VIRAL MENINGITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE CHINKIPORA SOPORE KASHMIR

MENINGITIS
By Dr Bashir Ahmed Dar
Associate Professor Medicine
Chinkipora Sopore Kashmir
Email- [email_address]

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.

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.

Sharing food, drinking glasses, eating utensils, tissues, or towels .

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

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

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

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.

through a person's stool, and someone who comes in contact with the stool — such as a child in day care .

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

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

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.

otitis media
mastoiditis
Osteomyelitic foci in the skull
sinusitis
Penetrating cranial injuries
Brain or spine surgery
Ventriculoperitoneal shun
lumbar puncture.

skull fractures
Extradural abscess
Subdural empyaema
Spinal epidural abscess.
Pachymeningitis

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

RISKS
Asplenia
drugs that suppress immune system
Immunocompromised
HIV, malignancy
malignancy
alcholism

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

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

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

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.

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

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.

Viral
HSV especially in infants
Enterovirus (coxsackie, echovirus)
HIV
Lymphocytic choriomeningitis virus
Arbovirus
Mumps
CMV
EBV
VZV
Adenovirus
Measles

Rubella
Rotavirus
Influenza and parainfluenza

Fungal
Cryptococcus
Coccidiodes
Histoplasmosis
Mucormycosis
Aspergilosis
Candidasis
With a particular prone settings etc

Parasitic/protozoal
Angiostrongylus
Toxoplamosis
Hydatid
Amoeba
Malaria
Cysticercosis

Rickettsial
Rocky mountain spotted fever

Others
Tuberculosis
Borrelia burgdorferi
Treponema pallidum
Mycoplasma pneumoniae
brucella
Chlamydia

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

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

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.

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.

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 (H flu) Strep pneumoniae

CSF-Gram stain:
Low power view showing many neutrophils.

CSF-Gram stain:
High power shows clusters of bacteria.
Neutrophils

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.)

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.

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

Ensuing inflammatory response increases blood-brain permeability
Cerebral edema
Increased ICP

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

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.

Bovine This brain shows irregular red spots which are areas of hemorrhage and necrosis caused by the bacteria, Histophilus somni .

Brain: 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.

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

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.

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 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.

Non-specific complaints
Fever
Headache
Nausea and vomiting
--Nuchal rigidity
Lethargy
Irritability
Restlessness
Poor feeding
Back pain
Altered mental status (seizure, coma)

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

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
ICP monitor (not routine)
Changes in pupils

Meningococcemia - Petechiae

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

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

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

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

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)

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).

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
Subfalcine (cingulate)
Transtentorial (uncal)
Tonsillar (foramen magnum)
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

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

Scarring
amputation of digits and limbs
Neurological damage

Visual impairment and blindness
Auditory impairment and deafness
Neuromotor disabilities
Seizure disorders
Behaviour problems
Learning difficulties

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

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

Psychosocial and emotional problems - low self esteem and difficulties coping
Subtle complications - poor concentration, clumsiness and mood swings
May be age-specific

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

Chemical meningitis: Rupture of tumor
intracranial haemorrage like
Epidural
subdural
Subarachnoid
intraparenchymal

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).

It then flows through the cerebellomedullary cistern down the spinal cord and over the cerebral hemispheres.

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.

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.

Ventricular puncture for the relief of increased ICP is one of the oldest practices in neurosurgery.

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.

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.

Indications
1. Diagnostic aid
2. Therapy for idiopathic intracranial hypertension
3. Infusion of anaesthetic (“spinal”), chemotherapy, or contrast agents (myelography)

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

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.

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

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)

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

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 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

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

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.

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.

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

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.

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.

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

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

VDRL
fungal culture
viral culture
PCR and /or antibody titers for Lyme ds.

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)

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

- 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.

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.

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.

Glucose: 2/3rd or < 40% of concurrent serum glucose or less than 2/3 rd of serum glucose (often absolute CSF glucose < 2.2 , (normal is 2.2 mmol to 4 mmol/l)
cells <5/cmm mostly lymphocyte

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.

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 protein levels (normal 15 to 45 mg/dL ) or < 1.5 g per L.

Culture provides definitive diagnosis as well as identificaiton of pathogenic organism and antibiotic susceptibilities
blood culture positive in 50% cases

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.

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.

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.

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.

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.

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 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

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.

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

5-7 weeks after completion of all therapy
Lumbar puncture repeated only if clinically indicated

LATE POST-THERAPY VISIT
5-6 months after completion of therapy
Emphasis on hearing/ development/ neurological findings
Behavioral difficulties should be documented as well

Persistence of pathogen at 24-36 hr. tap leading to additional therapy or change in therapy.

CSF evaluation decreased increased < 500 Fungal decreased increased <500 TB Low to normal increased <1000 Viral <2.2 m mol/l 100-500 or >1.5gm/l >1000K PMN’s Bacterial, acute >50 (2.2 mmol to 4 mmol/l) 5-45 <5 , lymphocytes mainly Normal Glucose (mg/dL) Protein (mg/dL) WBC Condition

CSF Diagnosis Elevated (>100 mg) Low Elevated (PMN’s early, lymphs late TB Meningitis Normal or slightly elevated Normal to low Elevated (PMN’s early, lymphocytes late) Aseptic Meningitis Elevated (>100 mg) Low >1000 PMN’s predominate Bacterial Meningitis 15 to 45 mg/dl 2/3 rd of serum glucose <5 (lymphocytes) Normal Protein Glucose WBC

CSF evaluation Normal Upto 100 <1000 Viral low Upto 500 <500 Fungal low Increased upto 500 mg/dl <500 TB Low Increased>more than 100 mg/d >1000 PMN’s Bacterial, acute >50 5-45 <5, lymph's mainly Normal Glucose (mg/dL) Protein (mg/dL) WBC Condition

Summary of Typical CSF Findings +TB Negative Positive Negative Culture Increased +/- Increased Increased 5-40 Protein < 30% Normal <40% 66% CSF plasma: Glucose ratio Decreased Normal Decreased 60-80 Glucose Increased Predominate Late 5 Lymphocytes +/- increased Early Predominate 0 Polymorphs <500 <1000 >1000 0-5 Cells TB Viral Bacterial Normal

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)

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.

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.

since SIADH has been reported. Fluid restriction, diuretics, and rarely hypertonic saline infusion may be used to correct the hyponatremia

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

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

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

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

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

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)

VIRAL MENINGITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE CHINKIPORA SOPORE KASHMIR

by Dr Bashir Ahmed Dar

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VIRAL MENINGITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE CHINKIPORA SOPORE KASHMIR Presentation Transcript

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