CNS infection 1

CNS INFECTIONS

CNS Infections classified Anatomically into:
Meningitis. Encephalitis Myelitis Meningoencephalitis
Abscesses: Brain Abscess Epidural Abscess Subdural Abscess
CNS Infections classified chronologically into:
Acute: which occurs acutely within hours to few days, Subacute: which ranges between days to two weeks, and Chronic: that has history more indolent for weeks to months.
CNS Infections classified etilogically into:
Infective: - bacterial - viral - fungal - protozoal
Non Infective: - Inflammatory - Malignant

INFECTION SPREAD to CNS occurs through:

1-Hematogenous Spread:
Distant Arterial Spread: as from respiratory, GIT, GUT and bacterial endocarditis.........etc
Venous Spread: as occurs from nearby pericranial sites like: paranasal sinuses, OM & mastoiditis and craniofacial & dental infections.
2- Penetrating head injuries.
3- Congenital & acquired defects in skull & spinal cord leading to recurrent meningitis.
4- Rarely lymphatic spread from spinal cord.

ACUTE PYOGENIC (BACTERIAL) MENINGITIS

Is acute purulent infection of leptomeninges (arachnoid & pia matters) and the subarachnoid spaces, associated with inflammatory exudative reaction affecting them.
EPIDEMIOLOGY: annual incidence >2.5 cases/ 100 000 population.
ETIOLOGY: the usual causative M.Os;
S.pneumonae >50% of adult cases.
N.meningitidis 20% of adult young cases.
H.influenzae 10% of all cases usually in unvaccinated patients.
S.aureus & epidermidis usually occurs in neurosurgical & head injured patients.
L.monocytogens should be suspected in every meningitic pt with:
Pregnancy b- extremes of age c-immune compromised & diabetic pt.
6-Enterobacteriace, S.agalactiae and B streptococci should be suspected in neonates, pt.s with debilitating diseases as DM, liver cirrhosis.
PATHOLOGY:
1-The bacteria COLONIZE the epithelial cells of nasopharynx.
2-Then transport through epithelium to the blood stream.
3-The bacteria reach the ventricular choroid plexus, infect it & spread to CSF.
4-The bacteria multiply, induce inflammatory reaction and exudation.
CLINICAL FEATURES:
The classical clinical triad of (Headache, Fever, Neck Stiffnees) should be present in meningitis case. Conscious may vary from lethargy to coma.
Constitutional symtoms are Nausea, vomiting, photophobia, lassitude.
Focal or generalised fits may occur.
CUSHING TRIAD as evidence of rised intracranial pressure: (bradycardia, hypertension and irregular respiration).
late sequelae: deteriorating conscious, papilloedema, poorly reacting pupils, abducens palsy and decerebrate posturing......etc as
On Examination signs of meningeal irritation.


INVESTIGATIONS:
CBC + ESR, Blood Culture and PCR should be done immediately.
2- Basic Biochemical tests. (RBS, RFT, S.E, LFT, GUE.....etc)
3- LP for CSF Examination, BUT neuroimaging with contrast CT or MRI is MUST in patients with: a- papilloedema b-focal neurological deficit
c- decreased level of consciousness d- Hx of recent head injury.
CSF shows: -under pressure>200mmH2O - turbidity
-Sugar<40mg% or <2/3 of RBS -Albumin >45mg%
-Gram stain +ve in 60-90 % of untreated pt
-Culture & sensitivity >80% +ve in untreated pt.
-CSF-PCR for bacterial antigens.
4-Other Ix like CXR, US of abdomen for hidden nidus for infection.
TREATMENT:
Our TARGET is to start Antibiotic therapy (3rd generation Cephalosporin & Acyclovir) within the first hour in the emergency dept. In combination with Dexamethazone after taking blood samples for microbiological Ix, and before awaiting for CSF.
Specific Antibiotic Therapy:
1-S.pneumonae: Ceftriaxone 2gm * 2 or Cefotaxime 2gm * 6, or Cefuroxime 2gm *4, If B lactamase producer add VANCOMYCIN 1gm*2. Alternative Chloramphenicol (all IV for 14 days)
2-N.meningitidis: Penicillin G 50 000u/kg *6, or Cefuroxime orCeftriaxone or Cefotaxime. Alternative Chloramphenicol. (IV for 7days)
3-H.influenzae:Cefriaxone or Cefotaxime. Alternative Chloramphenicol.
4-L.monocytogen: Ampicillin 2gm*6 plus Gentamycine 5mg/kg/day, or Cotrimoxazol 50mg/kg/day (IV for at least 21days).
5-S.aureus & epidermidis: Nafcillin 100mg/kg/day or vancomycin 1gm*2 in Penicillin Allergic Patients.
6-Enterobacteriacae and gram –ve bacilli:Ceftazidime or Ceftriaxone or Cefotaxime.
ROLE OF DEXAMETHAZONE IN ABM:
If started prior or with the 1st AB dose it decreases mortality and morbidity in paediatric age group, while it decreases morbidity in adult age groups.
PROPHYLAXIS:
1-Rifampicin Cap.: adults cap.s 300mg * 2 for 2 days.
Child: 1m-12 yr 10mg/kg *2 for 2days
Neonates 5mg/kg *2 for 2 days
2-Ciprofloxacin 750mg single oral dose.
3-Azithromycine 500mg single oral dose.
4-Ceftriaxone 250mg sinle IM dose.


COMPLICATIONS:
1-Convulsions. 2- Cerebral Vien Thrombosis. 3- Hydrocephalus
4- Brain Abscess. (exclusively in infants) 5- SIADHS
Stroke 7- Deafness 8- Gait impairment
9- Mental Retardation in paediatric ages.

PROGNOSIS: Bad Prognostic Factors are:

1-Age extremities. 2- Signs of high ICP
Seizures within 1st 24hours 4- Impaired conscious.
5- Comorbidity 6- Delay in AB initiation
MORTALITY IN ABM:
1-S.pneumonae: around 20%.
2-N.menigitidis, H.influenzae and group B streptococci: each around 3-7%
3-L.monocytogen: about 15%
CHRONIC MENINGITIS:
Septic Meningitis: ex,TBM , brucellosis.
Fungal meningitis: histoplasma, coccidiomycosis.
Parasites
Few Viruses: ex HIV, CMV.
Drugs: ex NSAID, AED....etc
Inflammatory Meningitis: - Connective Tissue Disease ex. SLE
Behcet disease.


Tuberculous Meningitis
Meningitis usually caused by acid & alcohol fast “Mycobacterium tuberculosis” and exceptionally by “Mycobacterium bovis”, affecting all ages, although more frequently adults, alcoholics and immune compromised patients as AIDS pts .
Pathogenesis:
1- Seeding of the tubercles (Gohns focus) in the meninges and subarachnoid spaces through blood stream.
2- Rupture of these tubercles and discharge of the bacteria through CSF stream.
3- Multiplication of the bacteria and inducing ventriculitis, basilor meningitis and meningoencephlaitis through the pial vessels.
50-60 % of pts have evidence of TB elsewhere in the body, as miliary or pulmonary TB.
Or it may be the primary focus in the brain
CLINICAL PRESENTATION:
We are endemic area in TB, we should have high index of suspicion, the clinical scenario passes into 3 stages:
1st stage: non specific symptoms of (headache, low grade fever, malaise and lethargy).
2nd stage: 1- signs of meningeal irritation (3).
2- Cranial nerve involvement(oculomotor nerves, facial nerve, deafness and papilloedema.
3-Cerebral Arteritis leading to focal neurological defecits secondary to ischemic or heamorrhagic strokes.
3-3rd stage: complications raise like:
Seizures
Progressive neurological deficits.
If untreated, deteriorating consciousness, coma and death ensues within 4-8 weeks.
Investigations:
CBC +ESR, Blood Culture, TB-PCR.
CXR, US.
Basic Biochemical tests.
Neuroimaging with contrast MRI or CT
CSF Study which shows
- Turbidity and cob web formation if sample left for 24 hours.
-opening pressure >200mmH2O
- Increased cell count 50-500 mainly lymphocytes
- Increased protein and may cause Froin Syndrome
- Decreased Glucose <40mg%
-AFB may be positive in 30% of pts only
- CSF Culture may be +ve 70% of pts
-CSF-TB-PCR may be +ve in up to 85% of pts
TREATMENT:
At least two months of 4 antiTB drugs (
- INH 100mg/kg/d max. 300mg/day plus Pyridoxine 10mg b.i.d,
- Rifampicin 10mg/kg to max. 600mg/day
- Pyrazineamide 20-30 mg/kg to max. 1500mg/day
- Either Ethambutol 15mg/kg/day Or Streptomycin 15mg/kg to max. 1gm/day.
Then at least 4 months of INH & Rifampicin.
ROLE OF ORAL STEROIDS IN TBM:
It decreases morbidity in TBM, Prednisolone 60mg/day for 4-6 weeks, or IV Dexamethazone & indicated in the following conditions:
Severe life threatening attack.
Spinal block & froin Syndrome


Prevention:
BCG vaccine
INH 5-10mg/kg/day with B6, for 6-12 months, for persons with close prolonged contacts with TB pts .

NEUROBRUCELLOSIS

Serious complication of brucella infection which is zoonitic disease might be manifested neurologically as: meningitis, encephalitis, neuritis & radiculitis, stroke, MS like picture, cranial nerve palsies, psychosis, mycotic aneurysms and even brain abscesses.
Neurobrucellosis may occur as part of clinical syndrome of brucellosis, or may be the sole manifestation of brucellosis; thence need high index of suspicion. As meningitis disorder full investigations should be done, CSF Study mimics bacterial meningitis in addition Brucella agglutination Antibodies and increased Gamma Globulin levels are present in CSF, and bacteria might be culteured there.
Treatment should be with three drugs Doxycycline , Aminoglycoside (IM streptomycine or IV Gentamycine) and either Trimethoprime / sulfamethoxazol or Ceftriaxone for 6 weeks.

BRAIN ABSCESS
Is encapsulated or free pus collection in the substance of brain after a focal purulent infection, staphylococci, streptococci, pseudomonas, and anaerobes are the usual offending organisms.
ETIOLOGY: brain abscesses usually results from:
Direct spread: from cranial infections like dental infections, sinusitis, mastoiditis and osteomyelitis of skull.
Infected skull fractures or neurosurgical procedures.
Haematogenous spread from septicaemia or infection elsewhere in the body.
Almost never from meningitis except in infants.
CLINICAL FEATURES:
Non localizing headache is the most common symptom.
Fever (less than 60% of pts) & seizures point to subdural empyema rather than brain abscess.
Focal signs and altered mental state in 50% of pts depending on location of the abscess.
Sudden worsening of headache & new nuchal rigidity signifies rupture of the abscess into the ventricular space.
INVESTIGATIONS:
Blood, biochemical, radiographic tests all should be done looking for the source of infection, neuroimaging with contrast CT or MRI should be done showing contrast ring enhanced lesion and CSF study is supportive.
TREATMENT
Empiric antibiotic therapy includes 3rd generation cephalosporin and metronidazole and additional antibiotic may be needed according to suspected organism. Surgical drainage with various techniques might be need.
PROGNOSIS:
Outcome without treatment is usually fatal, BUT with new advances in treatment it reaches about 30%.


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