| |
It is important for physicians to be familiar with the common types and manifestations of nervous system infections for several reasons. First, this category of neurologic illness can be quite acute in presentation. Additionally, some nervous system infections can have severe and potentially life-threatening consequences. Finally, for many infections, specific therapies are available, and tailored to the identified etiologic organism.
BACTERIAL INFECTIONS
Three common and important forms of bacterial nervous system infection are acute bacterial meningitis, brain abscess, and spinal epidural abscess.
ACUTE BACTERIAL MENINGITIS
Clinical Findings
Acute bacterial meningitis is a medical emergency. It is critical for all physicians to know its presentation, its initial diagnostic evaluation, and the urgency with which a potential case of bacterial meningitis needs to be addressed. The cardinal findings include headache, fever, and neck stiffness. Patients can also be confused or have a depressed level of consciousness, develop seizures, or have other focal neurologic symptoms or signs, depending on the extent to which the meningeal infection or inflammatory process also affects the brain parenchyma (thus causing meningoencephalitis). In immunosuppressed patients, as well as in the very elderly, there may be no fever, so it is vital to have a high degree of clinical suspicion in these populations. On exam, patients often have nuchal rigidity, that is, rigidity with flexing the neck forward. Two classically described physical signs associated with meningitis (Fig. 21-1), although not specific to the bacterial form, are:
FIGURE 21-1. Kernig sign is elicited by flexion of the hip at 90 degrees. If the patient experiences pain by extending the knee, the Kernig sign is positive. Brudzinski sign is elicited by flexing the patient’s neck. The sign is positive if the patient flexes the hips and knees in response. (Reused with permission from Lippincott’s Clinical Simulations. 1st ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.)
•Kernig sign: The patient lies supine, and the knee is extended passively while the hip is flexed. If the patient is unable to extend the knee because of pain, the sign is positive.
•Brudzinski sign: An involuntary flexion at the hips when the neck is flexed.
Etiology
The most common organisms causing bacterial meningitis vary depending on the patient’s age at presentation (Table 21-1). The introduction of vaccines against Streptococcus pneumoniae (“pneumococcus”), Neisseria meningitides (“meningococcus”), and Haemophilus influenzae has substantially reduced the incidence of acute bacterial meningitis among children in the United States. In most cases, bacteria reach the subarachnoid space by hematogenous spread from the respiratory tract, although bacterial meningitis may also be a direct sequela of traumatic or mechanical invasion of the subarachnoid space, such as after neurosurgical procedures or open head injury. It is also possible to have direct infiltration of the subarachnoid space from parameningeal foci, such as the sinuses.
TABLE 21-1. Common Causes of Meningitis by Age, and Empiric Antibiotic Treatment | ||
Age | Bacterial | Empiric Treatments |
0–3 mo | —Group B Streptococcus —Streptococcus pneumonia —Listeria monocytogenes —Escherichia coli | Ampicillin + cefotaxime OR ampicillin + an aminoglycoside |
3–24 mo | —S. pneumonia —Neisseria meningitides —Haemophilus influenza type B —Group B Streptococcus | Vancomycin + a third-generation cephalosporin |
2–18 y | —N. meningitides —S. pneumonia | Vancomycin + a third-generation cephalosporin |
Older adults | —S. pneumonia —N. meningitides —H influenza, type B —Group B Streptococcus —L. monocytogenes | Vancomycin + ampicillin + a third-generation cephalosporin |
Diagnostic Workup
The critical test in the diagnosis of acute bacterial meningitis is cerebrospinal fluid (CSF) analysis from a lumbar puncture (LP). Because of the concern that LP may precipitate brain herniation in the presence of a focal intracranial mass with increased intracranial pressure, head imaging (usually with computed tomography [CT], because it is available more readily) should be performed before LP when papilledema is present on fundoscopic examination or if there is any focal sign on neurologic examination suggesting the possibility of an intracranial lesion. Many neurologists advocate head imaging prior to LP under any circumstances with an acute presentation.
The characteristic CSF profile in acute bacterial meningitis includes an elevated white blood cell (WBC) count, with a predominance of polymorphonuclear leukocytes (generally never acceptable in a CSF sample), elevated protein, and low glucose (<40 mg/dL or less than two-thirds of a simultaneously measured serum glucose level) (Table 21-2). The differential on the CSF WBC must be interpreted with caution early in the course of meningitis because patients with bacterial meningitis may present initially with a lymphocytic predominance. Patients with viral meningitis may also have a neutrophil predominance early in the course. Severely immunosuppressed patients with pancytopenia may also not have classic CSF patterns. CSF Gram stain can demonstrate the bacteria and narrow the differential diagnosis of causative organisms. CSF cultures in acute bacterial meningitis can often identify the specific organism, which can then be tested for antibiotic sensitivity.
TABLE 21-2. Common Cerebrospinal Fluid Patterns in Different Forms of Meningitis | |||||
Bacterial | Viral | Fungal | TB | ||
Opening pressure | Elevated | Normal | May be normal or elevated | May be normal or elevated | |
WBC | ≥100 cells/µL | <100 cells/µL | <500 cells/µL | <500 cells/µL | |
Cell type | Polymorphonucleocytes | Lymphocytes | Lymphocytes | Lymphocytes | |
Glucose | Low | May be normal | Low | Low | |
Protein | Elevated | Elevated | Elevated | Elevated | |
TB, tuberculosis; WBC, white blood cells. | |||||
Because of the potentially life-threatening nature of acute bacterial meningitis, a prolonged delay in obtaining CSF may necessitate the institution of empiric antibiotic coverage prior to LP—using antibiotics that are effective against the most likely organisms, at doses that ensure adequate penetration into the subarachnoid space, or “meningitis doses.” In this case, CSF cultures may not grow organisms if they were not obtained until well after antibiotic therapy was begun, and it may be necessary to complete an entire course of empiric therapy.
Treatment
Appropriate antibiotic therapy needs to be administered promptly upon the diagnosis of acute bacterial meningitis, with specific drugs initially chosen on the basis of the most likely organisms, and subsequently modified on the basis of Gram stain or culture results (Table 21-1). In addition to the antibacterial therapy, some adjunctive therapies may also be helpful in certain situations. Corticosteroids are often used in children in an attempt to prevent some long-term complications of acute bacterial meningitis, such as deafness.
KEY POINTS
●Acute bacterial meningitis is a medical emergency.
●The typical clinical presentation consists of headache, fever, neck pain, or stiffness, and often, altered consciousness.
●Immunocompromised patients may lack some of the cardinal features of meningitis such as fever.
●The classic CSF profile of bacterial meningitis demonstrates a high WBC count (mostly polymorphonuclear leukocytes), high protein, and low glucose.
●Antibiotic treatment should be initiated early and is tailored on the basis of the identification of responsible organisms and penetration into the subarachnoid space.
BRAIN ABSCESS
Clinical Findings
Brain abscesses typically present much like any other focal intracranial lesions, with headache, focal neurologic signs (that depend on the location of the abscess), seizures, and potentially, signs of increased intracranial pressure. Fever may be present, but this is not invariable.
Etiology
Solitary brain abscesses often arise from invasion of the intracranial space from neighboring sites of infection, such as the sinuses, or from direct open trauma or mechanical instrumentation. The first stage of brain abscess development is often cerebritis in which there is an active infection in the brain but not yet walled off. CSF studies are abnormal, and imaging studies or electroencephalogram (EEG) or both may also be abnormal. In the second stage, the infection becomes organized and walled off to form a classic abscess. Multiple brain abscesses are typically the result of hematogenous dissemination, such as from infective bacterial endocarditis, or with immunocompromised states. Responsible organisms depend on the etiology: respiratory pathogens may invade from the sinuses; abscesses from trauma or instrumentation are often skin flora; multiple abscesses are often caused by organisms that cause infective bacterial endocarditis. Most abscesses contain multiple organisms, often a mixture of aerobic and anaerobic pathogens (Table 21-3).
TABLE 21-3. Causes of Brain Abscesses | |
Source of Infection | Bacterial Causes |
Traumatic brain injury | Staphylococcus aureus Staphylococcus epidermidis Pseudomonas aeruginosa Enterobacter species |
Neurosurgery | Staphylococcus aureus Staphylococcus epidermidis Pseudomonas aeruginosa Propionibacterium acnes Streptococcus species |
Hematogenous spread | Staphylococcus aureus Streptococcus viridans Klebsiella pneumoniae |
Ear | Proteus mirabilis Streptococcus milleri group organisms Streptococcus pneumonia |
Dental | Streptococcus species Bacteroides fragilisus |
Diagnostic Workup
The diagnosis of brain abscess is usually made by neuroimaging. CT or magnetic resonance imaging (MRI) with intravenous contrast agents will usually demonstrate a mass lesion, often surrounded by “ring enhancement” and signs of central necrosis within the brain parenchyma (Fig. 21-2). There may be surrounding edema. At the top of the radiologic differential diagnosis are malignant neoplastic lesions, which often have a similar ring-enhancing mass appearance. Sometimes, single photon emission computed tomography (SPECT) scanning can help differentiate a neoplastic process from an abscess. Depending on the source of the infection, blood cultures may identify the responsible organisms, but neurosurgical drainage is often necessary for definitive pathogen identification.
FIGURE 21-2. Presentation of brain abscess on CT and MRI. On noncontrast CT (A), the abscess appears hypodense (asterisk). On MRI (B), the edema (arrow) surrounding the abscess appears hyperintense, and contrast enhancement (C) visualizes the capsule (arrow). On diffusion-weighted imaging (D), the abscess cavity appears hyperintense (arrow). [CT, computed tomography; MRI, magnetic resonance imaging.] (Reprinted with permission from Scheld WM, Whitley RJ, Marra CM. Infections of the Central Nervous System. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2014. Figure 31.15.)
Treatment
Prolonged courses of intravenous antibiotics, either chosen empirically for broad-spectrum coverage of aerobic and anaerobic organisms or tailored specifically on the basis of culture results, are the mainstay of treatment for brain abscesses. If the lesion does not respond to antibiotics, surgical drainage may be required. If the lesion causes mass effect and the patient is at risk of herniation, surgical drainage may also be necessary.
CENTRAL NERVOUS SYSTEM EMPYEMA
Collections of pus, known as empyemas can occur in the central nervous system (CNS) as in other tissues. CNS empyemas most commonly occur in the subdural or epidural spaces. One must have a high degree of clinical suspicion because the empyema may be difficult to differentiate from a subdural hematoma on a scan. Consequently, these lesions are missed frequently. Patients may present with fever and headache. The infection typically arises from direct spread from an adjacent tissue (sinus, bone, or skin) or hematogenous spread (Fig. 21-3).
FIGURE 21-3. Frontal sinusitis with intracranial empyema. T1-weighted, contrast-enhanced image confirming likely subcortical infarction. Blue arrow: empyema. Violet arrow: subcortical infarct.(Reprinted with permission from Mancuso AA. Head and Neck Radiology. 1st ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010. Figure 13.16.)
SPINAL EPIDURAL ABSCESS
Clinical Findings
Spinal epidural abscesses typically present with the combination of neck or back pain and focal neurologic signs consistent with spinal cord compression or cauda equina involvement, depending on the spinal level of the abscess. For thoracic or lumbar abscesses, clinical signs may include leg weakness, sensory loss with a discernible sensory level on examination, and urinary and sexual dysfunction. Cervical abscesses may present with the same symptoms as those at lower levels, but the arms may be involved as well, resulting in arm weakness or sensory symptoms there, or both. Fever is not necessarily present. Symptoms may come on acutely or more insidiously; an acute, rapid presentation raises concern for a spinal cord infarction.
Etiology
Spinal epidural abscesses can be sequelae of spinal instrumentation, including epidural or spinal anesthesia or spine surgery. In these cases, the responsible organisms are often skin pathogens such as staphylococcal species. Abscesses can also be the result of spread from more anterior infections, including vertebral body osteomyelitis or diskitis.
Diagnostic Workup
If there is a clinical suspicion on the basis of history and exam, spine imaging should be obtained urgently because an intraspinal lesion such as an epidural abscess can cause cord compression with resulting paralysis. In general, the administration of contrast (with either CT or MRI) can help demonstrate the enhancing nature of spinal epidural abscesses (Fig. 21-4). LP is contraindicated in most situations before the anatomic extent of the lesion is defined clearly by imaging, because there is a theoretical possibility of seeding the subarachnoid space with bacteria using the spinal needle. As with intracranial abscesses, blood cultures can sometimes demonstrate the responsible organisms, but in many cases, radiologically guided biopsy or surgical drainage for microbiologic studies is necessary.
KEY POINTS
●Abscesses affecting the CNS are mass lesions that are often ring-enhancing on imaging studies with contrast.
●They present with focal neurologic signs that are dependent on their intracranial or spinal location.
●Prolonged courses of intravenous antibiotics are the mainstay of treatment, but surgical drainage is necessary sometimes.
●MRI or CT imaging should be obtained urgently in patients for whom there is a high clinical concern for epidural abscess, because there is a risk of cord compression from these lesions.
●Patients with evidence of cord compression or a cauda equina syndrome often require surgical decompression in addition to antibiotic treatment for the abscess.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
