that prompt treatment can be initiated
- Despite the complication, treatment usually begins with a change in antibiotic regimen or the initiation of parenteral antibiotics
- Myringotomy is important for both drainage of the infection and to obtain culture and sensitivity results for the inciting organism
- Mastoidectomy becomes useful in both eradicating middle ear disease and accessing and debriding areas of local extension of the infection
- Neurosurgical consultation should be initiated early if an intracranial complication is suspected
- Aggressive early treatment of these complications will likely offer the most favorable outcomes
