23. intracranial infection - prof sunartini

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  • 7/26/2019 23. Intracranial Infection - Prof Sunartini

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    Intracranial Infection

    in infant and children

    Sunartini

    INT Prog. FM UGM22042010

    Infections of the CNS

    two broad categories- those which involve primarily the meninges,

    and- those which are confined primarily to theparenchyma.

    Under the heading of meningeal infections, wewill consider general concepts after whichthree basic categories will be discussed:- pyogenic meningitis,- granulomatous meningitis,- lymphocytic meningitis.

    Infections of the CNS (2)

    Infection of the central nervous system (CNS)can be viral, bacterial, fungal, or parasitic inorigin. Infectious microorganisms most often

    enter the CNS by direct penetration aftertrauma or by travelling in the bloodstream

    There are three major categories of CNS infectionstreated by a neuro-ICU:

    Encephalitis Meningitis Brain Abscess

    Infections of the CNS(3)

    In contrast to the organization of meningeal infections,parenchymal infections have been organized in termsof the various types of organisms which include

    syphilis, parasites, fungi, viruses, and prions(scrapie, kuru & Creutzfeldt-Jakob disease).The definitions of at least two terms should be madeclear for parenchymal infections:

    cerebritis and encephalitis.

    Both of these terms imply inflammation of parenchymain the cerebrum, and on occasion are usedinterchangeably. However, by convention these termsdo have specific and different meanings among

    practicing neuropathologists

    Infections of the CNS (4)

    Cerebritis means inflammation of all tissues in thebrain substance, and is used to indicate a stagepreliminary to abscess formation. Thus, cerebritis is avery destructive process and implies bacterial infection.

    Encephaltitis, on the other hand, meansinflammation of brain tissue secondary to viral infection.Inflammation in encephalitis is not usually as intense asin cerebritis, and the destruction, while still profound, is

    not usually as great.

    Myelitis is the counterpart of encephalitis in the spinalcord.

    Encephalitis

    What is encephalitis?

    Encephalitis is defined as inflammation of the brain dueto an infection.

    This inflammation is commonly the result of a viral

    infection. Viruses can gain access to the centralnervous system (CNS) through the blood or by travelingwithin nerve cells (neurons).

    The neuro-ICU deals primarily with acute viralencephalitis.There are approximately 20,000 cases of encephalitisin America each year.

    In Indonesia no exact data.

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    MeningitisWhat is meningitis?Meninges is a membranous covering the innersurface of the skull of the brain

    A fluid known as cerebrospinal fluid (CSF) circulatesaround the brain and serves to cushion the brainagainst injury.

    Meningitis is an inflammation of the meninges dueto infection.It occurs when a foreign pathogen invades thesubarachnoid space and populates the CSF.The foreign microorganisms can either be bacteria orviruses. meningitis can be classified as eitherbacterialor viral.Since bacterial infection is much more serious, aneuro-ICU is specialized towards the treatment ofthis type of meningitis.

    Cont Epidemiology :

    1995 : bacterial as the etiology of 2800 cases ofmeningitis in children under 18 years in USA

    1986 :cases were children of 1 mo -5 yr old,in1995 meningitis cases in this group 87%decreased and median age of bacterialmeningitis bakterialis meningkat increased to15% in the age of 15 -25 yr old

    2001: India, from 54 of children with acutebacterial meningitis 78% were in the age of 1year and 52 % under 6 months old.

    What are the causes of bacterial meningitis?Generally, bacterial meningitis is more dangerous than

    the viral form and can constitute a medical emergency.

    Two of the major forms of bacteria* Streptococcus pneumoniaeand Neisseria meningitidis. ------>Therefore, bacterial meningitis usually occurs in either a

    pneumococcal or a meningococcal form.Pneumococcal meningitis is typically observed in adults.

    It can arise following brain trauma, and is predisposed bysickle cell anemia, alcoholism, and diabetes.

    Meningococcal meningitis most often occurs in children,adolescents, and young adults.

    Cont

    Etiologi : 1982- 2001 : bacterial the

    study in Public HealthLaboratory Service (PHLS)Neisseria meningitidis.

    3 type of bacterial cause ofacute bacterial meningitis ,are Streptococcuspneumoniae, Neisseria

    meningitidis, andHaemophilus influenzab(Hib).

    Organism Identified Most FrequentlyOrganism Identified Most Frequently

    as a Cause of Bacterial Meningitisas a Cause of Bacterial Meningitis

    Acute BacterialAcute BacterialMeningitisMeningitis

    Chronic BacterialChronic BacterialMeningitisMeningitis

    StreptococStreptococ.. pneumoniaepneumoniae

    HaemophilusHaemophilus influenzaeinfluenzae

    NeisseriaNeisseria meningitidismeningitidis

    Escherichia coliEscherichia coli

    Other gramOther gram--negatifnegatifbacillibacilli

    ListeriaListeria monocytogenesmonocytogenes

    Salmonella speciesSalmonella species

    LeptospiraLeptospira speciesspecies

    StaphylococcusStaphylococcus aureusaureus

    Group B streptococciGroup B streptococci

    MycobactMycobact. tuberculosis. tuberculosis

    TreponemaTreponema pallidumpallidum

    BorreliaBorrelia burgdorferiburgdorferi

    The Age distribution of 4 important types of acute bacterialThe Age distribution of 4 important types of acute bacterialmeningitis in a tropical African Country where meningococcalmeningitis in a tropical African Country where meningococcal

    meningitis is prevalent at a later age than in developed countrimeningitis is prevalent at a later age than in developed countrieses

    0 1 12 5 10 20 40 60 or >MONTHS YEARS

    AGE

    E. coli

    S. pneumoniae

    H. influenzae

    N. meningitis

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    Patofisiology

    Infection(ENT))

    Hematogenicspread out

    EntrancetpCNS

    Multiplicationof bscteria

    InflamationEdema

    CNS Dysfunction

    Severe HeadacgeNeckstiffnessPhotophobiaConvulsion(classic symptom)

    What are the clinical features of bacterialmeningitis?Bacterial meningitis presents as an acute disease.It is characterized by three main features:

    - headache,- high persistent fever, and- neck stiffness (an inability to bow the head, known as

    nuchal rigidity).Bacterial meningitis can also be accompanied by a varietyof other symptoms including- rashes,- nausea,- lethargy, and- general malaise.- In addition, seizures occur in about 20% of patients and- coma occurs in 5-10% of patients.The latter development is associated with a particularlypoor prognosis.

    Table 3. Diagnosis and treatment of meningitisDepend on the result of CSF examination

    CLINICAL PICTURE

    Cardinal Symptom Headache High fever persistent Neck stiffness (an inability to bow the head,

    known neckas nuchal rigidity)

    other symptoms including

    -rashes,

    - nausea,- lethargy, and- general malaise.- seizures occur in about 20% of patients- coma occurs in 5-10% of patients.

    The first signs : convulsion, irritabel,delirium, somnolent, letargi, & maybecoma

    Pathognomonis Sign : Meningeal Sign

    Neckstiffness, Brudzinsky I,II Sign, Kernig sign : (+)

    CLINICAL SIGN

    Specific Symptoms :Petechie & purpura: Meningococcemia

    some times H. infl.

    Progresive hemorrhage : MeningococcRash Str. PneumonieArthralgie : Meningococcemie & H. influenzae

    NeonatesNeonates

    High fever, vomiting, irritabel, convulsion,somnolent highpitch cry

    Specific : Large Fontanel bulging,tenderness Difficult to find meningeal sign e.gneck stiffness Brudzinsky and Kernig sign

    Baby (3Baby (3--1212 bulanbulan))

    Very difficult -- various clinical sign

    If there is a sign of sepsis --> consider

    intracranial infection

    Large fontanel : bulging

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    ..LUMBAR PUNCTURE : indication, contraindications,

    LCS: Oppalescent / unclear WBC increase Protein increase

    Glucose ratio between LCS : blood decerase

    Intracranial pressure on LCS increase

    Gram stain : positif bacteria

    Culture: Gold standard: positif

    Fast Diagnosis : latex partile agglutination

    DIAGNOSIS

    Laboratory Examination

    CSF Normal Baby BacterialMeningitis

    ViralMeningitis

    Leucocyte < 10 per m3 200-100.000/m3 25-1000/ m3

    Neutroph.

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    JAMA, 2007

    TREATMENT

    Fluid and electrolyte management

    Antibiotik

    Steroid dexametason

    Glucose 40%

    1.1. Nursing CareNursing Care

    2.2.In critical periodIn critical period ------> PICU> PICU

    3.3. treatmenttreatment

    a. Homeostasis ivfd

    b. Convulsion / st. convulsivus

    Stop seizure immediatelyStop seizure immediately

    Adequate OxygenationAdequate Oxygenation

    AirwayAirwayc. Corticosteroids for Bacterial M-is

    d. Antibiotics

    TREATMENT II. Antibiotic for Bacterial Meningitis

    Bacteriae Drugs

    N. Influensa

    S. Pneumonia

    N. Meningitis

    Gram Negatif

    Staphylococus

    -Kloramfenikol, ampisilin

    -Seftriakson, Sefotaksim

    -Penisilin, Kloramfenikol

    -Sefuroksim, Seftriakson

    -Vankomisin

    -Penisilin, Kloramfenikol

    -

    Sefuroksim, Seftriakson-Sebutaksim, Septazidin

    -Seftriakson, Amikasin

    -Gentamysin, netilmisin

    -Nafsilin, Vankomisin

    -Rifampisin

    THE PRINCIPAL OF ANTIBIOTIC

    1. Choose the proper AB

    2. Maintain the therapeutic level in CSF

    3. Use AB which can entrance through BBB

    4. The Ratio of AB level in CSF and blood are:

    KloramfenikolKloramfenikol 9 : 19 : 1 CefaloridinCefaloridin 1 : 701 : 70

    CefalotinCefalotin 1 : 71 : 7AmpisilinAmpisilin 1 : 561 : 56

    Influence withInfluence with

    Inflamation of meninges

    Protein bound

    ANTIBIOTIC ARE GIVEN IN 2 FASE

    I.vmin 5 DAYS (fever free), continued oral

    Culture (+) Drugs

    Neonates and babies:

    Combination of (1)

    or

    Neonates

    -(1) Ampisilin 200 400 mg/kg BB

    - + Kloramfenikol 100 mg/lg BB

    -(2) Ampisilin 200 400 mg/kg BB

    -+ Sefurokxim 100 200 mg/kg BB

    -Ampisilin 200 400 mg/kg BB

    -+ Gentamycin 6 mg/kg BB

    I. Result of culture : not yet ------> EMPIRICII. Result of culture positif : --> drugs sensitive

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    TABEL 4 Pengobatan yang direkomendasikan untukmeningitis aseptik

    Etiologi Pengobatan

    Cytomegalovirus Ganciclovir (Cytovene) (clinicalresearch trial)

    Enterovirus Immune globulin (possiblypleconaril)

    Herpes simplex virus Acyclovir (Zovirax)

    Hu manimmunodeficiency virus

    Multidrug antiretroviralregimens

    Lyme disease Ceftriaxone (Rocephin)

    Syphilis High -dose penicillin

    Toxoplasmosis Pyrimethamine (Daraprim) andsulfadiazine

    Tuberculosis Multidrug anti mycobacterialregimens

    Tunkelet al 2004

    How is bacterial meningitis treated in a neuro-ICU?The first step : to obtain a CSF sample via lumbar puncture and to then initiate antibiotic therapy.The antibiotic regimen should be specific to the type ofbacteria causing the meningitis.- a regimen of ampicillin and a third-generation

    cephalosporins such as ceftriaxone- Dehydration and/or shock ---> by blood volume

    expansion and the use of pressors to increase bloodpressure.

    - Cerebral edema and increased intracranial pressure- depressed level of consciousness,- severe headache, and- projectile vomiting.

    - ICP monitoring.- Seizures are treated by the use of rapid acting

    anticonvulsants such as diazepam and lorazepam.Lorazepam infusion is commonly followed-up with alonger lasting anticonvulsant known as phenytoin (Dilantin).

    Dose Guidelines of Intravenous Antimicrobials in Infantsand Children With Bacterial Meningitis

    Antibiotic

    Dose (mg/kg/d)

    IV

    Maximum Daily

    DoseDosing Interval

    Ampicillin 400 6-12 g q6h

    Vancomycin 60 2-4 g q6h

    Penicillin G 400,000 U 24 million q6h

    Cefotaxime 200-300 8-10 g q6h

    Ceftriaxone 100 4 g q12h

    Ceftazidime 150 6 g q8h

    Cefepime* 150 2-4 g q8h

    Imipenem 60 2-4 g q6h

    Meropenem 120 4-6 g q8h

    Rifampin 20 600 mg q12h

    *Minimal experience in pediatrics and not licensed for treatment of meningitis.

    Caution in use for treatment of meningitis because of possible seizures.

    Manajemen

    Admitted to the hospital, Antibioticin the dose of intracranial infectionFor bacterial meningitis : combination ofAmpicillin and Cefotaxime orChloramphenicol

    Empiric : acyclovir for neonates and babywith lesion in buccal or ginggiva /stomatitisor vesicle cause by herves virus, suspectedvirus ensefalitis, sepsis, without positifculture, or sepsis with HIV infection of theparent.

    Management Aseptic meningitis : symptomatic As general : minimize the symptom such as

    analgetics, fluid and treatment for prevention ofsequele

    Adequate oxigenation , fluid and electrolite

    Specific treatment for bactertial meningitisAntibiotics for Gram (+ and -) + Dexamethasone

    For virus used acyclovir or gancyclovir dependon the etiology with or without immunoglobulin

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    What is the prognosis for bacterialmeningitis?

    Prognosis directly depends on the speed with which therapyis initiated.It is also dependent on the identity of the invading bacteria- the age and- medical status of the patient.

    With rapid and effective treatment mortality ratesvary between 5-25%.

    Delayed long-term sequelae such as : deafness and intellectual deterioration. death.The earlier a diagnosis is made and treatment instituted, thegreater the chance of survival without neurologicaldisabilities.

    What are the complications of bacterialmeningitis?

    o) shock, a condition known as the Waterhouse-

    Friderichsen syndrome.p) cerebral edema.

    This can translate into a dangerous increase inthe pressure within the skull (the intracranial

    pressure or ICP). Both of these complicationsare life-threatening and mandate treatment inan intensive care unit.

    ENCEPHALITIS

    NN

    Herpes Simplex Encephalitis

    Herpes Simplex encephalitis is one of the mostserious complications of herpes simplex disease.There are two forms:

    Neonatal there is global involvement and the brainis almost liquefied. The mortality rate approaches100%.

    Focal disease the temporal lobe is most commonlyaffected. This form of the disease appears in childrenand adults. It is possible that many of these cases

    arise from reactivation of virus. The mortality rate ishigh (70%) without treatment.

    It is of utmost importance to make a diagnosis ofHSE early. It is general practice that IV acyclovir isgiven in all cases of suspected HSE before laboratoryresults are available.

    Neonatal Herpes Simplex (1)

    Incidence of neonatal HSV infection variesinexplicably from country to country e.g.from 1 in 4000 live births in the U.S. to 1 in10000 live births in the UK

    The baby is usually infected perinatallyduring passage through the birth canal.

    Premature rupturing of the membranes is awell recognized risk factor.

    Neonatal Herpes (2)

    The risk of perinatal transmission isgreatest when there is a florid primaryinfection in the mother.

    There is an appreciably smaller risk fromrecurrent lesions in the mother, probablybecause of the lower viral load and thepresence of specific antibody

    The baby may also be infected from othersources such as oral lesions from themother or a herpetic whitlow in a nurse.

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    Neonatal Herpes Simplex (3)

    The spectrum of neonatal HSV infection

    varies from a mild disease localized to theskin to a fatal disseminated infection.

    Infection is particularly dangerous inpremature infants.

    Where dissemination occurs, the organsmost commonly involved are the liver,adrenals and the brain.

    Where the brain is involved, the prognosisis particularly severe. The encephalitis isglobal and of such severity that the brainmay be liquefied.

    Neonatal Herpes (4)

    A large proportion of survivors of neonatalHSV infection have residual disabilities.

    Acyclovir should be promptly given in allsuspected cases of neonatal HSV infection.

    The only means of prevention is to offercaesarean section to mothers with florid

    genital HSV lesions.

    Other Manifestations..(1)

    Disseminated herpes simplex aremuch more likely to occur in immunocompromised individuals.

    The widespread vesicular resemblesthat of chickenpox. Many organs otherthan the skin may be involved e.g.

    liver, spleen, lungs, and CNS.

    Other Manifestation (2)

    Other cutaneous manifestations include

    eczema herpeticum which is potentially aserious disease that occurs in patients witheczema.

    Herpetic whitlow which arise from implantationof the virus into the skin and typically affect thefingers.

    zosteriform herpes simplex". This is a rarepresentation of herpes simplex where HSVlesions appear in a dermatomal distributionsimilar to herpes zoster.

    Laboratory Diagnosis (1)

    Direct Detection

    Electron microscopy of vesicle fluid - rapid result

    but cannot distinguish between HSV and VZV

    Immunofluorescence of skin scrappings - can

    distinguish between HSV and VZV

    PCR - now used routinely for the diagnosis of

    herpes simple encephalitis

    Laboratory Diagnosis.(2)

    Virus Isolation

    HSV-1 and HSV-2 are among the easiest viruses to

    cultivate. It usually takes only 1 - 5 days for a result

    to be available.

    Serology

    Not that useful in the acute phase because it takes

    1-2 weeks for before antibodies appear afterinfection. Used to document to recent infection.

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    Management

    At present, there are only a few indications ofantiviral chemo-therapy, with the high cost of

    antiviral drugs being a main consideration.Generally, antiviral chemotherapy is indicatedwhere the primary infection is especially severe,where there is dissemination, where sight isthreatened, and herpes simplex encephalitis.

    MANAGEMENT.

    Acyclovir this the drug of choice for most

    situations at present. It is available in a number offormulations:

    Intra Vena (HSV infection in normal and immuno

    compromised patients)

    Oral (treatment and long term suppression of

    mucocutaneous herpes and prophylaxis ofHSV in immunocompromised patients)

    Cream (HSV infection of the skin and mucousmembranes)

    Ophthalmic ointment

    Management

    Famciclovir and valacyclovir oral only, moreexpensive than acyclovir.

    Other older agents e.g. idoxuridine,

    trifluorothymidine, Vidarabine (ara-A).

    These agents are highly toxic and issuitable for topical use for opthalmic

    infection only

    Note acyclovir is effective in crrelation with thymidinekinase

    babi

    babi

    Dead-end host

    Human

    NyamukNyamuk

    Vector :Cx. tritaeniorhynchus

    Cx.gelidus

    Cx. pseudovishnuiCx. fuscocephalus

    Cx.wishnuiCx.annulirostris

    etc

    Nyamuk lainaedes sp.

    Bird

    Black crowned night heronSpring Fall

    Local winter reservoir

    Transporarialtransmission i n mosquitos

    Snake, birts bats

    Temperatur zone

    Bird migration

    Transmisi berlanjut

    , &

    .

    ,

    .

    414 .

    3

    24 , , , . , , , ,

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    , , ,

    (),

    , , ,

    , ,

    ,

    10 .

    ()

    ()

    Stadium ini dimulai bila suhu badandan sedimentation rate dari butir-

    butir darah merah normal.

    Gejala neurologi menunjukanadanya gejala-gejala perbaikanatau tetap tidak ada perubahan.

    Diagnosa laboratoium dapat dilakukandengan beberapa cara; secara serologi,biologi, identifikasi virus, pemeriksaandarah dan cairan sumsum.

    Secara serologis dapat dilakukanpemeriksaan Haemoglutination InhibitionTest (HI Test), Complement Fication Test(CFT), Neutralizing Antibody Test (NAT)pada anak mencit , ELISA, Agar GelDiffuion (AGD), Single Radial HaemolysisTest.

    ,

    ()

    ( )

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    ,

    ,

    ,

    (

    ).

    Gejala Klinik

    Nipah virus berhubungan dengan encephalitis(inflammation of the brain) ditandai denganfever dan drowsiness dan lebih serius padaSSP dapat menimbulkan coma, seizures, and

    inability to maintain breathing.

    Nipah virus terjadi 3-14 hari fever danheadache diikuti drowsiness and disorientationditandai dengan mental confusion.

    Tanda dan gejala dengan cepat menjadi komadari 24-48 jam beberapa pasien mengalami

    gangguan pernafasan sampai pertengahaninfeksi

    Penyakit nervous serius oleh nipah virus

    encephalitis telah perlihatkan ditunjukkanoleh beberapa sequelae, jugaconvulsions persistent dan personalitychanges.

    Dari tahun 1998-1999 (outbreak) : 40 %pasien terkena penyakit nervous seriusdan banyak menimbulkan kematian

    Cairan Serebrospinal tidak normal 75%kasus

    EEG menunjukkan diffuse secara pelan

    slow dengan abnormalities focal overtemporal regions (75%),

    Tomogram computer normal danmagnetic resonance otak sampai phaseakut menunjukkan perluasan sebaranlesi-lesi focal pada subcortical dan deep

    white matter.

    Diagnosis PENCEGAHAN

    Obat ribavirin menunjukkan hasil yangeffektif terhadap virus dalam uji coba invitro

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    DAFTAR PUSTAKA

    Petrus Nahak, SKM., Mkes, 2001Japanese Encephalitis (JE) BuletinEpidemiologi Propinsi NTT

    www.cdc.co.id/travel/ diseases/japence

    A Chaudhuri and P G E Kennedy 2002Diagnosis and treatment of viralencephalitis Postgraduate MedicalJournal 78:575-583

    REFFERENCES

    Shah,SS (editor) 2009 Pediatric Practice Infectious disease

    Krugman, 2003 Infectious disease

    mmmm

    Sunartini