Intratemporal and Intracranial Complications of Otitis Media

Alexander H. Arts

Meredith E. Adams

Otitis media (OM) is a heterogeneous disease with a wide spectrum of presentations and natural histories. The etiology, presentation, natural history, and management of acute and chronic otitis media (AOM and COM) are discussed in detail in other chapters. In this chapter, we discuss the complications, both intratemporal and intracranial, of AOM and COM and cholesteatoma, and their management. These complications are summarized in Table 149.1.

AOM is a common infection, estimated to represent up to 5.8% of all patient visits to physicians (1, 2). In the vast majority of cases, the pathologic process is self-limited, or resolves with antibiotic therapy. Indeed, although not universally agreed upon, some have recently considered observation alone for straightforward cases of AOM, with antibiotics reserved for refractory cases, or for prevention of complications in higher risk patients (3). AOM may resolve completely, resolve and recur, or evolve into one of many manifestations of COM. Complications of OM can occur directly from AOM or arise from COM. Although these complications are rare today, they occur in developed countries at approximately the same frequency as in underdeveloped countries, and are associated with high rates of serious morbidity and mortality (4). Prompt diagnosis and rapid, effective therapy are critical to minimizing these sequelae.

PATHOPHYSIOLOGY

Pathophysiology of OM

Both AOM and COM are bacterial infections involving the middle ear cleft. Risk factors can be complex and interrelated, but are primarily associated with (a) exposure to pathogens, (b) local anatomy, and (c) host response.

Exposure to pathogens can be increased or altered by exposure to day care environments, or crowded or unhygienic living situations. The specific microbiologic flora is strongly influenced by prior individual and community antibiotic treatment (5). Exposure to nasopharyngeal flora may be enhanced with patent eustachian tubes. In the case of COM, contamination by pathogens can occur via the external auditory canal via a tympanic membrane perforation or by direct contamination of debris within a cholesteatoma.

The latter can be enhanced by exposure to water from swimming or bathing. Different pathogens have varying degrees of pathogenicity and disease progression. The bacteriology of OM is summarized in Table 149.2. The primary anatomic variable affecting the development of OM is eustachian tube function. Eustachian tube function varies widely in otherwise normal individuals, but is reduced in patients with cleft palate, exposure to smoke (smokers and passive exposure), allergic rhinitis, neoplastic processes involving the cranial base, acromegaly, and many other conditions. Abnormally patent eustachian tubes result in reflux of nasopharyngeal contents into the middle ear. Mucosal disease such as nasal polyposis, ciliary dyskinesia, or cystic fibrosis results in reduced eustachian tube function. If a patient develops cholesteatoma, the local anatomy has a direct effect on how the cholesteatoma grows and what bony destruction it causes. The cholesteatoma and associated inflammation can then, in turn, directly or indirectly impact eustachian tube function.

Host response factors such as immunodeficiency, immunization status, ciliary dyskinesia, and history of bottle-feeding also play important roles in the development of OM.

Pathophysiology of Complications of OM

Similar factors influence the development of complications of OM, with the addition of many other variables. It is important to understand the anatomy in which these infections exist, their routes of spread, and the characteristic patterns of disease. Infection can spread via direct extension, via venous structures, or hematogenously. However, the primary pathogenesis seems to be a complex interaction between the specific organisms and the host (8).

TABLE 149.1

COMPLICATIONS OTITIS MEDIA

Intratemporal (extracranial)
	Mastoiditis
		Acute
		Coalescent
		Chronic
		“Masked”
		Associated with subperiosteal abscess
		Associated with deep neck abscess (Bezold abscess)
	Petrositis
	Labyrinthitis
		Serous or toxic
		Suppurative
			Otogenic
			Meningogenic
	Facial paralysis
	Labyrinthine fistula
Intracranial
	Extradural granulation tissue or abscess
	Sigmoid sinus thrombophlebitis
		Occluding
		Nonoccluding
	Brain abscess
	Otitic hydrocephalus
	Meningitis
	Subdural abscess

An important host response leading to complication is the production of tissue edema and granulation tissue that subsequently becomes obstructive to drainage and aeration. This creates an environment conducive to the growth of anaerobic organisms and the destruction of bone. Important microbiologic factors seem to pivot about the synergistic pathogenicity of anaerobic organisms (9).

The epidemiology and microbiologic behavior of the organisms found in complications offer some insight into the pathogenesis and pathophysiology of these complications (Table 149.2). For example, infections with Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis are the most common causes of acute suppurative OM (3, 10). Only about 4% of OM is caused by infection with H. influenzae type B; however, pediatric patients with OM occurring simultaneously with meningitis or other central nervous system infections were found to have an unusually high incidence of H. influenzae type B (10).

Uncomplicated chronic otorrhea characteristically cultures Pseudomonas aeruginosa, Staphylococcus aureus, and a variety of other Gram-negative organisms, such as Proteus sp., Klebsiella sp., and Escherichia coli. In contrast, mastoiditis associated with chronic suppurative otitis media (CSOM) frequently has a fetid odor and often cultures positive for Bacteroides fragilis (6). Multiple organisms are found in 57% of chronically draining ears with cholesteatoma, with an average of three different organisms. However, if these ears have a fetid discharge, characteristically 5 to 11 organisms are found, always including both anaerobes and aerobes. Malodorous discharge is a significant early sign of complication. Anaerobic organisms are a major cause of foulsmelling discharge.

TABLE 149.2 BACTERIOLOGY OF OM (PATHOGENS LISTED IN ORDER OF PREVALENCE) (6, 7)

Acute suppurative OM
	Streptococcus pneumoniae
	Haemophilus influenza (nontypeable)
	Moraxella catarrhalis
	Others (far less common)
		Group A Streptoccoci
		Staphylococcus aureus (infrequent)
		Gram-negative bacilli (infrequent)
Acute mastoiditis
	Streptococcus pneumonia
	Pseudomonas aeruginosa
	Group A beta-hemolytic Streptoccoci (e.g., Streptococcus pyogenes)
	Coagulase-negative Staphylococcus sp.
	Others (far less common)
		Staphylococcus aureus
		Proteus sp.
		Bacteroides sp.
Chronic otorrhea with or without cholesteatoma
	Mixed aerobic (also occasionally including S. pneumonia) and anaerobic organisms
			Foul-smelling ears (especially with cholesteatoma) may grow 5-11 organisms, always mixed aerobic and anaerobic
	Pseudomonas aeruginosa (most common aerobe)
	Staphylococcus aureus and Staphylococcus epidermidis
	Other aerobic organisms including Proteus sp., Klebsiella sp., Escherichia coli
	Various anaerobic organisms including Bacteroides fragilis
Intracranial abscesses (brain and subdural) of otogenic origin (mixed cultures)
	Streptococcus sp.
	Staphylococcus sp.
	Proteus sp.
	Anaerobic organisms (Peptococcus, Peptostreptococcus, Bacteroides fragilis)
Bacterial meningitis in children
	Streptococcus pneumonia
	Haemophilus influenzae, type B
	Neisseria meningitidis

β-Lactamase-producing organisms, such as S. aureus, H. influenzae, B. catarrhalis, and Bacteroides sp., not only survive β-lactam antibiotics but may also protect other potentially penicillin-susceptible pathogens from penicillin and other β-lactam antibiotics. Anaerobic organisms have recently been shown to play major roles in pathogenic synergism by protecting against host defenses, creating suitable environments for other organisms, and inactivating antibiotics (8, 9).

Anatomic variables are tremendously important in the development of complications. Eustachian tube function plays a critical role in not only the development of the original infection and its resolution but also the development of complications. The mucosal edema resulting from OM itself impairs eustachian tube function and inhibits resolution of the infection. Highly variable factors, such as the integrity of bone over the facial nerve or dura, influence access of the infection and its products to neurovascular structures and the intracranial space. Numerous venous channels traverse the bone between the mastoid and middle ear and the dural venous sinuses, sometimes associated with arachnoid granulations. Inflammation adjacent to these veins and venules can promote thrombosis. Thrombi and infection can then propagate to the dural venous sinuses and subarachnoid space. Cholesteatoma often results in patterns of bone destruction exposing the dura or facial nerve to the infectious process. Finally, prior surgery can result in areas of entrapped squamous epithelium or deficient areas of bone that act as sources of infection and routes for the infection to spread.

GENERAL PATTERNS OF PRESENTATION

Complications of OM tend to present in predictable patterns (Table 149.3). With the exception of meningitis in children and some cases of facial paralysis, which are usually associated with AOM, most complications tend to be associated with COM. Typically, mastoiditis is the initial complication, with more severe complications developing secondarily. Petrositis (petrous apicitis), for example, almost never occurs without preceding mastoiditis. Labyrinthine fistulae virtually always develop secondary to cholesteatoma. Granulation tissue in air cells adjacent to the sigmoid sinus can result in erosion of the bone overlying the sinus, with resultant sigmoid sinus exposure and possible sigmoid sinus thrombophlebitis. If the sigmoid becomes obstructed with thrombus, intracranial hypertension, that is, otitic hydrocephalus, can result (11). Retrograde thrombophlebitis may extend intracerebrally, resulting in a brain abscess. Subdural empyema rarely occurs due to COM, but is a more typical complication of meningitis in infants.

TABLE 149.3 PATTERNS OF PRESENTATION OF COMPLICATIONS OF OM

Origin of complication
	Acute infection
	Meningitis—infants and young children
	Meningitis—adults or children with occult CSF leaks
	Facial paralysis—children more commonly
	Labyrinthitis
Subdural abscess—infants more commonly
Subacute or chronic infection
	Mastoiditis
	Petrositis
	Facial paralysis
	Labyrinthitis
	Extradural abscess and granulations
	Sigmoid sinus thrombophlebitis
	Brain abscess
	Otitic hydrocephalus
	Meningitis
	Subdural abscess
Patterns of associated diseases and usual sequence
	Mastoiditis or petrositis
		Extradural granulation tissue and/or abscess
		Sigmoid sinus thrombophlebitis
		Brain abscess or otitic hydrocephalus
	Meningitis
		Subdural abscess—infants more commonly

Without a high index of suspicion, early evidence of an impending complication will be missed. Early symptoms and signs of complication are summarized in Table 149.4. Because antibiotic therapy may have a masking effect on the significant signs and symptoms of complications, a high level of clinical awareness is important for early diagnosis. Persistence of acute symptoms for 2 weeks or more or recurrence of symptoms or infection within 2 weeks is often the first sign of a potential complication. In chronically draining ears, acute exacerbation of pain or the new development of fetid drainage should be evaluated. Foulsmelling drainage that fails to respond to conservative treatment (debridement and topical antibiotics) portends an impending complication.

Once a complication has begun, signs and symptoms typically progress rapidly. Fever associated with COM implies some degree of extracranial cellulitis or intracranial infection. Postauricular edema/erythema, edema of the posterior-superior external auditory canal (EAC) wall, or anterolateral displacement of the pinna indicates mastoiditis associated with subperiosteal abscess. Retro-orbital pain in an infected ear is highly suggestive of petrositis (petrous apicitis). Vertigo and nystagmus in a patient with OM may indicate serous or suppurative labyrinthitis, or possibly a labyrinthine fistula. Facial paralysis ipsilateral to an infected ear may complicate AOM, or COM with cholesteatoma. Papilledema is an obvious sign of elevated intracranial pressure, but will go undetected without a fundoscopic examination. Headache and lethargy usually accompany an intracranial infectious complication. Meningismus is associated with meningitis, and focal neurologic signs or seizures are seen in brain abscess.

TABLE 149.4 EARLY SIGNS AND SYMPTOMS OF COMPLICATIONS

Impending complication
	Persistence of acute infection for 2 weeks or more
	Recurrence of symptoms within 2 weeks after initial resolution
	Acute exacerbation of chronic infection, especially if foul-smelling
	Foul-smelling discharge during treatment
	Haemophilus influenza type B or anaerobes
Complication (associated complication)
	Fever associated with a chronic perforation (intracranial infection or extracranial cellulitis)
	Pinna displaced inferolaterally and/or edema of the posterosuperior ear canal wall skin (subperiosteal abscess)
	Retro-orbital pain (petrositis)
	Vertigo in a patient with an infected ear (labyrinthitis or labyrinthine fistula)
	Facial paralysis ipsilateral to an infected ear (facial paralysis)
	Headache and lethargy (intracranial complication of any sort)
	Meningismus (meningitis or subdural abscess)
	Focal neurologic signs or seizure (brain abscess)
	Global neurologic signs (subdural abscess or meningitis)

SPECIFIC COMPLICATIONS

Intratemporal (Extracranial) Complications

Mastoiditis

As commonly used clinically, the term “mastoiditis” is nonspecific and often misleading. Since the mastoid air cell system is confluent with the middle ear space, any inflammatory process within the middle ear will also involve the mastoid. Although it may be pathologically correct to refer to purulent fluid within the mastoid secondary to OM as “mastoiditis,” it is not clinically meaningful or helpful, and does not represent a complication of OM. An example of this clinically misleading use of the term “mastoiditis” is the radiologic diagnosis of “mastoiditis” based on the presence of opacification or increased T2 signal intensity alone. This does not imply a complication and does not require additional therapy beyond that indicated for the primary middle ear process. True mastoiditis as a complication of OM implies an invasive or persistent infection involving the mastoid bone and/or surrounding structures, distinct from AOM or OM with effusion. With this in mind, mastoiditis can be subdivided into (a) acute mastoiditis, (b) coalescent mastoiditis, (c) chronic mastoiditis, and (d) masked mastoiditis. Clinically, there is often some overlap between these diagnostic categories.

Acute Mastoiditis

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