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Neurology›Condition·Updated Apr 17, 2026·v1

Meningitis

Meningitis is a critical inflammatory condition of the CNS membranes requiring urgent diagnosis via CSF analysis and immediate empiric treatment with broad-spectrum antibiotics and corticosteroids. While viral forms are common and often benign, bacterial and tuberculous forms carry high mortality and require intensive management of intracranial pressure and systemic inflammation.

High Evidence268 references·1,114 words·5 min read·v1
NeurologyInfectious DiseaseEmergency MedicineCritical CarePediatrics

Quick Reference

RxDrug of choiceCeftriaxone 2 g IV q12h + Vancomycin 15-20 mg/kg IV q8-12h
AltAlternativesMeropenem 2 g IV q8h (for cephalosporin allergy or resistant Gram-negatives)
⊘AvoidDelaying antimicrobial therapy to obtain neuroimaging or lumbar puncture
DxTest of choiceCSF analysis via Lumbar Puncture (Cell count, Glucose, Protein, Gram stain, PCR)
ScKey scoreGlasgow Coma Scale (GCS) for severity; PECARN rule for febrile infants
→When to referGCS < 12, focal neurological deficits, evidence of hydrocephalus, or suspected brain abscess
Meningitis is a medical emergency; treat with empiric antibiotics and steroids immediately upon suspicion to prevent death and permanent disability.
Meningitis is a life-threatening inflammation of the leptomeninges (arachnoid and pia mater) and the surrounding cerebrospinal fluid (CSF) that constitutes a true medical emergency. It is characterized by a diverse etiology including bacterial, viral, fungal, and parasitic pathogens, as well as non-infectious triggers like medications and autoimmune diseases. Bacterial meningitis, primarily caused by Streptococcus pneumoniae and Neisseria meningitidis, carries a high case-fatality rate and a 30% risk of permanent neurological sequelae, such as sensorineural hearing loss.

Overview and Recommendations

Background

  • •Define meningitis as the acute or chronic inflammation of the protective membranes surrounding the brain and spinal cord, specifically the leptomeninges. It is a critical global health challenge with significant geographic heterogeneity, such as the high burden seen in the African Meningitis Belt.
  • •Identify the primary infectious etiologies, which vary by age and risk factors: and dominate adult bacterial cases, while is the leading cause in neonates. Viral or 'aseptic' meningitis is most frequently caused by and is generally less severe but more common.
  • •Recognize the high morbidity associated with the condition, as more than 30% of survivors worldwide suffer from long-term neurological sequelae, including sensorineural hearing loss (SNHL), cognitive impairment, and seizure disorders.
  • •Distinguish between acute (hours to days) and chronic (more than 4 weeks) forms. Tuberculous meningitis (TBM) and cryptococcal meningitis often present subacutely and are major causes of mortality in immunocompromised populations, particularly those with HIV/AIDS.
  • •Consider non-infectious triggers such as drug-induced aseptic meningitis (DIAM)—often linked to NSAIDs or antibiotics—and systemic autoinflammatory diseases like (NPSLE) or GFAP astrocytopathy.

Evaluation

  • •Suspect meningitis in any patient presenting with fever, severe headache, and nuchal rigidity (neck stiffness), though be aware that this 'classic triad' is present in less than half of confirmed cases. In neonates, look for non-specific signs like irritability, poor feeding, bulging fontanelles, or hypothermia (Temperature ≤ 36.0°C).
  • •Perform a targeted physical exam for meningeal irritation using Kernig’s sign (resistance to knee extension with the hip flexed) and Brudzinski’s sign (involuntary hip flexion during passive neck flexion). Utilize the jolt accentuation of headache—increasing pain with rapid horizontal head rotation—as it is a highly sensitive sign for meningeal inflammation.
  • •Assess for 'red flags' that indicate high-risk complications, such as rapidly progressive purpura (suggestive of meningococcemia), focal neurological deficits, papilledema, or a Glasgow Coma Scale (GCS) score < 12.
  • •Order a non-contrast CT prior to performing a lumbar puncture (LP) only if specific contraindications are present: focal neurological deficits, new-onset seizures, papilledema, or known immunocompromise. Do not delay the first dose of antibiotics for imaging if an LP is deferred.
  • •Obtain blood cultures and a simultaneous serum glucose level immediately upon arrival. Blood cultures are positive in 50-80% of patients with bacterial meningitis and may provide a diagnosis if the LP is 'dry' or contraindicated.
  • •Perform a lumbar puncture to analyze cerebrospinal fluid (CSF) for opening pressure, cell count with differential, glucose, and protein. Typical bacterial findings include neutrophilic pleocytosis (>5 cells/μL), elevated protein, and a CSF/serum glucose ratio < 0.4.
  • •Utilize rapid molecular diagnostics such as the Meningitis/Encephalitis panel, which can identify 14 common pathogens via multiplex PCR within approximately one hour, significantly improving time-to-targeted-therapy.
  • •Evaluate for (TBM) in patients with subacute symptoms or high-risk backgrounds using CSF biomarkers (IFN-γ, IL-6) and molecular tools like CBNAAT or Loop-mediated isothermal amplification (LAMP), which has a sensitivity of ~62.5% in pediatric populations.
  • •Screen for cryptococcal antigen (CrAg) in all HIV-positive patients with a CD4 count < 100 cells/μL, as high blood CrAg titers are strongly predictive of concurrent meningitis and increased mortality.
  • •Rule out mimics such as (via CT or presence of xanthochromia in CSF) and autoimmune encephalitis (via MRI findings like linear perivascular radial enhancement in GFAP astrocytopathy).

Management

  • •Administer empiric antimicrobial therapy within 60 minutes of patient arrival; every hour of delay is associated with increased mortality. For most adults, initiate Ceftriaxone 2 g IV every 12 hours and Vancomycin 15-20 mg/kg IV every 8-12 hours.
  • •Add Ampicillin 2 g IV every 4 hours to the empiric regimen for patients over age 50, pregnant individuals, or those with immunocompromise to provide coverage for Listeria monocytogenes.
  • •Administer adjunctive Dexamethasone 0.15 mg/kg IV every 6 hours (maximum 10 mg) starting 10-20 minutes before or concurrently with the first dose of antibiotics to reduce the risk of hearing loss and neurological sequelae in bacterial cases.
  • •Continue dexamethasone for 4 days in patients confirmed to have Streptococcus pneumoniae meningitis; discontinue if the pathogen is found to be viral or a different bacterium where steroid benefit is less clear.
  • •Manage (TBM) with a standard 4-drug regimen (Rifampin, Isoniazid, Pyrazinamide, and Ethambutol) plus adjunctive dexamethasone for 6-8 weeks. Consider high-dose Rifampin 35 mg/kg/day to improve CNS penetration, though its mortality benefit is still debated.
  • •Treat HIV-associated cryptococcal meningitis using the AMBITION protocol: a single high dose of Liposomal Amphotericin B 10 mg/kg on Day 1, followed by 14 days of oral Flucytosine 100 mg/kg/day and Fluconazole 1200 mg/day.
  • •Monitor and manage increased intracranial pressure (ICP) using head elevation to 30 degrees and osmotic therapy (Mannitol 0.5-1.0 g/kg). Consider external ventricular drainage (EVD) for patients with refractory hypertension or symptomatic hydrocephalus.
  • •Implement seizure precautions and treat active seizures with benzodiazepines (e.g., Lorazepam 0.1 mg/kg IV), followed by maintenance anticonvulsants like Levetiracetam if cortical involvement is suspected.
  • •Provide post-exposure prophylaxis (PEP) to close contacts of patients with N. meningitidis or H. influenzae type b using Ciprofloxacin 500 mg PO (single dose) or Rifampin 600 mg PO twice daily for 2 days.
  • •Perform formal audiological diagnostic testing at the time of discharge or within 4 weeks of recovery to detect sensorineural hearing loss (SNHL), as early intervention is critical for preventing cognitive decline.
  • •Avoid the use of adjunctive corticosteroids in HIV-positive adults with TBM, as trials have shown they may not provide the same survival benefit as seen in HIV-negative populations.
  • •Refer to neurosurgery immediately if imaging reveals a (complicating ~1.9% of bacterial cases) or if there is evidence of obstructive hydrocephalus requiring a shunt.

Board Review — High Yield

  • •Jolt accentuation — The most sensitive physical exam maneuver for identifying meningeal irritation (worsening headache with horizontal head rotation).
  • •CSF/Serum Glucose Ratio < 0.4 — A classic laboratory finding strongly suggestive of bacterial, fungal, or tuberculous meningitis over viral causes.
  • •Waterhouse-Friderichsen syndrome — Adrenal insufficiency caused by bilateral adrenal hemorrhage, a catastrophic complication of meningococcemia.
  • •LTA4H genotype — A genetic marker that predicts whether a patient with tuberculous meningitis will benefit from adjunctive corticosteroids.
  • •AMBITION-cm Trial — Validated a single high-dose of liposomal amphotericin B as part of an effective, less toxic induction regimen for cryptococcal meningitis.
  • •Sensorineural hearing loss — The most common long-term sequela of bacterial meningitis, necessitating audiological follow-up for all survivors.
  • •Dexamethasone timing — Must be given before or with the first dose of antibiotics to be effective in reducing inflammatory neurological damage.
  • •Enterovirus — The most common cause of 'aseptic' meningitis, typically presenting with a benign, self-limiting course.

Deep Dive — Evidence Details

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