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Meningitis

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haneen khalil

on 26 October 2015

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Transcript of Meningitis

Meningitis
CSF Analysis
PathoPhysiology
Approach
Acute Viral Meningitis
Acute Bacterial Meningitis
Bacterial meningitis is an acute purulent infection within the sub-arachnoid space. It is associated with a CNS inflammatory reaction that may result in decreased consciousness, seizures, raised intracranial pressure (ICP), and stroke. The meninges, the subarachnoid space, and the brain parenchyma are all frequently involved in the inflammatory reaction (meningoencephalitis).


DD
-Viral meningoencephalitis (HSV)
-Rickettsial disease
-Focal suppurative CNS infections : empyema and brain abscess
-noninfectious CNS disorders:
Subarachnoid hemorrhage
chemical meningitis due to rupture of tumor contents into the CSF (e.g., from a cystic glioma or craniopharyngioma epidermoid or dermoid cyst)
drug-induced hypersensitivity meningitis; carcinomatous or lymphomatous meningitis;
- meningitis associated with inflammatory disorders such as: sarcoid, systemic lupus erythematosus (SLE), and Behçet's syndrome; pituitary apoplexy.
-subacutely evolving meningitis : include Mycobacterium tuberculosis , Cryptococcus neoformans , Histoplasma capsulatum , Coccidioides immitis, and Treponema pallidum .



(2)
decreased
glucose concentration and/or CSF/serum glucose ratio
(3)
increased
protein concentration
(4)
increased
opening pressure
* CSF bacterial cultures

are
positive
in
>80%
of patients.
* CSF Gram's stain
demonstrates organisms in
>60%.
Meningitis
Inflammation of the meninges, Meningitis can be caused by various infectious agents, including viruses, fungi, and protozoans, but bacteria produce the most life-threatening forms.
Meninges
Investigations for Bacterial Meningitis
* The CSF analysis:
(1)
(PMN) leukocytosis
Aseptic Meningitis
or sterile meningitis, is a condition in which the layers lining the brain, meninges, become inflamed and a pyogenic bacterial source is not to blame.
Viral Meningitis
Drug-induced aseptic meningitis
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Antimicrobials (e.g., trimethoprim-sulfamethoxazole, amoxicillin, isoniazid)
Muromonab-CD3 (Orthoclone OKT3)
Azathioprine
Intravenous immunoglobulin
Intrathecal methotrexate
Intrathecal cystine arabinoside
Vaccines
Allopurinol
Neoplastic meningitis
Neoplastic or malignant meningitis, also called meningitis carcinomatosa and leptomeningeal carcinomatosis, is the development of meningitis due to infiltration of the subarachnoid space by cancerous cells. Malignant cells come from primary cancer such as breast cancer or from a primary brain tumor like medulloblastoma. Neoplastic Meningitis (NM) was first reported in the 1870s with the most common cause being breast cancer, lung cancer, and malignant melanoma.
Fungal causes are as follows:

Cryptococcus neoformans
Histoplasma capsulatum
Coccidioides immitis
Blastomyces dermatitides
Parasites
Parasites that can cause aseptic meningitis are as follows:

Toxoplasma gondii
Taenia solium (cysticercosis)
Viral meningitis is not a nationally reportable disease; however, it has been estimated that
the incidence is
75,000 cases per year.
In temperate climates, there is an increase in cases during the summer and early fall months, reflecting the
seasonal
predominance of
enterovirus
and
arthropod-borne virus (arbovirus)
infections, with a peak monthly incidence of about
1
reported case per 100,000 population

Epidemiology
Less Common
Varicella zoster virus

Epstein-Barr virus

Lymphocytic choriomeningitis virus
most common viruses :
Enteroviruses (coxsackieviruses, echoviruses, and human enteroviruses 68–71)
Herpes simplex virus 2
Arthropod-borne viruses
HIV
CMV
Etiology
Enteroviruses - coxsackievirus, echovirus, poliovirus
Herpes simplex virus (HSV) types 1 and 2 (HSV-1, HSV-2)
Varicella-zoster virus
Arboviruses
Epstein-Barr virus
HIV
Influenza virus types A and B
Mumps virus
Coloradotick fever virus
Lymphocytic choriomeningitis virus (LCMV)
Rabies
Partially treated bacterial meningitis
Parameningeal infection
Endocarditis
Mycoplasma pneumoniae
Mycobacterium tuberculosis
Ehrlichiosis - monocytic, granulocytic
Borrelia burgdorferi
Treponema pallidum
Brucella species

Sarcoidosis
Leptomeningeal cancer
Posttransplantation lymphoproliferative disorder
Systemic lupus erythematosus
Wegener granulomatosis
CNS vasculitis
Behçet disease
Vogt-Koyanagi-Harada syndrome
Clinical Manifestations

Headache (frontal , retrofrontal)
Photophopia
Pain on moving the eyes
Fever,
Signs of meningeal irritation
Lethargy or drowsiness;mild
Nuchal rigidity which may be mild and
present only near the limit of neck anteflexion.
Constitutional signs can include:
malaise, myalgia, anorexia, nausea and
vomiting, abdominal pain, and/or diarrhea.
Acute, diffuse, inflammatory process affecting brain parenchyma
Most commonly viral
Acute flu-like prodrome
High fever, severe headache, N&V (with chronic low grade)
Altered consciousness (lethargic, drowsy, confused, coma)
(Seizures)
(Focal neurological signs)
Speech disturbances (dysphasia, aphasia)
Behavioural changes
Subacute and chronic presentations can be caused by CMV, VZV, HSV (immuno-compromised)
Any adult with seizure + fever or seizure from which they do not recover must be investigated for possible CNS infection


The signs and symptoms reflect the sites of infection and inflammation
Clinical Presentation
*N. meningitidis is the causative organism of
recurring epidemics of meningitis every 8 to 12 years.
*Staphylococcus occurs in those with recent neurosurgery.
*Bacterial meningitis is the most common form of suppurative CNS infection,
with an annual incidence in the United States of >2.5 cases/100,000 population. *The organisms most often responsible for community-acquired bacterial meningitis are :
Streptococcus pneumoniae (50%),
Neisseria meningitidis (25%),
group B streptococci (15%),
Listeria monocytogenes (10%).
Haemophilus influenzae type b accounts for <10% of cases .
Epidemiology
Treatment
Headache , fever, +- Nuchal regidity
Altered Mental State
Meningitis
Meningiencephalitis, Encepahopathy, Mass lesion.
Dexamethasone
Third-Fourth-Generation Cephalosporin
Vancomycin
Acyclovir
Doxycycline
ceftriaxone, cefotaxime, or cefepime
as HSV encephalitis is the leading disease in the D.D
during tick season to treat tick-borne bacterial infections
coverage for susceptible S. pneumoniae, group B streptococci, and H. influenzae and adequate coverage for N. meningitidis
against S. pneumoniae and N. meningitidis and greater activity against Enterobacter species and Pseudomonas aeruginosa, penicillin-sensitive pneumococcal and meningococcal meningitis .
Ampicillin
should be added to the empirical regimen for coverage of L. monocytogenes in individuals <3 months of age, those >55, or those with suspected impaired cell-mediated immunity because of chronic illness, organ transplantation, pregnancy, malignancy, or immunosuppressive therapy
penicillin-resistant pneumococci,
When ?
immediately after the performance of the lumbar puncture or, if a computed tomography (CT) scan is to be performed before LP, immediately after blood cultures are obtained
should be given shortly before or at the same time as the first dose of antibiotics, when indicated.
Adults in developed world in whom the organism is unknown or Streptococcus pneumoniae is confirmed, administration of dexamethasone is recommended . Dexamethasone should be continued if the CSF Gram stain and/or the CSF or blood cultures reveal S. pneumoniae.
What ?
How ?
No known immunodeficiency
Ceftriaxone
2g IV Q 12 hrs
Cefotaxime
2g IV Q4-6 hrs
Vancomycin
15-20 mg/kg Q 8-10 hrs
Ampicillin
2 g IV Q 4 hrs
If age > 50 yrs
Impaired immunity
Vancomycin
15-20 mg/kg Q 8-12 hrs
Ampicillin
2 g IV Q 4 hrs
Cefepime
2 g IV Q 8 hrs
Meropenem
2 g IV Q 8 hrs
Allergy to beta-lactams
Vancomycin
15-20 mg/kg Q 8-12 hrs
Moxifloxacin
400 mg IV once/day
Trimethoprim-Sulfamethoxazole
5mg/kg IV Q 6-12 hs
to cover Listeria in pt>50 yrs or with immunodefficincy
Empiric antimicrobial therapy
Supportive care
Therapy for Specific Pathogens
Empiric treatment
Regimes based upon Gram Stain
If
gram-positive cocci
are seen on the Gram stain of a patient with community-acquired meningitis,
S. pneumoniae

should be the suspected pathogen.

Vancomycin

plus a

third-generation cephalosporin.
If
gram-negative cocci
are seen,
N. meningitidis
is the probable pathogen.
If

gram-positive bacilli

suggest
L. monocytogenes
.
If
gram-negative bacilli
usually represent
Enterobacteriaceae

(eg, Klebsiella spp, Escherichia coli) in cases of community-acquired meningitis.
If there is a history of neurosurgery or head trauma within the past month or if a neurosurgical device is present,
ceftazidime, cefepime, or meropenem
since such patients are at greater risk for
P. aeruginosa
and
Acinetobacter spp
infection
((given issues of cephalosporin resistance with Acinetobacter spp, meropenem would be a more appropriate empiric choice when infection caused by this organism is suspected . If the Acinetobacter isolate is later found to be resistant to carbapenems, intravenous colistin or polymyxin B should be substituted for meropenem and should also be administered by the intraventricular or intrathecal route)).
Fluid management
Reduction of intracranial pressure
Induced hypothermia
REPEAT CSF ANALYSIS
no evidence of improvement by 48 hours after the initiation of appropriate therapy
Two to three days after the initiation of therapy of meningitis
Persistent fever for more than eight days without another explanation.
Investigations for Meningitis
*CSF Examination
*Polymerase Chain Reaction Amplification of Viral Nucleic Acid
*Viral Culture
*CBC
*LFT
*KFT
*ESR
*C-reactive protein, *Electrolytes, *Glucose, *Creatine kinase, *Amylase, and *Lipase
The typical profile is:
A lymphocytic pleocytosis
A normal or elevated protein
A normal glucose concentration,
Organisms are not seen on Gram's stain of CSF
wnv
mumps
Mumps
LCMV
is the diagnostic procedure of choice:

It is more sensitive than viral cultures
In patients with recurrent episodes of "aseptic" meningitis
Despite negative viral cultures
CNS viral infections caused by cytomegalovirus (CMV) Epstein-Barr virus (EBV), VZV, and human herpesvirus 6 (HHV-6)
useful in the diagnosis of CNS infection caused by Mycoplasma pneumoniae, which can mimic viral meningitis and encephalitis.
PCR
Treatment of Viral Meningitis
* Symptomatic ttt , Analgesics,Antipyretics , Antiemetics, Fluid & Electrolyte monitoring.
* Hspitalization for : Immunucompromized , alteration in consciousness,seizures, focal signs, atypical CSF pfile.
* Acyclovir with HSV ,EBV ,VZV (Oral /IV according the severity of illness ).
{ Acyclovir , famicyclovir, valacyclovir }
Normal CSF
Appearance:
Clear
Opening pressure:
10-20
cm

H 2 O
WBC count:
0-5
cells/µL (
< 2
polymorphonucleocytes [PMN]);
normal cell counts do not rule out meningitis or any other pathology
RBC count :
0
cells/ µL
Glucose level:
>60%
of serum glucose
Protein level:
< 45
mg/dL
D.D High WBCs
Bacterial meningitis (PMN)
Aseptic (viral) meningitis (lymph)
Protein
Infections
Intracranial Hge
Multiple sclerosis
Guillain Barré syndrome
Malignancies
Some endocrine abnormalities
Certain medication use
Inflammatory conditions
In presence of RBCs in a traumatic tap situation falsly elevation.
Glucose
CSF glucose is about 2/3 of the serum glucose
Presence of
RBCs

A sign of bleeding. ((Xanthochromia in SAH )
Due to traumatic tap (blood leaked into the fluid sample during collection)
may in :
Fungal meningitis (lymph)
Tuberculosis (early PMN then lymph)
Multiple sclerosis (early PMN then lymph)
Guillain Barré syndrome
Parazitic infection (eosinophils)
Repeated lumbar puncture
Chronic leak
Children between the ages 6m-2y in acute water intoxication
Idiopathic intracranial hypertension
CSF protein levels do not fall
in hypoproteinemia
Chemical meningitis
Inflammatory conditions as TB
Subarachnoid hge
Hypoglycemia
Elevated levels of blood glucose
*Depends on the virus
direct viral destruction of cells
Para or post-infectious inflammatory or immune-mediated response
*Most viruses primarily infect brain parenchyma and neuronal cells
*Some cause a vasculitis
*Demyelination may follow infection
Pathophysiology
Sporadic causes (not geographically restricted)
Herpes viruses
HSV-1, HSV-2, VZV, CMV, EBV, HHV6, HHV7
Enteroviruses
Coxsackie, echoviruses, enteroviruses 70/71, parechovirus, poliovirus
Paramyxoviruses
Measles, mumps
Others (rarer causes)
Influenza viruses, Adenovirus, parvovirus, lymphocytic choriomeningitis virus, rubella virus, rabies
Geographically restricted causes
Arboviruses — Japanese B, St Louis, West Nile, Eastern equine, Western equine, Venezuelan equine, tick borne encephalitis viruses
Bunyaviruses — La Crosse strain of California virus
Reoviruses — Colorado tick fever virus
Causes :
TB ENCEPHALITIS
Acute Viral Encephalitis
MANAGEMENT
Skin rashes, bites, injection sites
Examine chest, abdo, ears, genitals, urine for infection
Meningism, subtle motor seizures, focal neuro signs
NB ‘cold sores’ not diagnostic!
By Examination
INVESTIGATION
CSF analysis
WBC count: 50-500 cells/µL (early PMN then lymph)
Glucose level: Low
Protein level: Elevated
sensitivity and specificity of CSF-ADS for TBM diagnosis were 78% and 98% respectively
ADA estimation in CSF is simple, inexpensive, rapid and fairly specific method for making a diagnosis of tuberculous etiology in TBM
Moreover, the best cutoff point for differentiating between TBM and non-TBM was 9.5 U/L. In addition, CSF ADA activity was decreased in patients with TBM after antitubercular therapy in a time-dependent manner.
headache, stiff neck, fatigue, night sweats, and fever
In adults with suspected bacterial meningitis without the described risk factors, performing immediate spinal tap and blood culture is likely the best management. In the presence of baseline risk factors, management should be:
(1) blood culture (which may be positive even when spinal cultures are negative,
(2) intravenous antibiotics, then
(3) CT scan, followed by spinal tap unless the CT scan indicates increased risk for cerebral herniation.
Indications for performing brain CT scanning before lumbar puncture in patients with suspected meningitis include the following :

Patients who are older than 60 years
Patients who are immunocompromised
Patients with known CNS lesions
Patients who have had a seizure within 1 week of presentation
Patients with an abnormal level of consciousness
Patients with focal findings on neurologic examination
Patients with papilledema seen on physical examination, with clinical suspicion of an elevated ICP
Absolute contraindications for lumbar puncture:
the presence of infected skin over the needle entry site
the presence of unequal pressures between the supratentorial and infratentorial compartments.
Relative contraindications for lumbar puncture include the following:

Increased intracranial pressure (ICP)
Coagulopathy
Brain abscess
Cranial CT scanning should
be / not be ???
obtained before lumbar puncture in awake and alert SAH patients with a normal neurologic examination.
LP & CT
Papilledema &\or focal neurological deficit
immunocompromized ?
hx of recent head trauma?
known cancer? sinusitis?
Blood culture &
start empirical antimicrobial therapy
Head CT or MRI
Mass lesion
Abscess or Tumor
Appropriate medical/
surgical intervention
No Mass Lesion
White matter abnormalities
Focal on Generalize
Gray matter abnormalities or normal
Encephalitis
ADEM
Immediate Blood culture & Lumber Puncture
Pleocytosis with PMNs
Elevated Protein
Decreased Glucose
Gram's stain Positive
Bacterial Process
Pleocytosis with MNCs
Normal /elevated Protein
Normal / decreased Glucose
Gram's stain Negative
Viral : CSF PCR
CSF IgM for WNV
VIRAL CULTURE
SEROLOGY

Fungal :CSF cryptococcal Ag, fungal cultures
Bacterial: culture, PCR
Mycobacterial:CSF AFB stain,TB PCR ,culture, CXR.
Fungal
Systemic diseases
Bacterial causes:
Haematological and biochemical blood screen
Serology, blood cultures, HIV
Drug screen, urine analysis
CXR
CT head, MRI brain
EEG
LP (CSF ANALYSIS , CULTURE )
CSF PCR sensitivity(96%)and specificity(99%)ON HSV-1
((brain biopsy))used to be gold standard for diagnosis of HSV-1 encephalitis before PCR . May still have a role in undiagnosed pt who is deteriorating.
Adenosine Deaminase
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