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39 Brain Abscess
Allan R. Tunkel, H. Richard Winn, and W. Michael Scheld
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CHAPTER 39 Brain Abscess e189
neutropenia; chronic granulomatous disease; diabetes mellitus; injection site, thereby reducing tissue trauma with minimal (or
thermal injury; and the presence of a central venous catheter. no) infection in the subarachnoid space. This model also simu- 39
CNS aspergillosis is reported in 10% to 20% of patients with lated human infection in that the abscess was produced in the
invasive disease.81,83,85,86 The lungs are the usual primary site of white matter at the white and gray matter junction and migrated
infection, with dissemination to the CNS occurring by direct toward the ventricle, a shift in intracranial contents occurred, and
extension from an area that is anatomically adjacent to the brain. there was minimal histologic evidence of meningitis; the abscess
The most important underlying immune defect in patients with capsule was asymmetrical, being more complete on the cortical
invasive aspergillosis is neutropenia (i.e., in those who have an than on the ventricular side, perhaps because the increased vas-
underlying malignancy), but this infection may also be seen in cularity of normal cortical gray matter allowed greater fibroblast
patients with hepatic disease, diabetes mellitus, chronic granulo- proliferation and collagen helix formation. In addition, develop-
matous disease, Cushing syndrome, HIV infection, injection drug ment of the abscess paralleled clinical disease with the initial
use, organ transplantation, and bone marrow transplantation, as development of cerebritis and massive white matter edema fol-
well as after craniotomy and in patients receiving long-term cor- lowed by encapsulation.
ticosteroid therapy. In another animal model, brain abscess was produced in a rat
CNS infections caused by the Mucorales group are among the by direct intracerebral injection of agarose beads laden with S.
most fulminant infections known. Diabetes mellitus, usually asso- aureus.101 This method was also easy, reproducible, effective, and
ciated with acidosis, is the most common predisposing condition associated with a low mortality rate, and the histologic features
(≈70% of cases), but disease may also be seen in patients with of the experimental abscesses were similar to those observed in
acidemia from profound systemic illness (e.g., sepsis, severe dehy- other animal models and in humans. These models have been
dration, severe diarrhea, chronic kidney disease), hematologic useful in delineating the early events in brain abscess formation
neoplasms, renal transplantation, injection drug use, and use of with respect to bacterial virulence factors and the host defense
deferoxamine.83,87 Over the last two decades, this pathogen has mechanisms involved in brain abscess formation; these concepts
also emerged as an important cause of CNS disease in recipients are reviewed in greater detail subsequently.
of solid organ and hematopoietic stem cell transplantation.88
CNS disease results from direct extension from the rhinocerebral
form, after open head trauma, or after hematogenous dissemina-
Initiation of Infection
tion. Bilateral involvement of the basal ganglia has been reported The brain appears to be significantly more sensitive to infection
in injection drug users; Rhizopus arrhizus is the most common than many other tissues. In a rat model of experimental brain
isolate.89 abscess, injection of 104 colony-forming units (CFUs) of S. aureus
Scedosporium species may cause CNS disease in immunocom- or 106 CFUs of E. coli failed to cause infection in the skin, but
petent and immunocompromised hosts.83,90-94 These organisms abscess formation in brain tissue was induced by a level as low as
may enter the CNS by direct trauma, hematogenous dissemina- 102 CFUs of either organism.102 The brain may also be more
tion, or direct extension from infected sinuses. One case has also susceptible to infection by different organisms; in the experimen-
been reported in a patient after extracorporeal membrane oxy- tal rat model, strains of E. coli were more virulent (i.e., led to
genation.95 An association between near-drowning and subse- abscess formation at lower inocula) than P. aeruginosa, S. aureus,
quent CNS infection has been found because these organisms are or Streptococcus pyogenes.103 In addition, E. coli strains possessing
present in contaminated soil, water, and sewage. the K1 antigen were more infective than strains without this
Many other fungal species have been reported to cause brain antigen, thus indicating that certain encapsulated strains may be
abscess, including Cryptococcus neoformans, the endemic mycoses more virulent in brain abscess formation. Furthermore, inocula-
(Coccidioides spp., Histoplasma spp., and Blastomyces dermatitidis), tion of Bacteroides fragilis or streptococci such as Streptococcus
and many of the melanized, or dematiaceous, fungi.96 It is beyond intermedius failed to lead to abscess formation in rats even though
the scope of this chapter to review all fungal causes of brain these organisms account for a high percentage of isolates from
abscess, and more detail can be found in other sources.83,97 brain abscesses in humans; this finding may be explained by the
fact that brain abscess is often the result of a contiguous focus of
infection and the synergistic infectivity of mixed populations of
Experimental Models of Infection anaerobes plus a facultative organism may be necessary to estab-
Numerous animal models have been developed to study the lish infection.104,105 In an experimental dog model of brain abscess
pathogenesis and pathophysiology of brain abscess.98 Some large- formation, inoculation of B. fragilis with Staphylococcus epidermidis
animal models were created by direct implantation of bacteria in mixed culture caused a virulent reaction,106 although each
into the brain; however, these models were limited by lack of organism was not tested separately. The role of other bacterial
reproducibility, they required multiple steps and an agar vehicle virulence factors in the pathogenesis of brain abscess formation
to initiate infection, and they were quite expensive. Another has not been elucidated. However, the role of virulence factor
method used embolization of contaminated pliable cylinders production in the development of brain abscess was demon-
implanted into the carotid artery but required concomitant cere- strated by the inability of heat-inactivated S. aureus to induce
bral injury for abscess formation, and the accompanying brain proinflammatory cytokine or chemokine expression in an experi-
infarction caused a high mortality rate even in uninfected control mental mouse model; alpha toxin was identified as a key virulence
animals. factor for survival of S. aureus in the brain and subsequent devel-
A better animal model involved the use of mice or rats and opment of brain abscess.107
consisted of a simple, one-step, easily reproducible procedure for Brain abscess may also develop in patients with bacterial men-
consistent production of brain abscess. Infection was produced ingitis, a rare complication except in human neonates with men-
by the injection of 1 µL of saline containing a fixed inoculum of ingitis caused by C. diversus.57,58 Pathologically, there is cerebral
bacteria through a bur hole and into the frontal lobe of the necrosis and liquefaction, along with vasculitis of small vessels
brain.99,100 With this model, brain abscess was achieved in a one- and hemorrhagic necrosis of adjacent tissue with a propensity
step process at a specific site with the injection of bacteria alone, for contiguous inflammation in the cerebral white matter, which
the inoculum could be regulated in terms of both volume and may reflect the effects of endotoxin in the small penetrating
number of organisms, the number of injected bacteria and the vessels in this area; the typical abscess with capsule formation was
number of bacteria that remain viable in the tissue could be not present. The pathogenesis was investigated in an infant rat
quantified at a later time, and there was precise control of the model in which infection was initiated with the production of a
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e190 SECTION 1 Introduction and General Neurosurgery
high-grade bacteremia, infiltration of the leptomeninges, and the histopathologic sequence of brain abscess formation was
subsequent development of ventriculitis.108 Brain abscesses were found to be different in an experimental rat model after inocula-
found exclusively in the periventricular white matter, apparently tion with E. coli112; the histopathologic findings supported an
from disruption of the ventricular ependymal lining with direct alternative hypothesis that brain abscesses tend to rupture intra-
extension of the infection into the parenchyma. The virulence ventricularly because the infectious process is directed along the
factors responsible for the propensity of this organism to cause major white matter tracts (areas of lower tissue resistance) rather
brain abscess are undefined, although one study reports that a than as a result of asymmetric collagen deposition. However, the
minor 32-kD outer membrane determinant may be a marker for question of rupture of brain abscess requires further study.
strains that are more likely to produce ventriculitis and brain The histopathologic findings in brain abscesses after direct
abscess; strains that lacked the 32-kD outer membrane protein implantation differ from those produced by intracarotid emboli-
caused more bacteremia, meningitis, and death.109 zation because metastatic abscesses induce only transient midline
displacements, inflammatory cell infiltration is reduced, and col-
lagen formation is slower around proliferating capsular vessels;
Stages of Infection this difference may have patient care implications because a lower
The temporal course and pathologic consequences of brain level of encapsulation contributes to mortality.
abscess were examined in a canine model of infection after inocu-
lation with α-hemolytic streptococci. Four stages of infection
were identified (Table 39-2): early cerebritis, late cerebritis, early
Host Defense Mechanisms
capsule formation, and late capsule formation.110 These stages In the experimental models just described, bacteria were inocu-
are somewhat arbitrary but are useful in the classification and lated directly into the brain, thus bypassing the brain’s normal
comparison of virulence among different organisms in the pro- host defense mechanisms. The brain is generally protected from
duction of brain abscess. Similar neuropathologic findings were infection by an intact blood-brain barrier, but once infection is
described in an experimental model of anaerobic brain abscess,106 established, immune defenses are usually inadequate to control
but capsule formation could not be divided into early and late it. Local opsonization in the brain is deficient, allowing encapsu-
stages because of delayed encapsulation. S. aureus was found to lated bacteria such as B. fragilis and E. coli to escape efficient
be more virulent than α-hemolytic streptococci, with a greater phagocytosis; phagocytosis of Bacteroides species also requires
amount of necrosis and total area of involvement, a longer course heat-labile serum factors such as complement and lysozyme,
of progression to resolution, and longer times to reach a stable which are probably absent from the CNS.113,114 The outer mem-
size and to contain the necrotic region within a collagenous brane components of Bacteroides species may also be important in
capsule.111 Inflammation with histologic evidence of extension the inhibition of neutrophil chemotaxis, thereby reducing the
of inflammation, necrosis, and edema beyond the capsule was host response to brain abscess caused by this organism.115
also observed, findings similar to those after inoculation with As shown in Table 39-2, the border around the initial area of
B. fragilis. inoculation is composed of acute inflammatory cells during the
Capsule formation occurs in a delayed fashion (see Table early cerebritis stage, accompanied by the rapid development of
39-2). In all these studies, capsule formation was less prominent a perivascular infiltrate consisting of neutrophils, plasma cells,
on the ventricular than on the cortical surface.106,110,111 Differ- and mononuclear cells.106,110,111 In an experimental rat model of
ences in vascularity between the cortical gray and white matter brain abscess formation, production of the proinflammatory
might allow greater fibroblast proliferation more superficially cytokines interleukin-1α (IL-1α), IL-1β, IL-6, and tumor necro-
(i.e., on the cortical surface). Alternatively, fibroblasts responsible sis factor α (TNF-α) occurred as early as 1 to 6 hours after
for the capsule collagen may need to migrate from the menin- exposure to S. aureus.116 This was followed by enhanced concen-
ges,99 thereby accounting for the delay in capsule formation and tration of the CXC chemokine KC, which correlates with the
the greater density of the capsule on its superficial surface. This appearance of neutrophils in the abscess. The importance of
thinner aspect of the capsule on its “deeper” surface probably neutrophils in the initial containment of S. aureus in the brain
explain the tendency for brain abscesses to rupture into the ven- was established by the fact that mice that were transiently depleted
tricular system rather than into the subarachnoid space. However, of neutrophils before the implantation of bacteria-laden beads
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CHAPTER 39 Brain Abscess e191
had higher CNS bacterial burdens than control animals.117 Both TABLE 39-3 Initial Symptoms and Signs in Patients with Brain Abscess
macrophage inflammatory protein 2 (MIP-2) and KC/CXCL1, 39
Symptom or Sign Frequency Range (%)
two neutrophil-attracting CXC chemokines, were significantly
elevated in the brain after S. aureus exposure, thus indicating the Headache 49-97
importance of the CXC receptor 2 (CXCR2) ligands MIP-2 and Fever 32-79
KC, as well as neutrophils, in the acute host response. Focal neurological deficits* 20-66
The continued release of proinflammatory mediators by acti- Altered mental status 28-91
Seizures 13-35
vated glia and infiltrating peripheral immune cells may potentiate
Nausea and vomiting 27-85
the subsequent recruitment and retention of newly recruited Nuchal rigidity 5-52
inflammatory cells and glia,118 thereby perpetuating the antibac- Papilledema 9-51
terial inflammatory response. Later studies support this persistent
immune activation associated with experimental brain abscess in Data from references 1, 2, 8, 9-17, 102.
which increased concentrations of IL-1α, TNF-α, and MIP-2 *The specific deficit depends on the central nervous system location of
the abscess (see Table 39-4).
were detected between 14 and 21 days after S. aureus exposure,119
thus suggesting that intervention with anti-inflammatory com-
pounds, subsequent to bacterial neutralization, might minimize
damage to the surrounding brain parenchyma. Although Toll-like
receptor 2 (TLR2) has an important role in mediating S. aureus– immunosuppressed dogs. Although the decreased inflammatory
induced activation, additional receptors are involved in glial response and edema initially led to less mass effect, the eventual
responses to S. aureus. The functional importance of major size and area of the abscess may have become larger as a result
abscess-associated T-cell subsets in modulating ongoing innate of the diminished host response.
immune responses during infection has been assessed; manipulat-
ing Th1 and Th17 cells was found to expedite S. aureus clearance
from the CNS parenchyma and limit the extent of tissue
Clinical Findings
damage.120 Bacterial capsule was also shown to be involved in The clinical manifestations of brain abscess may run the gamut
modulation of innate immunity and complement system activa- from indolent to fulminant; most are related to the size and loca-
tion, in an experimental mouse model in which a capsular strain tion of the space-occupying lesion within the brain and the viru-
of S. aureus proliferated faster and caused early expression of the lence of the infecting organism.1-3,12-22 Common symptoms and
chemokine CXCL2, resulting in more polymorphonuclear leu- signs are presented in Table 39-3.4,21 Headache is generally
kocyte infiltration into the abscess area121 and potentially leading observed in 70% to 75% of patients; sudden worsening of the
to benefit in terms of survival. With progression to the late cere- headache, accompanied by new onset of meningismus, may
britis stage, the acute inflammatory cells become mixed with signify rupture of the abscess into the ventricular space.126,127 In
macrophages and fibroblasts, and reticulin formation surrounds one study of 33 consecutive patients with intraventricular rupture
the necrotic center. As the capsule begins to form, increased of brain abscess, severe headaches and signs of meningeal irrita-
numbers of fibroblasts and macrophages infiltrate the periphery, tion were prominent findings before rupture and were followed
and mature collagen is deposited to form a capsule. The necrotic by rapid clinical deterioration within 10 days.128 Intraventricular
center then continues to decrease while marked gliosis develops rupture appears to be more likely if the abscess is deep-seated,
outside the capsule. multiloculated, and in close proximity to the ventricular wall126;
Despite the presence of virulence factors in the organisms that a 1-mm reduction of the distance between the ventricle and the
resist host defense mechanisms, the host inflammatory response abscess increased the rupture rate by 10%. The classic triad, fever,
is important in containment of the abscess, as has been examined headache, and focal neurological deficits, is seen in less than 50%
with the use of immunosuppressed animals. Initial studies in a of patients with brain abscess. The specific neurological findings
dog model of experimental brain abscess with S. aureus or Proteus for brain abscess are also defined by location within the CNS
mirabilis demonstrated that the administration of dexamethasone (Table 39-4).1-3,13-20,129,130 In immunocompromised patients, the
slowed, but did not fully impair, capsule formation.122 In contrast, clinical findings may be masked by the diminished inflammatory
there was no evidence of capsule formation when dexamethasone response.
was given at the same time as inoculation of either S. pyogenes or The clinical manifestations of brain abscess may also be
S. aureus in another study.123 In an experimental rat model of E. defined by the infecting pathogen. For example, patients with
coli brain abscess,112 dexamethasone administration led to a reduc- nocardial brain abscess may have concomitant pulmonary, skin,
tion in macrophage and glial responses, collagen deposition, and or muscle lesions65,66,131; however, the CNS findings are more
host survival, with demonstration of an increased number of often nonspecific and associated with fever, headache, and focal
viable bacteria in the brain abscess. Coadministration of dexa- neurological deficits defined by location. Patients with Aspergillus
methasone also impaired the lymphocytic and fibroblastic brain abscess commonly manifest signs of a stroke syndrome as
response in a rat model of experimental S. aureus brain abscess,124 a result of ischemia or intracerebral hemorrhage, or both, that is
although it did not entirely halt the encapsulation or reduce the referable to the involved areas of the brain.83,85,86,132 Patients
associated cerebral edema. who are severely immunocompromised usually have nonspecific
Another study in dogs, which were immunosuppressed with findings shortly before death, whereas those who are less immu-
azathioprine and prednisone 7 days before the intracerebral nocompromised are more likely to have headache and focal neu-
inoculation of α-hemolytic streptococci, demonstrated that the rological deficits, but evidence of aspergillosis in other organ
immunosuppressed animals manifested a decreased inflammatory systems is usually apparent.
response characterized by a reduction in neutrophils and macro- Patients with rhinocerebral mucormycosis initially have
phages in the lesion, a decrease and delay in collagen deposition, symptoms referable to the eyes or sinuses and complaints of
and persistence of viable organisms into the late capsule stage.125 headache, facial pain, diplopia, lacrimation, and nasal stuffiness
Reduction of neutrophils, plasma cells, lymphocytes, and macro- or epistaxis.83,87 With continued infection and spread to contigu-
phages in the areas surrounding the necrotic center of the ous structures, necrotic lesions appear in the turbinates, nose,
abscess was observed, and cerebritis was also decreased outside paranasal skin, or hard palate; chemosis, proptosis, and external
the developing capsule. However, gliosis was markedly increased ophthalmoplegia may also occur. Cranial nerve involvement is
in the area surrounding the collagenous capsule in these common, and blindness may occur as a result of invasion of the
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e192 SECTION 1 Introduction and General Neurosurgery
Diagnosis
Magnetic resonance imaging (MRI) is the diagnostic neuro-
Figure 39-2. Axial fluid-attenuated inversion recovery (FLAIR) image
imaging procedure of choice in patients with brain abscess4; it
of the patient from Figure 39-1 demonstrating vasogenic edema
is more sensitive than computed tomography (CT) and offers
surrounding each lesion. (Courtesy of Stanley Lu, MD, Monmouth
significant advantages in the early detection of cerebritis, more
Medical Center, Long Branch, NJ.)
conspicuous demonstration of spread of inflammation into the
ventricles and subarachnoid space, and earlier detection of satel-
lite lesions (Figs. 39-1 and 39-2).22,134 On T1-weighted images,
the abscess capsule often appears as a discrete rim that is isoin- of the abscess. On diffusion-weighted images, restricted diffu-
tense to mildly hyperintense; administration of gadolinium– sion (bright signal) may be seen and may distinguish abscesses
diethylenetriaminepentaacetic acid helps clearly differentiate the from necrotic neoplasms.3 Proton MR spectroscopy is another
central abscess, surrounding enhancing rim, and cerebral edema. diagnostic modality that may assist in differentiating between
On T2-weighted images, the zone of edema that surrounds the malignant tumors and cerebral abscesses; when combined with
abscess demonstrates marked high signal intensity in which the diffusion-weighted imaging, MR spectroscopy can significantly
capsule appears as an ill-defined hypointense rim at the margin increase the diagnostic accuracy of conventional MRI.4,135 The
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CHAPTER 39 Brain Abscess e193
combined use of proton MR spectroscopy, diffusion-weighted diencephalic structures adjacent to the ventricles). At the time of
imaging, and diffusion tensor imaging has been shown to improve aspiration, specimens should be sent for Gram stain, routine 39
the specificity of the diagnosis of ring-enhancing lesions of the aerobic and anaerobic cultures, modified acid-fast smears, acid-
brain and to help differentiate brain abscess from other cystic fast smears and culture, and fungal smears and culture. In patients
lesions of the brain, including tumors.136 In one prospective study with histopathologic and Gram stain findings suggestive of a
of 115 patients with 147 cystic brain lesions, including 97 patients bacterial brain abscess but negative culture results, 16S ribosomal
with brain abscess, diffusion-weighted imaging had a sensitiv- RNA gene sequencing and amplification may be an important
ity of 96%, a specificity of 96%, a positive predictive value of adjunct.141,142 In one study, use of multiple ribosomal DNA
98%, and a negative predictive value of 92% in differentiation sequencing was found to dramatically increase the number of
of brain abscesses from primary or metastatic cancers.137 These infectious agents identified in cerebral abscesses.143 In a subse-
data point to the importance of diffusion-weighted imaging in quent study of 71 patients with brain abscesses, a metagenomic
the diagnostic approach to central nervous system mass lesions analysis identified 80 different bacterial taxa, including 37 that
(Fig. 39-3). In patients who cannot undergo MRI, CT with and were as yet uncultured, with the major sources being the sinuses
without intravenous contrast enhancement is recommended; and dental flora as part of a polymicrobial infection.144 However
a brain abscess characteristically has a hypodense center with more data are needed to determine the importance of many of
peripheral uniform ring enhancement after the intravenous injec- these organisms in patients with brain abscess.
tion of contrast material.138-140 Other findings include nodular In patients with Aspergillus brain abscess, appropriate stains
areas and regions of low attenuation without enhancement, the may reveal the presence of septate hyphae with acute-angle,
latter finding seen in the early cerebritis stage before abscess dichotomous branching, whereas in patients with mucormycosis,
formation. In later stages, contrast material no longer differenti- tissue specimens may reveal irregular hyphae with right-angle
ates the lucent center, and the CT appearance is similar to that branching. Histologic preparations of brain abscess specimens
of the early cerebritis stage. caused by Scedosporium species are indistinguishable from those
Neuroimaging may be quite sensitive in defining the findings caused by Aspergillus species. The hyphae of dematiaceous fungi
in patients with fungal brain abscess.83 In patients with CNS may be brownish on hematoxylin-eosin staining but are not dis-
aspergillosis, a cerebral infarct may be demonstrated, which typi- tinguishable from those of other molds. In patients with CNS
cally develops into either single or multiple abscesses; in immu- aspergillosis or other mold infections, detection of galactoman-
nocompromised patients, there may be little or no contrast nan antigen and 1,3-β-d-glucan in CSF may be helpful in estab-
enhancement on MRI.86 Characteristic changes may be seen on lishing a fungal diagnosis.145,146
MRI in patients with rhinocerebral mucormycosis, including
sinus opacification, erosion of bone, and obliteration of deep
fascial planes; cavernous sinus thrombosis may also be apparent.
Management
The lack of contrast enhancement in patients with mucormycosis The initial approach to management of a patient with a suspected
is a poor prognostic sign because it indicates failure of host brain abscess is a multidisciplinary one that involves a neurora-
defense mechanisms to control the offending agent. diologist, neurosurgeon, and infectious disease specialist.147 After
A major advance is the ability to perform stereotactic MRI- or neuroimaging, if single or multiple ring-enhancing lesions are
CT-guided aspiration to facilitate microbiologic diagnosis.3 found, prudent management involves either aspiration or excision
Current techniques afford the surgeon rapid, accurate, and safe of lesions larger than 2.5 cm in diameter, depending on brain
access to virtually all intracranial points, including those in deep location, under stereotactic guidance. For abscesses in the early
critical areas of the CNS (i.e., the brainstem, cerebellum, and cerebritis stage or if all lesions are 2.5 cm or less in diameter, the
A B C
Figure 39-3. A, Transverse axial T1-weighted magnetic resonance image shows a bilobed lesion in the right
frontal lobe and a second lesion in the left frontal lobe. B, Postcontrast T1-weighted image demonstrates
peripheral enhancement of two lesions and subtle enhancement of another lesion in right frontal lobe (arrow).
C, Trace diffusion-weighted MR imaging shows marked hypersignal, consistent with decreased water
diffusion, in the cores of all lesions, a finding consistent with multiple pyogenic brain abscesses. (Courtesy of
Glenn A. Tung, MD, Warren Alpert Medical School of Brown University, Providence, RI.)
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e194 SECTION 1 Introduction and General Neurosurgery
largest lesion should be aspirated by means of stereotactic tech- is suspected (e.g., after organ transplantation), trimethoprim-
nique for definitive diagnosis and identification of the organ- sulfamethoxazole or sulfadiazine should be added. If Aspergillus
ism.148 Although abscess size greater than 2.5 cm has been infection is suspected, voriconazole is recommended.4 In HIV-
recommended as an indicator for neurosurgical intervention,147 infected patients and in patients who are immigrants from or have
data from comparative studies are lacking, and this size cannot traveled to areas of the world where tuberculosis is endemic or
be regarded as a definitive indication for aspiration.4 With the who have know risk factors for tuberculosis, antituberculous
use of modern stereotactic neurosurgical techniques, most brain therapy should be considered pending further diagnostic evalua-
abscesses that measure at least 1 cm in diameter are amenable to tion. Once the infecting pathogen is isolated, antimicrobial
stereotactic aspiration, regardless of location4; stereotactic navi- therapy can be modified for optimal treatment (Table 39-6);
gation systems can be used for drainage, and images obtained recommended dosages of agents in patients with normal renal
with volumetric CT or MRI may be used to build a three- and hepatic function are shown in Table 39-7.
dimensional reconstruction of the patient’s brain. For patients in
whom abscesses cause brain shift leading to brain herniation,
neurosurgical intervention may be indicated irrespective of
Bacterial Brain Abscess
abscess size.4 Furthermore, drainage should be considered if an The principles of antimicrobial therapy for bacterial brain abscess
abscess is abutting the ventricular system, to prevent abscess are to use agents that are able to penetrate the abscess cavity and
rupture and resulting ventriculitis. have in vitro activity against the isolated pathogen,1,2,5,12,59,151-153
After aspiration of abscess material and submission of speci- although no randomized controlled trials have examined the effi-
mens for special stains, histopathologic examination, and culture, cacy of specific antimicrobial agents in the treatment of bacterial
empirical antimicrobial therapy should be initiated. Because anti- brain abscess. Few studies have examined the penetration of spe-
microbial therapy before aspiration may reduce the yield of cific antimicrobial agents into brain abscess pus, and some anti-
bacterial cultures, it is reasonable to postpone initiation of anti- microbial agents that penetrate may be inactivated in a purulent
microbial therapy until after neurosurgery has been performed. environment. It is also important to note that depending on the
Delaying antimicrobial therapy should be considered only in pathogenesis, a mixed infection may be present even though only
clinically stable patients and, therefore, every effort should be one organism has been isolated, thus necessitating the use of
made to perform surgery in an expedited manner.4 more than one antimicrobial agent for therapy.4 A significant
The empirical approach to antimicrobial therapy in patients agent in the treatment of brain abscess is metronidazole, which
with bacterial brain abscess is based on results of stains of the has strong in vitro activity against strict anaerobes, an excellent
aspirated specimen and the probable pathogenesis of infection pharmacokinetic profile, and good oral absorption and penetra-
(Table 39-5).2,4 The combination of metronidazole plus a third- tion into brain abscess cavities149; metronidazole, however, must
generation cephalosporin is commonly used18,148,149; in patients in always be used in combination with an agent effective against
whom S. aureus is also considered a probable pathogen, vanco- streptococci because polymicrobial infections are common in
mycin is added pending identification of the organism and in patients with bacterial brain abscess. Vancomycin has also
vitro susceptibility testing.150 In patients in whom gram-negative achieved excellent penetration into brain abscess fluid after pro-
bacilli such as P. aeruginosa is likely, either ceftazidime, cefepime, longed therapy. In one study, simultaneous measurement of van-
or meropenem can be used. In patients with no clear predisposing comycin concentrations in serum and brain abscess fluid were
factors, a reasonable regimen to administer is the combination of obtained 1 hour after a 500-mg dose; vancomycin concentrations
vancomycin, metronidazole, and a third- or fourth-generation obtained before and during operative removal of the brain abscess
cephalosporin. In patients in whom infection caused by Nocardia were 15 µg/mL and 18 µg/mL, respectively, with a simultaneous
serum vancomycin concentration of 21 µg/mL.150 The third-
generation cephalosporins are another class of antimicrobial
agents that are useful, given their excellent in vitro activity against
TABLE 39-5 Predisposing Conditions and Empirical Antimicrobial
Therapy in Patients with Presumed Bacterial Brain Abscess
many etiologic agents that cause brain abscess and their demon-
strated success in small clinical studies154,155; when combined with
Predisposing Condition Antimicrobial Therapy metronidazole and used with surgical therapy (see later) in one
Otitis media or mastoiditis Metronidazole + a third-generation study, high doses of cefotaxime were effective in the treatment of
cephalosporin* bacterial brain abscess.156 Imipenem has been used successfully
Sinusitis (frontoethmoidal or Metronidazole + a third-generation for the treatment of pyogenic and nocardial brain abscess,157,158
sphenoidal) cephalosporin* + vancomycin† although it has been associated with an increased risk for seizures,
Dental infection Penicillin + metronidazole thus limiting the utility of this agent in patients with brain
Penetrating trauma or secondary Vancomycin + a third- or abscesses. Meropenem has been efficacious in isolated cases of
to a neurosurgical procedure fourth-generation cephalosporin‡
brain abscess, including one patient with a brain abscess caused
Lung abscess, empyema, or Penicillin + metronidazole + a
bronchiectasis sulfonamide§
by Enterobacter cloacae,159 so this agent may be especially valuable
Bacterial endocarditis Vancomycin|| in patients with infections caused by resistant pathogens. In one
Congenital heart disease Third-generation cephalosporin* 11-year retrospective study that compared intravenous cefotax-
Unknown Vancomycin + metronidazole + a ime and metronidazole with either intravenous imipenem or
third- or fourth-generation meropenem, meropenem therapy was associated with a signifi-
cephalosporin‡ cantly lower mortality rate and a lower seizure rate than imipe-
*Cefotaxime or ceftriaxone; the fourth-generation cephalosporin nem.160 The fluoroquinolones have also been used in isolated
cefepime may also be used. brain abscess cases, given their good CNS penetration161; further
†
Added if infection caused by methicillin-resistant Staphylococcus studies are needed to demonstrate their efficacy, however.
aureus is suspected, pending results of in vitro susceptibility testing. Surgical therapy is often required for the optimal approach to
‡
Ceftazidime or cefepime should be used if infection with patients with bacterial brain abscess.7,20,22,61,148,162 Procedures
Pseudomonas aeruginosa is suspected. include bur-hole aspiration and complete excision after craniot-
§
Trimethoprim-sulfamethoxazole should be included if infection caused omy, although no prospective trial comparing these two proce-
by Nocardia species is suspected.
|| dures has ever been performed. However, in one retrospective
Additional agent(s) may be added based upon other likely microbial
etiologies.
review of 47 studies from 1990 to 2008, patients who underwent
aspiration had a mortality of 6.6%, compared with 12.7% in
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CHAPTER 39 Brain Abscess e195
TABLE 39-6 Antimicrobial Therapy for Brain Abscess Based on Isolated Pathogen
39
Organism Standard Therapy Alternative Therapy(ies)
BACTERIA*
Actinomyces spp. Penicillin Clindamycin
Bacteroides fragilis Metronidazole Clindamycin
Enterobacteriaceae† Third- or fourth-generation cephalosporin Aztreonam, meropenem, fluoroquinolone, trimethoprim-
sulfamethoxazole
Fusobacterium spp. Metronidazole Clindamycin
Haemophilus spp. Third-generation cephalosporin‡ Aztreonam, fluoroquinolone, trimethoprim-sulfamethoxazole
Listeria monocytogenes Ampicillin§ or penicillin G§ Trimethoprim-sulfamethoxazole
Mycobacterium tuberculosis Isoniazid + rifampin + pyrazinamide + ethambutol
Nocardia spp.|| Trimethoprim-sulfamethoxazole Minocycline, imipenem, meropenem, a third-generation
cephalosporin, amikacin
Prevotella spp. Metronidazole Clindamycin, meropenem
Pseudomonas aeruginosa Ceftazidime,§ cefepime,§ or meropenem§ Aztreonam,§ fluoroquinolone§
Staphylococcus aureus:
Methicillin sensitive Nafcillin or oxacillin Vancomycin
Methicillin resistant Vancomycin Trimethoprim-sulfamethoxazole,†¶ daptomycin¶
Streptococcus anginosus (milleri) Penicillin G Third-generation cephalosporin,‡ vancomycin
group, other streptococci
FUNGI
Aspergillus spp. Voriconazole Amphotericin B deoxycholate, liposomal amphotericin B,
amphotericin B lipid complex, itraconazole,**
posaconazole**
Candida spp. Amphotericin B deoxycholate,†† liposomal Fluconazole
amphotericin B,†† amphotericin B lipid complex††
Cryptococcus neoformans Amphotericin B deoxycholate,†† liposomal Fluconazole
amphotericin B,†† amphotericin B lipid complex††
Mucorales Amphotericin B deoxycholate, liposomal Posaconazole**
amphotericin B, amphotericin B lipid complex
Scedosporium apiospermum Voriconazole Itraconazole,** posaconazole**
*Depending on the pathogenesis of brain abscess formation (see Table 39-1), combination therapy should be continued for the possibility of a mixed
aerobic/anaerobic infection.
†
Use of a specific agent depends on in vitro susceptibility testing of the isolated organism.
‡
Cefotaxime or ceftriaxone.
§
Addition of an aminoglycoside should be considered.
||
Combination therapy may be required in immunocompromised patients or in those in whom standard therapy fails (see text).
¶
No data on the efficacy of these agents in patients with methicillin-resistant S. aureus brain abscess.
**Considered for use as salvage therapy in nonresponding cases or patients intolerant of amphotericin B–based therapies; posaconazole may have a
role as follow-up therapy in patients with mucormycosis.
††
Addition of flucytosine should be considered.
those who underwent surgical excision.163 Aspiration ideally the preferred method of surgical treatment of cerebellar abscesses
should be performed under stereotactic neuroimaging guidance, in children,170,171 given that worse outcomes have been seen in
which affords the neurosurgeon rapid, accurate, and safe access those treated only by aspiration. However, bur-hole aspiration
to virtually any intracranial point.155,164-167 Stereotactic aspiration has also been suggested as a satisfactory method of drainage in
is a useful approach even for abscesses located in eloquent or patients with cerebellar abscesses.6 Drainage is important in such
inaccessible regions168; a second aspiration should be considered cases because precipitous neurologic deterioration can occur
if the initial aspiration proves ineffective or partially effective. within the relatively smaller volume of the posterior fossa in the
Intraoperative ultrasound guidance is also helpful for the aspira- presence of disproportionate edema, especially in children.172 In
tion of small abscesses and can delineate abscess pockets.169 In one retrospective review, there was a lower mortality in the exci-
one series of 142 patients with brain abscess,17 there were no sion group than in the aspiration group.173
significant differences in outcome among those who were treated Neurosurgeons have long debated the proper method of per-
by excision, by craniotomy with drainage, and by stereotactic forming a craniotomy for a brain abscess. Some have advocated
drainage, thus indicating that therapy must be individualized for using the more convenient “free” craniotomy, in which the over-
each patient. Recurrence rates after stereotactic aspiration range lying muscle (e.g., temporalis) is stripped from the bone (i.e.,
from 0% to 24%. creating an unattached craniotomy bone flap), thereby interrupt-
Complete excision by craniotomy is now infrequently per- ing the bone flap’s blood supply. In contrast, others have argued
formed because of the success of aspiration and closed-drainage for the use of an osteoplastic flap. In this technique, the muscle
techniques, although it may be required for patients with multi- is left attached to the bone flap, thus theoretically preserving
loculated abscesses in whom aspiration techniques have failed, for blood supply to the bone. The osteoplastic bone flap potentially
abscesses containing gas, or for abscesses that fail to resolve. would have a lower risk of osteomyelitis in general and especially
Excision is usually required for posttraumatic abscesses that in the setting of an infection. However, no randomized studies
contain foreign bodies or retained bone fragments to prevent have been performed that definitively resolve this procedural
recurrence, for abscesses that result from fistulous communica- question.
tions (e.g., secondary to trauma or congenital dermal sinuses), Intracranial pressure (ICP) monitoring and treatment of
and for those localized to one lobe of the brain and contiguous elevated ICP may be beneficial in patients with brain abscess.
with a primary focus.22 It has also been suggested that excision is Morbidity and especially mortality are usually consequences of
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e196 SECTION 1 Introduction and General Neurosurgery
TABLE 39-7 Recommended Dosages of Antimicrobial Agents in alone.130,174-176 Such groups include those with medical conditions
Adults with Brain Abscess and Normal Renal and Hepatic Function* that increase the risk associated with surgery, with multiple
abscesses, with abscesses in a deep or dominant location, with
Total Daily Dosage
Antimicrobial Agent (Dosing Interval in Hours)
coexisting meningitis or ependymitis, and with abscess size less
than 2.5 cm to 3 cm, and those in whom early reduction of the
Amikacin† 15 mg/kg (8) abscess led to clinical improvement after antimicrobial therapy.
Amphotericin B deoxycholate‡ 0.6-1 mg/kg (24) In one series, no abscess larger than 2.5 cm resolved without
Amphotericin B lipid complex 5 mg/kg (24)
surgical therapy.174 The best candidates for medical therapy alone
Ampicillin 12 g (4)
Aztreonam 6-8 g (6-8)
appear to be those with small abscesses (≤2.5 cm) who are in good
Cefepime 6 g (8) clinical condition with a Glasgow Coma Scale score higher than
Cefotaxime 8-12 g (4-6) 12 and in whom the abscess has a well-known etiology.177 Surgery
Ceftazidime 6 g (8) should be considered, however, if the patient’s clinical condition
Ceftriaxone 4 g (12-24) is worsening or in those without clinical or radiologic improve-
Ciprofloxacin 800-1200 mg (8-12) ment within 1 to 2 weeks.
Daptomycin 6-10 mg/kg (24) The optimal duration of medical treatment of bacterial brain
Fluconazole 400-800 mg (24) abscess is unclear but has traditionally been 6 to 8 weeks for
Flucytosine§ 100 mg/kg (6) high-dose intravenous antimicrobial therapy,1,2,22,175 which is
Gentamicin† 5 mg/kg (8)
Isoniazid§ 300 mg (24)
often followed by oral antimicrobial therapy for 2 to 3 months if
Itraconazole 400-800 mg (12) appropriate agents are available. However, the efficacy of and
Linezolid 1200 mg (12) necessity for additional oral antimicrobial therapy have not been
Liposomal amphotericin B 5-7.5 mg/kg (24) established. A combination of surgical aspiration or removal of
Meropenem 6 g (8) all abscesses more than 2.5 cm in diameter, 6 weeks or more of
Nafcillin 12 g (4) antimicrobial therapy, and weekly neuroimaging to document
Oxacillin 12 g (4) abscess resolution should lead to cure rates greater than 90%.6,178
Penicillin 24 million units (4) Patients should be monitored with neuroimaging until the abscess
Posaconazole§ 800 mg (6-12)†† has completely resolved. If the abscess enlarges after 2 weeks of
Pyrazinamide§ 15-30 mg/kg (24)
antimicrobial therapy, or fails to resolve after 3 to 4 weeks, further
Rifampin§ 600 (24)
Tobramycin† 5 mg/kg (8) surgical aspiration or excision should be performed. Courses of
Trimethoprim-sulfamethoxazole|| 10-20 mg/kg (6-12) 3 to 4 weeks of antimicrobial therapy may be adequate for patients
Vancomycin¶ 30-45 mg/kg (8-12) who have undergone surgical excision of the brain abscess,
Voriconazole** 8 mg/kg (12) whereas longer courses (up to 12 weeks with parenteral agents)
may be required in patients treated with antimicrobial therapy
*Unless indicated, therapy is administered intravenously.
†
Need to monitor peak and trough serum concentrations. alone. The Infection in Neurosurgery Working Party of the
‡
Doses up to 1.5 mg/kg per day may be required in patients with British Society for Antimicrobial Therapy recommends that
aspergillosis or mucormycosis. intravenous therapy be used for 1 to 2 weeks for bacterial brain
§
Oral administration. abscess179; depending on the clinical response, change to an oral
||
Dosage based on trimethoprim component. regimen can be considered. Although this approach has been used
¶
Need to monitor trough serum concentrations (maintain at 15 to in several series,18,180,181 it cannot be considered standard therapy
20 µg/mL). in most patients with bacterial brain abscess. Biweekly neuroim-
**Load with 6 mg/kg every 12 hr for two doses; maintain serum trough aging studies performed for up to 3 months after completion of
concentrations of 2-5 µg/mL.
†† therapy have been suggested to monitor for reexpansion of the
200 mg orally 4 times a day initially, then 400 mg orally twice a day.
abscess and failure of resolution.4,22,147
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CHAPTER 39 Brain Abscess e197
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e198 SECTION 1 Introduction and General Neurosurgery
all intracranial infections. The most common predisposing condi- infection (whether sinusitis or otitis media).220,235 The findings are
tions are otorhinologic infections, especially of the paranasal generally insidious because the dura is closely apposed to the
sinuses, which are affected in 40% to 80% of patients.220-226 The inner surface of the cranium such that the abscess usually enlarges
mastoid and middle ear are affected in 10% to 20% of patients, too slowly to produce the sudden onset of major neurological
who are usually living in geographic locales where patients with deficits seen in patients with cranial subdural empyema (see
otitis media are not properly treated. Other predisposing condi- earlier), unless there is deeper intracranial extension. The usual
tions are skull trauma, neurosurgical procedures, and infection of complaints are fever and headache, but the patient may not
a preexisting subdural hematoma.227 In a 20-year review of sub- appear acutely ill, thereby leading to a delay in diagnosis. Eventu-
dural empyemas in children,228 approximately 20% of the infec- ally, however, focal neurological signs and seizures may develop,
tions had occurred after head trauma or neurosurgery. Rare and as the abscess enlarges, papilledema and signs of increased
predisposing factors include cranial traction devices, nasal surgery, ICP may develop in untreated patients. If the epidural abscess is
ethmoidectomy, and nasal polypectomy.223 The infection is meta- near the petrous bone, Gradenigo’s syndrome may develop, a
static in 5% of cases, usually from a pulmonary source. This condition characterized by the involvement of cranial nerves V
pathophysiology may be operative in both adults and children. and VI and manifested clinically as unilateral facial pain and
Meningitis is an important predisposing condition in infants with weakness of the lateral rectus muscle.
cranial subdural empyema, which occurs in 2% to 10% of those
with bacterial meningitis.224 In one series of patients with infraten-
torial empyema, cases tended to cluster during the spring and
Diagnosis
summer months, with disease more commonly seen in males The diagnosis of cranial subdural empyema should be suspected
(65%) than females (35%).229 in any patient with meningeal signs and a focal neurological
The etiologic agents in patients with cranial subdural empyema deficit.220-224 MRI, the diagnostic imaging procedure of choice,
are usually microbial flora from those with chronic sinusitis, usually demonstrates a crescentic or elliptical area of hypoin-
and such agents include aerobic streptococci (25% to 45%), tensity (on T1-weighted images) below the cranial vault or
staphylococci (10% to 15%), aerobic gram-negative bacilli (3% adjacent to the falx cerebri.226,237,239 Depending on the extent
to 10%), and anaerobic streptococci and other anaerobes (33% of disease, there may also be an associated mass effect with
to 100% in some series in which careful culturing for anaerobes displacement of midline structures. MRI is superior to CT
was performed).222-225,230,231 If the predisposing condition is post- because it provides better clarity of morphologic detail and
operative or posttraumatic, the usual pathogens are staphylococci may detect the presence of a subdural empyema that is not
and aerobic gram-negative bacilli. Propionibacterium acnes may be seen on CT; it is particularly helpful in detecting a subdural
isolated from patients after trauma, neurosurgical procedures, or empyema at the base of the brain, along the falx cerebri, or in
dural allografts.232-234 Operative culture results are reported to be the posterior fossa.
negative in 7% to 53% of patients,226 but the variation in and MRI is also the diagnostic imaging procedure of choice in
high negative results may be related to the frequent use of pre- patients with cranial epidural abscess; it usually demonstrates a
culture/preoperative antimicrobial therapy. superficial, circumscribed area of diminished intensity with
Cranial epidural abscess refers to a localized collection of pus pachymeningeal enhancement.235 CT is used for imaging bone
between the dura mater and overlying skull; because the abscess or if MRI is not available, although MRI is superior in identifica-
can cross the cranial dura along emissary veins, an accompanying tion and delineation of the collection and is able to differentiate
subdural empyema may also be present.220,235 Therefore, the epidural abscesses from sterile effusions and hematomas that
pathogenesis and bacterial etiology are usually identical to those may be present in patients who have undergone cranial surgery
in patients with cranial subdural empyema (see earlier). Cranial or suffered head trauma.
epidural abscess may also occur after head trauma, fetal scalp The diagnosis of both subdural and epidural empyemas in
monitoring, halo pin penetration, and recent intracranial, trans- postcraniotomy patients is problematic and often delayed.240
nasal, or transmastoid surgical procedures.235,236 Symptoms and signs are protean and can be masked by expected
postoperative changes and laboratory findings. Sequential
imaging studies may be valuable for documenting subtle changes,
Clinical Findings but the most useful tool is a high degree of suspicion.
The clinical manifestations in patients with cranial subdural
empyema may be rapidly progressive, with symptoms and signs
related to increased ICP, meningeal irritation, or focal cortical
Management
inflammation.220-224,226,237,238 Most patients have fever and head- Cranial subdural empyema is a surgical emergency because
ache; vomiting is common as ICP increases. Altered mental status antimicrobial therapy alone does not reliably sterilize the
can occur and progress rapidly to obtundation and coma if the empyema. The goals of surgical therapy are to achieve adequate
infection is not treated. Focal neurological signs (e.g., hemipare- decompression of the brain and to evacuate the empyema com-
sis and hemiplegia, ocular palsies, dysphasia, homonymous hemi- pletely.220,237,241,242 The optimal surgical approach is controversial.
anopia, dilated pupils, and cerebellar signs) appear in 24 to 48 When comparing craniotomy drainage with drainage after place-
hours and progress rapidly, with eventual involvement of the ment of bur holes, some studies have demonstrated a lower mor-
entire cerebral hemispheres, although in one series, no focal signs tality rate in patients who have undergone craniotomy. However,
were observed in 41% of the 699 subjects.224 Seizures occur in selection bias may have played a role in these results because
25% to 80% of patients.226 Signs of meningeal irritation are seen patients who underwent drainage via bur-hole placement may
in about 80% of patients. In untreated patients, there is rapid have been more ill and had a greater surgical risk. If bur-hole
neurological deterioration with signs of increased ICP and cere- drainage is performed, multiple bur holes may be required to
bral herniation. However, these clinical findings may not be seen allow extensive irrigation. For patients undergoing craniotomy,
in patients in whom subdural empyema develops after cranial wide exposure is needed to permit surgical exploration of all areas
surgery or trauma, in those who have previously received antimi- where empyema is suspected. In a large series of 699 patients in
crobial therapy, in patients with infected subdural hematomas, or which the efficacy of drainage after CT-guided bur holes was
in those with metastatic infection to the subdural space. compared with craniectomy or craniotomy drainage,243 mortal-
The clinical manifestation of cranial epidural abscess may be ity rates were higher in patients treated by only drainage via
insidious and is usually overshadowed by the primary focus of bur holes (23.3%) than in those who underwent craniectomy
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CHAPTER 39 Brain Abscess e199
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e200 SECTION 1 Introduction and General Neurosurgery
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