Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (111 page)

BOOK: Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis
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   Subdural abscesses are localized in the space between the dura mater and arachnoid.

Organisms may be directly visualized and isolated from CSF in patients with meningitis, as discussed later. In localized parenchymal, epidural, and subdural abscesses, organisms may not have access to the CSF, so Gram stain and culture of CSF are often negative, unless the abscess ruptures into the subarachnoid space. On the other hand, the immune response to abscesses may result in inflammatory changes detectable in the CSF, like increased WBC (usually without clear PMN predominance) and mildly elevated protein; CSF glucose is typically normal.

CENTRAL NERVOUS SYSTEM ABSCESSES

As in other tissues, CNS abscesses are localized infections with formation of pus. Disease is caused by tissue destruction and the inflammatory response to the primary infection. The forces caused by swelling of the nervous system parenchyma against the rigid structures of the skull may cause trauma (e.g., herniation) or vascular compromise. The infection may occur in the parenchyma of the brain, in the epidural or subdural space, or in other anatomic sites in the CNS. Hematogenous seeding should be suspected in patients with multiple abscesses (see eBook Figure 4-35).

A very wide variety of pathogens have been implicated in the etiology of brain abscesses. Monomicrobial and polymicrobial infections are well defined. The etiology depends on a number of factors, including age of the patient, anatomic site of infection, immune status of the patient, site of primary infection or source of organisms, and virulence of the infecting organism(s).

A broad etiology must be considered, especially in immunocompromised patients, including fungal and parasitic pathogens.
Toxoplasma gondii
reactivation should be considered in patients with defects in cell-mediated immunity, like HIV infection. Other parasitic pathogens, like
Taenia solium
or
Entamoeba histolytica
, must be considered in patients who have emigrated from endemic areas. Patients with arteriovenous malformations or other right-to-left shunts are at significantly increased risk for brain abscess.

Anaerobic organisms are frequently isolated, often as part of a polymicrobial flora. The species reflect the primary source of infection, which is commonly related to oropharyngeal, intra-abdominal, or pelvic infections. Pathogens include
Bacteroides, Prevotella, Fusobacterium, Propionibacterium
, and other species.

A wide variety of aerobic species are also implicated, including
Streptococcus
species, enteric gram-negative bacilli, and
S. aureus
.
Citrobacter
species have been implicated in brain abscesses and meningitis in neonates.
Klebsiella pneumoniae
has been implicated in brain abscesses associated with primary liver abscess.

   Clinical Presentation

Severe, sometimes localized headache unrelieved by over-the-counter analgesics is the most common symptom of brain abscess. Patients may have neck stiffness. Vomiting, change in mental status, and focal neurologic signs are signs of severe disease.

   Diagnosis and Laboratory Findings

Definitive diagnosis is usually made by aerobic and anaerobic culture, with Gram stain, of infected material. Patients with CNS abscesses should be carefully evaluated for increased intracranial pressure, especially prior to collection of CSF by lumbar puncture.

Typical laboratory findings include the following:

   Aspirate of infected pus should be cultured for aerobic and anaerobic bacteria, fungi, and mycobacteria, with Gram, AFB, and fungal stains.
   Histopathologic examination may provide specific diagnosis.
   CSF shows signs of inflammation, typically:
   WBC approximately 25–300/μL with increased neutrophils and lymphocytes.
   CSF protein may be normal or minimally or markedly increased (75 to >300 mg/dL).
   CSF glucose is often normal.
   Bacterial cultures of CSF may be negative, but laboratory signs of acute purulent meningitis may be seen if the abscess ruptures.

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