Meningitis and Brain abscess

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    Meningitis and Brain abscess

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    CSF FLOW AND SPREAD OF

    INFECTION

    Produced by the Choroid plexus of the cerebralventricles

    Exits through narrow foramina into thesubarachnoid space

    Circulates around the base of the brain and over thecerebral hemispheres

    Resorbed by arachnoid villi projecting into the

    superior sagittal sinus.

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    CSF FLOW AND SPREAD OF

    INFECTION

    CSF flow provides a pathway for rapid spread ofinfectious and malignant processes over the brain,spinal cord, and cranial and spinal nerve roots.

    Spread from the subarachnoid space into brainparenchyma may occur via the arachnoid cuffs thatsurround blood vessels that penetrate brain tissue(Virchow-Robin spaces).

    .

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    Acute infections of the nervous

    system

    Acute bacterial meningitis

    Viral meningitis

    Encephalitis Focal infection: brain abscess, subdural

    empyema, infectious thrombophlebitis

    Fever & Headache

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    Meningitis

    Acute infection of meningitis, important medical problem

    Causes:

    Infective: Bacterial

    Viral: Enterovirus; mumps

    Fungal: cryptococcus; candida

    Protozoa: amoeba; toxoplasma; cysticercus

    Non infective: Malignant disease: breast CA; leukemia; lymphoma; Bronchial CA

    Inflammatory: Behcets disease; SLE; sarcoidosis

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    Acute bacterial meningitis

    Acute purulent infection of the sub-arachnoid

    space

    Epidemiology:

    Annual incidence: >2.5/100,000 population

    Common organisms (community acquired):

    Strep. pneumoniae: 50%

    N. meningitidis: 25% adults (50% in >2 and 50yrs with underlying dis.) Listeria monocytogens: 10%

    H influenza: < 10%

    Staph aureus: neurosurgical procedure

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    Causative organisms

    Age of onset Common Less common

    Neonate Gramve bacil

    Gr. B Strep.

    Listeria

    Pre school H. Influenza

    N meningitidis

    St. Pneumoniae

    Older childrenand adult

    N meningitidis

    St. Pneumoniae

    Listeria

    H influenza

    Staph aureus

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    Etiology

    Strep Pneumoniae: most common in > 20yrs

    Predisposing condn.

    - pneumonia, sinusitis, otitis media,

    - alcoholism, diabetes,

    - splenectomy,

    - hypogamma.,complement defn. Mortality: 20%

    Neisseria meningitidis 25% Children and young adults: 60%

    Petechial rash

    Disease can be fulminant

    Listeria monocytogens: < 1 month & >60 yrs; pregnancy, immunocompromised (all ages)

    Ingestion contaminated food : milk products, meat products

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    Pathophysiology

    Colonize nasopharynx

    Intravascular space

    Choroid plexus

    CSF

    Proliferation of bact.

    Avoids phagocytosis

    Absence effective host

    defense mech

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    Pathophysiology

    Most neuro. Manifest & complications: immune response to invadingpathogen and not direct bact. Induced injury

    Injury can progress even after CSF sterilized

    Lyse bacteriarelease of cell wall components (LPS, teicholic &peptidoglycan) in SA space cytokines (IL 1 & TNF)

    WCC & CSF protein

    Production of excitatory amino acids, reactive O2, nitrogen species

    permeability of BB barrier: vasogenic oedema; protein in SA space

    Sub arachnoid space exudates Obstruction of flow of CSF

    Decrease resorptive capacity

    Increase ICP

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    Clinical manifestations

    Onset: rapid (few hours) or subacute (worsens overdays)

    Classic clinical triad : Fever, headache, nuchual rigidity(Kernigs sign; Brudzinski sign)

    level of consciousness 75% (lethargy to coma) Nausea and vomiting

    Photophobia

    Seizure (20-40%)

    Focal: focal ischemia or infarction; cv thrombosis; focal edema Generalized: hyponatremia; cerebral anoxia; toxic effect of Penn.

    Rash: meningococcemia

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    Clinical manifestations

    ICP 90%

    Signs: level of consiousness

    PapilloedemaDilated and partly reacting pupils

    VI th nerve palsy

    Decerebrate posture

    Cushingss reflex: pulse rate, HTN, irreg. resp

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    Diagnosis

    Suspected blood culture empiricalAntibiotics

    Diagnosis by CSF examination

    LP safely done in: Immunocompetent person

    normal level of consiousnessNo PapilloedemaNo focal neurological signs

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    Cond. Cell Count Glucos Protein

    mg/dL

    Gram

    Normal Lymph 0-4 >60% bl 0 to 45 _

    Viral Lymph 10-2000 N N _

    Bact. Polym. 1000-5000

    N/ +

    TB Lymp/mixed

    50-5000 Often-

    Fungal Lymph 50-500 +/-

    Malig Lymph 0-100 N/ -

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    Diagnosis

    CSF in pyogenic meningitis PMN leucocytes (>100/microL) 90%

    glucose (< 40 mg/dL) 60%

    protein ( > 45 mg/dL) 90%

    pressure (> 180 mm H2O) 90%

    Gram stain: 60% Culture: >80%

    Causes of low CSF glucose Fungal

    TB

    CA

    Imaging : CT or MRI, latter preferred

    Biopsy of petechial lesions: Meningococcemia

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    Differential Diagnosis

    Viral meningo encephalitis: HS virus CSF: normal glucose and lymphocytosis

    MRI : high intensity signal lesions

    EEG

    Rickettsial disease fever, headache, myalgia and nausea and vomiting

    Rash in 96 hrs

    Focal suppurative CNS infection subdural and epidural empyema

    Brain abscess

    Non infectious diseases SAH

    Inflammatory

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    Treatment

    Start Antimicrobial: Goal, < 60 mins arrival to ER

    Empirical before CSF results Patients with typical meningococcal rash

    - Benzylpenicillin 4 megaunits 6 hrly

    Adults : 18 -50 without typical meningococcal rash- 3rd gen. Cephalosporin ( ceftriaxone 2 g 12 hrly)

    Penn resistant pneumocci suspected

    - 3rd gen. Cephalosporin + Vancomycin 1 g 12 hrly

    Listeria suspected ( < 3/12 and > 55 yrs)

    - 3rd gen. Cephalosporin + Ampicillin 2 g, 4 hrly H/O anaphylaxix to B lactam

    - Chloramphenicol 25mg/kg, 6 hr + Vancomycin 1 g 12 hrly

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    Adjunctive Treatment

    Dexamethasone: 20 minutes before antibiotic therapy.(Before the macrophages and

    microglia are activated by endotoxin)

    No benefit if started > 6 hrs after Ab therapy

    Dose: 10 mg, 6 hrly for 4 days

    Benefits synthesis of IL1 and TNF

    CSF outflow resistance

    stabilizing the BB barrier

    Reduce the number of unfavorable outcomes- unfavourable outcome 15% vs 25%

    - death: 7% vs 15%

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    Adjunctive Treatment

    Treatment of raised ICP

    Elevation of patients head 30-45 degrees

    Intubation and hyperventilation (PaCo2 25-30

    mmhg)

    Mannitol

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    Prognosis

    .

    Poor prognostic markers

    decrease level of cons.

    seizure in 24 hrs Sign of increase ICP

    Young age & >50 yrs

    Co morbid condn.

    Delay in starting treatment

    decrease CSF glucose (3 g/l)

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    Prevention of meningococcal

    infection

    Indication

    HH and other close contacts of pt. with

    meningococcal infections

    Drug:

    Rifampicin : 10 mg/kg, 12 hrly for 2 days

    Ciprofloxacin: 500 mg single dose

    Vaccines: available for prevention of

    Group A and C.

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    Course and prognosis

    Mortality: 3 to 20%

    Poor prognostic factors: level of consciousness

    Increase ICP Onset of seizure within 24 hrs

    Extremes of age

    Delay in treatment

    low CSF glucose (< 40 mg/dl)

    Sequele intellectual fxn

    memory impairment

    seizure Extremes of age

    Difficulty in gait

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    Viral meningitis

    Most common cause Usually benign and self limiting illness requiring notherapy

    Common organisms: echo & mumps

    C/F:

    Children or young adults affected Headache, irritability, fever and meningnism

    Focal neurological signs: rare

    Investigation; CSF: (verify that pt. has not received

    antibiotics lymphocytes

    Glucose normal

    Protein: normal or raised

    Treatment: No specific treatment. Recovery in few days

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    Brain abscess

    Pathogenesis & Etiology

    Penetrating injury, direct spread from paranasal

    sinus or middle ear

    Hematogenous spread: septicaemia

    Initial infection suppuration loculation of pus

    surrounding wall of gliosis

    Etiology

    StreptococciAnaerobes

    Staphylococci

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    Brain abscess

    Investigations LP hazardous

    CT: single or multiple low density areas with ring enhancement andsurrounding oedema

    DD: cerebral toxoplasmosis and tuberculoma

    Management Medical treatment: small abscess (