Bacterial seeding of the brain may exert its destructive effect at an early stage in the clinical course. Delay in diagnosis due to difficulty to appreciate nonspecific symptoms or, equally common, failure to act timely when signs become apparent contributes to later morbidity.1 Indeed, the vexing concern for any physician is to recognize a bacterial infection when obvious signs, such as fever, confusion, skin rash, and recent sinusitis or otitis, are absent. Without question, a medical debacle may evolve in the first hours after entry to the emergency department despite responding quickly and appropriately. Intracranial abscesses may be first unmasked only after a single seizure without fever. Purulent CSF is sometimes a physician's surprise in a patient with unexplained coma.
In adults, the most common causative organisms in community-acquired meningitis are Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, and Haemophilus influenzae.2,3 From the onset, it is clear that the priorities in evaluation (computed tomography [CT] or cerebrospinal fluid [CSF]) of a presumed bacterial meningitis are complicated.4 Also, management in bacterial meningitis caused by S. pneumoniae or N. meningitidis has become problematic with the emergence of organisms resistant to penicillin and cephalosporin. This chapter focuses on early aggressive management of common bacterial infections of the central nervous system. It emphasizes avoidance of pitfalls and provides guidelines to make simple and straight-forward clinical decisions.
Acute Bacterial Meningitis
The pathophysiology of bacterial meningitis involves many pathways that may, at least in the most severe cases, lead to cerebral edema, brain tissue displacement, and, probably most important, cerebral infarction.5 The consequences of meningeal inflammation are discussed in Box 16.1.
In most adults, a healthy state is first interrupted by an upper respiratory tract infection or ear infection, and antibiotic therapy does not make any major progress. Thus, potential sources for acute bacterial meningitis, such as pneumonia, paranasal sinusitis, and middle ear infection, should be sought. These sources are more prevalent in patients with profound comorbidity, such as diabetes mellitus, prior transplantation, long-term dialysis, splenectomy, alcoholism, and certain malignancies such as Hodgkin's disease.
Characteristic symptoms and signs of acute bacterial meningitis are fever, headache, and reduced alertness. The degree of fever in bacterial meningitis may vary. Most patients have so-called hectic temperature, with an increase to 39°C or 40°C, but low-grade fever (or none at all) may be present in the elderly, immunosuppressed patients, or patients who have been taking oral antibiotics or antipyretic drugs, all of whom may have greatly reduced mechanisms to mount this febrile response.2 Temperature is usually constantly elevated, and marked temperature oscillations may therefore suggest a localized collection of pus (e.g., tonsillar, mastoid, or middle ear abscess).
Box 16.1. Pathogenesis of Bacterial Meningitis and Its Consequences
A common sequence in the development of bacterial meningitis is as follows: Nasopharyngeal colonization occurs and is dependent on fimbriae and specific surface cell receptors. Attachment may be facilitated by previous viral infection. It is followed by development of bacteremia. The polysaccharide capsule should counter the classic complement pathway or alternative complement pathway (common in patients with underlying sickle cell disease and splenectomy) and defy phagocytosis. Next is meningeal invasion and entrance into the CSF through the choroid plexus, again facilitated by receptors. The bactericidal activity in the subarachnoid space is poor because the complement activity needed to initiate phagocytosis is low. Then, an inflammatory response is mounted by components of the lysed bacterial cell mass (teichoic acid endo-toxin), which induce production of inflammatory cytokines (tumor necrosis factor, interleukin-1, and macrophage inhibitory protein). Neutrophils invade, and blood-brain barrier permeability increases, finally causing vasogenic brain edema. The toxic oxygen metabolites cause cytotoxic edema, and CSF outflow resistance from protein-rich exudate in the subarachnoid space produces interstitial edema and hydrocephalus.
Cerebral infarcts from vasculitis, vasospasm of basal arteries, or thrombosis of the major venous sinuses may occur, possibly only in the most fulminant cases with virulent pathogens.6,7,8,9 The urokinase plasminogen activator system may be involved in breaching of the CSF-blood-barrier (Fig. 16.1).10
More than 75% of patients with bacterial meningitis are confused, irritable, or stuporous. Most patients can be roused with a forcible command or painful stimulus. Elderly patients may simply have a blank expression and be motionless and withdrawn.11,12
Figure 16.1 Pathophysiologic alterations causing a vicious cycle. BBB, blood-brain barrier; CBV, cerebral blood volume. (From Scheld et al., 2002,5 with permission.)
Nuchal rigidity is common in bacterial meningitis. Flexion of the neck causes flexion in the hips and knees (Brudzinski's sign of meningismus, see Chapter 8). Cranial nerve involvement may include abducens nerve palsy as a false localizing sign of increased intracranial pressure, facial nerve palsy associated with mastoiditis, and, most worrisome, inflammation of the cochlear nerve leading to permanent hearing loss, reducing response to voice.
Seizures are more prevalent in children and young adults but may occur in up to 10% of adults or the elderly. Seizures, particularly focal, can be attributed to focal edema, early cortical venous thrombosis, and cerebral infarction from occlusion of penetrating branches encased by the basal purulent exudate.
Generalized myoclonus may occur and should immediately prompt measurement of the level of penicillin or cephalosporin. It is common in patients with coexistent renal disease, which reduces excretion and allows penicillin or cephalosporins to accumulate to toxic levels.13
Rapidly developing coma with pathologic motor responses is uncommon in adults, but when present, it signals a fulminant variant with diffuse cerebral edema or multiple cerebral infarcts from secondary inflammatory vasculitis.14 Increased intracranial pressure leading to cerebral herniation syndromes occurs in approximately 10% of patients. Rarely, meningeal veins become necrotic or thrombosed, a condition leading to extensive hemorrhagic cortical infarction and bihemispheric swelling.
Meningococcal meningitis may progress to shock from adrenal hemorrhages. Petechiae, widespread purpuric rash with patches of necrotic skin (see Color Fig. 16.2 in separate color insert), conjunctival hemorrhage, and punctate lesions inside the mouth and on the lips are seen in conjunction with shock, profound hyponatremia and hyperkalemia (Addison's disease), and laboratory evidence of intravascular coagulation.
Tuberculous meningitis should be suspected in patients with human immunodeficiency virus (HIV) infection, malnutrition, drug abuse, home-lessness, or any immunosuppressed state. Prodromal symptoms of coughing, weight loss, and night sweats followed by confusion and rapidly developing coma with cranial nerve deficits are frequent but nonspecific. Choroidal tubercles at ophthalmoscopy, hilar adenopathy on chest radiographs, and hydrocephalus on CT scan are additional indicators of tuberculous meningitis. In a recent series, 32 of 48 patients with adult tuberculous meningitis had an extrameningeal tuberculous location.15 When younger patients are seen on admission, white cell counts of less than 10,000 × 103 per mL, age, and protracted history of illness are more common features seen with tuberculous meningitis than with bacterial meningitis.16 Clear CSF with moderate number of lymphocytes and monocytes and a reduced ratio of cerebral fluid-blood glucose were important differentiating factors in a large study of tuberculous meningitis from Vietnam.16
Interpretation of Diagnostic Tests
Computed Tomography and Magnetic Resonance Imaging
CT scanning could precede CSF examination because images can be acquired very quickly with modern CT scanners. If CT scan cannot be rapidly obtained, empiric therapy should be administered first, followed by CT scan and CSF, in that order. The nonspecific presentation of fever, seizures, and neck stiffness may indicate a subdural empyema or an intracranial abscess with ventricular rupture rather than bacterial meningitis. When CT scanning is deferred, either of these conditions may theoretically worsen with lumbar puncture. If diffuse cerebral edema is present, herniation may occur with lumbar puncture despite removal of a small amount of CSF (e.g., 5 mL) or the use of a smaller needle (e.g., 22 gauge), although herniation from fulminant meningitis may occur irrespective of lumbar puncture. CT scan images are typically normal in bacterial meningitis.
Mild obstructive hydrocephalus (see Chapter 11), cerebral edema, and hypodensities from ischemic strokes have been reported in a small proportion of patients with acute bacterial meningitis.3,17 However, CT scan findings are abnormal in 51% of patients with tuberculous meningitis. Ventricular dilatation, superficial meningeal enhancement, and hypodensity representing cerebral infarcts are common in tuberculous meningitis.
Magnetic resonance imaging (MRI), particularly fluid-attenuated inversion recovery (FLAIR) sequences, may reveal important findings in any type of bacterial meningitis because of its superb sensitivity; cerebral infarcts (Fig. 16.3) or the inflammatory exudate18 (Fig. 16.4) may be detected. MRI may also document involvement of vestibular and cochlear structures in patients with hearing loss.19
The CSF in acute bacterial meningitis is typically turbid or xanthochromic, with increased opening pressure (>200 mm H2O) and polymorphonuclear pleocytosis (>1000 cells/mm3). CSF leukocyte counts are increased less in meningitis associated with S. pneumoniae than in N. meningitidis, and could reflect a poor immunocompetent state.20 Increased CSF protein (often >100 mg/dL) and decreased CSF glucose concentration (<40 mg/dL) are typical findings. CSF glucose should be compared with serum glucose, which may be increased as a stress response to the acute neurologic illness (normal ratio of CSF glucose to serum glucose is 0.6). Decreased CSF glucose concentration is typical of bacterial meningitis but may occur in fungal, tuberculous, or carcinomatous meningitis, in neurosarcoidosis, or, rarely, as a reflection of marked hypoglycemia. When CSF is bloody, the total white blood cell count is falsely increased, complicating interpretation. Red blood cells from a traumatic puncture increase the total cell count of 1 white blood cell per 700 red blood cells.
Figure 16.3 Magnetic resonance image with fluid-attenuated inversion recovery (FLAIR) sequences in patient with fulminant pneumococcal meningitis. Bilateral thalamic infarcts (arrows) from penetrating branch occlusions produce coma. (From Vernino et al.18 By permission of the American Academy of Neurology.)
Figure 16.4 Magnetic resonance image with fluid-attenuated inversion recovery (FLAIR) sequences demonstrates purulent exudate (arrow) not visible on routine sequences or after gadolinium T1 enhancement. (From Vernino et al.18 By permission of the American Academy of Neurology.)
CSF lymphocytosis is most compatible with viral, fungal, and tuberculous meningitis. However, initial CSF lymphocytosis in bacterial meningitis was found in 6% of 428 patients and in 24% of patients with CSF leukocyte counts of fewer than 1000 cells/mm3, irrespective of previous antibiotic use.20 A predominant CSF lymphocytosis may occur early in the ictus, most often associated with L. monocytogenes meningitis in immunosuppressed patients. If glucose concentration is decreased, the presence of predominantly lymphocytes in the CSF formula should strongly point to the possibility of tuberculous or fungal meningitis.20 At least three CSF samples are needed to obtain material for a smear; an enzyme-linked immunosorbent assay may visualize the tuberculous bacilli in 40% of smears. CSF cultures require up to 6 weeks for growth. However, fungal meningitis may not be detected with any of these tests, and meningeal biopsy may be needed. Other diagnostic tests are available to complement CSF cultures (Box 16.2).
Box 16.2. Rapid Diagnostic Tests
Latex particle agglutination tests can rapidly detect bacteria) antigens in purulent CSF. The specificity is close to 100%; the sensitivity depends on the organism (H. influenzae, 78%–86%; S. pneumoniae, 69%–100%; N. meningitidis, 33%–70%). Experience with polymerase chain reaction in acute bacterial infection is limited. The technique is useful in certain unusual causes of bacterial infections, but processing takes from 12 hours to 3 days. It has a sensitivity of 70%–80% in Lyme disease.
Gram stain has a positive yield in 60%–80% of patients, but the yield is much lower (40%–50%) with previous antibiotic use. Acid-fast stain may diagnose tuberculosis in 35%–80% of cases.21
First Priority in Management
Cephalosporins and vancomycin should be given intravenously at once, before any further diagnostic tests are ordered and, in fact, when the first purulent spinal fluid drops appear in the test tube. Recommended empirical therapy is shown in Figure 16.5. The addition of vancomycin is important to immediately preempt cephalosporin-resistant S. pneumoniae, which has become increasingly frequent.22 Vancomycin administration should be closely monitored (aiming at a trough of 10 mg/mL and a peak serum level of 50 mg/mL) and continued for 14 days, if indicated. (Vestibular damage is uncommon from vancomycin and is much more likely from direct inflammation of the vestibular nerve due to meningitis.) Antibiotic therapy for specific organisms is summarized in Table 16.1.23A combination of three antituberculous drugs is additionally needed if tuberculous meningitis is likely on the basis of the initial CSF formula and clinical presentation.24 Dexamethasone is reserved for fulminant variants (e.g., brain edema, impending brain herniation), including tuberculous meningitis;25 and its use is proven in adult-onset bacterial meningitis26 due to penicillin-susceptible streptococcus meningitis. In other conditions, dexamethasone may seriously reduce penetration of cephalosporins and, particularly, vancomycin (Box 16.3).26 Nonetheless, dexamethasone, 10 mg every 6 hours for 4 days,26 just before administration of antibiotics should be very seriously contemplated, if not considered standard. Rifampin, 600 mg/day, may increase the bioavailability of vancomycin and should be added if penicillin resistance becomes obvious.
Figure 16.5 Empirical therapy for acute bacterial meningitis. CSF, cerebrospinal fluid; CT, computed tomography; DD, divided dose (intravenously); MRI, magnetic resonance imaging; PMN, polymorphonuclear cells.
Chemoprophylaxis is indicated in meningococcal meningitis and is administered to any person who had close contact with the patient. Recommendations for chemoprophylaxis, which should be discussed in the emergency department, are shown in Table 16.2.30,31,32,33
Predictors of Outcome
S. pneumoniae meningitis continues to cause sequelae such as hearing loss, seizures, personality change, and cognitive deficits.34 In well-recovered patients with adult bacterial meningitis, neuropsychologic tests have noted reduced reaction speed and executive functioning but no memory deficits.35 Drug-resistant strains of pneumococci cause significantly higher mortality than other pneumococcal bacteria. Coma at onset or focal seizures, focal neurologic deficits, and low CSF leukocyte counts increase the risk of poor outcome.36 Acute complications such as brain edema and cerebral infarcts significantly increase the chance of a persistent vegetative state. Many predictors of poor outcome have been identified in tuberculous meningitis, including extremes of age, malnutrition, miliary disease, hydrocephalus, documented ischemic stroke, and low total CD4 cell count in a subset with HIV infection.37
Table 16.1. Recommended Antimicrobial Therapy for Bacterial Meningitis
· Urgent otolaryngologic evaluation.
· Admission to a neurologic intensive care unit is indicated to monitor the development of cerebral edema or, more commonly, hydrocephalus.
· If seizures have occurred, loading with fosphenytoin or phenytoin, 20 mg/kg intravenously.
Subdural Empyema and Epidural Abscess
Sinusitis,38 recent sinus surgery, and, less commonly, otitis or traumatic brain injury are sources that may cause infection of the subdural space. Infection may spread directly, through erosion of the posterior wall of the frontal sinus or tegmen tympani of the middle ear, or indirectly, through retrograde extension of thrombophlebitis.39 This bacterial infection is uncommon in adults and often mistakenly diagnosed at first as bacterial meningitis.40,41
Epidural abscess is produced by sources similar to those in subdural empyema, but in this condition, the suppurative infection is localized between the dura and bone. Continuous infection is most common, and the abscess creates a mass effect, gradually lifting the dura from the overlying skull.
Patients (often men in the second or third decade) with subdural empyema are very ill with fever, vomiting, excruciating headache, and, most commonly, localizing neurologic deficits, such as aphasia, apraxia, visuospatial neglect, hemiparesis, and focal seizures.42 Most of these seizures arise in the premotor area of the frontal lobe (adversive seizures), with turning of the head and eyes, abduction of the contralateral arm, and flexion in the elbow with raised arm similar to the posture of a fencer. Other patients have speech arrest without impairment of consciousness or jacksonian seizures (the spread of the seizure reflects the cortical topography, beginning in the hand and moving to the face, the leg, and the foot).43
Clinical presentation is insidious and directly related to the mass effect, which may take weeks to become prominent and critical. Papilledema may be observed in patients with a comparatively slow-growing abscess. This allows time for increased intracranial pressure to be transmitted to the optic nerve sheaths, with subsequent venous stasis and resultant disk swelling. Nuchal rigidity is present; and if localizing neurologic signs are absent and the classic association with recent pyogenic sinusitis or surgery is not appreciated, bacterial meningitis is often incorrectly diagnosed. Misdiagnosis may also be more prevalent when the epidural empyema overlies or collects between the hemispheres. Headache and fever may be the only symptoms in these patients. An uncommon but localizing symptom complex of facial pain (trigeminal nerve involvement), facial palsy, and abducens paresis can be observed if the petrous bone is involved in the process (Gradenigo's syndrome).
Box 16.3. Dexamethasone in Bacterial Meningitis
Dexamethasone reduces the production of cytokines and thus reduces the inflammatory response. It may reduce permeability of the blood-brain barrier and thus reduce cerebral edema. However, reduction of meningeal inflammation may reduce the penetration of antibiotics that require an impaired blood-brain barrier.
Dexamethasone reduces mortality, deafness, and neurologic deficits in children with bacterial meningitis caused by H. influenzae. It also reduces morbidity in tuberculous meningitis but only in the most severe cases. In fulminant bacterial meningitis, dexamethasone is arbitrarily recommended for 4 days. Preferably, dexamethasone should be administered 30 minutes or less prior to the first antibiotic dose. Antibiotic therapy causes bacteriolysis and release of endotoxin. Dexamethasone may preempt production of tumor necrosis factor initiated after release of endotoxin.25,27,28,29 In adults, a dose of 10 mg q6h for 4 days reduces disability but not hearing loss.26
Interpretation of Diagnostic Tests
Computed Tomography and Magnetic Resonance Imaging
CT scanning or MRI demonstrates a fairly characteristic lesion (Fig. 16.6), usually supratentorially. Small collections may also be seen in the posterior fossa.44Noncontrast CT scanning shows a hypodensity over or between the hemispheres along the falx, but enhancement of the pus collection after contrast administration reveals the characteristic crescent shape of the mass. Imaging of the mastoid and paranasal sinuses to seek a potential source is imperative.45,46
MRI with gadolinium is superior to contrast CT because bone artifacts that may limit detection are absent.41,47 MRI also clearly distinguishes between hydroma (similar T1- and T2-weighted signals to CSF) and pus (hyperintensive to CSF on T2-weighted image and hypointense to CSF on T1).48 MRI may also detect parenchymal involvement and development of cerebral venous thrombosis, but a separate magnetic resonance venogram may be needed.
In a patient with an epidural abscess, a lentiform mass overlying the cerebral convexity without hemispheric involvement is clearly evident on CT scans with contrast and is not uncommonly found after a prior craniotomy (Fig. 16.7),49 MRI may further localize small locations and their extent.50 Lack of gadolinium enhancement of the dura below the mass strongly favors epidural localization.51
Table 16.2. Chemoprophylaxis Options for Meningococcal Meningitis
Figure 16.6 Computed tomographic scan showing subdural empyema with mass effect (arrows).
Lumbar puncture is contraindicated. One study suggested clinical deterioration after lumbar puncture.52 When available (as mentioned earlier, often when bacterial meningitis was suspected), the findings include variable total cell counts (10–500/mm3), increase in polymorphonucleated cells (fewer than 10 white blood cells may occur in 10% of patients), increased protein (60%–80% of patients), normal glucose in CSF (at least 50% of cases), but often negative Gram stain and sterile culture (>90% of patients).39,43 The CSF isolates are often Streptococcus milleri (otorhinogenic source), Staphylococcus aureus, or coagulase-negative staphylococcus (sinus, trauma, or surgery). When pneumonia is concomitantly present, S. pneumoniae, Escherichia coli, and H. influenzae are common infectious agents. Blood cultures are seldom diagnostic.
First Priority in Management
Surgical evacuation and immediate antibiotic coverage are therapeutic interventions in the first hours of presentation. Antibiotic therapy in the emergency department should start with a combination of a third-generation cephalosporin and metronidazole. However, anaerobic isolates are uncommon. Alternatively, a combination of piperacillin sodium and tazobactam sodium (Zosyn) can be considered (Table 16.3). Craniotomy rather than aspiration over multiple burr holes is preferred.53,54,55 In a patient with an epidural abscess, grafting may be needed if the dura is destroyed or penetrated by the inflammation. Parenteral antibiotic therapy should continue for 2–6 weeks. Conservative management is seldom considered and perhaps an option only in the remote clinical situation of full alertness, tiny fluid collections (<1 cm in diameter), and rapid clinical improvement after intravenous antibiotics.55 However, clinical deterioration may occur suddenly.
Figure 16.7 Computed tomographic scans and magnetic resonance image after frontal craniotomy show epidural pus collections (arrows).
Table 16.3. Empirical Antibiotic Therapy in Subdural Empyema and Epidural Abscess
Predictors of Outcome
Subdural empyema is a potential calamity if not treated quickly.56 Complacency leads to death in a matter of days, often from cerebral venous thrombosis as a result of cortical thrombophlebitis. Surgical drainage craniotomy rather than burr holes52 and intravenous antibiotics are mandatory, resulting in the greatest chance of recovery with a minimal neurologic deficit. In a review of 102 patients with subdural empyema, treatment before the patients lapsed into stupor increased the chance of survival, reducing mortality to 10%.57 Rhinogenic subdural empyema had the best prospects for good outcome.52
· Otolaryngologic evaluation.
· Start antibiotics and transport to the operating room.
· Consider mannitol, 1 g/kg, if CT scan shows a significant mass effect before transport.
· Intravenous loading with phosphenytoin or phenytoin, 20 mg/kg, if seizures have occurred.
In referral hospital emergency departments, the incidence of brain abscess may approximate 1 in 10,000 hospital admissions.58 The causes are listed in Table 16.4. The paranasal sinuses, middle ear, and teeth remain the most common sources of entry. One should expect the cause in 30% of patients with a bacterial brain abscess to remain unresolved. Hematogenous source from endocarditis, injected drugs, or tongue piercing should also be considered.59,60
Table 16.4. Brain Abscess: Predisposing Condition, Site of Abscess, and Microbiology
Brain abscess most often is manifested by dull headache and rarely by fever or papilledema.61
Neurologic signs depend on localization of the abscess and, as expected because of a lack of obvious symptoms, on localization of the frontal or occipital lobe. Clinical findings may become more evident if edema surrounds the mass and certainly if rupture into the ventricular system occurs. Sudden worsening of headache and stupor may then be common clinical features. Level of consciousness depends on the timing of referral, and now significantly more patients seen in the emergency department are fully alert, with headache alone.62 Seizures due to cerebral abscess are often generalized tonic-clonic seizures and have an estimated incidence of 40%.
Localization of an abscess in the cerebellum and brain stem is rare. The signs are ataxia, vomiting, appendicular dysmetria, and nystagmus.
Figure 16.8 A: Computed tomographic scans showing abscess in the frontal lobe with perilesional edema (arrows). B: Temporal lobe abcess associated with otitis media. Note absent air in mastoid and edema on magnetic resonance imaging (arrows).
Interpretation of Diagnostic Tests
CT scanning is diagnostic (Fig. 16.8).63 A common misinterpretation of the abnormality in a noncontrast CT scan image, lacking the ring configuration, is a cerebral infarct. MRI may further define mass effect and demonstrate additional lesions. In T1-weighted sequences, a hypodense center consisting of pus with a ring at the periphery is characteristic and may become evident only after contrast enhancement. T2-weighted images show a hyperintense signal with edema, which should be separated from the actual lesion in assessment of its size.64 MRI is also more sensitive in detecting newly developing lesions, particularly cerebritis, and it may demonstrate the proximity of the abscess to the ventricular system. Differentiation of brain abscess from cystic brain tumor remains difficult. In preliminary studies, results from magnetic resonance spectroscopy suggested that brain abscess could be distinguished on the basis of elevated acetate, succinate, and some amino acids.65,66,67 Using diffusion-weighted imaging, hyperintensity was noted in abscess and hypodensity in necrotic brain tumors.67
Table 16.5. Suggested Empirical Therapy for Brain Abscess by Presumed Source
First Priority in Management
Antibiotic therapy aimed at polymicrobial flora should be started immediately (Table 16.5). The decision to operate depends on several factors. Open craniotomy with debridement or stereotactic CT-guided aspiration is the first procedure in most cases. Early excision of an abscess should be considered if a thick, fibrotic capsule reduces the success of catheter drainage alone, predominantly in abscesses due to Mycobacterium tuberculosis and Nocardia. Impending rupture to the ventricular system is a reason for early surgical intervention.68 However, surgery can be deferred if multiple abscesses are present, if the diameter of the abscess is less than 3 cm on CT scan images, or if Toxoplasma is considered. Corticosteroids (dexamethasone, 10 mg intravenously q6h) with multipronged antibiotic coverage should be considered if edema is profound and signs of early herniation are developing. The dose should be tapered over 3–7 days. Aggressive ventricular drainage with intraventricular administration of antibiotics is needed in patients with ventricular pus from rupture into the ventricular system. If die abscess is localized in the brain stem, stereotactic drainage is more cumbersome. Empirical therapy with antibiotics lasting up to 3 months may be preferred to surgical drainage with identification of the organism, but both approaches are successful.
Predictors of Outcome
Important factors predicting poor outcome in cerebral abscess are symptoms of short duration, decreased consciousness, rapidly progressive neurologic deficit, number and size of abscesses, and ventricular rupture.69 Mortality is closely linked to initial presentation in coma, which increases the frequency to 50%–80% as opposed to a minimal risk of death in patients who are alert.
· To the operating room: patients with abscess and mass effect, close proximity to the ventricular system, or hydrocephalus.
· To the ward: patients with multiple small cerebral abscesses. Management is by intravenous administration of antibiotics with central venous catheter access.
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