Meningitis: Classification and External Resources
Meningitis: Classification and External Resources
Meningitis: Classification and External Resources
Meningitis
ICD-10 G00.–G03.
ICD-9 320–322
DiseasesDB 22543
MedlinePlus 000680
eMedicine med/2613 emerg/309emerg/390
MeSH D008581
Nuchal rigidity occurs in 70% of adult cases of bacterial meningitis. [6] Other signs of meningism include
the presence of positive Kernig's sign or Brudzinski's sign. Kernig's sign is assessed with the patient
lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain
limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes
involuntary flexion of the knee and hip. Although Kernig's and Brudzinski's signs are both commonly used
to screen for meningitis, thesensitivity of these tests is limited.[6][8] They do, however, have very
good specificity for meningitis: the signs rarely occur in other diseases. [6] Another test, known as the "jolt
accentuation maneuver" helps determine whether meningitis is present in patients reporting fever and
headache. The patient is told to rapidly rotate his or her head horizontally; if this does not make the
headache worse, meningitis is unlikely.[6]
[edit]Early complications
A severe case of meningococcal meningitis in which the petechial rash progressed to gangrene and requiredamputation of
all limbs. The patient,Charlotte Cleverley-Bisman, survived the disease and became a poster child for a meningitis
vaccination campaign in New Zealand.
People with meningitis may develop additional problems in the early stages of their illness. These may
require specific treatment, and sometimes indicate severe illness or worse prognosis. The infection may
trigger sepsis, a systemic inflammatory response syndrome of falling blood pressure,fast heart rate, high
or abnormally low temperature and rapid breathing. Very low blood pressure may occur early, especially
but not exclusively in meningococcal illness; this may lead to insufficient blood supply to other organs.
[1]
Disseminated intravascular coagulation, the excessive activation of blood clotting, may cause both the
obstruction of blood flow to organs and a paradoxical increase of bleeding risk. In meningococcal
disease, gangrene of limbs can occur.[1] Severe meningococcal and pneumococcal infections may result
in hemorrhaging of the adrenal glands, leading to Waterhouse-Friderichsen syndrome, which is often
lethal.[10]
The brain tissue may swell, with increasing pressure inside the skull and a risk of swollen brain
tissuegetting trapped. This may be noticed by a decreasing level of consciousness, loss of the pupillary
light reflex, and abnormal positioning.[4] Inflammation of the brain tissue may also obstruct the normal flow
of CSF around the brain (hydrocephalus).[4] Seizures may occur for various reasons; in children, seizures
are common in the early stages of meningitis (30% of cases) and do not necessarily indicate an
underlying cause.[3] Seizures may result from increased pressure and from areas of inflammation in the
brain tissue.[4] Focal seizures (seizures that involve one limb or part of the body), persistent seizures, late-
onset seizures and those that are difficult to control with medication are indicators of a poorer long-term
outcome.[1]
The inflammation of the meninges may lead to abnormalities of the cranial nerves, a group of nerves
arising from the brain stem that supply the head and neck area and control eye movement, facial muscles
and hearing, among other functions.[1][6] Visual symptoms and hearing loss may persist after an episode of
meningitis (see below).[1] Inflammation of the brain (encephalitis) or its blood vessels (cerebral vasculitis),
as well as the formation of blood clots in the veins (cerebral venous thrombosis), may all lead to
weakness, loss of sensation, or abnormal movement or function of the part of the body supplied by the
affected area in the brain.[1][4]
[edit]Causes
Type of
Glucose Protein Cells
meningitis
PMNs,
Acute bacterial low high
often > 300/mm³
mononuclear,
Acute viral normal normal or high
< 300/mm³
mononuclear and
Tuberculous low high
PMNs, < 300/mm³
usually
Malignant low high
mononuclear
Treatment
[edit]Initial treatment
Meningitis is potentially life-threatening and has a high mortality rate if untreated; [3] delay in treatment has
been associated with a poorer outcome.[4] Thus treatment with wide-spectrum antibiotics should not be
delayed while confirmatory tests are being conducted. [23] If meningococcal disease is suspected in
primary care, guidelines recommend that benzylpenicillin be administered before transfer to hospital.
[7]
Intravenous fluids should be administered if hypotension (low blood pressure) or shock are present.
[23]
Given that meningitis can cause a number of early severe complications, regular medical review is
recommended to identify these complications early,[23] as well as admission to an intensive care unit if
deemed necessary.[4]
Mechanical ventilation may be needed if the level of consciousness is very low, or if there is evidence
of respiratory failure. If there are signs of raised intracranial pressure, measures to monitor the pressure
may be taken; this would allow the optimization of the cerebral perfusion pressure and various treatments
to decrease the intracranial pressure with medication (e.g. mannitol).[4] Seizures are treated
withanticonvulsants.[4] Hydrocephalus (obstructed flow of CSF) may require insertion of a temporary or
long-term drainage device, such as acerebral shunt.[4]
[edit]Bacterial meningitis
[edit]Antibiotics
Structural formula of ceftriaxone, one of the third-generation cefalosporin antibiotics recommended for the initial treatment of
bacterial meningitis.
Empiric antibiotics (treatment without exact diagnosis) must be started immediately, even before the
results of the lumbar puncture and CSF analysis are known. The choice of initial treatment depends
largely on the kind of bacteria that cause meningitis in a particular place. For instance, inthe United
Kingdom empirical treatment consists of a third-generation cefalosporin such ascefotaxime or ceftriaxone.
[21][23]
In the USA, where resistance to cefalosporins is increasingly found in streptococci, addition
of vancomycin to the initial treatment is recommended.[3][4][21]Empirical therapy may be chosen on the
basis of the age of the patient, whether the infection was preceded by head injury, whether the patient
has undergone neurosurgery and whether or not a cerebral shunt is present. [3] For instance, in young
children and those over 50 years of age, as well as those who are immunocompromised, addition
of ampicillin is recommended to coverListeria monocytogenes.[3][21] Once the Gram stain results become
available, and the broad type of bacterial cause is known, it may be possible to change the antibiotics to
those likely to deal with the presumed group of pathogens. [3]
The results of the CSF culture generally take longer to become available (24–48 hours). Once they do,
empiric therapy may be switched to specific antibiotic therapy targeted to the specific causative organism
and its sensitivities to antibiotics.[3] For an antibiotic to be effective in meningitis, it must not only be active
against the pathogenic bacterium, but also reach the meninges in adequate quantities; some antibiotics
have inadequate penetrance and therefore have little use in meningitis. Most of the antibiotics used in
meningitis have not been tested directly on meningitis patients in clinical trials. Rather, the relevant
knowledge has mostly derived from laboratory studies in rabbits.[3]
Tuberculous meningitis requires prolonged treatment with antibiotics. While tuberculosis of the lungs is
typically treated for six months, those with tuberculous meningitis are typically treated for a year or longer.
[13]
In tuberculous meningitis there is a strong evidence base for treatment with corticosteroids, although
this evidence is restricted to those without AIDS.[36]
[edit]Steroids
Adjuvant corticosteroids have a different role in children than in adults. Though the benefit of
corticosteroids has been demonstrated in adults as well as in children from high-income countries, their
use in children from low-income countries is not supported by evidence; the reason for this discrepancy is
not clear.[39] Even in high-income countries, the benefit of corticosteroids is only seen when they are given
prior to the first dose of antibiotics, and is greatest in cases of H. influenzae meningitis,[3][40] the incidence
of which has decreased dramatically since the introduction of the Hib vaccine. Thus, corticosteroids are
recommended in the treatment of pediatric meningitis if the cause is H. influenzae and only if given prior
to the first dose of antibiotics, whereas other uses are controversial. [3]
A 2010 analysis of previous studies has shown that the benefit from steroids may not be as significant as
previously found. The one possible significant benefit is reduction of hearing loss in survivors. [41]
[edit]Viral meningitis
Viral meningitis typically requires supportive therapy only; most viruses responsible for causing meningitis
are not amenable to specific treatment. Viral meningitis tends to run a more benign course than bacterial
meningitis. Herpes simplex virus and varicella zoster virus may respond to treatment with antiviral drugs
such as aciclovir, but there are no clinical trials that have specifically addressed whether this treatment is
effective.[9] Mild cases of viral meningitis can be treated at home with conservative measures such as
fluid, bedrest, and analgesics.[42]
[edit]Fungal meningitis
Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of highly
dosed antifungals, such as amphotericin B andflucytosine.[25][43]