DEFINITION AND CLINICAL SIGNIFICANCE

Complications of acute or chronic suppurative ear disease manifest acutely and are medical and surgical emergencies. These complications are defined as a spread of infection beyond the confines of the pneumatized spaces of the temporal bone and the attendant mucosa. Complications are classified into two groups: aural (intratemporal) and intracranial. Aural complications include (1) mastoiditis, (2) petrositis, (3) labyrinthitis, and (4) facial paralysis. Intracranial complications include (1) extradural abscess or granulation tissue, (2) dural venous sinus thrombophlebitis, (3) brain abscess, (4) otitic hydrocephalus, (5) subdural abscess, and (6) meningitis (Fig. 15-1).¹

FIGURE 15-1 Intracranial complications. The predictable pattern of associated complications is numbered in order of progression with the ultimate outcome being brain abscess or otitic hydrocephalus or both. CSF, cerebrospinal fluid.

Because of the significant reduction in absolute numbers of complications, individual clinicians do not have extensive experience in treating patients with complications of suppurative ear disease. This limited experience contributes to decreased familiarity and recognition of otogenic complications.^2,3 The combination of lack of awareness and masking of early signs and symptoms leads to delay in diagnosis and subsequent treatment. Physician delay has been noted to be the most significant factor in late diagnosis and treatment of otogenic complications. Delay in diagnosis and treatment of complications of suppurative ear disease is associated with worsening morbidity and mortality.^2,4

ETIOLOGY AND PATHOGENESIS

The organisms responsible for otogenic complications in the acute setting are Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, and Haemophilus influenzae.⁵ Organisms that cause complications in chronic otitis media are frequently gram-negative or anaerobic, or both; the presence of anaerobes is significantly associated with complications.^6–9 Pseudomonas aeruginosa, Enterobacteriaceae, S. aureus, and anaerobic bacteria are most common in chronic mastoiditis; anaerobes tend to predominate in chronic mastoiditis when techniques allow their discovery.⁵

In patients with infratemporal complications, isolates from cultures of middle ear effusions, otorrhea, and mastoid have shown S. pneumoniae to be the most common organism,¹⁰ followed by P. aeruginosa, S. pyogenes,¹¹ S. aureus, and H. influenzae.^12,13 P. aeruginosa was the most common organism found in a review of 134 patients with acute mastoiditis.¹⁴

S. pneumoniae¹⁵ and H. influenzae type B are the most common causes of bacterial meningitis.¹⁶ Proteus mirabilis, P. aeruginosa, and staphylococcal organisms are common pathogens isolated in patients with intracranial complications.¹⁷ Gram-negative isolates have been major organisms in other series.^18,19 Polymicrobial cultures are common in brain abscess.⁸

These studies are important for a general reference; however, organisms change over time, and culture-specific treatment is important, as illustrated by the fact that a more recent study determined that methicillin-resistant S. aureus was the second most common organism in chronic suppurative otitis media.²⁰

Obstruction of the aditus ad antrum, congenitally preformed pathways through the oval or round window; obstruction of acquired pathways from fractures or chronic erosive infection, granulation tissue, or cholesteatoma, especially virulent organisms such as H. influenzae type B; and synergistic pathogenicity resulting from anaerobic organism microenvironmental changes all may play a role in the pathogenesis of complications (Fig. 15-2).^1,21 Clinically, several important observations can be made that help alert the physician to the possible occurrence of a complication and may reflect some of the pathobiology. Signs and symptoms of possible impending complications are (1) persistent acute infection for 2 weeks; (2) recurrent symptoms of infection within 2 weeks; (3) acute, fetid exacerbation of chronic infection; (4) fetid discharge during treatment; (5) H. influenzae type B or anaerobes cultured from the ear; and (6) fever in the presence of a chronically perforated tympanic membrane, with or without cholesteatoma.

FIGURE 15-2 Obstruction of the aditus ad antrum, key to the development of complications.

CLINICAL PRESENTATION

When the possibility exists that the patient has a complication from suppurative ear disease, the complete list of the 10 complications and the fact that more than one complication is likely can be overwhelming. The complications tend to manifest in obvious or predictable clinical patterns, however.

Less Obvious Complications

Classic mastoiditis is easily recognized; however, without such obvious signs, masked mastoiditis (defined as radiographic evidence of bone destruction) may manifest as mild discomfort in the ear, with or without mastoid tenderness. The pathophysiologic and diagnostic key to occult complications is mastoiditis. Without careful medical care, the classic presentation of acute coalescent mastoiditis with subperiosteal abscess predominates and is quickly diagnosed. Masked mastoiditis may occur in patients with seemingly adequate care, however, and is much harder to diagnose promptly, and consequently can be much more devastating and is more often associated with intracranial complications.^23,24 Patients with any of the signs and symptoms of impending complication, particularly with a recurrence of deep, although not severe, pain, may have masked mastoiditis. If bone destruction is present, the diagnosis is made. Masked mastoiditis may exist, however, without early evidence of radiographic bone destruction. If pain persists despite seemingly adequate culture-guided antibiotic administration, surgical mastoid exenteration with facial recess approach to the middle ear creating a posterior tympanotomy, deep mastoid cultures with sensitivities for aerobes and anaerobes, and aggressive medical treatment may be indicated.

Rarer subperiosteal or soft tissue abscesses can occur in the deep neck (Bezold’s abscess) or zygoma (Luc’s abscess). If purulent debris escapes through eroded bone and along vessels from the medial tip cells (medial to the digastric ridge and muscle) and diploetic bone and enters the neck through the incisura digastrica (the digastric groove on the inferior surface of the temporal bone), a Bezold’s abscess is formed. Purulent debris deep to the fascial planes of the sternocleidomastoid and trapezius muscles is difficult to localize by palpation.²⁵ If pus tracks along the external auditory canal and accumulates under the temporalis muscle, a rare Luc’s abscess is formed.²⁶

Other, less obvious complications follow. Subdural abscesses are extremely rare, usually obvious by coma and focal neurologic signs and easily seen by magnetic resonance imaging (MRI). If there is any doubt that a catastrophic intracranial lesion exists, the chance of a subdural abscess being present is remote.

Otitic hydrocephalus characteristically manifests with headache, some degree of lethargy, and severe papilledema. Almost without exception, otitic hydrocephalus is associated with occlusive sigmoid sinus thrombophlebitis and extradural abscess or granulation tissue.

Petrositis manifests with retro-orbital pain; however, the patient may not volunteer this symptom. It is crucial to ask about retro-orbital pain to be assured of its absence. Petrositis is rarely, if ever, present without mastoiditis. Intracranial complications are more frequent with petrositis. The full classic triad of Gradenigo (ear infection, ipsilateral retro-orbital pain, and abducens palsy), often thought to be pathognomonic of petrositis, is rarely present in petrositis unless an extradural intracranial medial petrous abscess is present that compresses the abducens nerve in Dorello’s dural canal.

Four silent, but extremely serious complications occur together in predictable patterns: (1) mastoiditis (classic or masked), (2) extradural abscess or granulation tissue, (3) dural venous sinus thrombophlebitis, and (4) brain abscess. Mastoiditis may occur alone, but often results in a silent accumulation of extradural abscess or granulation tissue. The extradural infection may occur, in the case of cholesteatoma, in the middle fossa at the tegmen, but it characteristically occurs along the extraluminal surface of the lateral wall of the sigmoid sinus, creating an often silent, nonoccluding phlebitis of the sinus wall and an induced mural thrombus, sigmoid sinus thrombophlebitis. In every case of suspected or operated mastoiditis, extradural granulation tissue and sigmoid sinus thrombophlebitis should be sought, preoperatively and intraoperatively. Brain abscess occurs as a result of retrograde thrombophlebitis of cerebral or cerebellar veins that are tributaries to the inflamed sigmoid sinus or other adjacent dural sinuses.

Brain abscesses have four stages, as follows:

1. Invasion: The initial onset of cerebritis. This stage creates vague symptoms of mild headache, lethargy, and malaise that last several days and then resolve.

2. Localization: The stage of quiescence and latency. This stage is totally silent for weeks.

3. Enlargement: The stage in which most abscesses manifest with seizures or focal neurologic signs.

4. Termination: The stage in which the abscess catastrophically ruptures into the ventricle or subarachnoid space.

Brain abscesses are silent; take weeks from onset to be detectable, even with imaging; and can be devastating. It is prudent to look for brain abscesses in cases of mastoiditis initially and again 3 to 4 weeks later (Fig. 15-3).

FIGURE 15-3 A and B, Mechanism of development of brain abscess by retrograde thrombophlebitis of cerebral vessels, usually above the tentorium, from inflamed sigmoid and transverse sinus secondary to mastoid and extradural granulations.

DIAGNOSIS

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