Acute bacterial infection of the sella turcica is a rare event (153-161). Whereas in many instances the pathogenesis of pituitary infection is not apparent, those instances in which an etiology has been established suggest that pituitary abscess arises in two clinical settings. The first is the result of secondary extension from a preexisting anatomically contiguous purulent focus. Acute sphenoid sinusitis, osteomyelitis of the sphenoid bone, mastoiditis, cavernous sinus thrombophlebitis, peritonsillar abscess, purulent otitis media, and bacterial meningitis have all been implicated as the primary infectious source. The other principal pathogenetic mechanism relates to generalized sepsis and hematogenous dissemination from a variety of distant septic foci (pneumonia, osteomyelitis, endocarditis, retroperitoneal abscess, tooth abscess). Isolated pituitary abscesses are extremely rare. More commonly (although still extremely unusual) abscesses have been reported in association with pre-existing sellar lesions (pituitary adenoma, craniopharyngioma, Rathke's cyst) (154,160). Why such lesions should be especially vulnerable to abscess formation is unclear but may be related to the impaired vascularity and/or areas of necrosis within such lesions.
The symptoms of pituitary abscess are nonspecific and frequently indistinguishable from those of other sellar mass lesions (headache, visual field deficits, hypopituitarism). When these symptoms are accompanied by fever, leukocytosis, and meningismus, the possibility of a pituitary abscess should be strongly considered. Admittedly, so florid an infectious presentation tends to occur in only a minority of patients, being present in only a third of the 24 examples of Vates et al. (160). In only 20% of their patients could the correct diagnosis be made preoperatively. Most patients will have some radiologic evidence of sellar pathology, the result of either a preexisting lesion or of the abscess itself. The bacteriology of pituitary abscess is variable. When organisms have been isolated, Staphylococcus aureus, Diplococcus pneumoniae, group A Streptococcus, Klebsiella species, Escherichia coli, and Citrobacter divercusis are most frequently reported (160). In this series, definitive organisms were isolated in fewer than 60% of cases, whereas in the remainder, it was either intraoperative appearance or histopathologic evidence of necrosis and inflammation that prompted a diagnosis of pituitary abscess. One must recognize, however, that both intraoperative appearance and inflammatory histopa-thology can be misleading, particularly when dealing with certain cystic pathologies in the sella (notably Rathke's cleft cysts and craniopharyngiomas) whose cyst contents may fully mimic the appearance, consistency, and texture of suppuration. Accordingly, one must exercise caution in labeling a sellar process as being infectious when neither the clinical presentation nor the microbiologic diagnosis are confirmatory.
The management of a suspected pituitary abscess includes transsphenoidal exploration of the sella, drainage of the inflammatory mass, and antibiotic therapy. Selection of antimicrobial agents is based ideally on culture reports; however, empiric broad-spectrum therapy should include a combination of a third-generation cephalosporin, a synthetic penicillin, and metronidazole for their Gram-negative, staphylococcal, and anaerobic sensitivities, respectively. The optimal duration of antibiotic therapy has not been established.
Because pituitary abscesses are rare, recent data concerning long-term outcome are not available. Based on their review of 29 cases, Domingue and Wilson identified an overall mortality rate of 28% for pituitary abscess, which further increased to 45% if meningitis was also present (154). In a more contemporary series of Vates et al., which also included seven patients reported by Domingue and Wilson, the overall mortality rate was 8.3% (160).
A variety of other rare nonbacterial or atypical bacterial infective agents may also be responsible for pituitary and sellar region infection. Tuberculosis, still endemic in certain areas, has historically been an important etiology for destructive granulomatous inflammatory lesions involving the hypothalamus and sellar region (162-164). In most instances, parasellar involvement has been a complication of its dense plaque-like basilar meningitis. Such "tuberculomas" are often associated with near-total anterior and posterior pituitary failure, are frequently calcified, and often, but not invariably, associated with evidence of active tuberculosis elsewhere (Fig. 6).
Brucellosis, a common zoonosis in many parts of the world, has in rare instances presented as a sellar mass (165,166).
Syphilis, now extremely uncommon in its consummate forms, represents another granulomatous infection involving the hypothalamus and sellar region (153). Historical accounts suggest that the clinical features of syphilitic gumma in the sellar region were typical of other destructive processes of the sella and were usually associated with syphilitic lesions elsewhere in the neuroaxis.
Mycotic infection, notably aspergillosis, has also been reported to involve the sellar, parasellar, and orbital regions, often presenting as a discrete inflammatory mass (167,168). Rare examples of candidal abscess in the pituitary are also known to occur (169). Parasitic infiltration of the sellar and parapituitary regions by cystercosis (170) and echinococcus (171) have both produced a mass in this region. Finally, in the context of AIDS and other immunosuppressed states, an additional spectrum of pituitary infection has emerged, including agents such as Pneumocystis carinii, Toxoplasma gondii, and cytomegalovirus (172).
Mucoceles are benign slowly expansile mucous-filled cystic lesions that arise in paranasal sinuses. Their neurosurgical relevance derives primarily from their occasional tendency to erode intracranially, wherein they may present as an intracranial mass or, less frequently, offer a source for intracranial infection. Although mucoceles arising in the maxillary sinus are numerically the most frequent, and those arising in the frontal and anterior ethmoid sinuses are clinically the most significant, this discussion concerns those rare mucoceles arising from the sphenoid or posterior ethmoid sinuses, whose intracranial involvement brings them into the realm of parasellar pathology.
Mucoceles of the sphenoid and posterior ethmoid sinuses (spheno-ethmoid mucoceles) are rare. Rarer still is the occasion when these mucoceles erode through the sellar floor and present as intrasellar, parasellar, or suprasellar masses (173-176). In some instances their clinical features are indistinguishable from those of a nonfunctioning pituitary adenoma (NFPA); the sella is eroded, showing balloon-like enlargement, and a chiasmal syndrome attendant to suprasellar extension is documented. In other cases there may be more extensive intracranial involvement, with extensions into the orbital apex and superior orbital fissure. In such cases additional symptoms of exophthalmos and oculomotor palsies may also be present. Hypopituitarism is rarely a feature of sellar region mucoceles. On CT scanning, most mucoceles appear isodense, although their walls may exhibit contrast enhancement of varying degree. Bone windows reveal the extent of bony erosion and/or destruction. Their MRI signal characteristics are variable, depending on the viscosity of contents.
Pathologically, mucoceles are encapsulated masses whose walls are composed of the mucoperiosteal lining of the involved sinus. Their pathogenesis remains conjectural. Although postinflammatory obstruction of the sinus ostia is the most commonly invoked mechanism underlying their development, mucoceles appear to be neither a common nor an inevitable result of such obstruction. Whatever the basis for their initiation, mucoceles are generally chronic lesions, frequently exhibiting years of subclinical growth before causing symptoms. Ongoing accumulation of mucoid material gives rise to expansile growth, causing bony erosion of the sinus walls, and eventual access to the intracranial compartment. Mucoceles that become infected are known as "mucopyoceles" and, unexpectedly, have an abruptly accelerated course, often with rapid bony destruction and an increased risk of intracranial or intraorbital infection (Fig. 7).
Sphenoido-ethmoidal mucoceles are effectively treated by transsphenoidal or transethmoidal exploration, depending on their sinus of origin. Drainage of mucocele contents and mucosal exenteration of the involved sinus is generally curative. Radical removal of the intracranial portion of the mucocele wall is neither necessary nor advisable.
Rarely, mucoceles are a complication of previous transsphenoidal or more particularly trans-ethmoidal surgery.
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