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Meningitis
Last Updated: July 25, 2005

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AUTHOR INFORMATION

Section 1

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Author: Marjorie Lazoff, MD, Medical Editor, Medical Computing Today; Contributing Editor, MSR's N
Marjorie Lazoff, MD, is a member of the following medical societies: Alpha Omega Alpha, American C
Emergency Physicians, and Society for Academic Emergency Medicine
Editor(s): Mark S Slabinski, MD, Director, Emergency Services, Southeastern Ohio Regional Medica
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Eric L Weiss, MD, DTM&H
Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of
Medicine and Infectious Diseases, Stanford University School of Medicine; John Halamka, MD, Chie
Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency M
Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Cra
FACEP, FAAEM, FACPh, Director, National Institute for Medical Informatics, Director, Federal Projec

Director of Informatics, Washington National Medical Center, Director, National Center for Emergency
Informatics
Disclosure

INTRODUCTION

Section 2 of 1

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Background: Meningitis is an inflammation of the leptomeninges and underlying subarachnoid cereb

(CSF). It can be useful to divide symptom onset into acute, subacute, and chronic categories. Unlike
chronic (>7 d) meningitis, which have myriad infectious and noninfectious etiologies, acute meningitis
always a bacterial infection caused by one of several organisms. Depending on age and general cond
ill patients present acutely with signs and symptoms of meningeal inflammation and systemic infectio
day's duration. Patients may decompensate quickly and require emergency care, including antimicrob
30 minutes of emergency department (ED) presentation.

Not all bacterial meningitis is acute. Approximately 75% of patients with bacterial meningitis present s
patients still require urgent ED diagnosis and care.

The emergence of resistant strains has prompted changes in antibiotic protocols in some countries, in
Apart from dexamethasone, neuronal cell protectants still hold only future promise as adjunctive thera

The challenges for emergency physicians when treating meningitis are to (1) identify and treat patien
bacterial meningitis, (2) assess whether a central nervous system (CNS) infection is present in those
subacute or chronic meningitis, and (3) identify the causative organism. Bacterial meningitis must be
Emergency physicians should be aware that future therapies will be based on improved understandin
pathogenesis of acute bacterial meningitis and may include caspase inhibitors, antioxidants, poly (AD
polymerase inhibitors, inhibitors of lipid peroxidation, and metalloproteinase inhibitors, in addition to a
steroids.

Pathophysiology: A number of factors influence the development of bacterial meningitis, including v

strain, host defenses, and bacteria-host interactions.

Bacterial seeding usually occurs by hematogenous spread. In those without an identifiable source of
tissue and bloodstream invasion by bacteria colonized in the nasopharynx may be a common source
contiguous structures invade via septic thrombi or osteomyelitic erosion; meningeal seeding also may
bacterial inoculate during trauma, neurosurgery, or instrumentation. Meningitis in the newborn is trans
from colonized pathogens in the maternal intestinal or genital tract or horizontally from nursery person

at home.

Once in the CSF, the paucity of antibodies, complement components, and white blood cells (WBCs) a
infection to flourish. Bacterial cell wall components initiate a cascade of complement- and cytokine-m
result in at least 3 critical events: increased permeability of the blood-brain barrier, cerebral edema, a
toxic mediators in the CSF. Replicating bacteria, increasing numbers of inflammatory cells, cytokine-in
in membrane transport, and increased vascular and membrane permeability perpetuate the infectious
account for the characteristic changes in CSF cell count, pH, lactate, protein, and glucose. Exudates
the CSF, particularly to the basal cisterns, damaging cranial nerves (eg, cranial nerve VIII, with resulta
obliterating CSF pathways (causing obstructive hydrocephalus), and inducing vasculitis and thrombop
local brain ischemia).

As intracranial pressure (ICP) continues to rise and brain edema progresses, CNS autoregulatory pro
fail. This pivotal event may occur when the transient increase in cerebral blood flow (CBF) reverses a
decrease. CBF reduction correlates with the patient's decreasing alertness and changes in mental sta

Without medical intervention, the cycle of decreasing CBF, worsening cerebral edema, and increasing
unchecked. Ongoing endothelial injury may result in vasospasm and thrombosis, further compromisin
lead to stenosis of large and small vessels. Systemic hypotension (septic shock) also may impair CBF
soon dies from systemic complications or from diffuse CNS ischemic injury.

The pathophysiologies of nonbacterial pathogens are less well understood. Fungal meningitis is thou
manner similar to but less acute than bacterial meningitis.
Frequency:

In the US: The incidence of bacterial meningitis is 2-3 per 100,000. Recent statistics show an
persons aged 60 years and older independent of other factors. In 1995, incidence by major pa
per 100,000) was as follows:
Streptococcus pneumoniae (1.1) in all except neonates
Neisseria meningitidis (0.6), usually local outbreaks among young adults, epidemics internatio
incidence in late winter or early spring
Group B streptococci (0.3), in newborns
Listeria monocytogenes (0.2) in newborns, elderly, and immunocompromised
Haemophilus influenzae, type b (0.2) in unvaccinated children and adults

Internationally: Meningococcal meningitis is endemic in parts of Africa, India, and other devel
Periodic epidemics occur in the so-called sub-Saharan "meningitis belt" as well as among relig
traveling to Saudi Arabia for the Hajj.

Mortality/Morbidity: Morbidity and mortality depend on pathogen, patient's age and condition, and s
illness.

Among bacterial pathogens, pneumococcal meningitis causes the highest rates of mortality (21
(15%).

Mortality rate is 50-90% and morbidity even higher if severe neurologic impairment is evident a
presentation (or with extremely rapid onset of illness), even with immediate medical treatment.

Race: Statistically, blacks are at greater risk than other races, although race may not be an independ
Sex: In neonates, male-to-female ratio is 3:1. No sex preference exists among adults.
Age: Median age is 25 years. In 1986, it was 15 months.

Excluding meningococcal meningitis, patients younger than 5 years and older than 60 years ar

Newborns are at highest risk for acute bacterial meningitis. After the first month of life, the pea
infants aged 3-8 months.

CLINICAL

Section 3 of 1

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

History: Distinguishing acute, subacute, and chronic meningitis helps identify the pathogen. Approxim
patients with bacterial meningitis present acutely within 24 hours of onset of symptoms. Other patient
meningitis and most patients with viral meningitis present with subacute neurologic symptoms develo
Chronic symptoms lasting longer than 1 week suggest meningitis caused by some viruses as well as
syphilis, fungi (especially cryptococci), and carcinomatous meningitis.

Classic symptoms (not evident in infants or seen often in the elderly) include the following:
o

Headache

Nuchal rigidity (generally not present in children <1 y or in patients with altered mental s

Fever and chills

Photophobia

Vomiting

Prodromal upper respiratory infection (URI) symptoms (viral and bacterial)

Seizures (30-40% in children, 20-30% in adults)

Focal neurologic symptoms (including focal seizures)

Altered sensorium (confusion may be sole presenting complaint, especially in elderly)

Symptoms in infants
o

Fever

Lethargy and/or change in level of alertness

Poor feeding and/or vomiting

Respiratory distress, apnea, cyanosis

Partially treated meningitis: As many as 40% of patients with meningitis were treated previousl
antibiotics. Seizures may be the sole presenting symptom; fever and changes in level of alertn
status occur less commonly than in untreated meningitis.

Low-grade ventriculitis associated with ventriculoperitoneal shunt: Patients may have a less dr
than those with acute meningitis, with headache, nausea, minimal fever, and malaise.

Fungal meningitis: Headache, low-grade fever, and lethargy are the primary symptoms; the co
with fluctuating symptoms, especially in immunocompromised patients.

Tuberculous meningitis: Fever, weight loss, night sweats, and malaise, with or without headach
meningismus are common symptoms; this infection may follow a protracted course with vague
presentation.

Physical: Otherwise healthy patients within age extremes present with clinically obvious acute bacte
contrast, most patients with subacute bacterial meningitis present a diagnostic challenge. Systemic e
occasionally reveals a pulmonary or otitis media co-infection.

Signs of meningeal irritation

o

Nuchal rigidity or discomfort on neck flexion

Kernig sign: Passive knee extension in supine patient elicits neck pain and hamstring re

Brudzinski sign: Passive neck or single hip flexion is accompanied by involuntary flexion

Papilledema is present in only one third of meningitis patients with increased ICP; it takes at le
develop.

Focal neurologic signs

Isolated cranial nerve abnormalities (principally III, IV, VI, VII) in 10-20% of patients

Associated with a dramatic increase in complications from lumbar puncture (LP) and po
outcome

Systemic findings
o

Extracranial infection (eg, sinusitis, otitis media, mastoiditis, pneumonia, urinary tract inf
noted.

Arthritis is seen with N meningitidis, less commonly with other bacteria.

Nonblanching petechiae and cutaneous hemorrhages are seen classically with N menin
these also can occur with other bacterial and viral infections.

Endotoxic shock with vascular collapse is characteristic of severe N meningitidis infectio

Altered mental status, from irritability to somnolence, delirium, and coma

Infants
o

Bulging fontanelle (if euvolemic)

Paradoxic irritability (ie, quiet when stationary, cries when held)

High-pitched cry

Hypotonia

Examine skin over entire spine for dimples, sinuses, nevi, or tufts of hair, which may ind
anomaly communicating with the subarachnoid space.

Causes: Meningitis is caused by the following pathogens in each age group:

Neonates - Group B or D streptococci, nongroup B streptococci, Escherichia coli, and L monoc

Infants and children - H influenzae (48%), S pneumoniae (13%), and N meningitidis

Adults - S pneumoniae, (30-50%), H influenzae (1-3%), N meningitidis (10-35%), gram-negativ

staphylococci (5-15%), streptococci (5%), and Listeria species (5%)

Risk factors
o

Aged 60 years or older

Aged 5 years or younger, especially children with diabetes mellitus, renal or adrenal ins
hypoparathyroidism, or cystic fibrosis

Immunosuppressed patients are at increased risk of opportunistic infections and acute b

Immunosuppressed patients may not show dramatic signs of fever or meningeal inflamm

Crowding (eg, military recruits and college dorm residents) increases risk of outbreaks o
meningitis.

Splenectomy and sickle cell disease increase the risk of meningitis secondary to encap

Alcoholism and cirrhosis: Multiple etiologies of fever and seizures in these patients mak
challenging to diagnose.

Diabetes

Recent exposure to others with meningitis, with or without prophylaxis

Contiguous infection (eg, sinusitis)

o
o

Dural defect (eg, traumatic, surgical, congenital)

Thalassemia major

Intravenous (IV) drug abuse

Bacterial endocarditis

Ventriculoperitoneal shunt

Malignancy (increased risk of Listeria species infection)

Some cranial congenital deformities

DIFFERENTIALS
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Brain Abscess

Section 4 of 1

Delirium Tremens
Encephalitis
Herpes Simplex
Herpes Simplex Encephalitis
Neoplasms, Brain
Pediatrics, Febrile Seizures
Pediatrics, Meningitis and Encephalitis
Subarachnoid Hemorrhage
Other Problems to be Considered:
All causes of altered mental status and coma
Leptospirosis
Subdural empyema

WORKUP
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography

Lab Studies:

Complete blood count (CBC) with differential

Serum electrolytes to determine dehydration or syndrome of inappropriate secretion of antidiur

Serum glucose as baseline for determining normal CSF glucose; may be low if glycogen store
with diabetes

BUN and/or creatinine and liver profile to assess organ functioning and adjust antibiotic dosing

Coagulation profile and platelets in patients with chronic alcohol use, liver disease, or if dissem
suspected. (Patients may require platelets or fresh frozen plasma [FFP] prior to LP.)

Urinary electrolytes if SIADH is suspected

Serum cryptococcal antigen, especially if baseline is known (less diagnostic than India ink and

Cultures prior to instituting antibiotics may be helpful if diagnosis is uncertain: blood (50% posi
S pneumoniae, N meningitidis); nasopharynx, respiratory secretions, urine, and skin lesions.

Latex agglutination or counter immunoelectrophoresis (CIE) of blood, urine, and CSF for speci
occasionally if diagnosis is challenging or in patients with partially treated meningitis.

Serum test for syphilis is indicated if neurosyphilis is in differential diagnosis. (Cases have bee
negative for Venereal Disease Research Laboratory test [VDRL].)

Imaging Studies:

Head CT scan with contrast or MRI with gadolinium

o

Imaging is indicated in patients with evidence of head trauma, altered mental status, or

Presence of papilledema and inability to fully assess fundi or neurologic status are indic

Obtain blood cultures and initiate treatment before imaging studies and LP in patients w

Results may be normal or demonstrate small ventricles, effacement of sulci, and contra

Late findings include venous infarction and communicating hydrocephalus.

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