Cerebral abscess can be defined as a focal pyogenic infection of the brain, typically bacterial, less commonly fungal and parasitic.
There are four main pathologic stages:
Early cerebritis (first ~5 days): Represents early focal infection with localized polymorphonuclear leukocytes (PMNs), edema, scattered necrosis, and petechial hemorrhage. Toxic changes in neurons with perivascular infiltrates are present. The lesion is poorly demarcated from surrounding brain.
Late cerebritis (5–14 days): Reticular matrix formation begins leading to a rim of thin granulation tissue at the periphery. Necrotic foci also coalesce leading to the development of a necrotic center.
Early capsule (2 weeks–1 month): Lesion develops neovascularity. At this stage, there is a developed, liquefied necrotic center surrounded by a dense reticular network.
Late capsule (several months): The lesion wall thickens and contains collagen, granulation tissue, and macrophages. The central cavity begins to shrink as the wall of the abscess thickens. The lesion also induces peripheral gliosis at this stage.
Dissemination from primary site remote from the brain. (The chest is the most common.)
In 15% of cases, this leads to multiple abscesses, occurring at the gray–white junction.
The middle cerebral artery (MCA) territory (in the parietal lobe) is the most common site of dissemination.
No source can be identified in up to 25% of cases.
Common sites of primary infection include skin, dental abscess, osteomyelitis, septicemia (intravenous drug users), and right to left shunt due to congenital cardiac malformations.
The majority of these cases arise from the face, paranasal sinuses, and middle ear/mastoid infections.
Location provides clues as to the etiology (e.g., mastoiditis will cause abscesses in the cerebellum; otitis media will cause erosion through the temporal bone).
Infection spreads due to retrograde thrombophlebitis through valveless diploic veins leading to extracranial–intracranial communication.
Usually with penetrating craniocerebral trauma with retained foreign bodies
Rarely, a basal skull fracture with persistent cerebrospinal fluid (CSF) leak may lead to abscess formation.
Malignancy, organ transplant recipients, human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) and chronic steroid use
Twenty to 30% of abscesses are cryptogenic; postoperative etiologies should also be considered.
Brain abscess occurs at any age, but is most common in the third and fourth decades; 25% occur in patients younger than 15 years.
The condition is relatively rare: only 2,500 cases per year in the United States.
The male to female ratio is ~2 to 1.
Headache (90%) and nausea and/or vomiting are the most common presenting symptoms.
Fever (in 50% of cases, greater than 39° C is uncommon)
Seizures are seen in up to 50% of cases.
Focal neurologic deficits occur depending on the location and size of the abscess.
Altered mental status with nuchal rigidity may occur in cases of increased mass effect (which may lead to herniation) or in cases of intraventricular rupture of the abscess.
Diagnosis and Imaging
White blood cell (WBC) count (elevated in 50%, often demonstrates increased PMN)
Erythrocyte sedimentation rate (ESR; increased in 75% of cases)
Blood cultures (rarely positive initially)
First-line brain imaging: Computed tomography (CT) with and without contrast, magnetic resonance imaging (MRI) with and without contrast
Extracranial work (guided by clinical findings): Chest X-ray, sinus CT with and without contrast, CT chest/abdomen/pelvis with and without contrast, tagged white blood cell (WBC) scan
Common microorganisms include
Bacterial: Staphylococcus, Streptococcus, Pneumococcus (In ~30% of bacterial abscesses more than one organism is identified.)
In diabetic patients: Klebsiella pneumoniae
In patients with HIV: Toxoplasmosis, Mycobacterium tuberculosis
In immunosuppressed patients: Nocardia, Aspergillus, Candida
In neonates: Citrobacter, Proteus, Pseudomonas, Serratia, Staphylococcus aureus
Early cerebritis: May be normal. Lesion will demonstrate ill-defined hypodense subcortical lesion with mass effect. Contrast will demonstrate mild, patchy ring enhancement.
Late cerebritis: Demonstrates central low-density area with peripheral edema. Contrast will produce enhancing rim.
Early capsule: This stage will demonstrate the peak amount of edema. Distinct capsule enhancement (deepest part of the capsule is thinnest; the more superficial part is thickest).
Late capsule: Edema will be diminished, with a shrunken hypodense cavity. The capsule will be at its thickest point at this stage.
Early cerebritis: Poorly defined margins with a mixed intensity mass and patchy enhancement
Late cerebritis: Hypointense center with mildly hyperintense rim; intense but irregular rim enhancement
Early capsule: The rim is isointense to white matter with the center hyperintense to CSF. There will be a well-defined, thin-walled enhancing rim.
Late capsule: Shrunken cavity with thickened capsule and increased rim enhancement
Early cerebritis: Poorly defined hyperintense mass
Late cerebritis: Hyperintense center (cellular, debris) with hypointense, but irregular rim and hyperintense surrounding edema
Early capsule: Hypointense rim (related to collagen, hemorrhage, or paramagnetic free radicals)
Late capsule: Diminished hyperintensity around capsule and reduced mass effect
Diffusion-weighted images (DWIs)
Hyperintensity in both cerebritis and abscess
Dark on apparent diffusion coefficient (ADC) map centrally in the abscess
Central necrotic area may show acetate, lactate, alanine, succinate, pyruvate, and amino acids peaks.
Cerebral abscesses do not contain normal neurons; therefore, no peaks of N-acetylaspartate (NAA) or phosphocreatine/creatine (PCr/Cr) should be detected.
Radiographic differential diagnoses
Primary brain tumor: Typically low intensity on DWI
Resolving blood clot: History of trauma and dark on gradient echo sequence (GRE)
Demyelination: Typically enhancing incomplete ring in the presence of other lesions in the brain; minimal mass effect
Metastatic lesion: Typically low intensity on DWI and suspicious clinical history
Subacute infarct: History of stroke with lesion in vascular distribution with gyriform enhancement
Tips for diagnosis on MRI
Consider DWI sequences and MR spectroscopy to distinguish abscess from mimics.
T2 hypointense abscess rim resolves in successfully treated patients before resolution of the enhancement.
Treatment Options and Alternatives
Antibiotics alone for lesions < 2.5 cm in size and in the early phase of cerebritis (Antibiotics do not penetrate the abscess capsule well.)
For all other lesions, surgical drainage and/or excision are the primary therapeutic modalities.
Steroids can help treat edema.
Goals and Advantages of Selected Surgical Approach
Because a cerebral abscess can occur anywhere in the brain, the general surgical approach that would be most useful is a stereotactic-guided minicraniotomy for evacuation and drainage. The goals and advantages include
Greenberg or other self-retaining retractor system
High-speed drill, microdissectors
Microscope or loop magnification with headlight illumination
Antibiotic irrigation should be available.
Expert Suggestions / Comments
Image-guided needle aspiration combined with antibiosis has significantly improved the outcomes for patients with intracerebral abscesses (Fig. 114.1A-C).
Lumbar puncture is dangerous in the setting of intracranial mass effect.
The pathogen is rarely identified from a lumbar tap.
Hematogenous spread usually demonstrates multiple abscesses at the gray–white junction.
Absence of fever does not exclude brain abscess.
In patients with the appropriate clinical history, one must have a high index of suspicion for tuberculosis (TB) and investigate their respiratory system accordingly.
Great care must be taken when removing an abscess “en bloc” to avoid intraoperative rupture and spillage of purulent material, especially into the ventricles.
Excision may be considered as first-line treatment in traumatic abscesses or fungal lesions.
If using abscess aspiration as a treatment modality, repeated procedures may be required until the abscess is completely resolved.
Fig. 114.1 (A) Axial view showing patient positioning and stereotactic frame in place with site of skin incision determined based on the trajectory location and entry point as determined on preoperative imaging studies. Eloquent structures are avoided. A stereotactic biopsy and aspiration can be obtained to determine the offending organism and decompress a deeply located abscess. (B) Oblique front view of the same setup and positioning described in (A). (C) A minicraniotomy may also be performed in select cases with frameless stereotaxy and a guided small thin ultrasound probe can be driven down to the location of the abscess to better determine the nature of the lesion and achieve decompression. SI, S-shaped skin incision; CS, coronal suture.
Key Steps of the Procedure
The craniotomy procedure for abscess resection and or decompression will be described herein. The stereotactic-guided biopsy procedure is described in detail in another chapter.
Preoperative CT/MR images should be obtained including a stereotactic protocol. These films should be studied to plan the trajectory. This will aid in positioning, pin placement, as well as incision type and location. Patients should be placed under general anesthesia and then positioned where the planned craniotomy is facing up and toward the surgeon. Pins should be placed far out of the way of the operative site. An incision should be planned in a way that it can be extended if necessary. The hair should also be shaved or clipped in an adequate manner to accommodate this eventuality. The reference star or frame for neuronavigation should be placed directly on the headholder in a tight fashion so as to not migrate during the procedure. Once the system is registered and active, this can be used to further guide incision and approach plan.
Once a detailed “time out” is performed outlining the procedure type and site, local anesthetic can be injected into the planned incision site. One technique is to make a “lazy S” incision that is about one and a half times to twice the size of the planed craniotomy. Next, a 10-blade scalpel can be used to make the skin incision. Further tissue dissection can be performed using the Bovie electrocautery. A self-retaining retractor can be used such as a cerebellar retractor. Then, the image guidance probe should be used to redefine the minicraniotomy site. One or two burr holes are usually sufficient. These can be made with a high-speed drill. One should try to hide the burr holes under an area that can be covered with overlying muscle if possible. Now, a Penfield #3 dissector can be used to strip the dura from the underside of the bone that is to be removed. A side cutting apparatus/drill attachment can be used to turn a bone flap, which is passed off the field with care.
Once the bone flap is taken off and the dura exposed, the reference probe should be used to reconfirm the path to the abscess. The bone edges should be waxed and, depending on how large a craniotomy made, a few dural tack-up sutures are placed. One option is to open the dura in a cruciform fashion such that the opening can be extended if needed. The dura is opened using a 15-blade scalpel. The dural leaves are held off the field with 4-0 Nurolon suture. The operative microscope should be brought in at this point, and the Greenberg retractors (or other self-retaining retractor system) can be placed in case these become necessary. The image guidance should be used to guide entry into the brain parenchyma to minimize brain trauma. Once the abscess is encountered, one should keep in mind that the capsule can be rather resilient and may need to be opened with a scalpel (in cases of larger abscesses that need to be drained prior to resection). An attempt should be made to remove the abscess cyst in its entirety (in an “en-bloc” fashion). If this cannot be done safely then that cyst should at least be drained and a specimen sent to a microbiology laboratory for identification. The purulent fluid obtained from the abscess should be sent for routine aerobic and anaerobic cultures as well as fungal elements and acid-fast bacilli. Care should be taken not to rupture the abscess into the ventricle if it is located near that area (Fig. 114.2).
Fig. 114.2 A standard craniotomy is performed to remove a superficially located abscess in noneloquent brain. The abscess is accessed by completing a corticectomy along the expanded gyrus, as demonstrated on the stereotactic images obtained preoperatively.
Once resection/removal are complete, copious irrigation should be used with or without antibiotics (depending on the surgeon’s preference, as certain antibiotics have been shown to be neurotoxic). Meticulous hemostasis should be completed using the bipolar cautery and absorbable gelatin powder (GelfoamTM powder, Pfizer Inc., New York, NY) with thrombin. Strips of absorbable hemostat (SurgicelTM, Johnson & Johnson Inc., New Brunswick, NJ) can be placed in the resection cavity. The dura is reapproximated with 4.0 Nurolon. The bone flap is replaced and held in place with titanium microscrews and plates. The scalp flap is then closed using inverted 2.0 Vicryl suture for the galea, followed by staples for the final skin closure.
Avoidances / Hazards / Risks
Rupturing the abscess into the ventricle should be avoided.
A pathway should be chosen going through the least eloquent cortex.
Excessive brain retraction should be avoided and cyst drainage attempts should be considered to increase exposure.
Salvage and Rescue
If rupture of cyst into the ventricle occurs, copious irrigation should be used with or without antibiotics.
If a lesion is not fully accessible or complete removal is not possible, then the surgeon should try to remove as much lesion as safely possible and then abort the procedure. At least a specimen can be obtained and will guide specific treatment management.
If the craniotomy made was too small and does not offer adequate access, it can always be enlarged, but this eventuality should be anticipated at the onset of the procedure when choosing the incision type and location.
Outcomes and Postoperative Course
The patient is observed in an intensive care unit with frequent neurologic checks for at least the initial 24 hours postoperatively.
Follow-up imaging should be repeated every 2–4 weeks until the scan shows complete resolution.
Antiseizure medications are considered when lesions are in the cortex, especially in the temporal lobe.
C-reactive protein (CRP), ESR, complete blood count (CBC) with differential, and temperature should all be followed closely.
An infectious disease specialist should be formally consulted to make specific antibiotic recommendations. Antimicrobials should be tailored based on the sensitivities and culture results.
Cyst rupture into the ventricle
Postoperative or intraoperative hemorrhage
Retraction injury, stroke, cerebral edema
Spread of the infection: Recurrent abscesses, meningitis, ventriculitis
Long-term complications include cognitive dysfunction, delayed onset of seizures, and focal neurologic deficits.
Outcomes and Prognosis
The overall cure rate for single or multiple abscesses reported in the literature is ~90% with combined surgical and medical therapy.
Mortality is variable (ranging from 0–30%); prognosis depends on size, location of abscess, organism, and comorbidities.
Prognosis is worse with intraventricular rupture, ventriculitis, meningitis, or lesions causing significant mass effect.
Patients have the best outcomes when the abscess is discovered early, a pathogen is identified, antibiotics are tailored, and the patient does not have significant comorbidities such as a compromised immune system.
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