MENINGITIS Prof Mohammad Abduljabbar Prof Mohammad Abduljabbar.
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Transcript of MENINGITIS Prof Mohammad Abduljabbar Prof Mohammad Abduljabbar.
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MENINGITIS
Prof Mohammad
Abduljabbar
Prof Mohammad
Abduljabbar
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Definition
Meningitis is defined as an infection of the tow layers of meninges ( Pia And Arachnoid ) including the fluid in between namely cerebrospinal fluid (CSF)
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CAUSES
1-Bacterial
2-Viral
3-Fungal
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N. meningitides
G-ve diplococci
N. meningitides
G-ve diplococci
Streptococci-GBS
G+ve cocci
Streptococci-GBS
G+ve cocci
Strep. pneumoniae
G+ve diplococci
Strep. pneumoniae
G+ve diplococci
E.Coli
G-ve bacilli
E.Coli
G-ve bacilli
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Bacterial Meningitis - Organisms
• Birth - 4 wks: GBS, E.coli
• 4 - 12 wks: GBS, E.coli, Pneumococcus Salmonella, Listeria, H. Influenza
• 3 months - 3 yrs: Pneumococcus, Meningococcus H. Influenza
• 3 yrs+ adult: Pneumococcus, Meningococcus
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(Bacterial Meningitis) Pathogenesis
• Infection of upper respiratory tract
• Invasion of blood stream (bacteraemia)
• Seeding & inflammation of meninges
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Clinical PresentationTriad of Meningitis
• Headache
• Fever
• Neck pain
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Meningitis: Clinical features
Newborn & Infants: non-specific symptoms including:
• Fever
• Irritability
• Lethargy
• Poor feeding
• High pitched cry and bulging AF
• Convulsions and opisthotonus
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Meningitis: older children
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Kernig’s sign
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Brudzinski’s sign
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Acute Meningococcaemia• Neisseria meningitidis: serotype Grp B
commonest • Endotoxin causes vascular damage
vasodilatation, third spacing, severe shock • Severe complication:
Waterhouse-Friderichsen syndrome: massive haemorrhage of adrenal glands secondary to sepsis: adrenal crisis-low B.P, shock, DIC, purpura, adreno-cortical insufficiency
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Purpura fulminans
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Clinical features
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Clinical features
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Clinical features•
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DIAGNOSISHistory and physical examination
Investigations:•CBC•Renal profile•CRP•Coagulation•Blood gas•Glucose
• Blood C/S • Skin scrapings• PCR • CXR• Skin test
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Diagnosis
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CSF FINDINGS Bacterial Viral TB
Cells 10-100,000 <2,000 250-500
Polys lymph lymph
Glucose low Normal Very low
Protein N or High Normal High
G-Stain gen +ve -ve +ve Zn
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Bacterial Meningitis Management
• Medical emergency
• Early diagnosis essential
• Immediate optimum treatment
• Intensive supportive therapy
• Rehabilitation
• Prophylaxis to family
• Notification to GP & Public Health
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Bacterial Meningitis/Meningococcaemia Management
• ABC• ICU admission• Fluid management: aggressive resuscitation• Dexamethasone: only in Pneumococcal and
H I bacteria, given before antibiotics• Inotropes: increasing aortic diastolic
pressure and improving myocardial contractility
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Antibiotics
Less than 2 months of age:• Ampicillin + Cefotaxime+/- Gentamicin• Treat for 3 weeks (neonate)
Over 2 months:• Cefotaxime• Treat for 7-10 days
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Prophylaxis
1- Rifampicin:
Children: 5mg/kg bid x 2/7
Adults: 600 mg bid x 2/7
2- Cefuroxime:
IM x 1 dose in
Pregnant contact
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Meningitis Complications
• Septic shock - DIC
• Cerebral oedema
• Seizures
• Arteritis/venous thrombosis
• Subdural effusions
• Hydrocephalus . Abscess . Brain damage
• Deafness
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Meningococcemia poor prognosis
• Onset of Petechial within 12 hrs
• Absence of meningitis signs
• Shock (BP 70 or less)
• Normal or low WBC
• Normal or low ESR
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Subdural Effusion
• Failure of temperature to show progressive reduction after 72 hours
• Persistent positive spinal cultures after 72 hours
• Occurrence of focal/ persistent convulsions• Persistence/recurrence of vomiting• Development of focal neurological signs• Clinical deterioration after 72 hours especially
ICP
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Partially treated meningitis
• 50% cases prior antibiotic ( alters the findings in bacterial meningitis )
Accurate history is vital• CSF mainly lymphocytic (usual polys)
• Can have normal glucose
• Positive cultures reduced by 30%
• Gram stain reduced by 20%
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Viral meningitis
• Most common infection of CNS especially in <1yr• Causes: enterovirus (commonest, meningitis
occurring in 50% of children <3mth ) herpes, influenza, rubella, echo, coxsackie, EBV, adenovirus
• Mononuclear lymphocytes in CSF• Symptomatic treatment. Complications associated
with encephalitis and ICP
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Herpes simplex Encephalitis
• The most commonly identified cause of acute, sporadic viral encephalitis:10 to 20% of all cases
• Subtype 1 virus causes more than 95% of cases of HSV encephalitis
• In children and young adults, primary HSV infection may result in encephalitis (virus enters the central nervous system (CNS) by neurotropic spread from the periphery via the olfactory bulb)
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Herpes simplex Encephalitis
In about 25% of the patients, the HSV-1 strains from the oropharynx and brain tissue of the same patient differ (some cases may result from reinfection with another strain of HSV-1 that reaches the CNS)
Most adults with HSV encephalitis have clinical or serologic evidence of mucu-cutaneous HSV-1 infection before the onset of the CNS symptoms. HSV DNA has been demonstrated in brain tissue from healthy adults. ( = reactivation)
Most adults with HSV encephalitis have clinical or serologic evidence of mucu-cutaneous HSV-1 infection before the onset of the CNS symptoms. HSV DNA has been demonstrated in brain tissue from healthy adults. ( = reactivation)
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Herpes simplex Encephalitis
Diagnosis
CSF
WBC: 20-300 cells/mm3 (rarely < 5)
Protein: mildly elevated, median 80 (normal<60)
Glucose usually normal
EEG: spike and slow wave activity from the temporal lobe. Sensitivity 85%. Specificity 33%.
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Herpes simplex Encephalitis
Diagnosis
CT: Edema in the temporal lobe
hemorrhagic necrosis midline shift
First 5 days: CT sensitivity 73%, specificity 89%
>5 days: CT sensitivity 90%, specificity 92%
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HSE: MRI is more sensitive, especially for identifying edema. The neuroimaging technique of choice!!!
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Herpes simplex Encephalitis
confirmation of etiology
Brain biopsy (complications 3%)
Serologic analysis in serum and CSF: low sensitivity in the first 10 days.
CSF Cultures: negative
PCR in CSF: highly sensitive and specific. The diagnostic procedure of choice.
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Detection of intrathecal anti-HSV antibodies
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PCR of HSV DNA from CSF samples
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HSE: acute, focal, necrotizing encephalitis with cerebral edema and petechial hemorrhages
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Herpes simplex Encephalitis
Treatment
IV acyclovir (10 mg/kg x 3/day over 1 hour) is effective in reducing the rates of death (70% 24%) and morbidity
Early therapy is a critical factor in outcome!!!
In suspected cases: start acyclovir empirically
If PCR negative and no other support for HSE, stop acyclovir
Long-term cognitive abnormalities
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TB Meningitis
• Usually insidious: difficult to diagnose in early stages (fever 30%, URTI 20%)
• Rare in children in developed countries• If untreated is usually fatal• Meningitis usually occurs 3-6mths after primary
infection• 1 stage ( lasts 1-2wk, fever malaise, headache )• 2 stage (+/- suddenly, meningeal signs )• 3 stage (worsening neurological condition, death )
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Mortality/Morbidity• Bacterial meningitis: Overall mortality 5-10%• Neonatal meningitis: 15-20%• Older children: 3-10%• Strep. pneumonia: 26-30%• H. influenza type B: 7-10%• N. meningitidis: 3.5-10%• 30% neurological complications• 4% Profound bilateral hearing loss (sensory
neural) in all bacterial meningitis
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Mortality/Morbidity
• Viral meningio-encephalitis: Enteroviral fewer complications
• Tuberculous meningitis: related to stage of disease
• Stage I (30%) morbidity.
• Stage II (56%)
• Stage III (94%)
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