MENINGITIS Prof Mohammad Abduljabbar Prof Mohammad Abduljabbar.

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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%)