MENINGITIS Prof Mohammad Abduljabbar Prof Mohammad Abduljabbar.
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Transcript of MENINGITIS Prof Mohammad Abduljabbar Prof Mohammad Abduljabbar.
MENINGITIS
Prof Mohammad
Abduljabbar
Prof Mohammad
Abduljabbar
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)
CAUSES
1-Bacterial
2-Viral
3-Fungal
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
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
(Bacterial Meningitis) Pathogenesis
• Infection of upper respiratory tract
• Invasion of blood stream (bacteraemia)
• Seeding & inflammation of meninges
Clinical PresentationTriad of Meningitis
• Headache
• Fever
• Neck pain
Meningitis: Clinical features
Newborn & Infants: non-specific symptoms including:
• Fever
• Irritability
• Lethargy
• Poor feeding
• High pitched cry and bulging AF
• Convulsions and opisthotonus
Meningitis: older children
Kernig’s sign
Brudzinski’s sign
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
Purpura fulminans
Clinical features
Clinical features
Clinical features•
DIAGNOSISHistory and physical examination
Investigations:•CBC•Renal profile•CRP•Coagulation•Blood gas•Glucose
• Blood C/S • Skin scrapings• PCR • CXR• Skin test
Diagnosis
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
Bacterial Meningitis Management
• Medical emergency
• Early diagnosis essential
• Immediate optimum treatment
• Intensive supportive therapy
• Rehabilitation
• Prophylaxis to family
• Notification to GP & Public Health
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
Antibiotics
Less than 2 months of age:• Ampicillin + Cefotaxime+/- Gentamicin• Treat for 3 weeks (neonate)
Over 2 months:• Cefotaxime• Treat for 7-10 days
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
Meningitis Complications
• Septic shock - DIC
• Cerebral oedema
• Seizures
• Arteritis/venous thrombosis
• Subdural effusions
• Hydrocephalus . Abscess . Brain damage
• Deafness
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
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
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%
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
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)
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)
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%.
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%
HSE: MRI is more sensitive, especially for identifying edema. The neuroimaging technique of choice!!!
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.
Detection of intrathecal anti-HSV antibodies
PCR of HSV DNA from CSF samples
HSE: acute, focal, necrotizing encephalitis with cerebral edema and petechial hemorrhages
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
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 )
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
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%)