Central Nervous System Infections



Central Nervous System Infections


Benjamin H. Schnapp

Corlin Jewell



THE CLINICAL CHALLENGE

Infections of the central nervous system (CNS) can be rapidly fatal and require prompt intervention in order to maximize good outcomes. Providers are forced to act quickly to provide treatment, often without knowing the exact underlying pathology. Many patients will have a nonspecific presentation with a wide differential diagnosis. Although fever is common in pathologies such as meningitis (inflammation of the meninges) or encephalitis (inflammation of the brain), it may not be present in other types of CNS infections, such as neurocysticercosis or opportunistic fungal infections in immunocompromised patients.

More than half of cases of bacterial meningitis in the United States are caused by Streptococcus pneumoniae.1 However, Neisseria meningitidis, Escherichia coli, Haemophilus influenzae, and Listeria monocytogenes also represent frequently isolated bacterial species. Even with treatment, mortality is as high as 16%.2 Mycobacterium tuberculosis also represents a common cause of meningitis worldwide, with as many as 1% to 2% of patients with active tuberculosis (TB) being affected by CNS infection. As with many CNS infections, meningitis secondary to M tuberculosis is more frequently seen in patients with compromised immune systems, such as those afflicted by human immunodeficiency virus (HIV).

Viral meningitis is the most common CNS infection; it is generally associated with lower morbidity and mortality than bacterial meningitis. Enteroviruses are the most common infectious pathogens, particularly in warmer seasons. However, other important pathogens include herpes simplex virus (HSV), varicella-zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and HIV. Often, the exact pathogen is not identified. Owing to modern vaccination practices, rates of certain previously common etiologies of viral meningoencephalitis, such as measles and mumps, have decreased. Although viral infections are typically less severe and often have excellent outcomes, many features of bacterial and viral meningitis overlap, making the distinction between them difficult, especially at the onset of disease.

Certain fungal species can also invade the CNS. The most common being Cryptococcus neoformans, followed by Coccidioides immitis. Mucormycosis can also spread to the CNS; diabetic patients are at higher risk for this severe invasive infection. Other common invasive fungal species, such as Aspergillus and Candida, only rarely cause meningitis. Fungal CNS infections were previously found mainly in patients with HIV/acquired immunodeficiency syndrome (AIDS), but the
incidence has been increasing because of the greater numbers of patients on chronic immunosuppression for transplanted organs and autoimmune conditions.

The most common parasitic CNS infection worldwide is neurocysticercosis, mostly occurring in lower income countries.2 This is caused by ingestion of the larva of the tapeworm Taenia solium, classically from eating undercooked infected pork products. Another common CNS parasite is Toxoplasma gondii; Although widely prevalent in the population, it generally causes no symptoms but can cause active infection in patients with decreased immunity. Infrequently, other species of worms, such as Strongyloides, can also cause meningitis.

Infectious encephalitis, a more severe infection, can caused by bacterial, viral, fungal, or parasitic infections and will commonly present with focal neurologic symptoms, behavioral change, cognitive deficits, or even seizures.3 The most common causes of meningoencephalitis are summarized in Table 18.1.

Intracranial abscesses are distinct from the granulomas that form secondary to parasitic and TB infections and most often occur in those with immune disorders or recent surgery. Rarely, they can occur in healthy individuals with normal immune systems. Infections are most commonly caused by Streptococcus species, followed by Staphylococcus (predominantly S aureus) and gram-negative bacteria (Proteus, E coli, etc.). Mortality rate, although still relatively high, has declined to as low as 10% in recent years, likely secondary to advanced diagnostic and treatment modalities.4

The epidural space represents another site where CNS abscesses can occur. Unlike many of the other types of CNS infections discussed in this chapter, the incidence of epidural abscess has been increasing in recent years, likely caused by an increase in spinal procedures, increasing numbers of immunocompromised patients, and high numbers of intravenous (IV) drug users. S aureus is the most common pathogen involved in epidural abscesses, with a high proportion of methicillin-resistant S aureus (MRSA). Although rare, mycobacteria and fungi also can cause spinal epidural abscesses.

Finally, prions represent an unusual form of CNS infection. They are transmissible misfolded proteins that, once acquired, induce progressive, fatal CNS disease. They induce a group
of disorders known as transmissible spongiform encephalopathies (TSEs). TSEs are very rare, but include Kuru, Creutzfeldt-Jakob disease (CJD), and fatal familial insomnia (FFI), with CJD being the most common.9











PREHOSPITAL CONCERNS

The focus for prehospital providers is on recognizing critical patients and transporting them to the closest appropriate hospital. Given that many CNS pathologies can result in altered mental status and loss of protective airway mechanisms, an assessment of the patient’s airway and ability to oxygenate should be completed first following local emergency medical service (EMS) protocols. If there is a concern for bacterial meningitis (eg, a febrile patient with a headache and altered mental status), the patient and crew should maintain droplet precautions by using personal protective equipment to prevent the spread of the disease. If possible, IV access should be obtained and crystalloid fluid resuscitation started.

If seizures occur prior to arrival at the emergency department (ED), abortive therapy with intramuscular (IM) midazolam or lorazepam, or IV lorazepam is recommended. There is no evidence supporting the use of prehospital antibiotics; sepsis studies on prehospital antibiotics have not demonstrated improved mortality, and we currently do not recommend prehospital antibiotic treatment. If bacterial meningitis from meningococcus is confirmed, providers in close contact with the patient’s respiratory secretions (eg, the provider who intubated) should receive antibiotic prophylaxis (see discussion below and Table 18.2).5


APPROACH


Meningitis

Classically, bacterial meningitis presents with fever, nuchal rigidity, and headache from the systemic and localized inflammatory responses. The majority of patients will present with at least one of these classic signs.1 However, relatively few patients present with all three components of this triad. Other common symptoms include nausea, vomiting, fatigue, and body aches. Viral meningitis presents similarly, but symptoms are typically less severe and more subacute in onset.

Risk factors for meningitis include immunocompromise (including diabetes), malignancy, pulmonary disease, and residence in a group home.6 All patients with suspected meningitis should have a focused history taken with attention to the symptoms and risk factors above, along with a full neurologic examination. Although patients with meningitis may initially appear altered because of lethargy
or severe headache, they generally do not exhibit focal neurologic deficits. If these signs are present, then infection of the brain parenchyma itself, that is, encephalitis, should be considered. In addition to the comprehensive neuro examination, jolt accentuation (worsening of the headache in response to rapid horizontal movements of the head) as well as the Kernig and Brudzinski maneuvers can be performed. A positive Kernig sign refers to an inability of the examiner to fully extend the knee secondary to resistance and hamstring pain when the patient is lying supine with their hip flexed to a right angle. Brudzinski sign is considered positive if attempts to passively flex the neck are accompanied by unintentional flexion of the hips. If Kernig and Brudzinski signs are negative, it should not be taken as evidence against CNS infection; these signs have been found to have very poor sensitivity (<5%) though are highly specific (>95%) for CSF pleocytosis (an elevation in leukocytes strongly suggestive of meningitis).7








Unless there are complicating factors such as suspected spinal epidural abscess, bleeding tendency (including anticoagulated status), findings suggestive of increased intracranial pressure, or overlying skin infection, patients with suspected meningitis should have a lumbar puncture (LP) performed. Prior to the LP, computed tomography (CT) without contrast of the head should be considered in certain situations (see Table 18.3).8 CSF cultures, in addition to blood cultures, should be obtained to determine bacterial species and provide susceptibility information.

An opening pressure should be measured with the patient in a supine position, and ideally three to four vials containing at least 1 mL of CSF obtained for analysis. In addition to cultures, CSF cell counts, glucose, and protein should be sent on all patients at a minimum. Serum glucose should be obtained as well to allow for interpretation of the CSF level (normal CSF glucose reading is approximately two-thirds of serum glucose in a normoglycemic individual). Table 18.4 shows common CSF profiles of various etiologies of meningoencephalitis. Additional testing, including further viral polymerase chain reaction (PCR) (eg, HSV, VZV) studies, and fungal testing can be ordered on those in whom specific additional diseases are suspected when it will alter management,
such as in immunocompromised individuals. Figure 18.2 shows a purulent CSF sample, a highly abnormal finding concerning bacterial meningitis. Serum procalcitonin, CSF lactate, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) may also have a role as adjunct means to differentiate bacterial from viral meningitis (see Evidence section).

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Jun 23, 2022 | Posted by in EMERGENCY MEDICINE | Comments Off on Central Nervous System Infections
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