3. Meningitis is caused by:
Bacteria
Viruses
Parasites,
Fungi
Noninfectious conditions including inflammatory disorders (e.g.,
SLE or Kawasaki disease) and neoplasia (e.g., leukemic
meningitis)
Chemical meningitis (NSAIDs, IV immunoglobulin,
trimethoprim, sulfonamides, and OKT3 monoclonal antibodies
can cause a drug-induced hypersensitivity meningitis.)
2
4. Types of meningitis:
Acute
Aseptic (misnomer, mostly viral)
Chronic (TB, Crypto, Spirochetal/ syphilis)
Meningitis due to viruses and certain other nonbacterial pathogens
is assigned as aseptic meningitis.
Chronic meningitis refers to duration greater than 4 weeks.
3
6. Meningitis is the diffuse inflammation of the leptomeninges.
Meninges = Dura mater (outer thick fibrous membrane) +
Arachnoid mater (thin) + Pia mater (thin)
Leptomeninges = Pia + Arachnoid (thin membranes = lepto)
CSF is b/n pia and arachnoid mater (subarachnoid space) in
addition to ventricular system.
Therefore meningitis is the inflammation of the Leptomeninges plus
CSF in the subarachnoid space.
If the inflammation is limited to dura (thick) mater it is known as
pachy meningitis.
DEFINITIONS
5
7. Encephalitis is diffuse/ generalized inflammation of brain
parenchyma.
Cerebritis is localized inflammation of brain parenchyma.
Cerebral abscess is localized inflammation of brain parenchyma
with capsule formation.
6
8. Bacterial meningitis is an acute purulent infection within the
subarachnoid space (SAS).
It is associated with a CNS inflammatory reaction that may result in
decreased consciousness, seizures, raised ICP, and stroke.
The meninges, SAS, and brain parenchyma are all frequently
involved in the inflammatory reaction (meningoencephalitis).
BACTERIAL MENINGITIS
7
9. Common etiologies of community-acquired bacterial meningitis:
Streptococcus pneumoniae (~50%),
Neisseria meningitidis (~25%),
Group B streptococci (~15%),
Listeria monocytogenes (~10%).
Haemophilus influenzae type b (<10%)
ETIOLOGY
8
10. Streptococcus pneumoniae
It is the most common cause in adults >20 years of age.
Predisposing factors:
Pneumococcal pneumonia (most important), pneumococcal
sinusitis or otitis media,
Alcoholism,
DM
Splenectomy, hypogammaglobulinemia, complement deficiency,
Head trauma with basilar skull fracture and CSF rhinorrhea.
The mortality rate is ~20% despite therapy.
9
11. N. meningitidis
The incidence has decreased with immunization of 11-18-year-olds
with the quadrivalent (serogroups A, C, W-135, and Y) vaccine.
The vaccine doesn’t contain serogroup B, which causes 1/3rd.
The Advisory Committee on Immunization Practices (ACIP)
recommends that adults aged 16–23 years may be vaccinated with
the serogroup B meningococcal (MenB) vaccine.
In some patients the disease is fulminant, progressing to death
within hours of symptom onset.
N. meningitidis causes epidemics of meningitis every 8–12 years.
10
12. Gram-negative bacilli
In chronic and debilitating diseases such as DM, cirrhosis, or
alcoholism and in those with chronic UTIs.
It can complicate neurosurgical procedures, particularly craniotomy,
and head trauma associated with CSF rhinorrhea or otorrhea.
After endocarditis may be due to viridans streptococci, S. aureus,
Streptococcus bovis, the HACEK group (Haemophilus sp.,
Actinobacillus actinomycetemcomitans, Cardiobacterium hominis,
Eikenella corrodens, Kingella kingae), or enterococci.
11
13. L. monocytogenes
It is an important cause of meningitis in:
Neonates,
Pregnant,
Alcoholics
Age >60 years, and
Immunocompromised individuals.
Acquired by ingesting foods contaminated by Listeria.
Contaminated coleslaw, milk, sox cheeses, and several types of
“ready-to-eat” foods, including delicatessen meat and uncooked
hotdogs.
12
14. H. influenzae type b
Causes meningitis in unvaccinated children and older adults, and
non-b is an emerging pathogen.
Hib meningitis in children has declined due to the vaccine, although
rare cases in vaccinated children have been reported.
S. aureus and coagulase-negative staphylococci are important
causes of meningitis that occurs following invasive neurosurgical
procedures, particularly shunting procedures for hydrocephalus, or
as a complication of the use of subcutaneous Ommaya reservoirs
for administration of intrathecal chemotherapy.
13
15. Amebic meningoencephalitis caused by Naegleria fowleri
Follows aspiration of water contaminated with trophozoites or cysts
or the inhalation of contaminated dust, leading to invasion of the
olfactory neuroepithelium.
Common among children or young adults, who often report recent
swimming in lakes or heated swimming pools.
After an incubation period of 2–15 days, severe headache, high
fever, nausea, vomiting, and meningismus develop.
Photophobia and palsies of the third, fourth, and sixth cranial nerves
are common.
Rapid progression to seizures and coma may follow.
Naegleria fowleri
14
16. It should be considered in patient who has purulent meningitis
without evidence of bacteria on Gram’s staining, antigen detection
assay, and culture.
Dx is by detecting motile trophozoites in wet mount of CSF.
Other laboratory findings resemble those for bacterial meningitis,
WBC (up to 20,000/ μL ), and elevated protein and low glucose.
Antibodies to Naegleria species have been detected in healthy
adults; serologic testing is not useful in the diagnosis.
The prognosis is uniformly poor: most patients die within a week.
Recently, two surviving children were treated with miltefosine.
15
19. Meningitis associated with sinusitis, otitis, or mastoiditis may be
due to streptococci, anaerobes, Staph. aureus, Haemophilus, or
Enterobacteriaceae.
Meningitis in the post neurosurgical may be due to staphylococci,
gram-negative bacilli, or anaerobes.
S.aureus is a common causative organism in penetrating head
trauma.
An interval of many years may separate an episode of significant
closed head trauma and the onset of meningitis.
18
20. The organism causing bacterial meningitis in immunocompromised
varies with the type of immune deficiency.
Cell-mediated immunity defect- includes very young infants,
pregnant, elderly, organ transplantation, malignancy, AIDS, or
medications, have an increased prevalence of meningitis due to L.
monocytogenes or mycobacteria.
Humoral immune defect (and those who undergone splenectomy)
are at risk of S.pneumoniae or, less frequently, N. meningitidis.
Patients with neutropenia are susceptible to meningitis caused by
Pseudomonas aeruginosa and gram negative enteric bacteria.
19
22. Chronic meningitis presenting acutely
A number of etiologic organisms that typically cause a subacute or
chronic meningitis may present with acute onset of symptoms.
This is especially true for TB meningitis but may occasionally
occur with fungal meningitides due to Cryptococcus neoformans,
Histoplasma capsulatum, Coccidioides immitis, or other agents.
The most urgent of these is tuberculous meningitis, and
presumptive treatment should be initiated if the condition is
suspected.
21
23. Bacterial meningitis is the most common form of suppurative CNS
infection.
Annual incidence in United States >2.5 /100,000 population.
EPIDEMIOLOGY
22
26. Outbreak: case definition
≥3 cases in <3 months
Reside in the same area but not close contacts
Primary attack rate >10cases/100,000
Strain isolate- N. meningitides of same type.
25
27. PATHOPHYSIOLOGY
The bacteria reach the intraventricular
choroid plexus, directly infect choroid
plexus epithelial cells, and gain access to
the CSF
The bacteria multiplies rapidly within CSF because of
the absence of effective host immune defense in the
CSF (no neutrophil CSF).
28. Normal CSF contains few WBCs (<5) and small amounts of
complement proteins and immunoglobulins.
The paucity of the latter two prevents effective opsonization of
bacteria, a prerequisite for phagocytosis.
Phagocytosis is further impaired by the fluid nature of CSF, which
is less conducive to phagocytosis than a solid tissue substrate.
A critical event in the pathogenesis of bacterial meningitis is the
inflammatory reaction induced by the invading bacteria.
Many of the neurologic manifestations and complications result
from the immune response to the invading pathogen.
27
29. TNF-α and IL-1β act synergistically to increase the permeability of
the BBB, resulting in induction of vasogenic edema and the leakage
of serum proteins into the SAS.
The subarachnoid proteinaceous material and leukocytes obstruct
the flow of CSF through the ventricular system and diminish the
resorptive capacity of the arachnoid granulations in the dural
sinuses, leading to obstructive and communicating hydrocephalus
and concomitant interstitial edema.
Cerebral herniation results from the cerebral edema, either focal or
generalized; hydrocephalus and dural sinus or cortical vein
thrombosis may also play a role.
28
30. Meningitis can present as an acute fulminant illness that progresses
rapidly in a few hours or as a subacute infection that progress over
several days.
The classic clinical triad is fever, headache, and nuchal rigidity, but
the triad may not be present.
Although one or more of these findings are absent in many patients,
virtually all patients (99 to 100%) have at least one of the triad.
Nausea, vomiting, and photophobia are also common complaints.
A decreased level of consciousness occurs in >75% of patients.
Patients may also present with septic shock (10–25%), especially
those with meningococcal meningitis.
CLINICAL PRESENTATION
29
31. Nuchal rigidity is the pathognomonic sign of meningeal irritation
and is present when the neck resists passive flexion.
Kernig’s and Brudzinski’s signs are also classic signs of meningeal
irritation.
Both may be absent or reduced in very young or elderly,
immunocompromised, or severely depressed mental status.
The high prevalence of cervical spine disease in older individuals
may result in false-positive tests for nuchal rigidity.
30
32. Seizures occurs in 20–40% of patients.
Focal seizures due to focal arterial ischemia or infarction, cortical
venous thrombosis, or focal edema.
Generalized seizure and status epilepticus may be due to
hyponatremia, cerebral anoxia, or, less commonly, the toxic effects
of antimicrobial agents.
31
33. A specific aetiology may be
suggested by Hx and PE.
A petechial rash (non blanching) in
75% of Meningococcal Meningitis.
=Meningococcemia
The presence of Otitis Media
suggests pneumococcal meningitis
Petechiae are found on the trunk,
L.extremities, mucous membranes
and conjunctiva, and occasionally
on the palms and soles.
20/12/2017
32
34. > 90% of patients have a CSF opening pressure >180 mmH2O, and
20% have >400 mmH2O.
Signs of increased ICP (reduced level of consciousness,
papilledema, dilated poorly reactive pupils, 6th nerve palsy,
decerebrate posturing, and the Cushing reflex (bradycardia,
hypertension, and irregular respirations).
The most disastrous complication of increased ICP is cerebral
herniation (1-8%)
Meningitis may be deceptively asymptomatic in the elderly,
alcoholic and the only sign may be confusion or altered
responsiveness in a patient with dementia.
33
35. Although bacterial meningitis is suspected based on the clinical
presentation, definitive diagnosis is made by analysis of the CSF.
If LP is delayed, empirical antibiotic should be initiated after blood
cultures are obtained.
The yield of CSF Gram’s stain and culture may be diminished by
antimicrobial therapy given several hours (not early) prior to LP,
but it will not affect the CSF WBC count and glucose.
In addition, antimicrobial therapy will not affect the result of the
PCR, which detects nucleic acid of bacteria in CSF.
DIAGNOSIS
34
38. Headaches occur after LP with standing up and are often relieved
with bedrest.
Low-pressure headaches after LP generally resolve spontaneously.
However, rarely they persist and require placement of a epidural
blood-patch, which is accomplished by injecting the patient’s own
blood to close the hole in the dura.
Postsurgical and posttraumatic leakage of CSF can cause low-
pressure headaches, and occasionally a spontaneous tear occurs.
Diagnosis of a spontaneous leak can at times be difficult and may
require injection of radiolabeled substances or contrast agents into
the CSF
37
40. The classic CSF abnormalities in bacterial meningitis are:
Increased opening pressure (>180 mmH2O in 90%).
Cloudy (WBC, RBC, bacteria, protein)
PMN leukocytosis (>100 cells/μL in 90%),
Decreased glucose (<40 mg/dL) or ratio of <0.4 in ~60%.
Increased protein (>45 mg/dL in 90%), and
A CSF/serum glucose ratio <0.4 is highly suggestive of bacterial
meningitis but may also be seen in other conditions, including
fungal, tuberculous, and carcinomatous meningitis.
CSF cultures are positive in >80% of patients, and CSF Gram’s
stain demonstrates organisms in >60%.
39
41. It takes 30 min to several hours for the CSF glucose to reach
equilibrium with blood glucose levels; therefore, administration of
glucose prior to LP, is unlikely to alter CSF glucose concentration
significantly unless more than a few hours have elapsed.
The CSF LA test has a specificity of 95–100% for S. pneumoniae
and N. meningitidis, However, the sensitivity is only 70–100% for
S. pneumoniae and 33–70% for N. meningitidis antigens, so a
negative test does not exclude infection by these organisms.
The Limulus amebocyte lysate assay is a rapid diagnostic test for
gram-negative endotoxin in CSF. The test has a specificity of 85–
100% and a sensitivity approaching 100%.
40
43. Almost all patients with bacterial meningitis will have
neuroimaging studies performed during the course of their illness.
MRI is preferred over CT because of its superiority in
demonstrating cerebral edema and ischemia.
In patients with bacterial meningitis, diffuse meningeal
enhancement is often seen after the administration of gadolinium.
Meningeal enhancement is not diagnostic of meningitis but it occurs
in any CNS disease associated with increased BBB permeability.
Petechial skin lesions, should be biopsied. The rash is due to dermal
seeding of the organisms with vascular endothelial damage, and
biopsy reveals the organism on Gram’s stain.
42
44. Blood cultures are valuable to detect the causative organism and
susceptibility patterns if CSF cultures are negative or unavailable.
Blood culture positivity differs for each causative organism: 50 to
90% of H. influenzae, 75% of pneumococcal, and 60% of adult
patients with meningococcal.
The yield of blood cultures was decreased by 20% in pretreated
patients in two studies.
Complement levels and immunoglobulin levels should be part of
the evaluation of every patient with bacterial meningitis.
43
45. Viral meningoencephalitis, particularly HSV encephalitis, can
mimic the clinical presentation of bacterial meningitis.
HSV encephalitis typically presents with headache, fever, altered
consciousness, focal neurologic deficits (e.g., dysphasia(aphasia),
hemiparesis), and focal or generalized seizures.
The findings on CSF, neuroimaging, and EEG distinguish HSV
encephalitis from bacterial meningitis.
The typical CSF profile with viral infections is a lymphocytic
pleocytosis with a normal glucose concentration.
DIFFERENTIAL DIAGNOSIS
44
46. The CSF HSV PCR has a 96% sensitivity and a 99% specificity
when examined 72 h following symptom onset, and in the first
week of therapy.
MRI abnormalities (other than meningeal enhancement) are not
seen in uncomplicated bacterial meningitis.
By contrast, in HSV encephalitis, on T2-weighted, fluid-attenuated
inversion recovery (FLAIR) and diffusion-weighted MRI images,
high signal intensity lesions are seen in the orbitofrontal, anterior,
and medial temporal lobes in the majority of patients within 48 h of
symptom onset.
Some patients with HSV encephalitis have a distinctive periodic
pattern on EEG.
45
47. A number of noninfectious CNS disorders can mimic bacterial
meningitis.
Subarachnoid hemorrhage; is generally the major consideration.
Other possibilities include medication-induced hypersensitivity
meningitis; chemical meningitis due to rupture of tumor contents
into the CSF (e.g., from a cystic glioma or craniopharyngioma
epidermoid or dermoid cyst); carcinomatous or lymphomatous
meningitis; meningitis associated with inflammatory disorders such
as sarcoid, SLE, and Behçet’s syndrome; pituitary apoplexy; and
uveomeningitic syndromes (Vogt- Koyanagi -Harada syndrome).
Occasionally, subacutely evolving meningitis may be considered.
46
48. In conclusion, concentrations of CRP and procalcitonin in serum
have been evaluated for their usefulness in determining the
diagnosis of bacterial meningitis; although elevated concentrations
can be suggestive of bacterial infection, they aren’t specific.
Some viruses may have PMN predominance in CSF, Eg. West Nile
Virus
47
49. When bacterial meningitis is suspected, blood culture should be
obtained and empirical Ax and dexamethasone should be started..
EMPIRICAL ANTIMICROBIAL THERAPY
Bacterial meningitis is a medical emergency.
Begin antibiotics within 60 min of arrival in the emergency room.
Empirical therapy of community-acquired bacterial meningitis
should include dexamethasone, a 3rd or 4th -generation
cephalosporin, and vancomycin, plus acyclovir, as HSV
encephalitis is the leading disease in the differential diagnosis, and
doxycycline during tick season to treat tick-borne infections.
TREATMENT
48
50. Ampicillin should be added to cover L. monocytogenes in
individuals <3 months, those >55, or impaired cell-mediated
immunity because of chronic illness, organ transplantation,
pregnancy, malignancy, or immunosuppressive therapy.
Metronidazole is added to the empirical regimen to cover gram-
negative anaerobes in patients with otitis, sinusitis, or mastoiditis.
In hospital-acquired meningitis, particularly following
neurosurgical procedures, staphylococci and gram-negative
organisms including P. aeruginosa are the most common etiologic
organisms. In these patients, empirical therapy should include a
combination of vancomycin plus ceftazidime / meropenem.
49
52. Meningococcal Meningitis
Although ceftriaxone / cefotaxime provide adequate coverage for N.
meningitidis, penicillin G remains the antibiotic of choice.
Patients with meningococcal meningitis must be isolated for the
first 24 hours after initiation of antibiotic therapy and treated with
rifampin 600 mg every 12 hours for 2 days after they finish a course
of IV Ax to eradicate nasopharyngeal colonization.
SPECIFIC ANTIMICROBIAL
THERAPY
51
53. Pneumococcal Meningitis
S. pneumoniae is considered susceptible to penicillin with a MIC
<0.06 μg/mL and resistant when the MIC is >0.12.
Sensitive to cephalosporins with MICs ≤0.5. Those with MICs of 1
μg/mL are considered to have intermediate resistance, and those
with ≥2 are considered resistant.
For MIC >1 μg/mL, vancomycin is the antibiotic of choice.
Rifampin can be added to vancomycin for its synergistic effect.
52
54. Patients should have a repeat LP 24–36h after the initiation of
therapy to document sterilization of the CSF.
Failure to sterilize after 24–36 h should be considered presumptive
evidence of resistance.
Patients with penicillin- and cephalosporin-resistant strains of S.
pneumoniae who do not respond to IV vancomycin alone may
benefit from the addition of intraventricular vancomycin.
The intraventricular route is preferred over the intrathecal route
because adequate concentrations in the cerebral ventricles are not
always achieved with intrathecal administration.
53
55. Listeria Meningitis
Treated with ampicillin for at least 3 weeks.
Gentamicin is added in critically ill patients (2 mg/kg loading dose,
then 7.5 mg/kg per day given tid ).
The combination of trimethoprim (10–20 mg/kg per day) and
sulfamethoxazole (50–100 mg/kg per day) given qid may provide
an alternative in penicillin-allergic patients.
54
56. Staphylococcal Meningitis
S. aureus or coagulase-ve staphylococci is treated with nafcillin.
Vancomycin is the drug of choice for methicillin-resistant
staphylococci and for patients allergic to penicillin.
In these patients, the CSF should be monitored during therapy.
If the CSF is not sterilized after 48 h of intravenous vancomycin
therapy, then either intraventricular or intrathecal vancomycin, 20
mg once daily, can be added.
55
57. Gram-Negative Bacillary Meningitis
The 3rd -generation cephalosporins are efficacious, with the
exception of P. aeruginosa.
A 3-week course of intravenous antibiotic therapy is recommended.
56
59. Because of the limitation in antibiotic penetration into the CSF, all
patients should be treated with IV Ax
Exception: Rifampin which is useful as a synergistic agent for
treatment of meningitis caused by beta-lactam-resistant S.
pneumoniae or coagulase-negative staphylococcus.
ROUTE OF Ax
58
60. Inpatient Ax for 6 days and absence of fever for at least 48 h
No significant neurologic dysfunction, focal findings, or seizure
Clinical stability or improving condition
Ability to take fluids by mouth
Access to home health nursing for Ax administration
Daily availability of a physician
Patient and/or family compliance with the program
Confirmed viral meningitis if appropriate contact and can be
ensured.
OUTPATIENT CRITERIAs
59
61. Dexamethasone inhibits the synthesis of IL-1β and TNF-α,
decreases CSF outflow resistance, and stabilizes the BBB.
It should be given 20 min before or with Ax to inhibit the
production of TNF-α by macrophages and microglia before these
cells are activated by endotoxin.
It doesn’t alter TNF-α production once it has been induced.
It is unlikely to be of significant benefit if started >6 h after Ax.
The results of trials of dexamethasone in meningitis due to H.
influenzae, S.pneumoniae, and N. meningitidis have demonstrated
its efficacy in decreasing inflammation and neurologic sequelae
such as the incidence of sensorineural hearing loss.
ADJUNCTIVE THERAPY
60
62. The benefits were most striking in pneumococcal meningitis.
Dexamethasone10 mg IV qid for 4 days
It should be continued for 4 days if the Gram stain reveals S.
pneumoniae or if the CSF or blood culture grows S. pneumonia
There is no proven benefit from dexamethasone in meningitis due to
other pathogens, mostly meningococcus.
Dexamethasone decreases the penetration of vancomycin into CSF.
As a result, give 45–60 mg/kg per day or administeer by the
intraventricular route.
61
63. The efficacy of dexamethasone in preventing neurologic sequelae is
different between high- and low-income countries.
Three large randomized trials in low-income countries (sub-Saharan
Africa, Southeast Asia) failed to show the benefit.
The lack of efficacy in these trials may be due to late presentation,
antibiotic pretreatment, malnutrition, infection with HIV, and
treatment of patients with not proven meningitis.
The results of these trials suggest that patients in low-income
countries with negative CSF Gram’s stain and culture should not be
treated with dexamethasone.
62
64. Some experts administer dexamethasone if the patient had
moderate-to-severe disease (GCS <11).
Dexamethasone should not be given to patients who have already
received Ax, in this circumstance it is unlikely to improve outcome.
Problems with dexamethasone:
hippocampal cell injury and reduced learning capacity.
(experimental models)
Decreased absorption of Vancomycin.
65. Indications to do repeated LP:
When no improvement by 48 hours after Ax.
Persistent fever for more than eight days without another
explanation.
Two to three days after the initiation of Ax in meningitis due to
resistant organisms to standard agents (eg, penicillin-resistant
pneumococcal infection), and for infection caused by a gram-
negative bacillus.
S. pneumonia infection, Coagulase –ve staph.
FOLLOW UP
64
66. Careful management of fluid and electrolyte is important, since
both over- and under-hydration can cause adverse outcomes.
Thus, there is evidence that the use of maintenance fluids is
preferred to restricted fluid intake in the first 48 hours in settings
with high mortality rates and where patients present late.
65
67. Surgery may be required to drain an accompanying brain abscess or
parameningeal focus of infection.
Decompressive craniectomy is not used in meningitis because the
cerebral involvement is diffuse rather than focal.
SURGICAL THERAPY
66
68. Treatment of viral meningitis.
Most cases of viral meningitis resolve spontaneously.
The headache may persist for months and can be managed with
amitriptyline and nonsteroidal anti-inflammatory agents.
Acyclovir is efficacious in treating HSV meningitis, and
prophylactic therapy with acyclovir, valacyclovir, or famciclovir is
efficacious in preventing recurrent meningitis due to HSV-2.
67
70. IMMIDIATE Vs DELAYED
immediate
coma Loss
of
airway
reflexe
s
seizure
s
Cerebral
edema
Vasomotor
collapse
DIC
Respirator
y arrest
Dehydratio
n
Pericardial
effusion
death
71. Mild to moderate increase in ICP typically cause headache,
confusion, irritability, nausea, and vomiting.
More severe increases can produce:
Altered mental status
Bradycardia with hypertension (the Cushing reflex)
Papilledema, sometimes with loss of vision, which has been
described in 4 to 9 percent of adults
Cranial nerve palsy, particularly involving the abducens nerve
Change in pupil (constricts….then dilates)
Herniation of the cerebellar tonsils leading to death
ICP
70
72. Raised ICP in patients with meningitis is primarily due to cerebral
edema, which can be caused by vasogenic, cytotoxic, or interstitial
mechanisms.
Vasogenic edema results from increased permeability of the BBB.
Cytotoxic factors released from neutrophils and bacteria can
directly produce cerebral edema.
The inflammation can impede the absorption of CSF from the
subarachnoid space via the arachnoid villi.
71
73. MGT OF ICP
Elevate of the head of the bed to 30-45 degrees.
Hyperventilation to a PCO2 of 27 - 30 mm Hg will cause
intracranial vasoconstriction and may reduce ICP.
This usually requires intubation and paralysis, and in some cases
the patient will already be hyperventilating to that level.
Osmotic diuresis: mannitol 1gm/kg loading dose then 0.25-
0.5gm/kg every 4-6 hours
72
75. Occurs in 15 to 30 percent
Early-onset seizures are more common in alcoholic patients.
Seizures can be generalized or focal.
Seizure is often a poor prognostic sign in adults.
The pathogenesis of seizures in meningitis is not well understood.
Bacterial toxins or secondary neurochemical changes are
presumably the cause of most seizures.
In one study, the occurrence of seizures correlated with colony
counts of >10 colony-forming units in the CSF prior to treatment.
SEIZURE
74
76. In 20 to 50 percent of cases
Onset is usually within the first 24 hours
The rate is higher with pneumococcal meningitis
The deficits include:
Cranial nerve palsy
Monoparesis or Hemiparesis
Gaze preference
Visual field defects
Aphasia, and ataxia
Most focal deficits resolve with successful treatment of the
meningitis, but long-term disability can occur.
FOCAL N.DEFICIT
75
77. Cranial Nerve palsy
Due to compression from brain swelling or from perineuritis due to
the adjacent meningeal inflammatory reaction
The abducens nerve is the most commonly affected in meningitis,
probably because its long intracranial segment adjacent to the
brainstem is highly vulnerable to the elevated ICP and
inflammatory reaction
Cranial nerves III, IV and VII also can be impaired.
Bacterial meningitis can induce arachnoiditis around the optic
nerve, which can lead to transient or permanent visual loss.
Optic atrophy that results in irreversible total blindness is a rare
complication of severe meningitis.
76
78. Hemiparesis
4 to 13 percent
Due to cortical vein or sagittal vein thrombosis, cerebral artery
spasm, subdural hematoma, hydrocephalus, a cerebral infarct or
abscess, and cerebral edema.
77
79. Cerebrovascular Complications
Thrombosis, vasculitis, acute cerebral hemorrhage, and aneurysm
formation of large, medium or small cerebral vessels are potential
complications of bacterial meningitis.
CT can reveal the following abnormal findings:
Vessel wall irregularities and focal dilatations
Arterial occlusions
Focal arterial bleeding
Thrombosis of the superior sagittal and cortical veins
78
80. Due to thrombocytopenia & hypofibrogenemia
Especially with meningococcal meningitis.
Thrombosis may produce peripheral gangrene
(combination of endotoxemia and severe hypotension initiates the
coagulation cascade resulting in thrombosis )
DIC
79
81. Sensorineural Hearing Loss
May be transient or permanent
Transient hearing loss: is usually 2ry to a conductive disturbance,
Permanent hearing loss: can result from damage to the 8th cranial
nerve, cochlea, or labyrinth induced by direct bacterial invasion
and/or the inflammatory response.
Studies in adults have shown hearing loss in 12- 14 %, with a
higher rate in pneumococcal meningitis.
80
82. Intellectual Impairment
In 32% of patients
Dexamethasone does not appear to alter the incidence of cognitive
impairment.
81
83. A number of other rare cerebrovascular complications have been
described including hemorrhagic stroke and thrombotic infarction
and/or subarachnoid hemorrhage into the brainstem.
Hemorrhagic strokes presumably occur when the inflammatory
reaction in the subarachnoid space produces either vessel erosion or
aneurysm formation.
82
84. Unusual Complications
Extraaxial fluid collections that are infected (subdural empyemas)
or sterile (subdural effusions or hygromas).
Drainage is mandatory if subdural empyema develops.
Spinal cord complications such as transverse myelitis or infarction,
presumably as a direct result of local vascular changes with
secondary cord ischemia.
Brain abscesses and focal cerebritis
Severe permanent hydrocephalus.
83
85. Ventriculitis
Hyponatremia may be caused by cerebral salt wasting, the SIADH,
or IV fluids
Waterhouse- Friedrichson Syndrome
Hemorrhagic adrenalitis
Is defined as adrenal gland failure due to bleeding into the
adrenal glands caused by severe bacterial or rarely viral infection
most commonly meningococcus
84
86. Mortality is 3–7% for H. influenzae, N. meningitidis, or group B
streptococci; 15% for L. monocytogenes; and 20% for S.
pneumoniae.
In general, the risk of death increases with (poor prog.):
Decreased level of consciousness on admission,
Signs of increased ICP,
Onset of seizures within 24 h of admission,
Age >50,
Delay in the initiation of treatment.
Comorbid conditions including shock and/or the need for MV,
PROGNOSIS
85
87. CSF glucose <40 mg/dl and markedly increased protein > 300
mg/dL have been predictive of increased mortality and poorer
outcomes in some series.
Moderate or severe sequelae occur in ~25% of survivors, although
the exact incidence varies with the infecting organism.
Common sequelae include decreased intellectual function, memory
impairment, seizures, hearing loss, and gait disturbances.
86
88. The pneumococcal polysaccharide vaccine is recommended for age
>65, those with asplenia, and those with increased risk for
pneumococcal disease due to chronic illness.
Most adults have protective antibody levels for 5 years, but
antibody concentrations should be monitored in patients with
recurrent bacterial meningitis
The index case and all close contacts of Neisseria should receive
chemoprophylaxis, rifampin 600 mg PO bid for 2 days.
Rifampin is not recommended in pregnant.
Alternatively, one dose of azithromycin (500 mg) or one IM dose of
ceftriaxone (250 mg) can be given.
PREVENTION
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