Management of Suppurative Intracranial and After Craniotomy Infections

Introduction

Intracranial suppurations may be primary or occur as a secondary complication of surgery. Postsurgical intracranial suppuration may be considered a mode of direct inoculation (iatrogenic) of infective agent into the craniotomy surgical field. It may be subdural or intracerebral or involve only the meninges. Intracranial infections and suppurations complicate the postoperative course, possibly leading to serious consequences affecting patient recovery and well-being. Such complications may lead to adverse outcomes of surgery, with significant added cost and less favorable neurological results. This paradigm has global implications for neurosurgical care, with relevant peri-operative preventative measures and postoperative approaches for management, elucidated in this chapter.

Pathogenesis of Brain Abscess

Pyogenic brain abscess is a focal collection of pus within the brain. This potentially fatal condition continues to be the subject of neurosurgical concern and global discussion. The incidence of pyogenic brain abscesses is 8% of intracranial masses in the developing countries, whereas in the West the incidence is 1% to 2%, with male predominance. ^, This condition is rare, largely because of the brain’s natural resistance to infection, a property mediated by its abundant vascular supply, the relative impermeability of the blood-brain barrier, and improvement in the treatment of ear, sinus, and orofacial infections during the latter half of the 20th century. An active neurosurgical service in a hospital in a developed country can expect to see 4 to 10 cases annually. ^, Peak ages vary depending on predisposing factors.

Brain abscess development is often characterized by four stages with a generally predictable window for each phase (elucidated later in the text): early cerebritis (1 to 4 days); late cerebritis (4 to 10 days); early capsule formation (11 to 14 days); and late capsule formation (>14 days). ^, Brain abscess formation is initiated when bacteria gain entry into cerebral tissues with trauma, contiguous spread from a suppurative focus, or hematogenous dissemination from a distant infection. Imaging modalities are the mainstay for staging abscess formation (discussed below). Many cases (40% to 60%) are the result of contiguous spread of infection from the middle ear, oropharynx, and paranasal sinuses ( Fig. 128.1 ). These lesions are usually solitary, and their distribution in the brain reflects the predisposing lesion ( Table 128.1 ). Seeding the brain probably occurs via the valveless emissary veins draining contiguous areas, allowing microorganisms to flow into the venous system of the brain from adjacent sites. Middle ear infections, chronic otitis media, or chronic mastoiditis can lead to temporal lobe or cerebellar abscesses by direct spread via the tegmen tympani or by translabyrinthine spread. Paranasal sinusitis can lead to frontal or temporal lobe abscesses by retrograde thrombophlebitis of the diploic veins. Frontal sinus infection can also lead to frontal lobe brain abscess when complicated by osteomyelitis of the frontal bone of the skull with dehiscence of the posterior table. Suppurative chronic obstructive pulmonary disease and dental infections are important sources of disseminated hematological spread into the intracranial cavity. ^,

Clinical Considerations

Many risk factors can predispose patients to bacterial brain abscess across a range of circumstances. Various considerations for classification criteria include: age (i.e., neonatal, pediatric, adult, and elderly), source of infection (i.e., direct penetrating inoculation, local extension of nearby infection, and hematological spread from distant location), comorbidities (i.e., immune status), and causative organism (i.e., bacterial, fungal, parasitic, and mixed).

Penetrating cranial trauma (such as open cranial fracture with dural tear) is a well-described, though relatively infrequent, cause of pyogenic brain abscess, accounting for less than 10% of these infections. ^{, ,} A distinctive form of posttraumatic brain abscess that occurs largely in young children results from penetrating injuries secondary to a foreign body injury, such as to the orbital region, transnasal-tansethmoid and, less commonly, other areas of the skull, from pencil tips, wooden sticks, and sharp toys. The interval from injury to clinical presentation varies, and may extend from days to years. Treatment, as in other penetrating cranial injuries, often involves early surgical debridement.

An increasingly important problem occurs in intravenous drug users with infected valvular vegetations delivering septic emboli, resulting in cerebral infarction, cerebral hemorrhage, brain abscess formation, and spinal epidural abscesses. This population is also prone to toxin-mediated diseases (tetanus and botulism) with inoculation of these agents at injection sites. In general, however, transient bacteremia is unlikely to result in brain abscess in the absence of breaches in the blood-brain barrier that predispose cerebral lesions, such as previous stroke or primary or metastatic neoplasms. ^,

Pediatric brain abscesses are most common between the ages of 4 to 7 years, and the minority of these children have congenital heart disease. Cerebral abscess complicates cyanotic congenital heart disease in 2% to 6% of cases. Cyanotic congenital heart disease is a leading underlying cause of pediatric brain abscess, accounting for 6% to 50% of cases. Tetralogy of Fallot and transposition of the great vessels underlie most cases, although any cardiac defect that results in significant right-to-left shunting appears to increase the risk. The pathogenesis probably involves increased blood viscosity as a result of chronic hypoxemia (due to right-to-left shunting), leading to areas of microinfarction within the brain that act as nidi for infection. The mortality from pyogenic brain abscess in this setting is high. Intrasellar, brain stem, basal ganglia, and thalamic abscesses are rare.

Intrasellar abscesses generally occur in the setting of preexisting pituitary or sellar lesions, such as adenomas, craniopharyngiomas, or Rathke cleft cysts, or as a complication of trans-sphenoidal surgery. ^, These lesions may also occur as a result of intrasellar extension from sphenoid sinusitis. Abscesses of the brain stem are generally hematogenous in origin and may extend longitudinally over several levels of the brain stem. The incidence of these lesions appears to have decreased over the past decades, probably as a result of improvements in the management of pediatric ear and sinus infections. Twenty percent of such brain abscesses are cryptogenic; many of these cases are the result of non-treated dental infections.

Bacteriology

The bacteriology of intracranial infection is determined by the initial site of infection (see Table 128.1 ). Streptococci ( Streptococcus milleri and Streptococcus viridans ) are the most common cause of pyogenic brain abscesses, involved in nearly two thirds of cases, because of their extension from the nasopharynx and oropharynx, as well as from endocarditis (S. viridans). ^, Staphylococcus aureus accounts for 10% to 21% of cases, generally in the setting of trauma and postoperatively, but it is also seen among patients with brain abscesses resulting from endocarditis. ^, Methicillin-resistant S. aureus (MRSA) should be considered in hospitalized patients or among those who were known as MRSA colonized. Anaerobic bacteria ( Bacteroides, Prevotella, Peptostreptococcus, Fusobacterium, and Actinomyces species) are also major causes of brain abscesses, usually as a part of polymicrobial infection. Brain abscesses due to Actinomyces species are commonly associated with pulmonary and odontogenic infections. Gram-negative bacilli such as Klebsiella pneumoniae, Escherichia coli, Pseudomonas aeruginosa, Serratia species, and Proteus species are associated with genitourinary or intra-abdominal infections, as well as commonly isolated from brain abscesses following head trauma and postoperative infection. ^{, ,} Pseudomonas species can cause brain abscess that results from otitis media or otitis externa. ^, Other bacterial species may be cultivated from brain abscesses in various clinical settings: Clostridium species, in association with an underlying malignancy or hemolytic–uremic syndrome ; Propionibacterium acnes in the postneurosurgical patient ; Nocardia species such as N. asteroides and N. farcinica comprise 1% to 2% of all cerebral abscesses, with a mortality rate of 31%. They are frequently seen in immunocompromised patients but can occur in immunocompetent patients. Nocardia brain abscess ( Fig. 128.2 ) may be an isolated cranial pathology or may result from dissemination of cutaneous or pulmonary infection. The number of case reports describing Nocardia brain abscess have been increasing; this may be related to better diagnostic techniques, but it is most likely due to increased incidence. Fungal brain abscesses can be caused by yeast such as Candida or Cryptococcus species; dimorphic fungi such as Histoplasma, Coccidioides, or Blastomyces species; and molds such as Aspergillus or Rhizopus species, which are associated with immunocompromised states. Protozoa and helminths can cause parasitic brain abscesses and may be relevant in certain cases, such as cat exposure or endemic areas. Toxoplasma gondii can cause central nervous system (CNS) toxoplasmosis and brain abscess ( Fig. 128.3 ), and Taenia solium can cause neurocystcercosis.

Brain abscess in the neonatal period has a distinctive bacteriologic profile, with most of these lesions caused by Proteus species and Citrobacter diversus. In contrast to meningitis caused by other pathogens, neonatal meningitis caused by these organisms is complicated by brain abscess in 40% to 75% of cases, so early computed tomography (CT) evaluation of neonates with meningitis or bacteremia caused by Proteus or Citrobacter species is recommended. Interestingly, the most common bacterial causes of acute pyogenic meningitis ( Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis ) are rarely associated with brain abscess. ^,

Clinical Presentation

Most patients with pyogenic brain abscess have symptoms for less than 2 weeks, although the disease can present indolently. The presenting features of brain abscess depend on the size and location of the lesion(s), the virulence of the infecting agents, the immunologic status of the host, and the cerebral edema elicited by the expanding intracranial mass lesion. The classic triad of fever, headache, and focal neurologic deficit is present in less than 50% of cases. Headache, usually dull and poorly localized, is present in 50% to 70% of cases yet is nonspecific and a potential cause of diagnostic delays. ^{, , , , ,} Sudden worsening of a preexisting headache in a patient with a brain abscess, especially if accompanied by the acute onset of meningeal signs, suggests either herniation or intraventricular rupture of the abscess.

Fever occurs in 25% to 50% of adults ^{, , , , ,} and is more common in children. Symptoms and signs related to any underlying disease (e.g., paranasal sinusitis or otitis media), if present, may aid in the diagnosis. Altered levels of consciousness are often present. Focal neurologic signs depend on the location of the lesions within the brain and the extent of cerebral edema : frontal and parietal lobe abscesses are commonly associated with hemiparesis and aphasia; temporal lobe presentations may include aphasia or visual field disturbances; intrasellar lesions tend to mimic pituitary tumors, and cerebellar abscesses often present with ataxia and nystagmus. Seizures occur in roughly 30% of cases, without a clear distribution pattern. Patients present with multiple brain abscesses in approximately 10% of cases.

Diagnosis of Brain Abscess