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Dr. Sunil Pahari , 3rd year resident
Yangtze university , jingzhou central hospital , hubei , china
1/19/20181
Meningitis General
Overview
MENINGITIS
Clinical description
1/19/20182
 Meningitis is a disease caused by the inflammation of
the protective membranes covering the brain and spinal
cord known as the meninges.
 The inflammation is usually caused by an infection of the
fluid surrounding the brain and spinal cord.
 Meningitis can be life-threatening because of the
inflammation's proximity to the brain and spinal cord;
therefore the condition is classified as a medical
emergency.
Meninges
1/19/20183
The meninges is the system of membranes which
envelops the central nervous system.
It has 3 layers:
1. Dura mater
2. Arachnoid mater
3. Pia mater
Subarachnoid
space - is the space
which exists
between the
arachnoid and the
pia mater, which is
filled with
cerebrospinal
Causes of Meningitis
1/19/20184
- Bacterial
- Viral
- Fungal
- Ricketsial (Rocky mountain spotted fever)
- Parasitic/ protozoal
- Physical injury
- Cancer
- Certain drugs ( mainly, NSAID’S)
 Severity/treatment of illnesses differ depending
on the cause. Thus, it is important to know the
specific cause of meningitis.
1/19/20185
1/19/20186
1/19/20187
Bacterial
- Haemophilus influenzae
- Listeria
- Meningococcus
- Pneumococcus
- Group A Streptococcus
- Group B Streptococcus
1/19/20188
 Bacterial meningitis may present
acutely (symptoms evolving rapidly
over 1-24 hours), sub acutely
(symptoms evolving over 1-7days), or
chronically (symptoms evolving over
more than 1 week).
1/19/20189
1/19/201810
 Premature babies and newborns (< 3 months): E.
coli. group B streptococci, .
 Older children: Neisseria meningitidis and
Streptococcu pneumoniae and those under five
by Haemophilus influenzae type B
 Adults: N. meningitidis and S. pneumoniae (80% of
all cases) of bacterial meningitis, with increased risk
of L. monocytogenes (>50yrs)
Bacterial
Route of infection
1/19/201811
 Major routes of leptomeninges
infection
 Bacteria are mainly from blood.
 Uncommonly, meningitis occurs by direct
extension from nearly focus (mastoiditis,
sinusitis) or by direct invasion (dermoid sinus
tract, head trauma, meningo-myelocele).
pathogenesis
1/19/201812
 Susceptibility of bacterial infection on
CNS in the children
Immaturity of immune systems
 Nonspecific immune
 Insufficient barrier (Blood-brain barrier)
 Insufficient complement activity
 Insufficient chemo taxis of neutrophils
 Insufficient function of monocyte-
macrophage system
 Blood levels of diminished interferon (INF) -
γand interleukin -8 ( IL-8 )
pathogenesis
1/19/201813
 Susceptibility of bacterial infection on CNS in
the children
Specific immune
 Immaturity of both the cellular and
Humoral immune systems
 Insufficient antibody-mediated protection
 Diminished immunologic response
Bacterial virulence
1/19/201814
 Bacterial toxics and Inflammatory
mediators are released.
 Bacterial toxics
 Lipopolysaccharide, LPS
 Teichoic acid
 Peptidoglycan
 Inflammatory mediators
 Tumor necrosis factor, TNF
 Interleukin-1, IL-1
 Prostaglandin E2, PGE2
1/19/201815
 Bacterial toxics and inflammatory mediators
cause Suppurative inflammation.
 Inflammatory infiltration
 Vascular permeability alter
 Tissue edema
 Blood-brain barrier destroy
 Thrombosis
 Csf exudates result into hydrocephalus.
 Brain cell death
1/19/201816
Triad of meningitis
1/19/201817
 Fever
 Headache
 Neck stifness
Symptoms of meningitis
1/19/201818
Meningitis and
meningococcal
septicemia may not
always be easy to
detect, in early stages
the symptoms can be
similar to flu. They may
develop over one or two
days, but sometimes
develop in a matter of
hours
It is important to
remember that
symptoms do not
Clinical manifestation
1/19/201819
 Bacterial meningitis may
present acutely (symptoms
evolving rapidly over 1-24
hours) in most cases.
 Symptoms and signs of
upper respiratory or
gastrointestinal infection
are found before several
days when the clinical
manifestations of bacterial
meningitis happen.
 Some patients may access
suddenly with shock and
DIC.
 Toxic symptom all
over the body
 Hyperpyrexia
 Headache
 Photophobia
 Painful eye movement
 Fatigued and weak
 Malaise, myalgia,
anorexia,
 Vomiting, diarrhea and
abdominal pain
 Cutaneous rash
 Petechiae, purpura
Clinical manifestation
1/19/201820
 Clinical
manifestation of
CNS
 Increased
intracranial pressure
 Headache
 Projectile vomiting
 Hypertension
 Bradycardia
 Bulging fontanel
 Cranial sutures
diastasis
 Coma
 Cerebral hernia
 Meningeal irritation
sign
 Neck stiffness
 Positive Kernig’s sign
 Positive Brudzinski’s
sign
1/19/201821
 Clinical manifestation of CNS
 Transient or permanent paralysis of cranial
nerves and limbs may be noted.
 Deafness or disturbances in vestibular
function are relatively common.
 Involvement of the optic nerve, with blindness,
is rare.
 Paralysis of the 6th cranial nerve, usually
transient, is noted frequently early in the
course.
1/19/201822
 Kernig’s sign ;
One of the physically demonstrable symptoms
of meningitis is Kernig's sign. Severe stiffness
of the hamstrings causes an inability to
straighten the leg when the hip is flexed to 90
degrees.
Brudzinski's sign
1/19/201823
 Another physically demonstrable symptoms
of meningitis is Brudzinski's sign. Severe
neck stiffness causes a patient's hips and
knees to flex when the neck is flexed.
Skin rashes
1/19/201824
• Is due to small skin bleed
• All parts of the body are affected
• The rashes do not fade under pressure
• Pathogenesis:
a. Septicemia
b. wide spread endothelial damage
c. activation of coagulation
d. thrombosis and platelets aggregation
e. reduction of platelets (consumption )
f. BLEEDING 1.skin rashes
2.adrenal hemorrhage
Adrenal hemorrhage is called Waterhouse-
Friderichsen Syndrome.It cause acute
adrenal insufficiency and is uaually fatal
‘Glass Test’
1/19/201825
A rash that does not
fade under pressure
will still be visible
when the side of a
clear drinking glass is
pressed firmly against
the skin.
If someone is ill or
obviously getting
worse, do not wait for
a rash. It may appear
late or not at all.
A fever with a rash that
does not fade under
pressure is a medical
emergency.
Aseptic meningitis
1/19/201826
Definition: A syndrome characterized by acute
onset of meningeal symptoms, fever, and
cerebrospinal fluid pleocytosis, with
bacteriologically sterile cultures.
Laboratory criteria for diagnosis:
CSF showing ≥ 5 WBC/cu mm
No evidence of bacterial or fungal meningitis.
Case classification
Confirmed: a clinically compatible illness
diagnosed by a physician as aseptic meningitis,
with no laboratory evidence of bacterial or
fungal meningitis
Comment
Aseptic meningitis is a syndrome of multiple
etiologies, but most cases are caused by a viral
agent
Viral
- Enterovirus (coxsackie, echovirus)
- Arboviral (mosquito-borne diseases)
- Influenza
- Herpes simplex virus type2 ( especially in
infants)
- Varicella zoster
- HIV
- Mumps
- measles
1/19/201827
Viral Meningitis
1/19/201828
Etiological Agents:
Enteroviruses (Coxsackie's and echovirus): most common.
-Adenovirus
-Arbovirus
-Measles virus
-Herpes Simplex Virus
-Varicella
Reservoirs:
-Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex,
and Varicella
-Natural reservoir for arbovirus birds, rodents etc.
Modes of transmission:
-Primarily person to person and arthopod vectors for Arboviruses
Incubation Period:
-Variable. For enteroviruses 3-6 days, for arboviruses 2-15 days
Treatment: No specific treatment available.
Most patients recover completely on their own.
Fungal
Cryptococcus
Coccidiodes
Histoplasma
Mucormycosis
Aspergillus
Candida (yeasts)
Parasitic/protozoal
Angiostrongylus
Toxoplama
Hydatid
Amoeba
Plasmodium
Cysticercosis
1/19/201829
Symptoms can be the same for Viral
and Bacterial
1/19/201830
COMPLICATIONS
1/19/201831
 subdural effusion
 Hydrocephalous
 Hyponatrenia ( SIADH) damage
 hearing loss /blindnessnd brain (subdural
effusion)
 Hearing loss
 seizureHydrocephal
 Mental retardnessure
DIAGNOSIS
1/19/201832
Tests that may be done include:
 For any patient who is suspected of having
meningitis, lumbar puncture ("spinal tap") is done for
CSF examination .
• Blood culture
 Chest x-ray
 CSF examination for cell count, glucose, and protein
 CT scan of the head
 Gram stain, other special stains, and culture of CSF
DIAGNOSIS (contd..)
1/19/201833
 Specimen: CSF, blood, urine culture
 Blood tests and imaging
 Blood tests are performed for markers of inflammation
(e.g. C-reactive protein, complete blood count), as well
as blood cultures.
 Most important is CSF examination by LP. Blood tests are
done when it is C/I
 In severe forms of meningitis, monitoring of blood
electrolytes may be important; for
example, hyponatremia is common in bacterial
meningitis.
DIAGNOSIS
(contd..)Lumbar puncture
A lumbar puncture is done by positioning the patient, usually lying on
the side, applying local anesthetic, and inserting a needle into the dural
sac. CT or MRI scan is recommended prior to the lumbar puncture.
The CSF sample is examined for presence and types of white blood
cells, red blood cells, protein content and glucose level. Gram staining of
the sample may demonstrate bacteria in bacterial meningitis (60% cases).
C/I: Mass in the brain (tumor or abscess) or the intracranial
pressure (ICP) is elevated.
Gram stain of meningococci from a
culture showing Gram negative (pink)
bacteria, often in pairs
1/19/201834
1/19/201835
1/19/201836
 Latex agglutination - The clumping of
cells such as bacteria or RBCs in the presence of an
antibody. The antibody or other molecule binds
multiple particles and joins them, creating a large
complex. Positive in meningitis caused
by Streptococcus pneumoniae, Neisseria
meningitidis, Haemophilus influenzae, Escherichia
coli and group B streptococci.
.
DIAGNOSIS (contd..)
1/19/201837
• Limulus amebocyte lysate (LAL): An aqueous
extract of blood cells (amoebocytes) from the
horseshoe crab, (Limulus polyphemus).
 LAL reacts with bacterial endotoxin or
lipopolysaccharide (LPS), which is a membrane
component of “Gram negative bacteria”.
• Polymerase chain reaction(PCR) is a technique used
to amplify small traces of bacterial DNA
DIAGNOSIS (contd..)
TREATMENT: ANTIBIOTIC
1/19/201838
 Therapeutic principle
Good permeability for Blood-brain
barrier
Drug combination
Intravenous drip
Full dosage
Full course of treatment
ANTIBIOTIC THERAPY
1/19/201839
 Selection of antibiotic
 No Certainly Bacterium
 Community-acquired bacterial infection
 Nosocomial infection acquired in a hospital
 Broad-spectrum antibiotic coverage as noted below
 Children under age 3 months
o Cefotaxime and ampicillin
o Ceftriaxone and ampicillin .
 Children over 3 months
o Cefotaxime or Ceftriaxone or ampicillin and
chloramphenicol
ANTIBIOTIC THERAPY
1/19/201840
 Certainly Bacterium
 Once the pathogen has been
identified and the antibiotic
sensitivities determined, the
most appropriate drugs
should selected.
 N meningitides : penicillin, -
cephalosporin
 S pneumoniae: penicillin, -
cephalosporin, Vancomycin
 H influenza: ampicillin,
cephalosporin
 S aureus: penicillin, nefcillin,
Vancomycin
 E coli: ampicillin,
chloramphenicol, -
cephalosporin
Course of treatment
7 days for meningococcal
infection
10~14 days for H
influenza or S pneumoniae
infection
More than 21 days for S
aureus or E coli infection
14~21 days for other
organisms
1/19/201841
COMPLICATION TREATMENTS
1/19/201842
 Subdural effusions
 Subdural pricking
 Draw-off effusions on one
side is 20-30ml/time.
 Once daily or every other
day is requested.
 Ependymitis
 Ventricular puncture —
drainage
 Pressure in ventricle be
depressed.
 Ventricular puncture may
give ventricle an injection of
antibiotic.
Hydrocephalus
Operative treatment
Adhesiolysis
By-pass operation of
cerebrospinal fluid
Dilatation of aqueduct
SIADH (Cerebral
hyponatremia)
Restriction of fluid
supplement of serum
sodium
diuretic
MENINGOCOCCAL
1/19/201843
 PENICILLIN G is DOC
 In case of resistance – Ceftriaxone,cefotaxime
 Uncomplicated course--7 day course.
 All close contacts should receive
chemoprophylaxis – 2 day regimen of
rifampicin 600 mg every 12 hrs *
2days/ciprofloxacin 750 mg od/azithromyxin
500 mg OD/ceftriaxone 250 mg OD
 Who are close contacts --- nasopharyngeal
secretions,kissing,toys,beverages use.
1/19/201844

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meningitis

  • 1. Dr. Sunil Pahari , 3rd year resident Yangtze university , jingzhou central hospital , hubei , china 1/19/20181 Meningitis General Overview MENINGITIS
  • 2. Clinical description 1/19/20182  Meningitis is a disease caused by the inflammation of the protective membranes covering the brain and spinal cord known as the meninges.  The inflammation is usually caused by an infection of the fluid surrounding the brain and spinal cord.  Meningitis can be life-threatening because of the inflammation's proximity to the brain and spinal cord; therefore the condition is classified as a medical emergency.
  • 3. Meninges 1/19/20183 The meninges is the system of membranes which envelops the central nervous system. It has 3 layers: 1. Dura mater 2. Arachnoid mater 3. Pia mater Subarachnoid space - is the space which exists between the arachnoid and the pia mater, which is filled with cerebrospinal
  • 4. Causes of Meningitis 1/19/20184 - Bacterial - Viral - Fungal - Ricketsial (Rocky mountain spotted fever) - Parasitic/ protozoal - Physical injury - Cancer - Certain drugs ( mainly, NSAID’S)  Severity/treatment of illnesses differ depending on the cause. Thus, it is important to know the specific cause of meningitis.
  • 7. 1/19/20187 Bacterial - Haemophilus influenzae - Listeria - Meningococcus - Pneumococcus - Group A Streptococcus - Group B Streptococcus
  • 8. 1/19/20188  Bacterial meningitis may present acutely (symptoms evolving rapidly over 1-24 hours), sub acutely (symptoms evolving over 1-7days), or chronically (symptoms evolving over more than 1 week).
  • 10. 1/19/201810  Premature babies and newborns (< 3 months): E. coli. group B streptococci, .  Older children: Neisseria meningitidis and Streptococcu pneumoniae and those under five by Haemophilus influenzae type B  Adults: N. meningitidis and S. pneumoniae (80% of all cases) of bacterial meningitis, with increased risk of L. monocytogenes (>50yrs) Bacterial
  • 11. Route of infection 1/19/201811  Major routes of leptomeninges infection  Bacteria are mainly from blood.  Uncommonly, meningitis occurs by direct extension from nearly focus (mastoiditis, sinusitis) or by direct invasion (dermoid sinus tract, head trauma, meningo-myelocele).
  • 12. pathogenesis 1/19/201812  Susceptibility of bacterial infection on CNS in the children Immaturity of immune systems  Nonspecific immune  Insufficient barrier (Blood-brain barrier)  Insufficient complement activity  Insufficient chemo taxis of neutrophils  Insufficient function of monocyte- macrophage system  Blood levels of diminished interferon (INF) - γand interleukin -8 ( IL-8 )
  • 13. pathogenesis 1/19/201813  Susceptibility of bacterial infection on CNS in the children Specific immune  Immaturity of both the cellular and Humoral immune systems  Insufficient antibody-mediated protection  Diminished immunologic response Bacterial virulence
  • 14. 1/19/201814  Bacterial toxics and Inflammatory mediators are released.  Bacterial toxics  Lipopolysaccharide, LPS  Teichoic acid  Peptidoglycan  Inflammatory mediators  Tumor necrosis factor, TNF  Interleukin-1, IL-1  Prostaglandin E2, PGE2
  • 15. 1/19/201815  Bacterial toxics and inflammatory mediators cause Suppurative inflammation.  Inflammatory infiltration  Vascular permeability alter  Tissue edema  Blood-brain barrier destroy  Thrombosis  Csf exudates result into hydrocephalus.  Brain cell death
  • 17. Triad of meningitis 1/19/201817  Fever  Headache  Neck stifness
  • 18. Symptoms of meningitis 1/19/201818 Meningitis and meningococcal septicemia may not always be easy to detect, in early stages the symptoms can be similar to flu. They may develop over one or two days, but sometimes develop in a matter of hours It is important to remember that symptoms do not
  • 19. Clinical manifestation 1/19/201819  Bacterial meningitis may present acutely (symptoms evolving rapidly over 1-24 hours) in most cases.  Symptoms and signs of upper respiratory or gastrointestinal infection are found before several days when the clinical manifestations of bacterial meningitis happen.  Some patients may access suddenly with shock and DIC.  Toxic symptom all over the body  Hyperpyrexia  Headache  Photophobia  Painful eye movement  Fatigued and weak  Malaise, myalgia, anorexia,  Vomiting, diarrhea and abdominal pain  Cutaneous rash  Petechiae, purpura
  • 20. Clinical manifestation 1/19/201820  Clinical manifestation of CNS  Increased intracranial pressure  Headache  Projectile vomiting  Hypertension  Bradycardia  Bulging fontanel  Cranial sutures diastasis  Coma  Cerebral hernia  Meningeal irritation sign  Neck stiffness  Positive Kernig’s sign  Positive Brudzinski’s sign
  • 21. 1/19/201821  Clinical manifestation of CNS  Transient or permanent paralysis of cranial nerves and limbs may be noted.  Deafness or disturbances in vestibular function are relatively common.  Involvement of the optic nerve, with blindness, is rare.  Paralysis of the 6th cranial nerve, usually transient, is noted frequently early in the course.
  • 22. 1/19/201822  Kernig’s sign ; One of the physically demonstrable symptoms of meningitis is Kernig's sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
  • 23. Brudzinski's sign 1/19/201823  Another physically demonstrable symptoms of meningitis is Brudzinski's sign. Severe neck stiffness causes a patient's hips and knees to flex when the neck is flexed.
  • 24. Skin rashes 1/19/201824 • Is due to small skin bleed • All parts of the body are affected • The rashes do not fade under pressure • Pathogenesis: a. Septicemia b. wide spread endothelial damage c. activation of coagulation d. thrombosis and platelets aggregation e. reduction of platelets (consumption ) f. BLEEDING 1.skin rashes 2.adrenal hemorrhage Adrenal hemorrhage is called Waterhouse- Friderichsen Syndrome.It cause acute adrenal insufficiency and is uaually fatal
  • 25. ‘Glass Test’ 1/19/201825 A rash that does not fade under pressure will still be visible when the side of a clear drinking glass is pressed firmly against the skin. If someone is ill or obviously getting worse, do not wait for a rash. It may appear late or not at all. A fever with a rash that does not fade under pressure is a medical emergency.
  • 26. Aseptic meningitis 1/19/201826 Definition: A syndrome characterized by acute onset of meningeal symptoms, fever, and cerebrospinal fluid pleocytosis, with bacteriologically sterile cultures. Laboratory criteria for diagnosis: CSF showing ≥ 5 WBC/cu mm No evidence of bacterial or fungal meningitis. Case classification Confirmed: a clinically compatible illness diagnosed by a physician as aseptic meningitis, with no laboratory evidence of bacterial or fungal meningitis Comment Aseptic meningitis is a syndrome of multiple etiologies, but most cases are caused by a viral agent
  • 27. Viral - Enterovirus (coxsackie, echovirus) - Arboviral (mosquito-borne diseases) - Influenza - Herpes simplex virus type2 ( especially in infants) - Varicella zoster - HIV - Mumps - measles 1/19/201827
  • 28. Viral Meningitis 1/19/201828 Etiological Agents: Enteroviruses (Coxsackie's and echovirus): most common. -Adenovirus -Arbovirus -Measles virus -Herpes Simplex Virus -Varicella Reservoirs: -Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex, and Varicella -Natural reservoir for arbovirus birds, rodents etc. Modes of transmission: -Primarily person to person and arthopod vectors for Arboviruses Incubation Period: -Variable. For enteroviruses 3-6 days, for arboviruses 2-15 days Treatment: No specific treatment available. Most patients recover completely on their own.
  • 30. Symptoms can be the same for Viral and Bacterial 1/19/201830
  • 31. COMPLICATIONS 1/19/201831  subdural effusion  Hydrocephalous  Hyponatrenia ( SIADH) damage  hearing loss /blindnessnd brain (subdural effusion)  Hearing loss  seizureHydrocephal  Mental retardnessure
  • 32. DIAGNOSIS 1/19/201832 Tests that may be done include:  For any patient who is suspected of having meningitis, lumbar puncture ("spinal tap") is done for CSF examination . • Blood culture  Chest x-ray  CSF examination for cell count, glucose, and protein  CT scan of the head  Gram stain, other special stains, and culture of CSF
  • 33. DIAGNOSIS (contd..) 1/19/201833  Specimen: CSF, blood, urine culture  Blood tests and imaging  Blood tests are performed for markers of inflammation (e.g. C-reactive protein, complete blood count), as well as blood cultures.  Most important is CSF examination by LP. Blood tests are done when it is C/I  In severe forms of meningitis, monitoring of blood electrolytes may be important; for example, hyponatremia is common in bacterial meningitis.
  • 34. DIAGNOSIS (contd..)Lumbar puncture A lumbar puncture is done by positioning the patient, usually lying on the side, applying local anesthetic, and inserting a needle into the dural sac. CT or MRI scan is recommended prior to the lumbar puncture. The CSF sample is examined for presence and types of white blood cells, red blood cells, protein content and glucose level. Gram staining of the sample may demonstrate bacteria in bacterial meningitis (60% cases). C/I: Mass in the brain (tumor or abscess) or the intracranial pressure (ICP) is elevated. Gram stain of meningococci from a culture showing Gram negative (pink) bacteria, often in pairs 1/19/201834
  • 36. 1/19/201836  Latex agglutination - The clumping of cells such as bacteria or RBCs in the presence of an antibody. The antibody or other molecule binds multiple particles and joins them, creating a large complex. Positive in meningitis caused by Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Escherichia coli and group B streptococci. . DIAGNOSIS (contd..)
  • 37. 1/19/201837 • Limulus amebocyte lysate (LAL): An aqueous extract of blood cells (amoebocytes) from the horseshoe crab, (Limulus polyphemus).  LAL reacts with bacterial endotoxin or lipopolysaccharide (LPS), which is a membrane component of “Gram negative bacteria”. • Polymerase chain reaction(PCR) is a technique used to amplify small traces of bacterial DNA DIAGNOSIS (contd..)
  • 38. TREATMENT: ANTIBIOTIC 1/19/201838  Therapeutic principle Good permeability for Blood-brain barrier Drug combination Intravenous drip Full dosage Full course of treatment
  • 39. ANTIBIOTIC THERAPY 1/19/201839  Selection of antibiotic  No Certainly Bacterium  Community-acquired bacterial infection  Nosocomial infection acquired in a hospital  Broad-spectrum antibiotic coverage as noted below  Children under age 3 months o Cefotaxime and ampicillin o Ceftriaxone and ampicillin .  Children over 3 months o Cefotaxime or Ceftriaxone or ampicillin and chloramphenicol
  • 40. ANTIBIOTIC THERAPY 1/19/201840  Certainly Bacterium  Once the pathogen has been identified and the antibiotic sensitivities determined, the most appropriate drugs should selected.  N meningitides : penicillin, - cephalosporin  S pneumoniae: penicillin, - cephalosporin, Vancomycin  H influenza: ampicillin, cephalosporin  S aureus: penicillin, nefcillin, Vancomycin  E coli: ampicillin, chloramphenicol, - cephalosporin Course of treatment 7 days for meningococcal infection 10~14 days for H influenza or S pneumoniae infection More than 21 days for S aureus or E coli infection 14~21 days for other organisms
  • 42. COMPLICATION TREATMENTS 1/19/201842  Subdural effusions  Subdural pricking  Draw-off effusions on one side is 20-30ml/time.  Once daily or every other day is requested.  Ependymitis  Ventricular puncture — drainage  Pressure in ventricle be depressed.  Ventricular puncture may give ventricle an injection of antibiotic. Hydrocephalus Operative treatment Adhesiolysis By-pass operation of cerebrospinal fluid Dilatation of aqueduct SIADH (Cerebral hyponatremia) Restriction of fluid supplement of serum sodium diuretic
  • 43. MENINGOCOCCAL 1/19/201843  PENICILLIN G is DOC  In case of resistance – Ceftriaxone,cefotaxime  Uncomplicated course--7 day course.  All close contacts should receive chemoprophylaxis – 2 day regimen of rifampicin 600 mg every 12 hrs * 2days/ciprofloxacin 750 mg od/azithromyxin 500 mg OD/ceftriaxone 250 mg OD  Who are close contacts --- nasopharyngeal secretions,kissing,toys,beverages use.