viral meningitis by dr bashir ahmed dar associate professor medicine chinkipora sopore kashmir

MENINGITIS

By Dr Bashir Ahmed DarBy Dr Bashir Ahmed Dar Associate Professor MedicineAssociate Professor Medicine Chinkipora Sopore KashmirChinkipora Sopore Kashmir Email- Email- [email protected]@gmail.com

What is meningitis?What is meningitis?

Meningitis is an infection of the pia-arachanoid and the CSF Meningitis is an infection of the pia-arachanoid and the CSF fluid that surrounds the brain. Meningitis is usually caused by an fluid that surrounds the brain. Meningitis is usually caused by an infection with a infection with a virusvirus, with a , with a bacteriumbacterium or even with or even with fungifungi..

How is Meningitis Caused

Colonization of nasopharynx by bacteria or Colonization of nasopharynx by bacteria or viruses viruses

Is an important way of spreading meningitis Is an important way of spreading meningitis by way of cribriform fossa or viremia or by way of cribriform fossa or viremia or bacteriaemia and can spread to others by bacteriaemia and can spread to others by coughing etc.coughing etc.


contagious, spread via tiny drops of fluid contagious, spread via tiny drops of fluid from the throat and nose of someone who is from the throat and nose of someone who is infected. The drops may become airborne infected. The drops may become airborne when the person coughs, laughs, talks, or when the person coughs, laughs, talks, or sneezes. They then can infect others when sneezes. They then can infect others when people breathe them in or touch the drops people breathe them in or touch the drops and then touch their own noses or mouths.and then touch their own noses or mouths.


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


spread between people who are in close contact, spread between people who are in close contact, such as those who live together or people who are such as those who live together or people who are exposed by kissingexposed by kissing

N. meningitidis cause epidemics of meningitis. In N. meningitidis cause epidemics of meningitis. In particular in a crowded day-care situation or a particular in a crowded day-care situation or a military recruit in a crowded training military recruit in a crowded training camp,schools,colleges has fallen ill with camp,schools,colleges has fallen ill with meningococcal meningitismeningococcal meningitis


Meningococcus is the bacteria that has Meningococcus is the bacteria that has caused outbreaks across North America caused outbreaks across North America over the last 8 - 10 years including most over the last 8 - 10 years including most recently. Understandably the presence of a recently. Understandably the presence of a meningitis epidemic in a community is very meningitis epidemic in a community is very scary to parentsscary to parents


Most of the viruses that cause meningitis Most of the viruses that cause meningitis live in the intestines and tend to be passed live in the intestines and tend to be passed on as a result of poor hygiene. Many on as a result of poor hygiene. Many different viruses can cause viral meningitis, different viruses can cause viral meningitis, most commonly enteroviruses that normally most commonly enteroviruses that normally live harmlessly in people's bowelslive harmlessly in people's bowels


L. monocytogenes has been associated with such L. monocytogenes has been associated with such foods as raw milk, pasteurized fluid milk,cheeses foods as raw milk, pasteurized fluid milk,cheeses (particularly soft-ripened varieties), ice cream, raw (particularly soft-ripened varieties), ice cream, raw vegetables, fermented raw-meat sausages, raw and vegetables, fermented raw-meat sausages, raw and cooked poultry, raw meats (of all types), and raw cooked poultry, raw meats (of all types), and raw and smoked fish. Its ability to grow at and smoked fish. Its ability to grow at temperatures as low as 0°C permits multiplication temperatures as low as 0°C permits multiplication in refrigerated foods. In refrigeration temperature in refrigerated foods. In refrigeration temperature such as 4°C the amount of ferric iron promotes the such as 4°C the amount of ferric iron promotes the growth of L. monocytogenes.growth of L. monocytogenes.


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

How is Meningitis Caused HematogenousHematogenous Many of the bacteria and viruses that cause Many of the bacteria and viruses that cause

meningitis are fairly common and are typically meningitis are fairly common and are typically associated with other routine illnesses.associated with other routine illnesses.

infection of the skin, urinary system, infection of the skin, urinary system, gastrointestinal or respiratory tract can spread by gastrointestinal or respiratory tract can spread by the bloodstream the bloodstream


A person may have another type of A person may have another type of infection (of the lungs, throat, or tissues of infection (of the lungs, throat, or tissues of the heart) caused by an organism that can the heart) caused by an organism that can also cause meningitisalso cause meningitis


Direct infectionDirect infection skull fractures possess abnormal openings to the skull fractures possess abnormal openings to the

sinuses, nasal passages, and middle ears. sinuses, nasal passages, and middle ears. Organisms can pass through openings and cause Organisms can pass through openings and cause infection. surgical procedures or who have had infection. surgical procedures or who have had foreign bodies surgically placed within their skulls foreign bodies surgically placed within their skulls (such as tubes to drain abnormal amounts of (such as tubes to drain abnormal amounts of accumulated CSF) have an increased risk of accumulated CSF) have an increased risk of meningitis.meningitis.


otitis mediaotitis media mastoiditismastoiditis Osteomyelitic foci in the skullOsteomyelitic foci in the skull sinusitissinusitis Penetrating cranial injuriesPenetrating cranial injuries Brain or spine surgeryBrain or spine surgery Ventriculoperitoneal shunVentriculoperitoneal shun lumbar puncture.lumbar puncture.


skull fracturesskull fractures Extradural abscessExtradural abscess Subdural empyaemaSubdural empyaema Spinal epidural abscess. Spinal epidural abscess. PachymeningitisPachymeningitis


NeurotropicNeurotropic also via an uncommon but interesting method called also via an uncommon but interesting method called

intraneural spread. This involves an organism invading intraneural spread. This involves an organism invading the body at a considerable distance away from the the body at a considerable distance away from the head, spreading along a nerve, and using that nerve as head, spreading along a nerve, and using that nerve as a kind of ladder into the skull, where the organism can a kind of ladder into the skull, where the organism can multiply and cause meningitis. Herpes simplex virus is multiply and cause meningitis. Herpes simplex virus is known to use this type of spread, as is the rabies virus.known to use this type of spread, as is the rabies virus.

RabiesRabies HSVHSV


RISKSRISKS AspleniaAsplenia drugs that suppress immune systemdrugs that suppress immune system ImmunocompromisedImmunocompromised HIV, malignancyHIV, malignancy malignancymalignancy alcholismalcholism


Patients with cardiac and pulmonary anomalies may Patients with cardiac and pulmonary anomalies may spread septic foci,bronchiectasis, occasionally spread septic foci,bronchiectasis, occasionally pneumonia). Common with pulmonary AV fistulae pneumonia). Common with pulmonary AV fistulae and R to L cardiac defectand R to L cardiac defect

T-cell defects (HIV)T-cell defects (HIV) Neural tube defects- Staph aureus, enteric organismsNeural tube defects- Staph aureus, enteric organisms Terminal compliment deficiency- NeisseriaTerminal compliment deficiency- Neisseria septic foci from thrombophibitisseptic foci from thrombophibitis iv drug abusersiv drug abusers


Immune-compromised Patients are also Immune-compromised Patients are also prone for fungal infections and the fungal prone for fungal infections and the fungal infections that can result in meningitis areinfections that can result in meningitis are

AspergillusAspergillus CandidaCandida MucorMucor Protozoal,Ameba infections,ToxoplasmaProtozoal,Ameba infections,Toxoplasma

Organisms Causing Meningitis

BacterialBacterial ViralViral Fungal Fungal Ricketsial Ricketsial Parasitic/ProtozoalParasitic/Protozoal


Purulent bacterial meningitisPurulent bacterial meningitis etiologyetiology newborns Group B Strep ,E. coli newborns Group B Strep ,E. coli children - H. influenzae , Str. pneumoniaechildren - H. influenzae , Str. pneumoniae HIB vaccine has reduced incidence of H influnza HIB vaccine has reduced incidence of H influnza

infectioninfection adults - meningococccal (small epidemies - army, adults - meningococccal (small epidemies - army,

holiday camps,school going holiday camps,school going students),pneumococcalstudents),pneumococcal


Streptococcus agalactiae (also known as Group B Streptococcus agalactiae (also known as Group B streptococcus) is a beta-hemolytic gram-positive streptococcus) is a beta-hemolytic gram-positive streptococcus.streptococcus.

S. agalactiae is a species of the normal flora of the S. agalactiae is a species of the normal flora of the female urogenital tract and rectum. Its chief female urogenital tract and rectum. Its chief clinical importance is that it can be transferred to a clinical importance is that it can be transferred to a neonate passing through the birth canal and can neonate passing through the birth canal and can cause serious group B streptococcal infection. cause serious group B streptococcal infection.


In the western world, S. agalactiae is a In the western world, S. agalactiae is a major cause of bacterial septicemia of the major cause of bacterial septicemia of the newborn, which can lead to death or long-newborn, which can lead to death or long-term sequelae such as hearing loss. S. term sequelae such as hearing loss. S. agalactiae can also cause neonatal agalactiae can also cause neonatal meningitis, which does not present with the meningitis, which does not present with the hallmark sign of adult meningitis, a stiff hallmark sign of adult meningitis, a stiff neckneck


rather, it presents with nonspecific rather, it presents with nonspecific symptoms such as fever, vomiting and symptoms such as fever, vomiting and irritability and can consequently go irritability and can consequently go undiagnosed until it is too late. Somewhat undiagnosed until it is too late. Somewhat more rarely, S. agalactiae can also cause more rarely, S. agalactiae can also cause invasive group B streptococcal disease of invasive group B streptococcal disease of the adult in the pregnant, elderly, or the adult in the pregnant, elderly, or immunosuppressed.immunosuppressed.


ViralViral HSV especially in infants HSV especially in infants Enterovirus (coxsackie, echovirus)Enterovirus (coxsackie, echovirus) HIVHIV Lymphocytic choriomeningitis virusLymphocytic choriomeningitis virus ArbovirusArbovirus MumpsMumps CMVCMV EBVEBV VZVVZV AdenovirusAdenovirus MeaslesMeasles


RubellaRubella RotavirusRotavirus Influenza and parainfluenzaInfluenza and parainfluenza


FungalFungal CryptococcusCryptococcus CoccidiodesCoccidiodes HistoplasmosisHistoplasmosis MucormycosisMucormycosis AspergilosisAspergilosis CandidasisCandidasis With a particular prone settings etcWith a particular prone settings etc


Parasitic/protozoalParasitic/protozoal AngiostrongylusAngiostrongylus ToxoplamosisToxoplamosis HydatidHydatid AmoebaAmoeba MalariaMalaria CysticercosisCysticercosis


RickettsialRickettsial Rocky mountain spotted feverRocky mountain spotted fever


Others Others TuberculosisTuberculosis

Borrelia burgdorferiBorrelia burgdorferi Treponema pallidumTreponema pallidum Mycoplasma pneumoniaeMycoplasma pneumoniae brucellabrucella Chlamydia Chlamydia


viral meningitisviral meningitis fairly common disease but rarely fatalfairly common disease but rarely fatal lymphocytic predominance ie mononuclear lymphocytic predominance ie mononuclear

cells (but may see neutrophils if CSF cells (but may see neutrophils if CSF sampled early in course - up to 48hrssampled early in course - up to 48hrs

glucose not reducedglucose not reduced


may follow Temporary, flu-like symptoms with may follow Temporary, flu-like symptoms with running nose sneezing etc., headache, low grade running nose sneezing etc., headache, low grade fever and stiff neck. fever and stiff neck.

Goes away on its own usually within three to 10 Goes away on its own usually within three to 10 daysdays

Bed rest, paracetamolBed rest, paracetamol Enteroviruses, the most common type of viral Enteroviruses, the most common type of viral

meningitismeningitis Strict isolation is not necessaryStrict isolation is not necessary


Since most cases are due to enteroviruses Since most cases are due to enteroviruses that may be passed in the stool, people that may be passed in the stool, people diagnosed with viral meningitis should be diagnosed with viral meningitis should be instructed to thoroughly wash their hands instructed to thoroughly wash their hands after using the toilet.after using the toilet.


The incidence of viral meningitis drops with age.The incidence of viral meningitis drops with age. Neonates are at greatest risk and have the most Neonates are at greatest risk and have the most

significant risk of morbidity and mortality.significant risk of morbidity and mortality.

The incidence during the first year of life is 20 The incidence during the first year of life is 20 times higher than in older children and adults.times higher than in older children and adults.


CRP much more elevated in bacterial than CRP much more elevated in bacterial than in viral meningitis (ie, 50-150 in bacterial in viral meningitis (ie, 50-150 in bacterial meningitis group vs <20 in viral meningitis meningitis group vs <20 in viral meningitis group).group).

Treatment for viral meningitis is mostly Treatment for viral meningitis is mostly supportive.supportive.

Neisseria meningitidisNeisseria meningitidis

Hemophilus influenza(H flu)

Strep pneumoniae

CSF-Gram stain:

Low Low power power view view showing showing many many neutrophineutrophils.ls.

CSF-Gram stain:

High High power power shows shows clusters of clusters of bacteria.bacteria.

NeutrophilNeutrophilss

CSF-Gram stain:

High High power power shows shows clusters of clusters of bacteria.bacteria.

NeutrophilNeutrophil

CSF-Gram stain:

Observe Observe Paired Paired rounded rounded bacteria – bacteria – (diplococci) (diplococci) staining staining pink (gram pink (gram negative)negative)

Pathogenesis of Meningitis

The virus or bacteria replicates in the initial The virus or bacteria replicates in the initial organ system (ie, respiratory or organ system (ie, respiratory or gastrointestinal mucosa) and gains access to gastrointestinal mucosa) and gains access to the bloodstream. Primary viremia or the bloodstream. Primary viremia or bacteremia introduces the virus or bacteria bacteremia introduces the virus or bacteria to the reticuloendothelial organs (liver, to the reticuloendothelial organs (liver, spleen, and lymph nodes.)spleen, and lymph nodes.)


If the replication persists despite If the replication persists despite immunologic defenses, secondary immunologic defenses, secondary bacteremia or viremia occurs, which is bacteremia or viremia occurs, which is thought to be responsible for seeding of the thought to be responsible for seeding of the CNS. Rapid viral replication likely plays a CNS. Rapid viral replication likely plays a major role in overcoming the host defenses.major role in overcoming the host defenses.


There occurs local immune response to There occurs local immune response to bacteria or virusbacteria or virus

Increased vascular permeabilityIncreased vascular permeability oozing of fluid exudate,inflammatory cellsoozing of fluid exudate,inflammatory cells Neutrophils migrate from capillaries and Neutrophils migrate from capillaries and

release toxinsrelease toxins TNF-a and IL-B1 produced by activated TNF-a and IL-B1 produced by activated

macrophages and endothelial cellsmacrophages and endothelial cells


Ensuing inflammatory response increases Ensuing inflammatory response increases blood-brain permeability blood-brain permeability

Cerebral edemaCerebral edema Increased ICPIncreased ICP


cellular damage and loss of cellular homeostasis cellular damage and loss of cellular homeostasis and worsen cerebral edemaand worsen cerebral edema

damage to vessels lead to vasculitis and bleed or damage to vessels lead to vasculitis and bleed or thrombose leading to infaraction or haemorrahagethrombose leading to infaraction or haemorrahage

exudate formation etc can obstruct CSF flow and exudate formation etc can obstruct CSF flow and lead to hydrocephalous lead to hydrocephalous

ICP lead to herniationICP lead to herniation


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

damage to neurons can take place if extending to damage to neurons can take place if extending to brain cells resulting in their degeneration.brain cells resulting in their degeneration.

The white appearance of this calf brain is caused by neutrophils within themeninges – 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 hemorrhageand necrosis caused by the bacteria, Histophilus somni.

Brain:

meningitis.


if infection becomes localised in brain then can if infection becomes localised in brain then can lead to abcess formation especially in case of lead to abcess formation especially in case of direct infections.direct infections.

immune system tries to confine this localised immune system tries to confine this localised infection therefore may develop fibrous wall infection therefore may develop fibrous wall around it with perivascular chronic inflamatory around it with perivascular chronic inflamatory cells around it,leading to brain abcess with central cells around it,leading to brain abcess with central suppuration and liqufication due to death of suppuration and liqufication due to death of cells .healing may occur with fibrous scar.cells .healing may occur with fibrous scar.

The Evolution of the Abscess is as follows An area of cerebritis begins, in which An area of cerebritis begins, in which

Polymorphonuclear leukocytes are Polymorphonuclear leukocytes are attracted to the invading bacteria. attracted to the invading bacteria.

Liquefaction of brain tissue rapidly Liquefaction of brain tissue rapidly ensues, and at the periphery, a thin rim ensues, and at the periphery, a thin rim of granulation tissue composed of new of granulation tissue composed of new capillaries and fibroblasts is formed. capillaries and fibroblasts is formed.

Evolution of the Abscess

With time, a connective tissue capsule With time, a connective tissue capsule is formed by collagen laid down by is formed by collagen laid down by infiltrating fibroblasts. Often this is more infiltrating fibroblasts. Often this is more perfectly formed on the outer aspect of perfectly formed on the outer aspect of the abscess, presumably due to the the abscess, presumably due to the contribution of the reservoir of potential contribution of the reservoir of potential in the adjacent meninges. in the adjacent meninges.


Due to the poor encapsulation of the Due to the poor encapsulation of the medial aspect of an abscess, which medial aspect of an abscess, which abuts upon or is located within the abuts upon or is located within the cerebral white matter, the infection cerebral white matter, the infection tends to form daughter or satellite tends to form daughter or satellite abscesses medially which may abscesses medially which may eventually rupture into the ventricular eventually rupture into the ventricular systemsystem


Such rupture may lead to rapid death, and in Such rupture may lead to rapid death, and in any event, is usually followed by severe any event, is usually followed by severe ventriculitis and massive meningitis as ventriculitis and massive meningitis as infected CSF pours into the subarachnoid infected CSF pours into the subarachnoid space. space.

Antibiotic therapy greatly decelerates the Antibiotic therapy greatly decelerates the growth of an abscess, and may allow time for growth of an abscess, and may allow time for a complete capsule to form after which the a complete capsule to form after which the abscess may be removed surgically.abscess may be removed surgically.


The image above shows a large abscess in The image above shows a large abscess in the brain. The purulent center is surrounded the brain. The purulent center is surrounded by a capsule. Often a zone of hyperemia is by a capsule. Often a zone of hyperemia is present adjacent to the wall and there is present adjacent to the wall and there is marked swelling of the adjacent brain tissuemarked swelling of the adjacent brain tissue

Evolution of the AbscessAbscess-CerebralGross:

Abscess-CerebralMRI

Meningial enhancementMeningial enhancement in a Bacterial meningitis - CT Scan Image

Meningial enhancement

Signs & symptoms of Meningitis

Acute (<1 day)- common with S. Acute (<1 day)- common with S. pneumoniae and N. meningitidespneumoniae and N. meningitides

Subacute (2-3 days)- preceding URI like Subacute (2-3 days)- preceding URI like symptoms, more common with H. flu and symptoms, more common with H. flu and other pathogens.other pathogens.

Signs & symptoms of Meningitis Non-specific complaintsNon-specific complaints

FeverFever Headache Headache Nausea and vomitingNausea and vomiting --Nuchal rigidity--Nuchal rigidity LethargyLethargy IrritabilityIrritability RestlessnessRestlessness Poor feedingPoor feeding Back painBack pain Altered mental status (seizure, coma)Altered mental status (seizure, coma)


FebrileFebrile stiff neck causing may causearched position stiff neck causing may causearched position

OpisthotonosOpisthotonos Focal neurologic signsFocal neurologic signs Petechia/purpura- DIC with N. menigitidisPetechia/purpura- DIC with N. menigitidis Positive Kernig’s and Brudniski’s i.e. , Positive Kernig’s and Brudniski’s i.e. , Meningismus Meningismus

(stiff neck + Brudzinski + Kernig signs)(stiff neck + Brudzinski + Kernig signs) ShockShock Disseminated intravascular coagulation (DIC)Disseminated intravascular coagulation (DIC) Cerebral edemaCerebral edema

Kernig’s Sign

Patient placed supine with hips flexed 90 Patient placed supine with hips flexed 90 degrees. Examiner attempts to extend the degrees. Examiner attempts to extend the leg at the kneeleg at the knee

Positive test elicited when there is Positive test elicited when there is resistance to knee extension, or pain in the resistance to knee extension, or pain in the lower back or thigh with knee extensionlower back or thigh with knee extension

Brudzinski’s Sign

Patient placed in supine position and neck is Patient placed in supine position and neck is passively flexed towards the chestpassively flexed towards the chest

Positive test is elicited when flexion of neck Positive test is elicited when flexion of neck causes flexion at knees and/or hips of the causes flexion at knees and/or hips of the patientpatient

Normal fundus

Increased intracranial pressure (ICP)

PapilledemaPapilledema Cushing’s triadCushing’s triad

BradycardiaBradycardia HypertensionHypertension Irregular respirationIrregular respiration Severe headacheSevere headache herniationherniation vomittingvomitting

ICP monitor (not routine)ICP monitor (not routine) Changes in pupilsChanges in pupils

Meningococcemia - Petechiae


Is due to small skin bleedIs due to small skin bleed All parts of the body are affecedAll parts of the body are affeced The rashes do not fade under pressureThe rashes do not fade under pressure Pathogenesis:Pathogenesis: a. Septicemiaa. Septicemia b. wide spread endothelial damage b. wide spread endothelial damage c. activation of coagulationc. activation of coagulation d. thrombosis and platelets aggregationd. thrombosis and platelets aggregation


e. reduction of platelets (cosumption )e. reduction of platelets (cosumption ) f. BLEEDING 1.skin rashesf. BLEEDING 1.skin rashes 2.adrenal hemorrhage 2.adrenal hemorrhage Arenal hemorrhage is called Waterhouse-Arenal hemorrhage is called Waterhouse-

Friderichsen Syndrome.It cause acute Friderichsen Syndrome.It cause acute adrenal insufficiency and is uaually fataladrenal insufficiency and is uaually fatal

Meningococcemia - Purpura fulminans


May also look like bruises,echymosis .May also look like bruises,echymosis .

Complications and Outcome of Meningitis Infection can spreading to Infection can spreading to Dura – pachymeningitisDura – pachymeningitis Leptomeninges - leptomeningitisLeptomeninges - leptomeningitis Brain – encephalitisBrain – encephalitis Spinal cord – myelitisSpinal cord – myelitis Ventricles - ventriculitisVentricles - ventriculitis

Complications and Outcome of Meningitis Disseminated intravascular coagulation (DIC) Disseminated intravascular coagulation (DIC)

Cerebral edemaCerebral edema

Adrenal hemorrhage is called Waterhouse-Adrenal hemorrhage is called Waterhouse-Friderichsen Syndrome.It cause acute adrenal Friderichsen Syndrome.It cause acute adrenal insufficiency and is uaually fatalinsufficiency and is uaually fatal

septicaemia and infection spreading to other septicaemia and infection spreading to other organsorgans

motor and neurological deficitsmotor and neurological deficits

Complications and Outcome of Meningitis SeizuresSeizures SIADHSIADH Subdural effusions & empyemaSubdural effusions & empyema Septic sinus or cortical vein thrombosis Septic sinus or cortical vein thrombosis Arterial ischemia / infarction (inflammatory Arterial ischemia / infarction (inflammatory

vasculitis)vasculitis) CNs Palsies (esp deafness)CNs Palsies (esp deafness) Septic shock / multi-organ failure from bacteremia Septic shock / multi-organ failure from bacteremia

(esp meningococcus & pneumococcus)(esp meningococcus & pneumococcus)

Complications and Outcome of Meningitis risk of adrenal hemorrhage with hypo-risk of adrenal hemorrhage with hypo-

adrenalism (Waterhouse-Friderichsen adrenalism (Waterhouse-Friderichsen syndrome)syndrome)

Serum sodium level may be abnormal Serum sodium level may be abnormal because of dehydration or the rare because of dehydration or the rare occurrence of syndrome of inappropriate occurrence of syndrome of inappropriate antidiuretic hormone secretion (SIADH).antidiuretic hormone secretion (SIADH).

Complications and Outcome of Meningitis Serum amylase level may be elevated in Serum amylase level may be elevated in

cases caused by mumps even in the absence cases caused by mumps even in the absence of parotitis.of parotitis.

Focal infarctions/microinfarcts due to Focal infarctions/microinfarcts due to endarteritis oblitreransendarteritis oblitrerans

Formation of intracranial massFormation of intracranial mass Cranial nerve palsiesCranial nerve palsies

Increased intracranial pressure

HeadacheHeadache

VomitingVomiting

Decreased Level of Decreased Level of ConsciousnessConsciousness

PapilledemaPapilledema

HerniationHerniation

TYPES OF HERNIATION

1.1. Subfalcine Subfalcine (cingulate)(cingulate)

2.2. Transtentorial Transtentorial (uncal)(uncal)

3.3. Tonsillar Tonsillar (foramen (foramen magnum)magnum)

4.4. ExtracranialExtracranial

TRANSTENTORIAL (UNCAL) HERNIATIONSHIFT OF THE BRAIN FROM THE MIDDLE TO THE SHIFT OF THE BRAIN FROM THE MIDDLE TO THE

POSTERIOR FOSSA THROUGH THE TENTORIAL POSTERIOR FOSSA THROUGH THE TENTORIAL INCISURAINCISURA

MAY BE UNILATERAL OR “CENTRAL”MAY BE UNILATERAL OR “CENTRAL”SECONDARY EFFECTS INCLUDE:SECONDARY EFFECTS INCLUDE:

Compression of the third cranial nerve(s)Compression of the third cranial nerve(s)Duret hemorrhages in midline rostral brainstemDuret hemorrhages in midline rostral brainstemCompression of the contralateral cerebral peduncle Compression of the contralateral cerebral peduncle (Kernohan’s notch)(Kernohan’s notch)Compression of the posterior cerebral artery with Compression of the posterior cerebral artery with infarction of the medial occipital lobeinfarction of the medial occipital lobe

HYDROCEPHALUS

DILATATION OF THE VENTRICULAR DILATATION OF THE VENTRICULAR SYSTEMSYSTEM

NONCOMMUNICATING: Due to obstruction NONCOMMUNICATING: Due to obstruction within the ventricular system, e.g., tumor, within the ventricular system, e.g., tumor, aqueductal stenosisaqueductal stenosis

COMMUNICATING: Due to obstruction of CSF COMMUNICATING: Due to obstruction of CSF flow in the subarachnoid space with decreased flow in the subarachnoid space with decreased reabsorptionreabsorption

Complications and Outcome of Meningitis Consequences of meningitis can be mild, Consequences of meningitis can be mild,

moderate or severe,moderate or severe, with many survivors being left with permanent with many survivors being left with permanent

disabilitydisability Septicaemia and shock can lead to skin grafting Septicaemia and shock can lead to skin grafting and scarring, amputations and in severe cases and scarring, amputations and in severe cases

neurological deficits neurological deficits Meningitis can lead to damage in various areas of Meningitis can lead to damage in various areas of

the brain resulting in loss of sight, hearing and the brain resulting in loss of sight, hearing and neurodevelopmental deficitsneurodevelopmental deficits

Complications and Outcome of Meningitis ScarringScarring amputation of digits and limbsamputation of digits and limbs Neurological damageNeurological damage

Complications and Outcome of Meningitis Visual impairment and blindnessVisual impairment and blindness Auditory impairment and deafnessAuditory impairment and deafness Neuromotor disabilitiesNeuromotor disabilities Seizure disordersSeizure disorders Behaviour problemsBehaviour problems Learning difficultiesLearning difficulties

Complications and Outcome of Meningitis The complications associated with septic shock The complications associated with septic shock

can result in irreversible tissue damage and can result in irreversible tissue damage and gangrenegangrene

Tissue damage occurs as a result of inadequate Tissue damage occurs as a result of inadequate tissue perfusion and oxygenation from tissue perfusion and oxygenation from hypotension and coagulopathy hypotension and coagulopathy

Skin grafting and amputation may be necessarySkin grafting and amputation may be necessary

Complications and Outcome of Meningitis Damage to various areas of the brain as a Damage to various areas of the brain as a

consequence of inflammation in the subarachnoid consequence of inflammation in the subarachnoid spacespace

This appears as exudate covering the surface of This appears as exudate covering the surface of the brainthe brain

Many complications are due to cranial nerve Many complications are due to cranial nerve damagedamage

Complications and Outcome of Meningitis Psychosocial and emotional problems - Psychosocial and emotional problems - low low

self esteem and difficulties copingself esteem and difficulties coping

Subtle complications - Subtle complications - poor concentration, poor concentration, clumsiness and mood swingsclumsiness and mood swings

May be age-specificMay be age-specific

Complications and Outcome of Meningitis TirednessTiredness

Recurring headachesRecurring headaches

Memory loss, which may be severeMemory loss, which may be severe

Difficulties in concentrationDifficulties in concentration Anger outburstsAnger outbursts ClumsinessClumsiness

Differential Diagnosis of Meningitis Brain abscessBrain abscess EncephalitisEncephalitis Tumor like Tumor like

ASTROCYTOMAS,OLIGODENDROGLIOMAS,EPASTROCYTOMAS,OLIGODENDROGLIOMAS,EPENDYMOMASENDYMOMAS

MIXED GLIOMASMIXED GLIOMAS Metastatic tumor Metastatic tumor Subdural and epidural empyemaSubdural and epidural empyema subduralsubdural subarachnoidsubarachnoid

Differential Diagnosis of Meningitis Chemical meningitis: Rupture of tumorChemical meningitis: Rupture of tumor intracranial haemorrage likeintracranial haemorrage like EpiduralEpidural subduralsubdural SubarachnoidSubarachnoid intraparenchymalintraparenchymal

Differential Diagnosis of Meningitis metabolic encephalopathymetabolic encephalopathy hyperglycaemic comahyperglycaemic coma uremiauremia hepatic encephalopathyhepatic encephalopathy vit B deficienciesvit B deficiencies vascular diseases (amyloid angiopathy, vascular diseases (amyloid angiopathy,

vasculitis, berry aneurysms, A-V vasculitis, berry aneurysms, A-V malformationsmalformations

CSF & LUMBER PUNCTURE

It is produced in the brain by modified ependymal It is produced in the brain by modified ependymal cells in the choroid plexus (approx. 50-70%), and cells in the choroid plexus (approx. 50-70%), and the remainder is formed around blood vessels and the remainder is formed around blood vessels and along ventricular walls. It circulates from the along ventricular walls. It circulates from the choroid plexus through the interventricular choroid plexus through the interventricular foramina (foramen of Monro) into the third foramina (foramen of Monro) into the third ventricle, and then through the cerebral aqueduct ventricle, and then through the cerebral aqueduct (aqueduct of Sylvius) into the fourth ventricle, (aqueduct of Sylvius) into the fourth ventricle, where it exits through two lateral apertures where it exits through two lateral apertures (foramina of Luschka) and one median aperture (foramina of Luschka) and one median aperture (foramen of Magendie). (foramen of Magendie).


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


The cerebrospinal fluid is produced at a rate The cerebrospinal fluid is produced at a rate of 500 ml/day. Since the brain can only of 500 ml/day. Since the brain can only contain from 135-150 ml, large amounts are contain from 135-150 ml, large amounts are drained primarily into the blood through drained primarily into the blood through arachnoid granulations in the superior arachnoid granulations in the superior sagittal sinus. Thus the CSF turns over sagittal sinus. Thus the CSF turns over about 3.7 times a day. about 3.7 times a day.


Direct cranial measurement of ICP.Direct cranial measurement of ICP.

ICP monitoring requires admission to the hospital. ICP monitoring requires admission to the hospital. A small pressure monitor is inserted through the A small pressure monitor is inserted through the skull into the brain or ventricles to measure the skull into the brain or ventricles to measure the ICP. pressure monitoring (either by lumbar ICP. pressure monitoring (either by lumbar catheter or the intracranial method) can detect an catheter or the intracranial method) can detect an abnormal pattern of pressure waves.abnormal pattern of pressure waves.


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


The "gold standard" technique for ICP The "gold standard" technique for ICP monitoring is a catheter inserted into the monitoring is a catheter inserted into the lateral ventricle, usually via a small right lateral ventricle, usually via a small right frontal burr hole. This can be connected to a frontal burr hole. This can be connected to a standard pressure transducer via a fluid-standard pressure transducer via a fluid-filled catheter in neurosurgery.filled catheter in neurosurgery.


Indirect measurement of ICP by lumber puncture.Indirect measurement of ICP by lumber puncture. The two principal objections to lumbar puncture in The two principal objections to lumbar puncture in

the diagnosis of intracranial hypertension have the diagnosis of intracranial hypertension have been the danger of inducing brain-stem been the danger of inducing brain-stem compression through tentorial or tonsillar compression through tentorial or tonsillar herniation and the contention that spinal fluid herniation and the contention that spinal fluid pressure is not always an accurate reflection of pressure is not always an accurate reflection of ICP. ICP.


IndicationsIndications

1. Diagnostic aid1. Diagnostic aid 2. Therapy for idiopathic intracranial 2. Therapy for idiopathic intracranial

hypertensionhypertension 3. Infusion of anaesthetic (“spinal”), 3. Infusion of anaesthetic (“spinal”),

chemotherapy, or contrast agents chemotherapy, or contrast agents (myelography)(myelography)


ContraindicationsContraindications - INR > 1.4 or other coagulopathy- INR > 1.4 or other coagulopathy - platelets < 50- platelets < 50 - infection at desired puncture site- infection at desired puncture site - obstructive / non-communicating hydrocephalus- obstructive / non-communicating hydrocephalus - intracranial mass- intracranial mass - high intracranial pressure (ICP) / papilloedema - high intracranial pressure (ICP) / papilloedema


An LP may safely be performed without An LP may safely be performed without first doing a CT head in a young previously first doing a CT head in a young previously healthy patient with no history of seizures, a healthy patient with no history of seizures, a normal level of consciousness and a normal normal level of consciousness and a normal neurological exam.neurological exam.


AnatomyAnatomy

Intercristal line is an imaginary line that Intercristal line is an imaginary line that connects the superior border of the iliac connects the superior border of the iliac crestscrests

- L4/5 interspace is the first interspace - L4/5 interspace is the first interspace caudal to the intercristal linecaudal to the intercristal line


MaterialsMaterials sterile gloves and masksterile gloves and mask LP kit (contains: syringe, 25 and 22G needles, 1% LP kit (contains: syringe, 25 and 22G needles, 1%

lidocaine, sterile drapes, sponges and gauze, 22G lidocaine, sterile drapes, sponges and gauze, 22G LP needle, stopcock and manometer, 4 collection LP needle, stopcock and manometer, 4 collection tubes and band-aid)tubes and band-aid)

- sterilization solution (chlorhexidine or - sterilization solution (chlorhexidine or proviodine)proviodine)


TechniqueTechnique 1. Obtain patient consent1. Obtain patient consent 2. Position the patient,close to edge of bed as 2. Position the patient,close to edge of bed as

possiblepossible 3.Pillow under head and between legs3.Pillow under head and between legs 4.Head flexed and legs curled up towards 4.Head flexed and legs curled up towards

chest,ask patient to bulge out lumbosacral spinechest,ask patient to bulge out lumbosacral spine 5.Carefully open LP kit and put cleaning solution 5.Carefully open LP kit and put cleaning solution

in reservoir.in reservoir.

Positioning

INCORRECT CORRECT


6.Put on mask and sterile gloves.6.Put on mask and sterile gloves. 7.Sterilize the field using the sterilizing 7.Sterilize the field using the sterilizing

solution and sponges provided. Clean a 6 solution and sponges provided. Clean a 6 inch area around the desired entry site, inch area around the desired entry site, proceeding outward in concentric circles. proceeding outward in concentric circles. Do this 3 separate times. Place sterile drape Do this 3 separate times. Place sterile drape over the field.over the field.

Skin Preparation Overlying skin cleaned Overlying skin cleaned

with povidone-iodinewith povidone-iodine

Sterile drape placed Sterile drape placed with an opening over with an opening over the LSthe LS

Spinal Needle Insertion Local anesthesia infiltrated Local anesthesia infiltrated 20 or 22 gauge spinal needle 20 or 22 gauge spinal needle

with stylet with stylet Advance spinal needle slowly, Advance spinal needle slowly,

angling slightly toward the angling slightly toward the headhead

Flat surface of bevel of needle Flat surface of bevel of needle

positioned to face patient’spositioned to face patient’s flanksflanks


8. Ensure all items in LP tray are ready for 8. Ensure all items in LP tray are ready for use. E.g.. 1% or 2% lidocaine loaded into use. E.g.. 1% or 2% lidocaine loaded into syringe, collection tubes open, test to see syringe, collection tubes open, test to see that the stylet slides in/out of LP needle that the stylet slides in/out of LP needle easily, stopcock and manometer for opening easily, stopcock and manometer for opening pressure measurement readypressure measurement ready


9.Local anaesthesia. Using a 25G needle, 9.Local anaesthesia. Using a 25G needle, inject 1% or 2% lidocaine under the skin at inject 1% or 2% lidocaine under the skin at the desired entry site. A small bleb under the desired entry site. A small bleb under the skin is sufficient. Switch the needle tip the skin is sufficient. Switch the needle tip to the 22G needle and anaesthetize deeper to the 22G needle and anaesthetize deeper structures by inserting the needle further, structures by inserting the needle further, injecting lidocaine while proceeding injecting lidocaine while proceeding forward.forward.


10.Insert LP needle. The bevel should be parallel 10.Insert LP needle. The bevel should be parallel to the spinal column. Always advance the needle to the spinal column. Always advance the needle with the stylet in place. Aim needle in the midline, with the stylet in place. Aim needle in the midline, slightly cephalad, towards the patient’s umbilicus. slightly cephalad, towards the patient’s umbilicus. Advance needle slowly until it is inserted 2-3 cm, Advance needle slowly until it is inserted 2-3 cm, then withdraw the stylet to check for CSF return. then withdraw the stylet to check for CSF return. Continue to advance the needle, periodically Continue to advance the needle, periodically checking for CSF return. Often a "pop'' is checking for CSF return. Often a "pop'' is appreciated as the needle pierces the dural appreciated as the needle pierces the dural membrane.membrane.


If the needle meets bone or if blood returns If the needle meets bone or if blood returns (hitting the venous plexus anterior or (hitting the venous plexus anterior or posterior to the spinal canal), withdraw the posterior to the spinal canal), withdraw the needle to the skin and redirect the needleneedle to the skin and redirect the needle


11.Once CSF flow is obtained, measure the 11.Once CSF flow is obtained, measure the opening pressure by attaching first the opening pressure by attaching first the stopcock to the LP needle and then the stopcock to the LP needle and then the manometer to the stopcock.manometer to the stopcock.


12.Collect CSF fluid into sequential tubes. 12.Collect CSF fluid into sequential tubes. about 2 ml in each tube is sufficient for about 2 ml in each tube is sufficient for basic investigations. More fluid will need to basic investigations. More fluid will need to be collected for special tests e.g. viral PCR, be collected for special tests e.g. viral PCR, cytology etccytology etc

13.Reinsert stylet. Withdraw needle. Place 13.Reinsert stylet. Withdraw needle. Place band-aid over insertion site.band-aid over insertion site.


What to order What to order The basicsThe basics Tube #1 Cell count and differentialTube #1 Cell count and differential

Tube #2 Chemistry (protein, glucose)Tube #2 Chemistry (protein, glucose)

Tube #3 Culture and Gram stainTube #3 Culture and Gram stain

Tube #4 reserve with csf in itTube #4 reserve with csf in it


Other tests to considerOther tests to consider - Will need to collect extra fluid for these - Will need to collect extra fluid for these

tests in tube #3 or #4.tests in tube #3 or #4. India ink and / or Cryptococcal Ag (for India ink and / or Cryptococcal Ag (for

Cryptococcus neoformans)Cryptococcus neoformans) AFB and / or PCR for TBAFB and / or PCR for TB Viral PCR (includes HSV, CMV, EBV)Viral PCR (includes HSV, CMV, EBV) arbovirus / WNV, echovirusarbovirus / WNV, echovirus


VDRLVDRL

fungal culturefungal culture

viral cultureviral culture

PCR and /or antibody titers for Lyme ds.PCR and /or antibody titers for Lyme ds.


oligoclonal banding (3-4 ml)oligoclonal banding (3-4 ml)

IgG index, IgG :albumin ratioIgG index, IgG :albumin ratio

cytology (must be collected in cytology fixative) cytology (must be collected in cytology fixative) (8-10ml)(8-10ml)

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


How much CSF to withdraw?How much CSF to withdraw?

- CSF is produced at a rate of 0.3 ml/min in - CSF is produced at a rate of 0.3 ml/min in adults or 450 ml/24hadults or 450 ml/24h

- CSF volume is approximately 150 ml in - CSF volume is approximately 150 ml in an adultan adult


- For basic investigations, only require 4-8 - For basic investigations, only require 4-8 mlml

- May require more volume for special tests. - May require more volume for special tests. Maximum to be removed at one time should Maximum to be removed at one time should probably not exceed 20 ml.probably not exceed 20 ml.


Normal opening pressure ranges 50 to 200 Normal opening pressure ranges 50 to 200 mm H20 in adults and up to 250 mm H20 in mm H20 in adults and up to 250 mm H20 in obese women patients or 5-20 cm of H20.obese women patients or 5-20 cm of H20.

2 Intracranial hypotension is defined as an 2 Intracranial hypotension is defined as an opening pressure of less than 50 mm H20. opening pressure of less than 50 mm H20.


Normal CSF is crystal clear. However, as Normal CSF is crystal clear. However, as few as 200 white blood cells (WBCs) per few as 200 white blood cells (WBCs) per mm3 or 400 red blood cells (RBCs) per mm3 or 400 red blood cells (RBCs) per mm3 will cause CSF to appear turbid.mm3 will cause CSF to appear turbid.


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

cells <5/cmm mostly lymphocytecells <5/cmm mostly lymphocyte


Xanthochromia is a yellow, orange, or pink Xanthochromia is a yellow, orange, or pink discoloration of the CSF, most often caused discoloration of the CSF, most often caused by the lysis of RBCs resulting in by the lysis of RBCs resulting in hemoglobin breakdown to oxyhemoglobin,hemoglobin breakdown to oxyhemoglobin,

methemoglobin, and bilirubin. methemoglobin, and bilirubin.


Discoloration begins after RBCs have been Discoloration begins after RBCs have been in spinal fluid for about two hours, and in spinal fluid for about two hours, and remains for two to four weeks.remains for two to four weeks.

Xanthochromia is present in more than 90 Xanthochromia is present in more than 90 percent of patients within 12 hours of percent of patients within 12 hours of subarachnoid hemorrhage subarachnoid hemorrhage


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


Culture provides definitive diagnosis as Culture provides definitive diagnosis as well as identificaiton of pathogenic well as identificaiton of pathogenic organism and antibiotic susceptibilitiesorganism and antibiotic susceptibilities

blood culture positive in 50% casesblood culture positive in 50% cases


The Xpert EV test, approved for use in March The Xpert EV test, approved for use in March 2007, can rapidly test for enteroviral meningitis. 2007, can rapidly test for enteroviral meningitis. The test uses a reverse-transcription PCR The test uses a reverse-transcription PCR disposable cartridge on which CSF is applied, and disposable cartridge on which CSF is applied, and enteroviral genetic material is identified if present. enteroviral genetic material is identified if present. Results are ready in 2.5 hours, as opposed to days Results are ready in 2.5 hours, as opposed to days to weeks in traditional PCR studies.to weeks in traditional PCR studies.


CT scan with contrast helps in ruling out CT scan with contrast helps in ruling out intracranial pathology. Contrasted scans should be intracranial pathology. Contrasted scans should be obtained to evaluate for any enhancement along obtained to evaluate for any enhancement along the meninges.the meninges.

ct scan also excludes intracranial abscess, subdural ct scan also excludes intracranial abscess, subdural empyema, or other lesions. Alternatively, and if empyema, or other lesions. Alternatively, and if readily available, an MRI of the brain should be readily available, an MRI of the brain should be done.done.


MRI with contrast is the criterion standard MRI with contrast is the criterion standard in visualizing intracranial pathology in viral in visualizing intracranial pathology in viral encephalitis HSV-1 commonly affects basal encephalitis HSV-1 commonly affects basal frontal and temporal lobes with a typical frontal and temporal lobes with a typical picture of diffusely enhancing bilateral picture of diffusely enhancing bilateral lesions.lesions.


All patients whose condition is not All patients whose condition is not improving clinically within 24-48 hours improving clinically within 24-48 hours should have more extensive work-up to should have more extensive work-up to discern the cause of meningitis.discern the cause of meningitis.

Blood, feces, and throat swabs may be sent Blood, feces, and throat swabs may be sent for viral serology and cultures.for viral serology and cultures.


Acid-fast staining of CSF should be Acid-fast staining of CSF should be performed and the remaining fluid should performed and the remaining fluid should be sent for PCR testing for HIV and CMV.be sent for PCR testing for HIV and CMV.

Serum titers of antibodies against HIV and Serum titers of antibodies against HIV and toxoplasma should be obtained.toxoplasma should be obtained.


EEG may be performed if encephalitis or EEG may be performed if encephalitis or subclinical seizures are suspected in the subclinical seizures are suspected in the altered patient. Periodic lateralized altered patient. Periodic lateralized epileptiform discharges (PLEDs) are often epileptiform discharges (PLEDs) are often seen in herpetic encephalitis.seen in herpetic encephalitis.


CSF Lactate ConcentrationCSF Lactate Concentration

normally 14 mg/dl normally 14 mg/dl in bacterial meningitis is usually <25 mg/dl in bacterial meningitis is usually <25 mg/dl PCR for microbial DNA may become PCR for microbial DNA may become

sensitive and specific method for bacterial sensitive and specific method for bacterial identificationidentification


CT Scanning sould be done and preferred choice CT Scanning sould be done and preferred choice before Lumbar Puncture in Suspected Meningitisbefore Lumbar Puncture in Suspected Meningitis

Acid-fast staining of CSF should be performed Acid-fast staining of CSF should be performed and the remaining fluid should be sent for PCR and the remaining fluid should be sent for PCR testing for HIV and CMV.testing for HIV and CMV.

Serum titers of antibodies against HIV and Serum titers of antibodies against HIV and toxoplasma should be obtained.toxoplasma should be obtained.


Additional serum collection 10-21 days later may Additional serum collection 10-21 days later may aid in discerning rising titers in the antibodies aid in discerning rising titers in the antibodies against specific viral pathogens; a 4-fold increase against specific viral pathogens; a 4-fold increase in viral antibodies confirms the diagnosis. This is in viral antibodies confirms the diagnosis. This is particularly useful for arboviral and LCMV cases, particularly useful for arboviral and LCMV cases, but also is helpful in ruling out toxoplasmosis, but also is helpful in ruling out toxoplasmosis, leptospirosis, borreliosis, and rickettsial infections. leptospirosis, borreliosis, and rickettsial infections. Although some of these studies do not yield an Although some of these studies do not yield an immediate result for clinical decision making, they immediate result for clinical decision making, they may be useful for prognostication.may be useful for prognostication.

CSF PRESSURE

Opening pressure: 5-20 cm water (only Opening pressure: 5-20 cm water (only valid in lateral decubitus position) or 50-valid in lateral decubitus position) or 50-200 mm of H20.200 mm of H20.

CSF PRESSURE

ICP is measured in millimeters of mercury ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 5–20 (mmHg) and, at rest, is normally 5–20 mmHg for a supine adult, and becomes mmHg for a supine adult, and becomes negative (averaging -10 mmHg) in the negative (averaging -10 mmHg) in the vertical position.vertical position.

CSF PRESSURE

Normal CSF pressure in the lower back is Normal CSF pressure in the lower back is between 50-200 mm water. between 50-200 mm water.

Normal Intracranial pressure(within the Normal Intracranial pressure(within the cranium) however is between 5-20 mmHg cranium) however is between 5-20 mmHg or 50-200 mm H2O in adults.or 50-200 mm H2O in adults.

Investigations & Diagnosis of Meningitis Repeat CSF analysis 24 to 36 hours Repeat CSF analysis 24 to 36 hours

(minimum of 24 hours) after initiation of (minimum of 24 hours) after initiation of therapytherapy

Changes in therapy/concomitant therapy as Changes in therapy/concomitant therapy as neededneeded

Evaluation of drug concentrations in CSFEvaluation of drug concentrations in CSF

Investigations & Diagnosis of Meningitis 5-7 weeks after completion of all therapy5-7 weeks after completion of all therapy Lumbar puncture repeated only if clinically Lumbar puncture repeated only if clinically

indicatedindicated

Investigations & Diagnosis of Meningitis LATE POST-THERAPY VISITLATE POST-THERAPY VISIT 5-6 months after completion of therapy5-6 months after completion of therapy Emphasis on hearing/ development/ Emphasis on hearing/ development/

neurological findingsneurological findings Behavioral difficulties should be Behavioral difficulties should be

documented as welldocumented as well

Investigations & Diagnosis of Meningitis Persistence of pathogen at 24-36 hr. tap Persistence of pathogen at 24-36 hr. tap

leading to additional therapy or change in leading to additional therapy or change in therapy. therapy.

CSF evaluation

ConditionCondition WBCWBCProtein Protein (mg/dL)(mg/dL)

Glucose Glucose (mg/dL)(mg/dL)

NormalNormal <5 , lymphocytes mainly<5 , lymphocytes mainly 5-455-45>50 (2.2 >50 (2.2 mmol to 4 mmol to 4 mmol/l)mmol/l)

Bacterial, Bacterial, acuteacute

>1000K PMN’s>1000K PMN’s100-500 or 100-500 or >1.5gm/l>1.5gm/l

<2.2 m <2.2 m mol/lmol/l

ViralViral<1000<1000 increasedincreased

Low to Low to normalnormal

TBTB <500<500 increasedincreased decreaseddecreased

FungalFungal < 500< 500 increasedincreased decreaseddecreased

CSF DiagnosisWBCWBC GlucoseGlucose ProteinProtein

NormalNormal <5 <5 (lymphocytes)(lymphocytes)

2/32/3rdrd of serum of serum glucoseglucose

15 to 45 15 to 45 mg/dlmg/dl

Bacterial Bacterial MeningitisMeningitis

>1000 PMN’s >1000 PMN’s predominatepredominate

LowLow Elevated Elevated (>100 mg)(>100 mg)

Aseptic Aseptic MeningitisMeningitis

Elevated Elevated (PMN’s early, (PMN’s early, lymphocytes lymphocytes late)late)

Normal to Normal to lowlow

Normal or Normal or slightly slightly elevatedelevated

TB TB MeningitisMeningitis

Elevated Elevated (PMN’s early, (PMN’s early, lymphs latelymphs late

Low Low Elevated Elevated (>100 mg)(>100 mg)

CSF evaluation

ConditionCondition WBCWBCProtein Protein (mg/dL)(mg/dL)

Glucose Glucose (mg/dL)(mg/dL)

NormalNormal <5, lymph's mainly<5, lymph's mainly 5-455-45 >50>50

Bacterial, Bacterial, acuteacute

>1000 PMN’s>1000 PMN’sIncreased>Increased>more than more than 100 mg/d100 mg/d

LowLow

TBTB <500<500 Increased Increased upto 500 upto 500 mg/dlmg/dl

lowlow

FungalFungal <500<500 Upto 500Upto 500 lowlow

ViralViral <1000<1000 Upto 100Upto 100 NormalNormal

Summary of Typical CSF Findings

NormalNormal BacterialBacterial Viral Viral TBTBCellsCells 0-50-5 >1000>1000 <1000<1000 <500<500PolymorphsPolymorphs 00 PredominatePredominate EarlyEarly +/- increased+/- increased

LymphocytesLymphocytes 55 LateLate PredominatePredominate IncreasedIncreased

GlucoseGlucose 60-8060-80 DecreasedDecreased NormalNormal DecreasedDecreased

CSF plasma:CSF plasma:

Glucose ratioGlucose ratio66%66% <40%<40% NormalNormal < 30%< 30%

ProteinProtein 5-405-40 IncreasedIncreased +/- Increased+/- Increased IncreasedIncreased

CultureCulture NegativeNegative PositivePositive NegativeNegative +TB+TB

TREATMENT of MENINGITIS

Empiric Antibiotics:Empiric Antibiotics: Cefotaxime 2g IV 6 hrlyCefotaxime 2g IV 6 hrly add Vancomycin 1-2 g IV 8-12 hrly in all patients add Vancomycin 1-2 g IV 8-12 hrly in all patients

(till possibility of Penicillin-resistant Strep (till possibility of Penicillin-resistant Strep pneumoniae has been ruled out)pneumoniae has been ruled out)

add Ampicllin 2g IV 6 hrly in elderly or add Ampicllin 2g IV 6 hrly in elderly or immunocompromised patients (for Listeria immunocompromised patients (for Listeria infections)infections)


for patients with serious penicillin allergies, for patients with serious penicillin allergies, Meropenem 1-2g IV 8hrly as alternativeMeropenem 1-2g IV 8hrly as alternative

Ceftazidime (2g IV 8 hrly or BD) + Vancomycin Ceftazidime (2g IV 8 hrly or BD) + Vancomycin for neurosurgical patients, those with shunts or for neurosurgical patients, those with shunts or CSF leaksCSF leaks

May consider adjunctive Acyclovir (10 mg/kg IV May consider adjunctive Acyclovir (10 mg/kg IV 8 hrly if normal renal function) in case of viral 8 hrly if normal renal function) in case of viral infection.infection.


Therapy can be modified as the results of Therapy can be modified as the results of Gram stain, cultures, and PCR testing Gram stain, cultures, and PCR testing become available. Patients in unstable become available. Patients in unstable condition need critical care unit admission condition need critical care unit admission for airway protection, neurologic checks, for airway protection, neurologic checks, and prevention of secondary complications.and prevention of secondary complications.


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


Cerebral edema does occur in cases of Cerebral edema does occur in cases of severe encephalitis and may require severe encephalitis and may require intracranial pressure control by infusion of intracranial pressure control by infusion of mannitol (1 g/kg initial dose followed by mannitol (1 g/kg initial dose followed by 0.25-0.5 g/kg 6 hrly), IV dexamethasone, or 0.25-0.5 g/kg 6 hrly), IV dexamethasone, or intubation and mild hyperventilation, with intubation and mild hyperventilation, with arterial PCO2 around 28-30 mm Hgarterial PCO2 around 28-30 mm Hg


Use of adjunctive corticosteroids:Use of adjunctive corticosteroids:

- prior to or along with initial antibiotics, - prior to or along with initial antibiotics, administer Dexamethasone 10 mg IV for administer Dexamethasone 10 mg IV for suspected bacterial meningitis (based on cloudy suspected bacterial meningitis (based on cloudy CSF, CSF WBC counts > 1000 or + Gram stain)CSF, CSF WBC counts > 1000 or + Gram stain)

- continue 10 mg IV 8 hrly x 4 days- continue 10 mg IV 8 hrly x 4 days


Isolation & Contact Prophylaxis:Isolation & Contact Prophylaxis:

- Generally isolate cases of bacterial - Generally isolate cases of bacterial meningitis for up to 48 hours of appropriate meningitis for up to 48 hours of appropriate antibioticsantibiotics

- Concern is to reduce transmission of - Concern is to reduce transmission of meningococcal infectionsmeningococcal infections


can be taken out of isolation after this time can be taken out of isolation after this time or if alternative pathogen identifiedor if alternative pathogen identified

- department of health should be notified of - department of health should be notified of pathogens in pyogenic meningitispathogens in pyogenic meningitis


Close contacts (family members, partners, Close contacts (family members, partners, co-workers or school children) should co-workers or school children) should receive prophylaxis if meningococcal or receive prophylaxis if meningococcal or haemophilus influenzae type B (if not haemophilus influenzae type B (if not vaccinated):vaccinated):

- rifampin 600 mg PO bid x 2d- rifampin 600 mg PO bid x 2d - ciprofloxacin 500 mg PO single dose- ciprofloxacin 500 mg PO single dose


dexamethasone 0.6 mg/kg/day IV 6-8 hrly dexamethasone 0.6 mg/kg/day IV 6-8 hrly for 4 days for 4 days

reduces incidence of neurologic sequelae, reduces incidence of neurologic sequelae, i.e., hearing loss i.e., hearing loss

electrolyte abnormalities - SIADH electrolyte abnormalities - SIADH

Prognostic Factors

1. Age1. Age 2. Level of Consciousness (50% mortality if 2. Level of Consciousness (50% mortality if

unresponsive or minimally responsive on unresponsive or minimally responsive on admission)admission)

3. Seizures early in course3. Seizures early in course 4. Strep. pneumoniae meningitis4. Strep. pneumoniae meningitis 5. CSF results (lower glucose & WBC 5. CSF results (lower glucose & WBC

counts, higher protein)counts, higher protein)

viral meningitis by dr bashir ahmed dar associate professor medicine chinkipora sopore kashmir

Health & Medicine