20 Surgery for Acute Intracranial Infection



10.1055/b-0035-121766

20 Surgery for Acute Intracranial Infection

P. B. Raksin

Introduction


Space-occupying intracranial infection may arise via contiguous spread from adjacent structures, through hematogenous dissemination, following operative neurosurgical procedures, or after head trauma. The same structural elements that define the various intracranial compartments—epidural, subdural, parenchymal, and ventricular—also dictate the pathways for spread of infection across those natural barriers. Management typically involves a combination of medical and surgical modalities.



Epidural Abscess


Infection within the space between the inner table of the calvarium and dura occurs most commonly as a complication of paranasal sinusitis, orbital cellulitis, mastoiditis, or chronic otitis media. It may also occur following traumatic fracture of the calvarium or following craniotomy. Rarely, epidural abscess may follow from fetal scalp monitoring or the application of halo pins to the skull. 1 Clinical presentation is often insidious. Headache may be accompanied by a relative paucity of other symptoms unless mass effect is present or the infectious process extends to the subdural space as well. Periorbital edema occurs in conjunction with bone osteomyelitis or orbital cellulitis. (Pott’s puffy tumor is the historical term applied to the clinical finding of forehead soft tissue swelling due to the presence of subgaleal fluid. 2 ) An infectious nidus adjacent to the petrous apex may present as Gradenigo syndrome. Streptococci (Streptococcus milleri group) predominate, though posttraumatic and postcraniotomy infections are more commonly associated with staphylococci. 3



Subdural Empyema


Infection within the potential space between dura and arachnoid mater arises either from the spread of infection via valveless emissary veins (in association with thrombophlebitis) or via extension of an osteomyelitis of the skull with an accompanying epidural abscess. Other predisposing conditions include skull trauma, infection of a preexisting subdural hematoma, or prior neurosurgical procedure. A small number are metastatic (often from a pulmonary source). Subdural empyema may also occur in up to 10% of infants with bacterial meningitis, presumably as the result of infection of a previously sterile subdural effusion. 4 Fever is present in most cases. Headache and vomiting are typical early findings. These symptoms may be accompanied by confusion, seizure, and focal neurologic deficits (most commonly hemiparesis). Neurologic decline may be rapid following symptom onset. On the other hand, postsurgical subdural empyema may present in a delayed fashion—up to 8 weeks following initial intervention. 3 A less fulminant course may be seen with prior antimicrobial therapy, as well as in the setting of metastatic spread to the subdural space or infection of an existing subdural hematoma. Bacterial isolates are similar to those found in epidural abscess cases. Polymicrobial infection is common. The incidence of culture-negative (27–29% in one series) cases is greater in subdural empyema 5 ; this may reflect the fastidious nature of many anaerobic organisms.



Intracerebral Abscess


Focal, encapsulated infection within the brain tissue may be single or multifocal. A single abscess typically arises by direct extension of a paranasal sinus, mastoid, or middle ear infection; a solitary focus may also arise following penetrating trauma. Multifocal disease more commonly results from hematogenous dissemination of primary cardiac, pulmonary, periodontal, abdominal, or dermatologic infection. Less than 50% of patients will present with the classic triad of headache, fever, and focal neurologic deficit. 6 In fact, patients may present with headache or nausea alone. Fever, when present, is typically low-grade; a temperature of greater than 101.5° F (38.6° C) should raise suspicion for a systemic infection. Focal neurologic symptoms reflect the location of the pathology. Hemiparesis is common. 7 New onset of meningismus, associated with sudden neurologic worsening, may indicate rupture into the ventricular space. Mortality in such cases is high. 8 Isolated pathogens are predominantly bacterial, commonly polymicrobial, and reflect the site of origin. Streptococci are isolated in up to 70% of cases. Bacteroides and Prevotella are present in 20–40% of cases and often occur in mixed culture. Staphylococcus aureus is present in 10–15% of brain abscesses—usually posttrauma or in the setting of endocarditis—and is usually monomicrobial. Enteric Gram-negative bacilli are present in up to 22–33% of cases, often in association with otic foci, bacteremia, or prior neurosurgical procedure. 9 Diagnostic considerations must be expanded in cases of immunocompromise. Gram-negative organisms and fungal isolates are common in cases of neutrophil deficiency, while Listeria, Nocardia, Cryptococcus, and Toxoplasma are encountered in the setting of T-cell deficiency.



Indications


The indications for surgical intervention are dictated by size, anatomic location, and accessibility, as well as by known or presumed pathogen. In all cases, surgical intervention must be coupled with appropriate intravenous (and, in certain cases, intrathecal) antimicrobial therapy.



Epidural Abscess


Most cases require open neurosurgical debridement. Bur hole drainage generally is ineffective given the tenacity of the purulent material; however, in select cases where a very small collection is present, trial bur hole drainage may be attempted. The participation of Otolaryngology may be necessary for simultaneous debridement of the affected sinus(es).



Subdural Empyema


The vast majority of cases require open neurosurgical debridement. More limited bur hole drainage may be considered in cases of parafalcine empyema, critically ill patients in septic shock, and children presenting with empyema secondary to meningitis. 10 Repeated drainage and/or conversion to craniotomy may be necessary in such cases.



Intracerebral Abscess


Several factors dictate the indications for and extent of neurosurgical intervention. Primary considerations include the maturity of the capsule, size, and location. Britt and Enzmann sought to define stages in the maturation of the abscess capsule. 11 Cortical inflammation—or, cerebritis—alone is not a surgical disease. Demarcation of an abscess cavity with respect to the surrounding parenchyma begins about 10 days after the onset of infection. The capsule wall, however, remains thin and discontinuous at this time. Abscesses may be amenable to cannulation and drainage—without attempted resection of the wall—during this early encapsulation phase. This strategy may also be appropriate in the setting of a more mature lesion in a less accessible location. With further maturity comes greater collagen deposition and, consequently, a capsule more consistent with that of a metastatic lesion. Consideration may be given to drainage—with resection of capsule—in the case of a mature and accessible lesion. This is generally feasible after ~ 2 weeks.


The size of the lesion also may influence treatment strategies. It has been suggested that abscesses of a certain size (1.7 cm or less) may be treated by medication alone, whereas lesions of greater than 2.5 cm rarely resolve without surgical intervention. 9 , 12


Medical therapy alone may be considered in cases of multifocal disease, lesions in eloquent areas, concomitant meningitis, coexistent hydrocephalus where shunt placement risks contamination, or where medical contraindications to invasive intervention may exist. 13


In a patient with documented bacteremia and a positive culture, consideration may be given to a trial of systemic antimicrobial therapy, provided the chosen agent(s) offers good central nervous system penetration. If the diagnosis is in question and/or there is a question of a polymicrobial infection in an immunocompromised host, consideration should be given to early biopsy to permit tailoring of medical therapy.



Preprocedure Considerations



Radiographic Imaging




  • CT head pre- and post-contrast will provide basic information regarding lesion location, the degree of associated edema/mass effect, and bony involvement. Cerebritis will appear as a nonspecific region of hypodensity. A more mature abscess will demonstrate ring-enhancement with associated perilesional edema. CT of the sinuses (with coronal and sagittal reconstructions) may be a necessary adjunct if contiguous extension is suspected.



  • MRI brain pre- and post-gadolinium may provide additional information to assist diagnosis and therapeutic interventions. MRI may define the stage of abscess or cerebritis. In cases of epidural or subdural empyema, magnetic resonance venography (MRV) will define the extent of sinus thrombosis, if present. Magnetic resonance diffusion images are useful in diagnosing subdural empyema, which often shows hyperintense signal indicating diffusion restriction. 14



  • Magnetic resonance spectroscopy or positron emission tomography may help distinguish an infectious from a neoplastic process.



  • Lumbar puncture generally is not necessary and, when a mass lesion is present, may be contraindicated. Given physical separation from the subarachnoid space, cerebrospinal fluid should be sterile (perhaps with nonspecific inflammatory changes) in the setting of epidural empyema.



  • Blood cultures should be drawn (preferably prior to initiation of antimicrobial therapy).



  • In the setting of bacteremia, an echocardiogram is indicated to exclude endocarditis as the etiology for intracranial infection.



  • HIV testing should be undertaken as the spectrum of infectious pathology (and the approach to treatment) in the immunocompromised population may differ.



  • A chest X-ray should be completed. A purified protein derivative skin test should be placed if tuberculosis is suspected.



  • A panoramic X-ray may define an odontologic etiology for intracranial infection.



  • Preoperative imaging ( Fig 20.1a–f ).

Fig 20.1a–f Axial CT (a) soft tissue and (b) bone windows, as well as (c) sagittal MRI post-gadolinium T1-weighted image demonstrating a Pott’s puffy tumor. Note the extracranial soft tissue collection in communication with the epidural space, via the frontal air sinus. (d) Axial MRI post-gadolinium T1-weighted image demonstrating a right frontal subdural empyema. (e) The diffusion-weighted imaging sequence, in this setting, demonstrates hyperintense signal, indicating diffusion restriction. (f) Axial MRI post-gadolinium T1-weighted image demonstrating an intracerebral abscess with loculations and peripheral enhancement, extending to the local meninges.


Medication




  • Empiric, broad-spectrum antimicrobial therapy should be initiated at the time of presentation. The source, and therefore likely pathogens, should be considered. The author prefers a regimen of vancomycin, ceftriaxone (cefepime if a nosocomial infection is suspected), and metronidazole, bearing in mind that the specific clinical circumstances of a given case may dictate modification of this regimen and/or the addition of antifungal or antituberculous coverage.



  • In cases where the pathogen is known, targeted antimicrobial therapy is the goal.



  • Corticosteroid therapy may be considered on an individual case basis for management of accompanying vasogenic edema. While the use of corticosteroids has been shown to be of some benefit in the setting of meningitis, 15 there exists no similar established role for steroids in the primary medical management of abscess.



  • Seizures are common in the setting of intracranial infection. Antiepileptic drug prophylaxis should be initiated upon p resentation.



Operative Field Preparation




  • The hair is cropped (not shaved) with an electric razor at the planned surgical site.



  • The skin is prepared initially with alcohol, followed either with a standard povidone iodine or chlorhexidine scrub.



  • The planned incision site is infiltrated with 1% lidocaine with 1:100,000 epinephrine.

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Jun 13, 2020 | Posted by in NEUROSURGERY | Comments Off on 20 Surgery for Acute Intracranial Infection

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