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686 PART 5: Infectious Disorders

due to involvement of the abducens, oculomotor, and trochlear nerves by extension into the temporal or occipital bone. Prolonged medical
and the ophthalmic division of the trigeminal nerve as they pass through therapy in conjunction with local debridement of granulation tissue
the orbital fissure. 25,26 and infected cartilage is effective in the majority of patients. In patients
Extension of infection from the maxillary sinus into the adjacent with more extensive disease involving the base of the skull and multiple
structures may result in osteomyelitis of the facial bones and prolapse cranial nerve palsies, therapy is not as successful, and up to 20 months
of the orbital antral wall with retro-orbital cellulitis, proptosis, and oph- of antimicrobial treatment may be required to achieve eradication of
thalmoplegia. Direct intracranial extension from the maxillary sinus is infection without relapse.
rare, except in rhinocerebral mucormycosis and other types of invasive
fungal sinusitis. ■ INTRACRANIAL SUPPURATION
Nosocomial sinusitis occurring after prolonged endotracheal intuba-
tion is a common complication of ventilation-associated pneumonia These dreaded complications that most commonly arise from chronic
and may present as fever of unknown origin in a substantial proportion sinusitis, mastoiditis, or deep fascial space infections are only briefly
of patients. The prevalence likely exceeds 15% in patients intubated reviewed here. Readers are referred to Chaps. 71 and 88 for a more
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longer than 5 days, and is probably more frequent following nasal than comprehensive description of these entities.
endotracheal or gastric intubation. CT studies of patients with pro- Brain Abscess: Most brain abscesses occur in association with three iden-
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longed intubation often demonstrate mucosal thickening or an air-fluid tifiable clinical settings: (a) a contiguous focus of infection, particularly
level, which by themselves do not establish the diagnosis of nosocomial sinusitis, otitis, or mastoiditis; (b) cranial trauma or postcraniotomy;
sinusitis. Sinus aspiration may be useful to identify the precise microbial and (c) hematogenous spread from an extracranial focus of infection,
etiology and guide antimicrobial therapy. The consequence of unrec- especially the lung and heart valves. Otogenic (eg, temporal lobe or
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ognized infection can be catastrophic, with intracranial extension and cerebellum) and sinusitis-related (eg, frontal lobe) brain abscesses
fulminant sepsis. account for approximately 50% of all pericranial sources of infection.
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Infections of the middle ear or mastoid within the petrous bone may Hematogenous brain abscesses are frequently multiple and located in
invade the middle fossa to involve the temporal lobe or into the poste- the distribution of the middle cerebral artery (ie, in the posterior frontal
rior fossa to involve the cerebellum or brain stem. The skull overlying or parietal lobes). The clinical presentations of brain abscesses are quite
the dura of the cerebrum is covered extracranially by the galea aponeu- variable and appear to be influenced primarily by the anatomic loca-
rotica. Pericranial infections, due either to head trauma or to a crani- tion of the abscesses; their proximity to the ventricles, cisterns, or dural
otomy, may result in a subgaleal abscess and cranial osteomyelitis, with sinuses; and major alterations in the intracranial pressure dynamics sec-
possible retrograde spread through the emissary veins to the epidural, ondary to the mass effect. Thus, a pontine abscess may bulge posteriorly
subdural, and subarachnoid spaces. and block the aqueduct of Sylvius acutely to cause obstructive hydro-
Rhinocerebral Mucormycosis and Malignant Otitis Externa: Rhinocerebral cephalus. An occipital lobe abscess could rupture or leak into the ven-
mucormycosis is a progressive and destructive infection of the parana- tricular system, causing ventriculitis, or it could involve the transverse
sal sinuses caused by fungi of the family Mucoraceae: Absidia, Mucor, sinus and cause septic thrombophlebitis or a subdural empyema. Four
Rhizomucor, and Rhizopus. 30,31 It occurs primarily in debilitated distinctive clinical presentations of a brain abscess can be recognized
patients with uncontrolled diabetes and ketoacidosis, in profoundly based on unique pathophysiologic events: (a) rapid focal mass expan-
dehydrated children, and in neutropenic patients receiving cytotoxic sion; (b) intracranial hypertension; (c) diffuse brain destruction; and
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therapy. The infection begins in the nose or nasopharynx and spreads (d) focal neurologic deficit. In the last category, temporal progression of
through the sinuses into the orbit or central nervous system. It may infection is so slow that it is often misdiagnosed as a neoplasm. Fever is
extend through the cribriform plate to involve the meninges and the present in only 45% to 50% of patients; therefore, absence of fever
adjacent frontal lobe and cranial nerves or it may extend through the should not be used to exclude the diagnosis of brain abscess.
nasolacrimal duct to involve the orbit, producing panophthalmitis. Subdural Empyema and Epidural Abscess: Intracranial subdural empy-
These fungi have a predilection for the walls of arteries, and infection ema in the adult usually results from a suppurative infection of the
spreads by this route, causing thrombosis and tissue infarction. The paranasal sinuses, mastoid, or middle ear (Fig. 73-2). An acute flare-
internal carotid artery or its major branches may be involved, as may up with local pain and increase in purulent nasal or aural discharge
the cavernous sinus. Clinically, black necrotic lesions may be found and onset of generalized headache and high fevers are the first indi-
on the nasal mucous membranes or the soft palate. When orbital cations of intracranial spread. They are followed within days by focal
involvement is seen, there is proptosis, ophthalmoplegia, blindness, neurologic findings such as unilateral motor seizures, hemiplegia,
chemosis, and corneal anesthesia. Extension into the cranial cavity hemianesthesia, or aphasia, and signs of increased intracranial pres-
is manifested by headache, meningismus, trigeminal or facial cranial sure with progressive lethargy and coma. The neck is stiff, but cere-
nerve palsy, seizures, and other focal neurologic signs. Progressive brospinal fluid (CSF) examination is more consistent with an aseptic
obtundation is seen, culminating in coma. The diagnosis is confirmed meningitis syndrome. In infants and young children, however, an
by the presence of broad, nonseptate hyphae in biopsy specimens and intracranial subdural empyema is almost invariably a complication
a positive culture. Treatment requires aggressive surgical debridement of bacterial meningitis. Early signs such as irritability, poor feeding,
and systemic amphotericin B. With early diagnosis, control of the or increased head size are nonspecific, but hemiparesis, convulsions,
underlying condition, and appropriate antimicrobial therapy com- stupor, and coma may rapidly ensue. S pneumoniae, Streptococcus
bined with surgical treatment, long-term survival has been reported agalactiae, and H influenzae are the most common causes.
in 70% of cases. 32 Cranial epidural abscess is usually associated with a postcraniotomy
Malignant otitis externa is a progressive and necrotizing infection of infection or a cranial osteomyelitis secondary to chronic sinusitis or
the external ear caused by P aeruginosa, with spread through the carti- middle ear infection. The onset of symptoms may be insidious and
laginous and bony canal to the base of the skull. Affected patients are overshadowed by the localized inflammatory process. Focal neurologic
usually debilitated and often have poorly controlled diabetes mellitus. findings are less common than in subdural empyema. Rarely, a fifth and
The infection is associated with severe otalgia, hearing loss, purulent sixth cranial nerve palsy may develop in association with infections of
discharge, edema, and granulation tissue or “polyp” in the cartilagi- the petrous portion of the temporal bone (Gradenigo syndrome).
nous portion of the external ear canal. Three stages of progression are
recognized clinically: (a) locally invasive disease; (b) disease associated Septic Intracranial Thrombophlebitis and Mycotic Aneurysm: Septic intra-
with facial palsy; and (c) disease associated with multiple cranial nerve cranial thrombophlebitis most frequently follows infection of the para-
palsies. In the latter stages, infection may involve the infratemporal fossa nasal sinuses, middle ear, mastoid, or oropharynx. If collateral venous
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