Laboratory and radiographic analysis
Baseline labs can be normal and without evidence of leukocytosis or azotemia. Cerebrospinal fluid (CSF) obtained by lumbar puncture (LP) is essential for the diagnosis of meningitis. The rare but serious consequence of LP is transtentorial herniation, which leads to rapid neurologic deterioration and death. This complication has been known anecdotally since the earliest use of LP, but modern series estimate occurrence in <1% of patients with bacterial meningitis. In addition, it is difficult to know if the herniation was a sequela of meningeal inflammation severity or a consequence of the procedure itself. Therefore, it is common clinical practice to obtain tomographic imaging of the brain to exclude mass effect or hydrocephalus (although robust studies at academic medical centers have shown this to be an unnecessary step that delays therapy by up to one hour and CSF analysis by up to two hours). Guidelines issued in 2004 by the Infectious Diseases Society of America recommend imaging only in patients with additional worrisome clinical factors, such as known immunocompromised state, previous history of central nervous system (CNS) disease, abnormal neurologic exam, or evidence of increased intracranial pressure (ICP) with papilledema (Table 2).
A common sequela of LP is post-procedure headache, which may sometimes be worse than the initial presenting complaints. The headache is believed to be caused by a low-level CSF leak at the site of the puncture and usually resolves with time. Observational data suggest that the risk of post-procedure headache can be reduced by keeping the patient supine for four to six hours after the LP has been performed. Other adjunct measures include oral and/or IV hydration. Caffeine has been used successfully in some circumstances. If all else fails, something called the “blood patch” can be performed by an anesthesiologist. In this unusual intervention, the patient’s blood is phlebotomized and then immediately injected into the subarachnoid space, providing immediate relief. This procedure has been done for decades, but there are few clinical data to support its efficacy.
The CSF should be analyzed for evidence of meningeal inflammation. If at all possible, ICP should be estimated with bedside manometry performed on the supine resting patient during the LP. Elevated pressures (normal ICP is one-sixth of a patient’s systolic BP, i.e., approximately 20 mm Hg) are highly suggestive of bacterial meningitis and may have prognostic value if more than double the normal level (>40 mm Hg). Routine studies should include protein and glucose determinations, WBC count and differential, and Gram’s stain and culture (Table 3). Because the results of culture are so crucial and the pathogens are exquisitely sensitive to antibiotics, the sample should be obtained prior to antibiotic administration. Use of polymerase chain reaction (PCR) for bacterial pathogens, although promising in the research setting, is not recommended at this time because of technical obstacles. If a timely LP cannot be done (either because of imaging-related delay or other complicating factors), blood cultures should be obtained and antibiotics given at once, despite the decrease in yield of CSF cultures. The approach to those with HIV infection or chronic immunosuppression because of solid organ or bone marrow transplantation is best handled with the assistance of a specialist.
Therapy
Empiric therapy should begin as soon as possible (Table 4). Antimicrobial choices will cover the usual suspects and will be modified once Gram’s stain and culture data become available. The use of dexamethasone, once considered controversial, has become the standard of care. Dexamethasone should be administered as soon as possible, as this agent has been shown to reduce morbidity as well as mortality in well-controlled trials in children as well as adults in many clinical settings. Note that the greatest benefit was seen in those patients with pneumococcal meningitis and worsened disease severity, so the use of corticosteroids in others may not be as important.
A diagnosis of bacterial meningitis requires respiratory isolation for 24 hours because of the possibility of meningococcal infection. If the clinician has evidence (e.g., Gram’s stain, CSF culture, or other clinical data) to suggest alternative causes, respiratory isolation may be discontinued. In the case of meningococcal disease, close contacts, defined as household members or those who were directly exposed to oral secretions (including respiratory therapists and other health-care personnel), should be offered chemoprophylaxis with rifampin, ciprofloxacin, ceftriaxone, or azithromycin. Additional information is available from the CDC (MMWR. 2005;54[RR07]:1-21. Available with a 2007 update for patients aged 11-18 years, both accessed October 10, 2008).
In persons exhibiting evidence of neurologic involvement, consider herpes simplex virus (HSV). HSV does not typically cause meningitis. (There is a rare disease known as Mollaret’s meningitis that may be associated with HSV; its prognosis is excellent.) However, HSV encephalitis can sometimes begin with headache, fever, and neurologic changes with little evidence on CNS imaging or the expected hemorrhagic pleiocytosis described in most clinical series. PCR for HSV has become widely available and allows for rapid testing from spinal fluid. Untreated, HSV encephalitis can be fatal. IV acyclovir is safe, so its addition to empiric therapy in the proper clinical context is encouraged until more information is obtained in patients whose Gram’s stain is negative. HSV is the only viral CNS infection that warrants empiric therapy. Other viral causes of meningitis, which outweigh bacterial causes by a factor of almost 10 in the general community, have a more benign course and are without any proven therapeutic options.
