Meningitis: viral and bacterial, signs, imaging, CSF analysis, management and sequelae

Overview

Meningitis is inflammation of the pia and arachnoid mater and the CSF between them. Infection reaches the meninges through the blood or by direct spread from the ear, sinuses, a skull fracture or a congenital defect.

Bacterial (purulent) meningitis is a medical emergency: it is fatal untreated and still kills about 15% of adults even with good care. Viral (aseptic) meningitis is common and usually benign. Tuberculous meningitis is common in Pakistan and is a slower, dangerous illness.

Causes

Bacteria by age and setting

Viral (aseptic) meningitis

Enteroviruses (Coxsackie, echovirus) are the commonest; also mumps, herpes simplex (HSV-2 can cause recurrent benign lymphocytic meningitis), varicella zoster, EBV and HIV seroconversion.

Other causes of a "sterile" or chronic meningitis

TB, fungi (Cryptococcus), syphilis, Lyme disease, partially treated bacterial meningitis, malignant meningitis, sarcoidosis, Behçet disease, drugs (NSAIDs, IVIG, co-trimoxazole) and blood after subarachnoid haemorrhage.

Pathology in brief

• Bacterial: pus in the subarachnoid space; cerebral oedema; adhesions that trap cranial nerves and block CSF flow (hydrocephalus); vasculitis causing infarcts.
• Viral: lymphocytic inflammation, no pus, little or no oedema.
• Tuberculous: thick grey-green basal exudate, tubercles, inevitable adhesions, obstructive hydrocephalus, vasculitic infarcts and cranial nerve palsies.

Clinical features

The meningitic syndrome

• Fever, headache and neck stiffness (the classic triad), with photophobia, vomiting and irritability.
• Bacterial meningitis develops over hours: rigors, high fever, severe headache, drowsiness, confusion, seizures, shock.
• Viral meningitis is milder; the patient is usually alert.

Signs of meningeal irritation

Clues to the organism

Warning features of complications

Falling consciousness, focal signs, seizures, papilloedema and cranial nerve palsies suggest raised intracranial pressure, abscess, venous sinus thrombosis, hydrocephalus or encephalitis (personality change, fits and confusion dominate; HSV affects the temporal lobes; treat with IV aciclovir).

Investigations

Immediate

• Blood cultures before antibiotics (but never delay antibiotics to get them), full blood count, CRP, glucose (for the CSF ratio), urea and electrolytes, clotting, lactate.
• Throat swab and PCR of blood (meningococcal and pneumococcal PCR stay positive after antibiotics).
• Gram stain of aspirate from a skin lesion.

When to do CT before lumbar puncture

LP is the key test but can cause coning (tonsillar herniation) if pressure is high from a mass. Scan first if there is:

• reduced or falling consciousness,
• focal neurological signs or new seizures,
• papilloedema,
• severe immunocompromise or suspected abscess.

Other contraindications to LP: shock, coagulopathy or low platelets, local skin infection at the site, and suspected meningococcal sepsis with a rash (diagnosis is clinical; LP is unnecessary and risky).

CSF analysis

Normal opening pressure is about 60–150 mm of CSF (raised in bacterial, TB and cryptococcal meningitis). Always send a paired blood glucose.

Organisms on stain: Gram-negative intracellular diplococci = meningococcus; Gram-positive diplococci = pneumococcus; Gram-negative coccobacilli = Haemophilus; Gram-positive rods = Listeria; India ink shows capsulated yeasts of Cryptococcus (also cryptococcal antigen).

Imaging (radiological findings)

• CT is often normal in uncomplicated meningitis; its job is to exclude a mass before LP and to detect complications.
• Contrast MRI/CT: meningeal (leptomeningeal) enhancement; in TB, basal meningeal enhancement, hydrocephalus, tuberculomas and infarcts (especially basal ganglia).
• Complications seen on imaging: hydrocephalus, cerebral oedema, abscess, subdural effusion or empyema, venous sinus thrombosis, infarction.
• Sinus and mastoid views or CT if a parameningeal source is suspected; chest X-ray for pneumonia or TB.

Management

Emergency treatment of bacterial meningitis

1. ABC, oxygen, IV access; treat septic shock with fluids and vasopressors.
2. Blood cultures, then antibiotics immediately. In the community, a suspected meningococcal rash means parenteral antibiotics at first contact (benzylpenicillin or a third-generation cephalosporin) before transfer.
3. Dexamethasone with or just before the first antibiotic dose.
4. CT if indicated, then LP.
5. Supportive care: fluids, treat seizures, monitor glucose, sodium (SIADH) and consciousness; ICU if needed.

Empirical antibiotics

Once the organism is known: meningococcus → benzylpenicillin or ceftriaxone if sensitive; pneumococcus → ceftriaxone, or penicillin if sensitive; Listeria → ampicillin ± gentamicin; Haemophilus → ceftriaxone. Treat for at least 5 days; the course is longer for pneumococcus, Listeria and Gram-negatives.

Dexamethasone

• Dexamethasone 0.6 mg/kg per day for 4 days (divided doses), given with or just before the first antibiotic dose.
• Reduces hearing loss and neurological sequelae, and mortality in pneumococcal meningitis in high-income settings.
• Stop it if the cause turns out not to be bacterial. Not useful once antibiotics have been running for a while, and not shown to help in low-income settings with late presentation and HIV.

Viral meningitis

Usually self-limiting in 4–10 days: rest, fluids, analgesia, antiemetics. Headache may linger for weeks. Give IV aciclovir if HSV or VZV encephalitis is possible (confusion, seizures, focal signs).

Tuberculous meningitis

• Subacute: weeks of headache, fever, malaise, vomiting, then confusion, cranial nerve palsies (VI commonest), papilloedema, hemiparesis, seizures and coma.
• CSF: lymphocytes, very high protein, low glucose; AFB rarely seen; GeneXpert/PCR helps but a negative result does not exclude it.
• Start treatment on suspicion: rifampicin, isoniazid, pyrazinamide (and usually a fourth drug in national regimens) for 2 months, then rifampicin and isoniazid, for about 9–12 months in total, plus corticosteroids (dexamethasone or prednisolone, tapered over several weeks).
• Treat hydrocephalus (shunt or drain).
• Mortality and disability remain high despite treatment.
• Follow the current National TB Control Programme (Pakistan) guideline, since regimens and durations change.

Cryptococcal meningitis

HIV with low CD4; headache with very high opening pressure; India ink and cryptococcal antigen; treat with amphotericin B + flucytosine, then fluconazole; repeated LPs to lower pressure.

Prevention

• Notify suspected meningococcal disease to public health.
• Chemoprophylaxis for close (household and kissing) contacts of meningococcal disease: rifampicin (short oral course) or single-dose ciprofloxacin; ceftriaxone in pregnancy. The patient also needs eradication if treated with penicillin alone.
• Vaccines: Hib (part of the pentavalent vaccine in Pakistan's EPI), pneumococcal conjugate vaccine (in EPI; polysaccharide vaccine for older adults and asplenia), meningococcal ACWY (required for Hajj and Umrah pilgrims), MenB and MenC where used. Schedules change: check the current EPI.

Sequelae and complications

Early (acute) complications

• Septic shock, DIC, Waterhouse-Friderichsen syndrome (bilateral adrenal haemorrhage in meningococcal sepsis), purpura fulminans with limb gangrene.
• Cerebral oedema and raised intracranial pressure, coning.
• Seizures.
• SIADH (hyponatraemia).
• Cranial nerve palsies (VI, III, VII, VIII).
• Hydrocephalus (communicating or obstructive).
• Subdural effusion (especially infants with Hib or pneumococcus) or subdural empyema.
• Venous sinus thrombosis, cerebral infarction (vasculitis), brain abscess, ventriculitis.

Long-term sequelae

• Sensorineural deafness: the commonest sequela, especially after pneumococcal and Hib meningitis. Every child should have a hearing test after bacterial meningitis.
• Epilepsy.
• Learning difficulty, cognitive and behavioural problems.
• Hemiparesis, spasticity, visual loss, hydrocephalus needing a shunt.
• Amputations and skin scarring after meningococcal sepsis.

Prognosis

• Viral: excellent, no lasting harm (unless encephalitis).
• Bacterial: mortality about 15% overall; worst with pneumococcus, older age, coma, shock and delayed treatment. Meningococcal meningitis alone has lower mortality than meningococcal septicaemia.
• Tuberculous: high death and disability rates, especially with late presentation.

Quick revision

• Triad: fever, headache, neck stiffness; Kernig and Brudzinski signs; petechial rash = meningococcus.
• Adults: meningococcus and pneumococcus; neonates: GBS, E. coli, Listeria; over 50/immunosuppressed: add Listeria.
• Antibiotics first: ceftriaxone/cefotaxime IV; + ampicillin for Listeria; + vancomycin for resistant pneumococci.
• Dexamethasone 0.6 mg/kg/day for 4 days with the first antibiotic dose; reduces deafness.
• CT before LP if reduced consciousness, focal signs, papilloedema, seizures or immunosuppression.
• CSF: bacterial = neutrophils, low glucose, high protein; viral = lymphocytes, normal glucose; TB = lymphocytes, very high protein, low glucose.
• Contacts: rifampicin or ciprofloxacin (ceftriaxone in pregnancy); vaccines Hib, PCV, MenACWY.
• Sequelae: deafness (commonest), epilepsy, hydrocephalus, cognitive and focal deficits.

Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).

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