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MENINGITIS

 By Dr Bashir Ahmed Dar


 Associate Professor Medicine
 Chinkipora Sopore Kashmir
 Email- drbashir123@gmail.com
What is meningitis?

 Meningitis is an infection of the pia-arachanoid and the CSF


fluid that surrounds the brain. Meningitis is usually caused by an
infection with a virus, with a bacterium or even with fungi.
How is Meningitis Caused
 Colonization of nasopharynx by bacteria or
viruses
 Is an important way of spreading meningitis
by way of cribriform fossa or viremia or
bacteriaemia and can spread to others by
coughing etc.
How is Meningitis Caused
 contagious, spread via tiny drops of fluid
from the throat and nose of someone who is
infected. The drops may become airborne
when the person coughs, laughs, talks, or
sneezes. They then can infect others when
people breathe them in or touch the drops
and then touch their own noses or mouths.
How is Meningitis Caused
 Sharing food, drinking glasses, eating
utensils, tissues, or towels .
How is Meningitis Caused
 spread between people who are in close contact,
such as those who live together or people who are
exposed by kissing

 N. meningitidis cause epidemics of meningitis. In


particular in a crowded day-care situation or a
military recruit in a crowded training
camp,schools,colleges has fallen ill with
meningococcal meningitis
How is Meningitis Caused
 Meningococcus is the bacteria that has
caused outbreaks across North America
over the last 8 - 10 years including most
recently. Understandably the presence of a
meningitis epidemic in a community is very
scary to parents
How is Meningitis Caused
 Most of the viruses that cause meningitis
live in the intestines and tend to be passed
on as a result of poor hygiene. Many
different viruses can cause viral meningitis,
most commonly enteroviruses that normally
live harmlessly in people's bowels
How is Meningitis Caused
 L. monocytogenes has been associated with such
foods as raw milk, pasteurized fluid milk,cheeses
(particularly soft-ripened varieties), ice cream, raw
vegetables, fermented raw-meat sausages, raw and
cooked poultry, raw meats (of all types), and raw
and smoked fish. Its ability to grow at
temperatures as low as 0°C permits multiplication
in refrigerated foods. In refrigeration temperature
such as 4°C the amount of ferric iron promotes the
growth of L. monocytogenes.
How is Meningitis Caused
 through a person's stool, and someone who
comes in contact with the stool — such as a
child in day care .
How is Meningitis Caused
 Hematogenous
 Many of the bacteria and viruses that cause
meningitis are fairly common and are typically
associated with other routine illnesses.
 infection of the skin, urinary system,
gastrointestinal or respiratory tract can spread by
the bloodstream
How is Meningitis Caused
 A person may have another type of
infection (of the lungs, throat, or tissues of
the heart) caused by an organism that can
also cause meningitis
How is Meningitis Caused
 Direct infection
 skull fractures possess abnormal openings to the
sinuses, nasal passages, and middle ears.
Organisms can pass through openings and cause
infection. surgical procedures or who have had
foreign bodies surgically placed within their skulls
(such as tubes to drain abnormal amounts of
accumulated CSF) have an increased risk of
meningitis.
How is Meningitis Caused
 otitis media
 mastoiditis
 Osteomyelitic foci in the skull
 sinusitis
 Penetrating cranial injuries
 Brain or spine surgery
 Ventriculoperitoneal shun
 lumbar puncture.
How is Meningitis Caused
 skull fractures
 Extradural abscess
 Subdural empyaema
 Spinal epidural abscess.
 Pachymeningitis
How is Meningitis Caused
 Neurotropic
 also via an uncommon but interesting method
called intraneural spread. This involves an
organism invading the body at a considerable
distance away from the head, spreading along a
nerve, and using that nerve as a kind of ladder into
the skull, where the organism can multiply and
cause meningitis. Herpes simplex virus is known
to use this type of spread, as is the rabies virus.
 Rabies
 HSV
How is Meningitis Caused
 RISKS
 Asplenia
 drugs that suppress immune system
 Immunocompromised
 HIV, malignancy
 malignancy
 alcholism
How is Meningitis Caused
 Patients with cardiac and pulmonary anomalies
may spread septic foci,bronchiectasis,
occasionally pneumonia). Common with
pulmonary AV fistulae and R to L cardiac defect
 T-cell defects (HIV)
 Neural tube defects- Staph aureus, enteric
organisms
 Terminal compliment deficiency- Neisseria
 septic foci from thrombophibitis
 iv drug abusers
How is Meningitis Caused
 Immune-compromised Patients are also
prone for fungal infections and the fungal
infections that can result in meningitis are
 Aspergillus
 Candida
 Mucor
 Protozoal,Ameba infections,Toxoplasma
Organisms Causing Meningitis
 Bacterial
 Viral
 Fungal
 Ricketsial
 Parasitic/Protozoal
Organisms Causing Meningitis
 Purulent bacterial meningitis
 etiology
 newborns Group B Strep ,E. coli
 children - H. influenzae , Str. pneumoniae
 HIB vaccine has reduced incidence of H influnza
infection
 adults - meningococccal (small epidemies - army,
holiday camps,school going
students),pneumococcal
Organisms Causing Meningitis
 Streptococcus agalactiae (also known as Group B
streptococcus) is a beta-hemolytic gram-positive
streptococcus.
 S. agalactiae is a species of the normal flora of the
female urogenital tract and rectum. Its chief
clinical importance is that it can be transferred to a
neonate passing through the birth canal and can
cause serious group B streptococcal infection.
Organisms Causing Meningitis
 In the western world, S. agalactiae is a
major cause of bacterial septicemia of the
newborn, which can lead to death or long-
term sequelae such as hearing loss. S.
agalactiae can also cause neonatal
meningitis, which does not present with the
hallmark sign of adult meningitis, a stiff
neck
Organisms Causing Meningitis
 rather, it presents with nonspecific
symptoms such as fever, vomiting and
irritability and can consequently go
undiagnosed until it is too late. Somewhat
more rarely, S. agalactiae can also cause
invasive group B streptococcal disease of
the adult in the pregnant, elderly, or
immunosuppressed.
Organisms Causing Meningitis
 Viral
 HSV especially in infants
 Enterovirus (coxsackie, echovirus)
 HIV
 Lymphocytic choriomeningitis virus
 Arbovirus
 Mumps
 CMV
 EBV
 VZV
 Adenovirus
 Measles
Organisms Causing Meningitis
 Rubella
 Rotavirus

 Influenza and parainfluenza


Organisms Causing Meningitis
 Fungal
 Cryptococcus

 Coccidiodes

 Histoplasmosis

 Mucormycosis

 Aspergilosis

 Candidasis

 With a particular prone settings etc


Organisms Causing Meningitis
 Parasitic/protozoal
 Angiostrongylus

 Toxoplamosis

 Hydatid

 Amoeba

 Malaria

 Cysticercosis
Organisms Causing Meningitis
 Rickettsial
 Rocky mountain spotted fever
Organisms Causing Meningitis
Others
 Tuberculosis
 Borrelia burgdorferi

 Treponema pallidum

 Mycoplasma pneumoniae

 brucella

 Chlamydia
Organisms Causing Meningitis
 viral meningitis
 fairly common disease but rarely fatal
 lymphocytic predominance ie mononuclear
cells (but may see neutrophils if CSF
sampled early in course - up to 48hrs
 glucose not reduced
Organisms Causing Meningitis
 may follow Temporary, flu-like symptoms with
running nose sneezing etc., headache, low grade
fever and stiff neck.
 Goes away on its own usually within three to 10
days
 Bed rest, paracetamol
 Enteroviruses, the most common type of viral
meningitis
 Strict isolation is not necessary
Organisms Causing Meningitis
 Since most cases are due to enteroviruses
that may be passed in the stool, people
diagnosed with viral meningitis should be
instructed to thoroughly wash their hands
after using the toilet.
Organisms Causing Meningitis
 The incidence of viral meningitis drops with age.
 Neonates are at greatest risk and have the most
significant risk of morbidity and mortality.

 The incidence during the first year of life is 20


times higher than in older children and adults.
Organisms Causing Meningitis
 CRP much more elevated in bacterial than
in viral meningitis (ie, 50-150 in bacterial
meningitis group vs <20 in viral meningitis
group).

 Treatment for viral meningitis is mostly


supportive.
Neisseria meningitidis
Hemophilus influenza Strep pneumoniae
(H flu)
CSF-Gram stain:

 Low
power
view
showing
many
neutrophi
ls.
CSF-Gram stain:

 High
power
shows
clusters of
bacteria.

 Neutrophil
s
CSF-Gram stain:

 High
power
shows
clusters of
bacteria.

 Neutrophil
CSF-Gram stain:

 High
power
shows
clusters of
bacteria.

 Neutrophil
CSF-Gram stain:

Observe
Paired
rounded
bacteria –
(diplococci)
staining
pink (gram
negative)
Pathogenesis of Meningitis
 The virus or bacteria replicates in the initial
organ system (ie, respiratory or
gastrointestinal mucosa) and gains access to
the bloodstream. Primary viremia or
bacteremia introduces the virus or bacteria
to the reticuloendothelial organs (liver,
spleen, and lymph nodes.)
Pathogenesis of Meningitis
 If the replication persists despite
immunologic defenses, secondary
bacteremia or viremia occurs, which is
thought to be responsible for seeding of the
CNS. Rapid viral replication likely plays a
major role in overcoming the host defenses.
Pathogenesis of Meningitis
 There occurs local immune response to
bacteria or virus
 Increased vascular permeability
 oozing of fluid exudate,inflammatory cells
 Neutrophils migrate from capillaries and
release toxins
 TNF-a and IL-B1 produced by activated
macrophages and endothelial cells
Pathogenesis of Meningitis
 Ensuing inflammatory response increases
blood-brain permeability
 Cerebral edema
 Increased ICP
Pathogenesis of Meningitis
 cellular damage and loss of cellular homeostasis
and worsen cerebral edema
 damage to vessels lead to vasculitis and bleed or
thrombose leading to infaraction or haemorrahage

 exudate formation etc can obstruct CSF flow and


lead to hydrocephalous
 ICP lead to herniation
Pathogenesis of Meningitis
 exudative pus of dead cells ,fluid,fibrin and
leucocytes (pus) cause thick whitish grey layer
that covers the leptomeninges over the surface of
brain and filling sulci and basal cisterns with
swollen edematous brain.

 damage to neurons can take place if extending to


brain cells resulting in their degeneration.
The white appearance of this calf brain is caused by neutrophils within the
meninges – a condition known as meningitis. This is usually due to a
bacterial infection.
This calf brain shows similar pathology. If a glass slide is pressed to the
surface of the brain and stained it would show high numbers of
neutrophils.
This brain shows irregular red spots which are areas of hemorrhage
Bovine
and necrosis caused by the bacteria, Histophilus somni.
Brain:
meningitis.
Pathogenesis of Meningitis
 if infection becomes localised in brain then can
lead to abcess formation especially in case of
direct infections.
 immune system tries to confine this localised
infection therefore may develop fibrous wall
around it with perivascular chronic inflamatory
cells around it,leading to brain abcess with central
suppuration and liqufication due to death of cells
.healing may occur with fibrous scar.
The Evolution of the Abscess is
as follows
 An area of cerebritis begins, in which
Polymorphonuclear leukocytes are
attracted to the invading bacteria.
 Liquefaction of brain tissue rapidly
ensues, and at the periphery, a thin rim
of granulation tissue composed of new
capillaries and fibroblasts is formed.
Evolution of the Abscess
 With time, a connective tissue capsule
is formed by collagen laid down by
infiltrating fibroblasts. Often this is more
perfectly formed on the outer aspect of
the abscess, presumably due to the
contribution of the reservoir of potential
in the adjacent meninges.
Evolution of the Abscess
 Due to the poor encapsulation of the
medial aspect of an abscess, which
abuts upon or is located within the
cerebral white matter, the infection
tends to form daughter or satellite
abscesses medially which may
eventually rupture into the ventricular
system
Evolution of the Abscess
 Such rupture may lead to rapid death, and in
any event, is usually followed by severe
ventriculitis and massive meningitis as
infected CSF pours into the subarachnoid
space.
 Antibiotic therapy greatly decelerates the
growth of an abscess, and may allow time for
a complete capsule to form after which the
abscess may be removed surgically.
Evolution of the Abscess
Evolution of the Abscess
 The image above shows a large abscess in
the brain. The purulent center is surrounded
by a capsule. Often a zone of hyperemia is
present adjacent to the wall and there is
marked swelling of the adjacent brain tissue
Evolution of the Abscess
Evolution of the Abscess
Evolution of the Abscess
Abscess-Cerebral
Gross:
Abscess-Cerebral
MRI
Meningial enhancement
Meningial
enhancement in a
Bacterial
meningitis - CT
Scan Image
Meningial enhancement
Signs & symptoms of Meningitis
 Acute (<1 day)- common with S.
pneumoniae and N. meningitides
 Subacute (2-3 days)- preceding URI like

symptoms, more common with H. flu and


other pathogens.
Signs & symptoms of Meningitis
 Non-specific complaints
 Fever

 Headache

 Nausea and vomiting

--Nuchal rigidity
 Lethargy

 Irritability

 Restlessness

 Poor feeding

 Back pain

 Altered mental status (seizure, coma)


Signs & symptoms of Meningitis
Febrile
 stiff neck causing may causearched position

Opisthotonos
 Focal neurologic signs

 Petechia/purpura- DIC with N. menigitidis

 Positive Kernig’s and Brudniski’s i.e. ,

Meningismus (stiff neck + Brudzinski +


Kernig signs)
 Shock
 Disseminated intravascular coagulation (DIC)
 Cerebral edema
Kernig’s Sign
 Patient placed supine with hips flexed 90
degrees. Examiner attempts to extend the
leg at the knee
 Positive test elicited when there is
resistance to knee extension, or pain in the
lower back or thigh with knee extension
Signs & symptoms of Meningitis
Brudzinski’s Sign
 Patient placed in supine position and neck is
passively flexed towards the chest
 Positive test is elicited when flexion of neck
causes flexion at knees and/or hips of the
patient
Normal fundus
Increased intracranial pressure
(ICP)
 Papilledema
 Cushing’s triad
 Bradycardia

 Hypertension

 Irregular

respiration
 Severe headache

 herniation

 vomitting
Meningococcemia - Petechiae
Signs & symptoms of Meningitis
 Is due to small skin bleed
 All parts of the body are affeced
 The rashes do not fade under pressure
 Pathogenesis:
 a. Septicemia
 b. wide spread endothelial damage
 c. activation of coagulation
 d. thrombosis and platelets aggregation

Signs & symptoms of Meningitis
 e. reduction of platelets (cosumption )
 f. BLEEDING 1.skin rashes
 2.adrenal hemorrhage
 Arenal hemorrhage is called Waterhouse-
Friderichsen Syndrome.It cause acute
adrenal insufficiency and is uaually fatal
Meningococcemia - Purpura
fulminans
Signs & symptoms of Meningitis
 May also look like bruises,echymosis .
Complications and Outcome of
Meningitis
 Infection can spreading to
 Dura – pachymeningitis
 Leptomeninges - leptomeningitis
 Brain – encephalitis
 Spinal cord – myelitis
 Ventricles - ventriculitis
Complications and Outcome of
Meningitis
 Disseminated intravascular coagulation (DIC)
Cerebral edema

 Adrenal hemorrhage is called Waterhouse-


Friderichsen Syndrome.It cause acute adrenal
insufficiency and is uaually fatal
 septicaemia and infection spreading to other
organs
 motor and neurological deficits
Complications and Outcome of
Meningitis
 Seizures
 SIADH
 Subdural effusions & empyema
 Septic sinus or cortical vein thrombosis
 Arterial ischemia / infarction (inflammatory
vasculitis)
 CNs Palsies (esp deafness)
 Septic shock / multi-organ failure from bacteremia
(esp meningococcus & pneumococcus)
Complications and Outcome of
Meningitis
 risk of adrenal hemorrhage with hypo-
adrenalism (Waterhouse-Friderichsen
syndrome)

 Serum sodium level may be abnormal


because of dehydration or the rare
occurrence of syndrome of inappropriate
antidiuretic hormone secretion (SIADH).
Complications and Outcome of
Meningitis
 Serum amylase level may be elevated in
cases caused by mumps even in the absence
of parotitis.

 Focal infarctions/microinfarcts due to


endarteritis oblitrerans
 Formation of intracranial mass
 Cranial nerve palsies
Increased intracranial pressure
Headache
Vomiting
Decreased Level of
Consciousness
Papilledema
Herniation
TYPES OF HERNIATION
1. Subfalcine
(cingulate)
2. Transtentorial
(uncal)
3. Tonsillar
(foramen
magnum)
4. Extracranial
TRANSTENTORIAL (UNCAL)
HERNIATION
SHIFT OF THE BRAIN FROM THE MIDDLE TO
THE POSTERIOR FOSSA THROUGH THE
TENTORIAL INCISURA
MAY BE UNILATERAL OR “CENTRAL”
SECONDARY EFFECTS INCLUDE:
Compression of the third cranial nerve(s)
Duret hemorrhages in midline rostral brainstem
Compression of the contralateral cerebral
peduncle (Kernohan’s notch)
Compression of the posterior cerebral artery with
infarction of the medial occipital lobe
HYDROCEPHALUS
DILATATION OF THE VENTRICULAR
SYSTEM

NONCOMMUNICATING: Due to obstruction


within the ventricular system, e.g., tumor,
aqueductal stenosis

COMMUNICATING: Due to obstruction of CSF


flow in the subarachnoid space with decreased
reabsorption
Complications and Outcome of
Meningitis
 Consequences of meningitis can be mild,
moderate or severe,
with many survivors being left with permanent
disability
 Septicaemia and shock can lead to skin grafting
and scarring, amputations and in severe cases
neurological deficits
 Meningitis can lead to damage in various areas of
the brain resulting in loss of sight, hearing and
neurodevelopmental deficits
Complications and Outcome of
Meningitis
 Scarring
 amputation of digits and limbs
 Neurological damage
Complications and Outcome of
Meningitis
 Visual impairment and blindness
 Auditory impairment and deafness
 Neuromotor disabilities
 Seizure disorders
 Behaviour problems
 Learning difficulties
Complications and Outcome of
Meningitis
 The complications associated with septic shock
can result in irreversible tissue damage and
gangrene

 Tissue damage occurs as a result of inadequate


tissue perfusion and oxygenation from
hypotension and coagulopathy

 Skin grafting and amputation may be necessary


Complications and Outcome of
Meningitis
 Damage to various areas of the brain as a
consequence of inflammation in the subarachnoid
space

 This appears as exudate covering the surface of


the brain

 Many complications are due to cranial nerve


damage
Complications and Outcome of
Meningitis
 Psychosocial and emotional problems - low
self esteem and difficulties coping

 Subtle complications - poor concentration,


clumsiness and mood swings

 May be age-specific
Complications and Outcome of
Meningitis
 Tiredness
 Recurring headaches
 Memory loss, which may be severe
 Difficulties in concentration
 Anger outbursts
 Clumsiness
Differential Diagnosis of
Meningitis
 Brain abscess
 Encephalitis
 Tumor like
ASTROCYTOMAS,OLIGODENDROGLIOMAS
,EPENDYMOMAS
 MIXED GLIOMAS
 Metastatic tumor
 Subdural and epidural empyema
 subdural
 subarachnoid
Differential Diagnosis of
Meningitis
 Chemical meningitis: Rupture of tumor
 intracranial haemorrage like
 Epidural
 subdural
 Subarachnoid
 intraparenchymal
Differential Diagnosis of
Meningitis
 metabolic encephalopathy
 hyperglycaemic coma
 uremia
 hepatic encephalopathy
 vit B deficiencies
 vascular diseases (amyloid angiopathy,
vasculitis, berry aneurysms, A-V
malformations
CSF & LUMBER PUNCTURE
 It is produced in the brain by modified ependymal
cells in the choroid plexus (approx. 50-70%), and
the remainder is formed around blood vessels and
along ventricular walls. It circulates from the
choroid plexus through the interventricular
foramina (foramen of Monro) into the third
ventricle, and then through the cerebral aqueduct
(aqueduct of Sylvius) into the fourth ventricle,
where it exits through two lateral apertures
(foramina of Luschka) and one median aperture
(foramen of Magendie).
CSF & LUMBER PUNCTURE
 It then flows through the
cerebellomedullary cistern down the spinal
cord and over the cerebral hemispheres.
CSF & LUMBER PUNCTURE
 The cerebrospinal fluid is produced at a rate
of 500 ml/day. Since the brain can only
contain from 135-150 ml, large amounts are
drained primarily into the blood through
arachnoid granulations in the superior
sagittal sinus. Thus the CSF turns over
about 3.7 times a day.
CSF & LUMBER PUNCTURE
 Direct cranial measurement of ICP.

ICP monitoring requires admission to the hospital.


A small pressure monitor is inserted through the
skull into the brain or ventricles to measure the
ICP. pressure monitoring (either by lumbar
catheter or the intracranial method) can detect an
abnormal pattern of pressure waves.
CSF & LUMBER PUNCTURE
 Ventricular puncture for the relief of
increased ICP is one of the oldest practices
in neurosurgery.
CSF & LUMBER PUNCTURE
 The "gold standard" technique for ICP
monitoring is a catheter inserted into the
lateral ventricle, usually via a small right
frontal burr hole. This can be connected to a
standard pressure transducer via a fluid-
filled catheter in neurosurgery.
CSF & LUMBER PUNCTURE
 Indirect measurement of ICP by lumber puncture.
 The two principal objections to lumbar puncture in
the diagnosis of intracranial hypertension have
been the danger of inducing brain-stem
compression through tentorial or tonsillar
herniation and the contention that spinal fluid
pressure is not always an accurate reflection of
ICP.
CSF & LUMBER PUNCTURE
 Indications

 1. Diagnostic aid
 2. Therapy for idiopathic intracranial
hypertension
 3. Infusion of anaesthetic (“spinal”),
chemotherapy, or contrast agents
(myelography)
CSF & LUMBER PUNCTURE
 Contraindications
 - INR > 1.4 or other coagulopathy
 - platelets < 50
 - infection at desired puncture site
 - obstructive / non-communicating hydrocephalus
 - intracranial mass
 - high intracranial pressure (ICP) / papilloedema
CSF & LUMBER PUNCTURE
 An LP may safely be performed without
first doing a CT head in a young previously
healthy patient with no history of seizures, a
normal level of consciousness and a normal
neurological exam.
CSF & LUMBER PUNCTURE
 Anatomy

 Intercristal line is an imaginary line that


connects the superior border of the iliac
crests

 - L4/5 interspace is the first interspace


caudal to the intercristal line
CSF & LUMBER PUNCTURE
 Materials
 sterile gloves and mask
 LP kit (contains: syringe, 25 and 22G needles, 1%
lidocaine, sterile drapes, sponges and gauze, 22G
LP needle, stopcock and manometer, 4 collection
tubes and band-aid)

 - sterilization solution (chlorhexidine or


proviodine)
CSF & LUMBER PUNCTURE
 Technique
 1. Obtain patient consent
 2. Position the patient,close to edge of bed as
possible
 3.Pillow under head and between legs
 4.Head flexed and legs curled up towards
chest,ask patient to bulge out lumbosacral spine
 5.Carefully open LP kit and put cleaning solution
in reservoir.
Positioning

INCORRECT CORRECT
CSF & LUMBER PUNCTURE
 6.Put on mask and sterile gloves.
 7.Sterilize the field using the sterilizing
solution and sponges provided. Clean a 6
inch area around the desired entry site,
proceeding outward in concentric circles.
Do this 3 separate times. Place sterile drape
over the field.
Skin Preparation
 Overlying skin cleaned
with povidone-iodine

 Sterile drape placed


with an opening over
the LS
Spinal Needle
Local anesthesia infiltrated
Insertion
 Local anesthesia infiltrated
 20 or 22 gauge spinal needle
with stylet
 Advance spinal needle slowly,
angling slightly toward the
head
 Flat surface of bevel of needle
positioned to face patient’s
flanks
CSF & LUMBER PUNCTURE
 8. Ensure all items in LP tray are ready for
use. E.g.. 1% or 2% lidocaine loaded into
syringe, collection tubes open, test to see
that the stylet slides in/out of LP needle
easily, stopcock and manometer for opening
pressure measurement ready
CSF & LUMBER PUNCTURE
 9.Local anaesthesia. Using a 25G needle,
inject 1% or 2% lidocaine under the skin at
the desired entry site. A small bleb under
the skin is sufficient. Switch the needle tip
to the 22G needle and anaesthetize deeper
structures by inserting the needle further,
injecting lidocaine while proceeding
forward.
CSF & LUMBER PUNCTURE
 10.Insert LP needle. The bevel should be parallel
to the spinal column. Always advance the needle
with the stylet in place. Aim needle in the midline,
slightly cephalad, towards the patient’s umbilicus.
Advance needle slowly until it is inserted 2-3 cm,
then withdraw the stylet to check for CSF return.
Continue to advance the needle, periodically
checking for CSF return. Often a "pop'' is
appreciated as the needle pierces the dural
membrane.
CSF & LUMBER PUNCTURE
 If the needle meets bone or if blood returns
(hitting the venous plexus anterior or
posterior to the spinal canal), withdraw the
needle to the skin and redirect the needle
CSF & LUMBER PUNCTURE
 11.Once CSF flow is obtained, measure the
opening pressure by attaching first the
stopcock to the LP needle and then the
manometer to the stopcock.
CSF & LUMBER PUNCTURE
 12.Collect CSF fluid into sequential tubes.
about 2 ml in each tube is sufficient for
basic investigations. More fluid will need to
be collected for special tests e.g. viral PCR,
cytology etc
 13.Reinsert stylet. Withdraw needle. Place
band-aid over insertion site.
CSF & LUMBER PUNCTURE
 What to order
 The basics
 Tube #1 Cell count and differential

 Tube #2 Chemistry (protein, glucose)

 Tube #3 Culture and Gram stain

 Tube #4 reserve with csf in it


CSF & LUMBER PUNCTURE
 Other tests to consider
 - Will need to collect extra fluid for these
tests in tube #3 or #4.
 India ink and / or Cryptococcal Ag (for
Cryptococcus neoformans)
 AFB and / or PCR for TB
 Viral PCR (includes HSV, CMV, EBV)
 arbovirus / WNV, echovirus
CSF & LUMBER PUNCTURE
 VDRL

 fungal culture

 viral culture

 PCR and /or antibody titers for Lyme ds.


CSF & LUMBER PUNCTURE
 oligoclonal banding (3-4 ml)

 IgG index, IgG :albumin ratio

 cytology (must be collected in cytology fixative)


(8-10ml)

 flow cytometry (3-4 ml) (NOT in fixative)


CSF & LUMBER PUNCTURE
 How much CSF to withdraw?

 - CSF is produced at a rate of 0.3 ml/min in


adults or 450 ml/24h

 - CSF volume is approximately 150 ml in


an adult
CSF & LUMBER PUNCTURE
 - For basic investigations, only require 4-8
ml

 - May require more volume for special tests.


Maximum to be removed at one time should
probably not exceed 20 ml.
CSF & LUMBER PUNCTURE
 Normal opening pressure ranges 50 to 200
mm H20 in adults and up to 250 mm H20 in
obese women patients or 5-20 cm of H20.
 2 Intracranial hypotension is defined as an
opening pressure of less than 50 mm H20.
CSF & LUMBER PUNCTURE
 Normal CSF is crystal clear. However, as
few as 200 white blood cells (WBCs) per
mm3 or 400 red blood cells (RBCs) per
mm3 will cause CSF to appear turbid.
CSF & LUMBER PUNCTURE
 Glucose: 2/3rd or < 40% of concurrent
serum glucose or less than 2/3rd of serum
glucose (often absolute CSF glucose < 2.2 ,
(normal is 2.2 mmol to 4 mmol/l)

 cells <5/cmm mostly lymphocyte


CSF & LUMBER PUNCTURE
 Xanthochromia is a yellow, orange, or pink
discoloration of the CSF, most often caused
by the lysis of RBCs resulting in
hemoglobin breakdown to oxyhemoglobin,
 methemoglobin, and bilirubin.
CSF & LUMBER PUNCTURE
 Discoloration begins after RBCs have been
in spinal fluid for about two hours, and
remains for two to four weeks.

 Xanthochromia is present in more than 90


percent of patients within 12 hours of
subarachnoid hemorrhage
CSF & LUMBER PUNCTURE
 CSF protein levels (normal 15 to 45
mg/dL ) or < 1.5 g per L.
CSF & LUMBER PUNCTURE
 Culture provides definitive diagnosis as
well as identificaiton of pathogenic
organism and antibiotic susceptibilities

 blood culture positive in 50% cases


CSF & LUMBER PUNCTURE

 The Xpert EV test, approved for use in March


2007, can rapidly test for enteroviral meningitis.
The test uses a reverse-transcription PCR
disposable cartridge on which CSF is applied, and
enteroviral genetic material is identified if present.
Results are ready in 2.5 hours, as opposed to days
to weeks in traditional PCR studies.
CSF & LUMBER PUNCTURE
 CT scan with contrast helps in ruling out
intracranial pathology. Contrasted scans should be
obtained to evaluate for any enhancement along
the meninges.

 ct scan also excludes intracranial abscess, subdural


empyema, or other lesions. Alternatively, and if
readily available, an MRI of the brain should be
done.
CSF & LUMBER PUNCTURE
 MRI with contrast is the criterion standard
in visualizing intracranial pathology in viral
encephalitis HSV-1 commonly affects basal
frontal and temporal lobes with a typical
picture of diffusely enhancing bilateral
lesions.
CSF & LUMBER PUNCTURE
 All patients whose condition is not
improving clinically within 24-48 hours
should have more extensive work-up to
discern the cause of meningitis.

 Blood, feces, and throat swabs may be sent


for viral serology and cultures.
CSF & LUMBER PUNCTURE
 Acid-fast staining of CSF should be
performed and the remaining fluid should
be sent for PCR testing for HIV and CMV.

 Serum titers of antibodies against HIV and


toxoplasma should be obtained.
CSF & LUMBER PUNCTURE
 EEG may be performed if encephalitis or
subclinical seizures are suspected in the
altered patient. Periodic lateralized
epileptiform discharges (PLEDs) are often
seen in herpetic encephalitis.
CSF & LUMBER PUNCTURE
 CSF Lactate Concentration

 normally 14 mg/dl
 in bacterial meningitis is usually <25 mg/dl
 PCR for microbial DNA may become
sensitive and specific method for bacterial
identification
CSF & LUMBER PUNCTURE
 CT Scanning sould be done and preferred choice
before Lumbar Puncture in Suspected Meningitis

 Acid-fast staining of CSF should be performed


and the remaining fluid should be sent for PCR
testing for HIV and CMV.
 Serum titers of antibodies against HIV and
toxoplasma should be obtained.
CSF & LUMBER PUNCTURE
 Additional serum collection 10-21 days later may
aid in discerning rising titers in the antibodies
against specific viral pathogens; a 4-fold increase
in viral antibodies confirms the diagnosis. This is
particularly useful for arboviral and LCMV cases,
but also is helpful in ruling out toxoplasmosis,
leptospirosis, borreliosis, and rickettsial infections.
Although some of these studies do not yield an
immediate result for clinical decision making, they
may be useful for prognostication.
CSF PRESSURE
 Opening pressure: 5-20 cm water (only
valid in lateral decubitus position) or 50-
200 mm of H20.
CSF PRESSURE

 ICP is measured in millimeters of mercury


(mmHg) and, at rest, is normally 5–20
mmHg for a supine adult, and becomes
negative (averaging -10 mmHg) in the
vertical position.
CSF PRESSURE
 Normal CSF pressure in the lower back is
between 50-200 mm water.
 Normal Intracranial pressure(within the
cranium) however is between 5-20 mmHg
or 50-200 mm H2O in adults.
Investigations & Diagnosis of
Meningitis
 Repeat CSF analysis 24 to 36 hours
(minimum of 24 hours) after initiation of
therapy
 Changes in therapy/concomitant therapy as
needed
 Evaluation of drug concentrations in CSF
Investigations & Diagnosis of
Meningitis
 5-7 weeks after completion of all therapy
 Lumbar puncture repeated only if clinically
indicated
Investigations & Diagnosis of
Meningitis
 LATE POST-THERAPY VISIT
 5-6 months after completion of therapy
 Emphasis on hearing/ development/
neurological findings
 Behavioral difficulties should be
documented as well
Investigations & Diagnosis of
Meningitis
 Persistence of pathogen at 24-36 hr. tap
leading to additional therapy or change in
therapy.
CSF evaluation
Protein Glucose
Condition WBC
(mg/dL) (mg/dL)

>50 (2.2
Normal <5 , lymphocytes mainly 5-45 mmol to 4
mmol/l)
Bacterial, 100-500 or <2.2 m
>1000K PMN’s
acute >1.5gm/l mol/l
Viral Low to
<1000 increased
normal
TB <500 increased decreased
Fungal < 500 increased decreased
CSF Diagnosis
WBC Glucose Protein
Normal <5 2/3rd of serum 15 to 45
(lymphocytes) glucose mg/dl
Bacterial >1000 PMN’s Low Elevated
Meningitis predominate (>100 mg)

Aseptic Elevated Normal to Normal or


Meningitis (PMN’s early, low slightly
lymphocytes elevated
late)
TB Elevated Low Elevated
Meningitis (PMN’s early, (>100 mg)
CSF evaluation
Protein Glucose
Condition WBC
(mg/dL) (mg/dL)

Normal <5, lymph's mainly 5-45 >50


Increased>
Bacterial,
>1000 PMN’s more than Low
acute
100 mg/d
TB <500 Increased
upto 500 low
mg/dl

Fungal <500 Upto 500 low


Viral <1000 Upto 100 Normal
Summary of Typical
CSF Findings
Normal Bacterial Viral TB
Cells 0-5 >1000 <1000 <500
Polymorphs 0 Predominate Early +/- increased

Lymphocytes 5 Late Predominate Increased

Glucose 60-80 Decreased Normal Decreased

CSF plasma: 66% <40% Normal < 30%


Glucose ratio
Protein 5-40 Increased +/- Increased Increased

Culture Negative Positive Negative +TB


TREATMENT of MENINGITIS
 Empiric Antibiotics:
 Cefotaxime 2g IV 6 hrly
 add Vancomycin 1-2 g IV 8-12 hrly in all patients
(till possibility of Penicillin-resistant Strep
pneumoniae has been ruled out)
 add Ampicllin 2g IV 6 hrly in elderly or
immunocompromised patients (for Listeria
infections)
TREATMENT of MENINGITIS
 for patients with serious penicillin allergies,
Meropenem 1-2g IV 8hrly as alternative

 Ceftazidime (2g IV 8 hrly or BD) + Vancomycin


for neurosurgical patients, those with shunts or
CSF leaks
 May consider adjunctive Acyclovir (10 mg/kg IV
8 hrly if normal renal function) in case of viral
infection.
TREATMENT of MENINGITIS
 Therapy can be modified as the results of
Gram stain, cultures, and PCR testing
become available. Patients in unstable
condition need critical care unit admission
for airway protection, neurologic checks,
and prevention of secondary complications.
TREATMENT of MENINGITIS
 since SIADH has been reported. Fluid
restriction, diuretics, and rarely hypertonic
saline infusion may be used to correct the
hyponatremia
TREATMENT of MENINGITIS
 Cerebral edema does occur in cases of
severe encephalitis and may require
intracranial pressure control by infusion of
mannitol (1 g/kg initial dose followed by
0.25-0.5 g/kg 6 hrly), IV dexamethasone, or
intubation and mild hyperventilation, with
arterial PCO2 around 28-30 mm Hg
TREATMENT of MENINGITIS
 Use of adjunctive corticosteroids:

 - prior to or along with initial antibiotics,


administer Dexamethasone 10 mg IV for
suspected bacterial meningitis (based on cloudy
CSF, CSF WBC counts > 1000 or + Gram stain)

 - continue 10 mg IV 8 hrly x 4 days


TREATMENT of MENINGITIS
 Isolation & Contact Prophylaxis:

 - Generally isolate cases of bacterial


meningitis for up to 48 hours of appropriate
antibiotics

 - Concern is to reduce transmission of


meningococcal infections
TREATMENT of MENINGITIS
 can be taken out of isolation after this time
or if alternative pathogen identified

 - department of health should be notified of


pathogens in pyogenic meningitis
TREATMENT of MENINGITIS
 Close contacts (family members, partners,
co-workers or school children) should
receive prophylaxis if meningococcal or
haemophilus influenzae type B (if not
vaccinated):
 - rifampin 600 mg PO bid x 2d
 - ciprofloxacin 500 mg PO single dose
TREATMENT of MENINGITIS
 dexamethasone 0.6 mg/kg/day IV 6-8 hrly
for 4 days
 reduces incidence of neurologic sequelae,
i.e., hearing loss

 electrolyte abnormalities - SIADH


Prognostic Factors
1. Age
 2. Level of Consciousness (50% mortality if
unresponsive or minimally responsive on
admission)
 3. Seizures early in course
 4. Strep. pneumoniae meningitis
 5. CSF results (lower glucose & WBC
counts, higher protein)

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