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The sequelae and complications of OM are vast, boasting a significant impact on both the pediatric and adult populations. Different types of complications result from AOM and OME as seen in Table 49–4.
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The spectrum of complications resultant from AOM ranges from the more common persistent TM perforation to the infrequent, but more severe intracranial complications. Critical complications of AOM arise in the modern antibiotic era generally due to poor access to medical care, poor compliance, or inappropriate diagnosis and management.
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Tympanic Membrane Perforation
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TM perforation can occur in the setting of AOM from accumulating inflammation and corresponding ischemia of the TM. The vast majority of perforations from AOM heal spontaneously within 48 to 72 hours. Non-healing perforations can lead to long-term sequelae such as conductive hearing loss or otorrhea.
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Acute mastoiditis, the most common intratemporal complication of AOM, occurs due to direct extension of disease from the middle ear cleft to the mastoid air cells. Classically, acute mastoiditis refers to the coalescent type with mastoid bone destruction and possible subperiosteal abscess formation lateral to the mastoid cortex. The patient typically presents with fevers, post-auricular erythema, and tenderness, ear proptosis, and AOM on otoscopy. Computerized tomography (CT) imaging demonstrates loss of mastoid air cell trabeculations, local bone destruction, and presence of soft tissue within the mastoid cavity and middle ear cleft.
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If infection escapes through the mastoid tip and tracks down the upper neck along the sheath of the sternocleidomastoid muscle (SCM), an abscess, known as Bezold's abscess, forms just deep to the SCM. Bezold's abscess occurs in older children with fully pneumatized mastoid tips, and in adults with mastoiditis or cholesteatoma. Similarly, when infection extends beyond the mastoid to penetrate the plane adjacent to the posterior belly of the digastric muscle, it is referred to as a Citelli's abscess.
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The term “masked mastoiditis” is used to describe granulation tissue and bony erosion of the mastoid in the absence of otorrhea. On otoscopy, the TM appears normal however a focus of infection (not responsive to antibiotics) continues to persist in the mastoid cavity. Patients may experience chronic postauricular pain with only slight tenderness on palpation of the mastoid. Furthermore, CT scan demonstrates localized opacification with an otherwise normal appearing mastoid.
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Patients with chronic mastoiditis classically present with purulent otorrhea, dull otalgia, often associated with multiple episodes of AOM, TM perforation, or cholesteatoma.
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Although exceptionally rare, petrositis is a known complication of AOM. Petrositis occurs when infection spreads within the temporal bone into the petrous apex. The classic triad, or Gradenigo's syndrome, is rare and characterized by retroorbital pain, AOM, and ipsilateral abducens nerve paresis. In conjunction with the clinical triad, diagnosis is confirmed with radiographic findings of bony destruction of the petrous apex.
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Facial nerve paresis can occur in the setting of AOM or OME, by two different mechanisms: (1) from the release of locally produced bacteria-mediated toxins or (2) from the direct effect of inflammatory tissue adjacent to the facial nerve as it transverses the mastoid cavity. Detecting the site of lesion can be a challenge especially in the setting of grossly inflammatory diseases such as AOM, cholesteatoma, or mastoiditis. The nerve excitability, maximum nerve excitability, electromyography, and electroneurography may be beneficial in identifying a neuro-destructive lesion. MRI with gadolinium can also provide additional information about inflammatory or neoplastic-mediated processes. In this context, the etiology of facial paresis differs when comparing the adult and pediatric populations. In adults, facial paresis most often occurs in the setting of cholesteatoma, whereas in children, AOM will precede the onset of facial paresis.
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Patients with labyrinthitis present with sudden sensorineural hearing loss, severe vertigo, and nystagmus accompanied by nausea and vomiting. In the setting of middle ear infection, bacterial infection can invade through the round window causing acute suppurative labyrinthitis. From the labyrinth, bacteria gain access to the cochlear aqueduct, forming a conduit between the perilymph and the cerebrospinal fluid (CSF) resulting in meningeal infiltration. It is important to diagnose and treat labyrinthitis early as to prevent the subsequent development of meningitis.
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Intracranial Complications
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Intracranial complications, including meningitis, encephalitis, otitic hydrocephalus, and abscess, are rare but serious, resulting from severe or neglected AOM (Figure 49–1). In children who develop fever, headache, photophobia, fluctuating mental status, and neck rigidity within hours of AOM, meningitis should be suspected. Furthermore, if patients also present with unilateral of bilateral congenital sensorineural hearing loss and vestibular symptoms, a Mondini malformation should be considered. Mondini malformations allow for communication between the CSF and the middle ear space through the stapes footplate or round window to the vestibule or cochlea. Meningitis secondary to AOM should be treated urgently with a myringotomy.
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Otitic hydrocephalus typically presents as headaches and lethargy without evidence of meningeal signs or intracranial abscess. Often associated with papilledema, otitic hydrocephalus is defined as increased intracranial pressure secondary to AOM or OME.
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Extradural, subdural, and brain abscesses are all severe, uncommon complications of untreated AOM. The most commonly cultured organisms from these abscesses include streptococci, Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas aeruginosa, Bacteroides fragilis, and Proteus. Once diagnosed, both brain and subdural abscesses require urgent neurosurgical intervention for drainage. In contrast, extradural abscesses can be approached via mastoidectomy while addressing underlying middle ear disease.
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The sigmoid (or lateral) sinus lies in close proximity to the mastoid cavity. If virulent AOM or mastoiditis penetrates the sigmoid sinus, sigmoid sinus thrombophlebitis may occur. Patients present classically with diurnal or “picket fence” fever curves, septicemia, and torticollis. Systemic signs and symptoms occur due to the showering of infected emboli both proximally and distally to the sigmoid sinus. MRI with gadolinium is considered to be the gold standard for diagnosis of sigmoid sinus thrombophlebitis.
Bluestone CD. Definitions, terminology, and classification. In: Evidence-Based Otitis Media. BC Decker; 1999. pp. 94–96 (Comprehensive, evidence-based book chapter outlining the historical progression of the definitions, terminology and classification of otitis media.)
Neely JG, Arts HA. Intratemporal and intracranial complications of otitis media. Bailey & Johnson Head & Neck Surgery—Otolaryngology, 4th ed. Lippincott, 2006. (Comprehensive, reference textbook in otolaryngology-head & neck surgery.)
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As noted above, substantial overlap exists in terms of complications resulting from AOM and OME. In contrast to the acute process, OME exhibits disease chronicity, symptoms expressed over longer periods of time.
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Conductive Hearing Loss & Speech Delay
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Conductive hearing loss is a well-studied complication of OME. Hsu et al. report “average duration of effusion in patients with chronic OME as 5.5 months” and “duration of AOM prior to referral as 9.3 months.” While OME-associated hearing loss is temporary, it is not fleeting and can have a significant impact on development. Studies suggest that the intermittent, fluctuating hearing loss caused by OME can influence certain aspects of language including articulation, receptive vocabulary, and phonologic awareness.
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Atelectasis in the setting of OME refers to either a grossly retracted or collapsed TM. TM retraction occurs when the negative pressure in the middle ear space accumulates, most often as a result of chronic Eustachian tube dysfunction. Over time, a retracted TM may lead to ossicular erosion and conductive hearing loss, which may be salvageable only through surgical repair. In the event that the TM is partially ateletatic, a localized retraction pocket can form leading to an altered migration pattern of squamous epithelium. This disruption of migration patterns predisposes to accumulation of debris and finally, cholesteatoma formation.
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With long-term tympanic retraction, acquired cholesteatoma development may occur. Acquired cholesteatoma, a consequence of AOM, OME or both, can be further divided into two categories: primary or secondary. Primary acquired cholesteatomas classically arise in the epitympanum adjacent to the pars flaccida component of the ear drum. In comparison, secondary acquired cholesteatomas migrate through a TM perforation into the middle ear. In the setting of chronic Eustachian tube dysfunction, the normal migration pattern of squamous epithelium in the external auditory canal is agitated. Disruption of squamous epithelium can lead to accumulation of debris and cholesteatoma formation. Cholesteatoma will expand locally destroying local bone in its path including the scutum, ossicles, mastoid cavity, tegmen, or otic capsule. This destruction can lead to long-term serious complications including facial paralysis, labyrinthitis, meningitis, and hearing loss.
Nittrourer S. The relation between speech perception and phonemic awareness: Evidence from low-SES children and children with chronic otitis media. J Speech Hear Res. 1996;39:1059–1070. (A retrospective controlled study exploring the development of speech perception and phonemic awareness in low-socioeconomic status children and children with otitis media.)
Vernon-Feagans PhD. Impact of otitis media on speech, language, cognition and behavior. In: Evidence-Based Otitis Media BC Decker; 1999. pp. 360–363 (Review of prospective studies examining the effects of otitis media on development of speech, language, cognition and behavior over time.)
Chole RA, Sudhoff HH. Chronic otitis media, mastoiditis, petrositis. Cummings: Otolaryngology: Head & Neck Surgery, 4th ed. Elsevier, 2005. (Comprehensive, reference textbook in otolaryngology-head & neck surgery.)