5. Pathophysiology
⢠Originate form
â Hematogenous spread
â infected thrombi
â direct extension from bacterially colonized cranial
structures adjacent to the meninges : surgical or
traumatic
⢠Parameningal foci of infection ď require
physical breach in the arachnoid
membraneď meningitis
7. Pathophysiology
⢠Effect of the bacteria within the CSF
â hyperemia of the meningeal vessels, followed rapidly
by migration of neutrophils into the subarachnoid
space
â The exudates increase quickly and extend to the
sheaths of cranial and spinal nerves and into the
perivascular spaces of the cortex
â Exudation of fibrinogen and other proteins from
blood continues
â Toward the end of the second week plasma cells
appear, and thereafter they increase as well
8. Pathophysiology
⢠Infections controlled early may leave no trace
on arachnoid structure, whereas those treated
after the infection has become solidly
established may leave behind a thickened,
cloudy, and adherent arachnoid membrane
⢠Cellular immune reaction in CSF ď endothelial
in small vessel swelling+adventitia infiltrates by
neutrophil ď necrosis of arterial wall
ď subarachnoid bleeding
9. Pathophysiology
⢠Vascular change can in ischemia and stroke
⢠Dysfunction of cranial and spinal nerves occurs
as the purulent exudate surrounds the nerves
⢠Spine : Chronic nerve root pain
⢠Foramina of Magendie and Luschka or the basal
cisterns : Hydrocephalus
⢠Brain : increase cortical microglia and astrocyte,
encephalopathy and seizure
10. Type of Bacterial Meningitis
⢠Most common â 75%
â Haemophilus influenza
â Neisseria meningitidis
â Streptococcus pneumoniae
⢠Less frequent
â Staphylococcus aureus
â Staphylococcus epidermidis
â Streptococcusgroup A, which usually occur after head
trauma neurosurgical procedures or with a brain or
epidural abscess
11. Type of Bacterial Meningitis
⢠Less frequent
â Streptococcusgroup B, which is seen in newborns;
â Enterobacteriaceae (Klebsiella, Proteus, and
Pseudomonas spp.), which occur after lumbar
puncture or shunt placement
â Meningococcal meningitis occurs most often in
children and adolescents but can be seen in
adulthood until the age 50
â Pneumococcal meningitis and Haemophilusmeningitis
both predominate in the very young and in elderly
adult
12. Clinical Features
⢠Adults and Older Children
â Early manifestations : fever, headache (typically
severe), generalized seizures, and impaired
sensorium
â Neck stiffness on flexion is common, Kernig sign and
Brudzinski sign are sometimes seen but are less
reliable
â if a petechial rash or ecchymosis accompanies the
onset of symptoms, meningococcus should be
suspected
13. Clinical Features
⢠Adults and Older Children
â In patients with preexisting infection of the lungs,
sinuses, or ears or in those who have disorders of the
heart valves, pneumococcus should be suspected
â The most common scenario for Haemophilus
meningitis is after an upper respiratory or ear infection
in a child
â In a young patient or in a comatose adult, signs of
meningeal irritation may be absent
14. Clinical Features
⢠Infants
â Infants have a greater incidence of meningitis than
adults do because of their less developed immune
system
â signs are nonspecific : fever, irritability, drowsiness,
vomiting, seizures, and a bulging fontanelle
â Risk factor : premature, prolong labour, UTI of mother
15. Clinical Testing
⢠Lumbar puncture
â Before instituting ATB
â Bleeding disorder : correct
â Increase intracranial pressure : CT, MRI
â Hydrocephalus : ventriculostomy with take CSF
⢠D
⢠d
16. Clinical Testing
⢠CSF
â C/S : positive 20 â 90 in untreated
â G/S
â ELISA, PCR if C/S negative
â LDH (isozymes 4,5 )rise in patients with bacterial
meningitis
â Lactic acid rise in bacterial or fungi but remain normal
in viral meningitis (higher than 35 mg/dL)
⢠Blood cultures should always be done
17. Radiologic Studies
⢠Radiograph of chest, skull, and sinuses
â in any patient suspected of having bacterial meningitis
without a known source
⢠CT of the skull
â sinus infection
â mastoiditis
⢠CT, MRI
â Hydrocephalus
â Infarction
â brain abscess or subdural empyema (or effusion)
18. Postcraniotomy meningitis
⢠Most common organisms
â S. Aureus
â S. Epidermidis
â Gram-negative organisms
⢠Signs and symptom
â fever, neck stiffness
â altered levels of consciousness
â increased risk for stroke secondary to venous
infarction
19. Postcraniotomy meningitis
⢠Lumbar puncture and CSF for cell count, diff,
glucose, protein
⢠Start ATB after LP
â Vancomycin 1 gm v q 8 hrs + ceftazidime 1-2 gm v q
8 hrs (Greenberg)
â For Pseudomonas add Gentamicin
⢠Role of prophylactic ATB remain controversial
20. Recurrent meningitis
⢠suspicion of an ongoing CSF leak through a
previous basilar skull fracture or surgical
procedure affecting the frontal, sphenoid, or
ethmoid sinuses or the cribriform plate
⢠Absent trauma, a congenital fistula between the
nasal sinuses and subarachnoid space may
be suspected.
21. Recurrent meningitis
⢠Difficult case to detect
â We have found the best method of detecting small
leaks to be injection of radioactive tracer (typically
99Tc or 111In) into the lumbar subarachnoid space
with placement of nasal pledgets.
â The patient is then imaged over the next 24 to 48
hours to observe gradual movement of the tracer to
the head (and if leak is present, into the nose
and stomach)
â The pledgets are removed after the first day and also
scanned; if a very slow leak is present, they may be
the only source of positive detection
22. Treatment
⢠ATB should be good penetration
â low molecular weight
â simple chemical structure of the drug
â low degree of ionization at physiologic pH
â high lipid solubility
â low degree of protein binding
⢠Duration
â bacterial meningitis : 10 â 14 days
â gram-negative bacteria and Listeria : 21 days
23. Treatment
⢠If a shunt is present, it will typically require
externalization or removal, or both, with
reinsertion done only when the meningitis has
been completely treated.
⢠Treatment is invariably by intravenous
administration, and in refractory cases or in
those with profound ventriculitis, intraventricular
therapy may additionally be needed
24. Treatment
⢠It is not necessary to repeat lumbar puncture at
intervals during therapy as long as progressive
clinical improvement suggests that the disease
is clearing
⢠Dexamethasone : 0.15 mg/kg every 6 hours
during the first 4 days of antibiotic therapy
⢠Anticonvulsants should be given when
seizures are present but need not be given
prophylactically
26. Prevention
⢠Strategies for prevention
â active immunization : Haemophilus vaccine
â passive immunization with immunoglobulins
â chemoprophylaxis
⢠Rifampin (10 to 20 mg/kg per day orally for 4
days to a maximal dose of 600 mg daily) should
be given to those who have had close
contact with the patient in the 2 weeks before
the diagnosis of meningococcal meningitis
27. Prognosis
⢠Mortality rate
â Haemophilus and meningococcal meningitis : 5 â 15
â Pneumococcal meningitis : 15 â 30 %
â Waterhouse-Friderichsen syndrome :
⢠Fulminant meningococcemia is possible with
or without meningitis and has a very high
mortality rate from vasomotor collapse
associated with adrenocortical hemorrhage
(Waterhouse-Friderichsen syndrome)
28. Prognosis
⢠Worse prognosis in
â Bacteremia
â Coma or Seizures
â Concomitant disease as alcoholism and diabetes
mellitus
⢠Those who recover from meningococcal
meningitis usually show no residual deficits, but
neurological injury occurs in 25% or more of
children with Haemophilusmeningitis and up to
30% of those with pneumococcal meningitis
29.
30. Tuberculous meningitis
⢠Inciden very low, 1 %
⢠Organism
â Mycobacterium tuberculosis
â Mycobacterium bovis
⢠Bacterial seeding to the brain ď formation
tubercles ď rupture and seed mycobacteria to
subarchnoid space
⢠Location : basal meninges, cerebral convexities
⢠Spread to along pia vessel to invade adjacent
brain tissue
31. Tuberculous meningitis
⢠Active tuberculosis elsewhere
⢠Alcholism is common
⢠Serous meningitis
â self-limited meningitis develop in cerebral
tuberculoma, mild symptom and tend to clear several
week
â CSF : modest pleocytosis, normal or elevated protein
levels, and normal glucose levels
32. Tuberculous meningitis
⢠Clinical feature : Headache, Stiff neck, lethargy,
confusion, fever, CN involvement
⢠Diagnosis :
â Lumbar puncture
⢠wbc 50-500, mononuclear cell predominate
⢠pressure normal to high
⢠glucose low but not usually very low levels seen in bacterial
meningitis
â CSF for Ziehl-Neelsen method(AFB), culture(1
month), PCR
33. Tuberculous meningitis
⢠Treatment
â Combination, at least three
â Isoniazid : side effect â neuropathy, hepatitis
â Ethambutol : side effect - optic neuropathy
â Corticosteroids are not generally used
â Intracerebral tuberculoma requires resection : mass
effect or if it fails to shrink with drug therapy
⢠Continues ATB for 18 â 24 Months
34. Treponemal (syphilitic) meningitis
⢠25% of patient with syphilis
⢠Asymptomatic, discover only by LP
⢠Different form other : Afebrile
⢠Rarely symptomatic : cranial nerve palsies,
seizures, and increased intracranial pressure
⢠2 year if no CNS invasion â 5 % will develop
5 year if no CNS invasion â 1 % will develop
35. Treponemal (syphilitic) meningitis
⢠CSF
â pleocytosis of 200 to 300 cells/mm mainly
lymphocytes and other mononuclear cells
â elevation of total protein to 40 to 200 mg/dL
â normal glucose content
â positive serologic tests
⢠VDRL : screen
⢠FTA-ABS test : confirm
36. Treponemal (syphilitic) meningitis
⢠Meningovascular syphilis
â more advanced form of the disease
â occurs 6 to 8 years after the original infection
â It should be considered when a relatively young
person has one or more cerebral infarcts
â CSF will show positive serology and pleocytosis
37. Treponemal (syphilitic) meningitis
⢠Treatment
â crystalline penicillin G : high doses intravenously for 2
weeks
â At 6 Mo
⢠Pt symptom free,CSF normal : no further treatment
⢠If CSF,pleocytosis or elevated glucose : penicillin
38. Meningitis from lyme disease
⢠Spirochetes of the genus Borrelia,
⢠tick bite with rash week to month
⢠asymptomatic meningitis, later neurological
abnormality : headache, stiff neck, nausea and
vomiting, malaise, and chronic fatigue and
fluctuates over a period of weeks to months
⢠CSF : pleocytosis 3000, lymphocyte, protein
300, glucose normal
⢠Treatment : high-dose penicillin or ceftriaxone
39. Fungal meningitis
⢠Less common than bacterial meningitis
⢠Hematogenous, infected paranasal sinus
⢠Occur in immunosuppression : diabetes
mellitus, hematopoietic malignancy, prolonged
immunosuppression in transplant patients, or
chronic steroid therapy
⢠Chronic meningitides : afebrile,cranial nerve
involvement, arteritis with thrombosis, infarction,
and hydrocephalus.
40. Fungal meningitis
⢠CSF
â Mirror to tuberculos meningitis
â Pressure elevate, moderate pleocytosis of
lymphocytic predominance,protein is elevated and
glucose is low
â KOH, culture, PCR
41. Fungal meningitis
⢠Coccidioidomycosis
â progresses from the typical influenza-like illness with
pulmonary infiltration to the disseminated form of the
disease
⢠Candidiasis
â Cause meningitis very rare
â parenchymal abscesses and noncaseating
granulomas
â Mortality rate very high
42. Fungal meningitis
⢠Cryptococcosis
â Headache, fever, stiff neck, increase intracranial
pressure, ataxia, confusion state
â CSF for india ink(60%), serumcryptcoccal Ag
â RX : amphotericin B IV(0.7 mg/kg), voriconazole for 2
Wk
â Positive culture after 2 Wks of Rx : predictive relapse
â LP for sign of increase intracranial pressure
⢠Daily LP : drain enough CSF to release typically ICP by 50%
⢠Daily LP may suspend when pressure are normal
⢠Lumbar drain : occasionally need for extremely high Ops(. 40
mmHg)
43. Uncommon meningitides
Rarely encountered
⢠Amebas of the genus Naegleria
â Swimming in ponds colonized by the organism
â Rapid characterized :severe headache, fever, nausea
and vomiting, and a stiff neck
â CSF similar to bacterial meningitis
â Treatment : amphotericin B
44. Uncommon meningitides
Rarely encountered
⢠Toxoplasmosis, Toxoplasma gondii
â HIV infection c rash, myocarditis, polymyositis,
seizures, confusion, coma
â CSF : increased protein and lymphocytic pleocytosis
â Treatment : sulfadiazine and pyrimethamine
45. Viral meningitis and encephalitis
⢠Route of entry
â viruses is either through the respiratory passages
(mumps, measles, varicella)
â through the gastrointestinal system (polioviruses and
other enteroviruses)
â through the oral or genital mucosa (herpes simplex),
â inoculation through the skin (arboviruses)
⢠Neurotropic infection is also thought possible
through retrograde movement of virus up the
axons of cranial or peripheral nerves, Rabies
46. Viral meningitis and encephalitis
⢠Virus attack leptomeninges ď aseptic meningitis
⢠Virus attack cell of brain ď encephalitis
⢠In herpes zoster and some cases of herpes
simplex, the virus stays latent within neurons for
prolonged periods until the immune defenses
falter as a result of either age or more active
instances of immunosuppression
⢠The basic clinical syndromes
â (1) aseptic meningitis
â (2) acute encephalitis meningoencephalitis
47. Aseptic meningitis
⢠Clinical syndrome : fever, headache, and mild
neck stiffness, photophobia
⢠CSF
â mononuclear pleocytosis
â slight rise in CSF protein
â cultures are negative ď aseptic meningitis.
â glucose is normal
⢠May be slight depression of CSF glucose
â mumps, varicellazoster, lymphocytic choriomeningitis,
or herpes simplex type 2
48. Aseptic meningitis
⢠Viral infection,most common
â entero virus family(echovirus, coxsackievirus, and
nonparalytic poliovirus) : children, fecal-oral route,
august to september
â Mump : any time in the yeay, often winter
â lymphocytic choriomeningitis : contact with infected
hamsters or food contaminated by mouse feces, most
common in late fall and winter
â Herpes simplex typre virus, and adenovirus.
⢠Leptospira : soil or water c contact urine mice
49. Aseptic meningitis
⢠Diagnosis of aseptic meningitis by exclusion
⢠Treatment
â Most cases of viral meningitis are not treated with
antiviral drugs but resolve on their own
â if herpesvirus or varicella-zoster is suspected,
treatment with acyclovir is commonly
recommended.
50. Aseptic meningitis
⢠Nonviral forms of aseptic meningitis that cause
lymphocytic or mononuclear reaction in the
leptomeninges with negative CSF cultures
⢠1. Bacterial infection adjacent to the
meninges, commonly referred to as a
parameningeal focus of infection : mastoiditis or
sinusitis.
51. Aseptic meningitis
⢠2. the organism is difficult to isolate : syphilis,
cryptococcosis, tuberculosis, brucellosis.
⢠The organism can rarely be cultured, and
detection depends on antibody titers in serum
and CSF ELISA.
52. Aseptic meningitis
⢠3. leptomeningeal carcinomatosis :
carcinomatous meningitis, leukemias and
lymphomas
⢠CSF : pleocytosis of lymphocytic
53. Aseptic meningitis
⢠4.autoimmune disease : Behçetâs disease
⢠classic triad : relapsing iritis, ulcers of mouth
and genitalia, and meningitis
⢠Neurological manifestations : recurrent
meningoencephalitis, recurring episodes of
dysfunction of the brainstem and diencephalon
mimicking vascular insufficiency
⢠CSF : pleocytosis, elevated protein, normal
glucose
Parameningeal : Infectious processes, including abscesses, effusions, and empyemas which occur in the epidural or subdural spaces surrounding the brain and spinal cord