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Meningitis and Brain abscess

CSF FLOW AND SPREAD OF INFECTION


Produced by the Choroid plexus of the cerebral ventricles Exits through narrow foramina into the subarachnoid space Circulates around the base of the brain and over the cerebral hemispheres Resorbed by arachnoid villi projecting into the superior sagittal sinus.

CSF FLOW AND SPREAD OF INFECTION


CSF flow provides a pathway for rapid spread of infectious and malignant processes over the brain, spinal cord, and cranial and spinal nerve roots. Spread from the subarachnoid space into brain parenchyma may occur via the arachnoid cuffs that surround blood vessels that penetrate brain tissue (Virchow-Robin spaces).

Acute infections of the nervous system


Acute bacterial meningitis Viral meningitis Encephalitis Focal infection: brain abscess, subdural empyema, infectious thrombophlebitis

Fever & Headache

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

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 <20 yrs) group B Strep: 15% (neonates, >50yrs with underlying dis.) Listeria monocytogens: 10% H influenza: < 10% Staph aureus: neurosurgical procedure

Causative organisms
Age of onset Common Less common

Neonate

Gram ve bacil Gr. B Strep. H. Influenza N meningitidis St. Pneumoniae N meningitidis St. Pneumoniae

Listeria

Pre school

Older children and adult

Listeria H influenza Staph aureus

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

Pathophysiology
Colonize nasopharynx Intravascular space Choroid plexus Absence effective host defense mech Avoids phagocytosis

CSF

Proliferation of bact.

Pathophysiology
Most neuro. Manifest & complications: immune response to invading pathogen 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

Clinical manifestations
Onset: rapid (few hours) or subacute (worsens over days) 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

Clinical manifestations
ICP 90% Signs:
level of consiousness
Papilloedema Dilated and partly reacting pupils VI th nerve palsy Decerebrate posture Cushingss reflex: pulse rate, HTN, irreg. resp

Diagnosis
Suspected blood culture empirical Antibiotics Diagnosis by CSF examination LP safely done in:
Immunocompetent person normal level of consiousness No Papilloedema No focal neurological signs

Cond.
Normal

Cell
Lymph

Count
0-4

Glucos
>60% bl

Protein mg/dL
0 to 45

Gram
_

Viral

Lymph

10-2000

Bact.

Polym.

10005000

N/

TB

Lymp/ mixed
Lymph

50-5000

N/

Often-

Fungal

50-500

+/-

Malig

Lymph

0-100

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

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

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

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%

Adjunctive Treatment
Treatment of raised ICP
Elevation of patients head 30-45 degrees Intubation and hyperventilation (PaCo2 25-30 mmhg) Mannitol

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 (<40 mg) & increased protein (>3 g/l)

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.

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

Viral meningitis
Most common cause Usually benign and self limiting illness requiring no therapy 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

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
Streptococci Anaerobes Staphylococci

Brain abscess
Investigations
LP hazardous CT: single or multiple low density areas with ring enhancement and surrounding oedema DD: cerebral toxoplasmosis and tuberculoma

Management
Medical treatment: small abscess (<2-3 cm) or non encapsulated Antibiotics - community acq: 3rd gen cephalosporin + metronidazole - penetrating injury: Ceftazidime+ vancomycin - duration: 6- 8 weeks Neuro Surgical intervention: diagnostic and therapeutic Prophylactic Anticonvulsants Mortality: 10-20%.