Surgery of Acute Infections and Their Complications

Definition and Clinical Significance

Infections of the mastoid or middle ear may spread beyond the confines of the pneumatized spaces of the temporal bone. When this occurs, the patient is at risk for significant morbidity or mortality. While these complications were more common before the antibiotic era, the potential harm to the patient is high, and the presentation may be subtle.

The complications of acute or chronic ear disease are classified as intracranial or extracranial. The intracranial complications include meningitis, brain abscess, and venous sinus thrombosis ( Fig. 15.1 ). The extracranial complications can be further divided into extratemporal, which includes abscesses of the surrounding soft tissue, and intratemporal, which includes facial paralysis, labyrinthitis, and mastoiditis.

Etiology and Pathogenesis

Fundamental to the development of complications of suppurative ear disease is the interaction of host factors and virulence of the offending organism(s). Once present in the mastoid or middle ear, the extension of infection beyond the ear follows the path of least resistance. Defects of the temporal bone may be present prior to infection, or the organism may cause them.

Host Factors

Preexisting defects within the temporal bone provide a route for infection to spread from the pneumatized bone of the ear to the surrounding structures. One of the clearest examples of this is the sign of the proptotic ear from acute mastoiditis. Infection spreads from the mastoid through the naturally porous bone of the MacEwan triangle to the postauricular subperiosteal plane. This subperiosteal abscess then pushes the ear forward.

Congenital defects of the temporal bone also present a risk. Defects of the inner ear, such as Mondini malformations, allow a more direct route for infection to spread from the cochlea into the cerebrospinal fluid of the internal auditory canal. Congenital bony tegmen defects, found in 20% to 34% of patients, may also provide a route for infection, although the dura itself may provide an additional barrier against spread.

Acquired defects of the temporal bone also remove barriers between the ear and the surrounding structures. These defects include temporal bone fractures, iatrogenic injury to the tegmen and dura, and erosion from cholesteatoma. Spontaneous cerebrospinal fluid leaks of the temporal bone, which are related to obesity and obstructive sleep apnea, ^, also provide a path for infection to ascend intracranially.

It has also been theorized that infection can spread via the mastoid emissaries and sigmoid sinus. Older works emphasize the role of local tissue inflammation from the infection as a trigger for complications. It was thought that granulation tissue obstruction of the eustachian tube or the atticus may trap infection, and this provided the rationale for early surgical intervention. The clinical significance of this granulation is unclear, however, particularly given that many patients with acute complications are successfully treated with more conservative therapy.

Age and race also influence the outcome. Immature immunity makes young children more susceptible to acute otitis media and acute mastoiditis, while adults are more frequently affected by chronic otitis media with or without cholesteatoma. Morbidity from acute complications, however, is associated with Black race and older age.

Pathogen Factors

The pathogens associated with acute otitis media are Streptococcus pneumoniae , nontypeable Haemophilus influenzae , and Moraxella catarrhalis . These occasionally cause intratemporal complications, such as facial nerve weakness. While acute mastoiditis is generally considered on a continuum with acute otitis media, the pathogens associated with acute mastoiditis differ slightly. These are S. pneumoniae , Streptococcus pyogenes , Staphylococcus aureus , H . influenzae , and Pseudomonas aeruginosa . S . pneumoniae and Fusobacterium necrophorum deserve specific mention.

S. pneumoniae is the most common of the pathogens involved in both acute otitis media and acute mastoiditis. While there was some initial promise that vaccination for S. pneumoniae would decrease the incidence of acute mastoiditis and its complications, this does not appear to have occurred. ^, This pathogen has some unique properties. It is associated with recurrent acute mastoiditis. It also has the potential to spread hematogenously; from the ear, it may enter the circulatory system, and then spread intracranially. ^,

F. necrophorum , an anaerobe, is an emerging pathogen for acute mastoiditis. Several groups in Europe and Israel have documented both its rise and virulence. ^, F . necrophorum mastoiditis is associated with a higher complication rate, particularly extracranial abscess and lateral sinus thrombosis. ^, Patients with a history of outpatient antibiotics prior to presenting with acute mastoiditis appear to be more likely to have F. necrophorum .

In chronic otitis media, the bacteria encountered in middle ear discharge are Pseudomonas aeruginosa, Proteus mirabilis, and S . aureus . Bacterial cultures do not appear to differ when cholesteatoma is present. Biofilms are frequently encountered in chronic otitis media and may challenge treatment with antibiotics. Bone erosion occurs through the induction of osteoclasts from inflammatory tissue adjacent to bone, and this activity may allow infection to spread beyond the ear.

Clinical Presentation and Diagnosis

Patients’ presentation depends on the complication encountered. Chronic or acute ear infections associated with fever, otalgia, purulent otorrhea, headache, neck stiffness, blurred vision, double vision, or failure to improve despite antibiotic treatment suggest complications. Papilledema may be identified if otitic hydrocephalus is present. Occasionally, obvious signs of facial weakness or vertigo in the presence of an ear infection may be present. Signs of inflammation in the bloodwork may be found. In one study, an elevated C-reactive protein (CRP) above 93.5 mg/L indicated intracranial complications from acute mastoiditis.

Suspicion for complications should prompt imaging. Computed tomography (CT) of the temporal bone provides evidence of erosion of the bony barriers between the mastoid and middle ear and surrounding structures. The tegmen, bone over the sigmoid sinus, and posterior fossa plate should be assessed for defects. Contrast enhancement of brain or temporal bone CTs can demonstrate abscess collection and venous thrombosis.

Magnetic resonance imaging (MRI) of the internal auditory canal or brain with contrast may also demonstrate the presence of abscess or thrombosis. MRI is recommended if there is any concern for intracranial complications, particularly because it allows a better evaluation than does CT for dural enhancement, cerebritis, cerebral edema, and intracranial granulation. Recent advances, particularly with non-echoplanar diffusion-weighted imaging, have allowed for the discrimination of cholesteatoma. These sequences are a valuable addition to assess the etiology. Further, if mastoiditis or, particularly, sigmoid sinus phlebitis is found, a repeat MRI 3 to 4 weeks after treatment may detect the subsequent development of an occult brain abscess.

Systemic Diagnostic Approaches

The complications of chronic or acute suppurative otitis media may occur alone or in combination. Extracranial complications, involving either the structures within the temporal bone or the surrounding soft tissue, are the most common. The three most common complications of acute suppurative otitis media, for instance, are acute mastoiditis, labyrinthitis, and facial paralysis. The complications are not always obvious, and a high index of suspicion is necessary for some of the more subtle and severe sequelae.