MENINGITIS Prof Mohammad Abduljabbar Prof Mohammad Abduljabbar.

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MENINGITIS Prof Mohammad Abduljabbar

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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