Central nervous system infections can cause meningitis or encephalitis. Bacterial meningitis is commonly caused by Streptococcus pneumoniae, Neisseria meningitidis, or Haemophilus influenzae type b. It presents with fever, headache, neck stiffness, and altered mental status. Diagnosis involves lumbar puncture showing pleocytosis and low glucose in CSF. Treatment involves antibiotics, corticosteroids, and supportive care to prevent increased intracranial pressure complications.
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Please find the power point on Meningoencephalitis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Acute meningoencephalitis Powerpoint presentation.
It comprises of acute meningitis and acute encephalitis, their clinical features, physical assesment, diagnosis and treatment.
Please find the power point on Meningoencephalitis. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
Meningitis is a severe CNS pathology and early and appropriate intervention is needed to prevent adverse outcome including mortality and long term complications. This presentation focuses on the different types of meningitis and the appropriate management options
Central nervous system (CNS) infections are extremely serious group of diseases.
The cerebral cortex and spinal cord are confined within the restricted boundaries of the skull and bony spinal canal.
Infection, inflammation and oedema therefore have serious consequences, often leading to tissue infarction that in turn results in permanent neurologic damage or death.
Therefor, early diagnosis and prompt treatment is very important
openings allow microbial colonization of the central nervous systemRotRot8
Therefore, the CNS is an arsenic environment-it has no normal microbiota.
Pathogens may access the CNS
through breaks in the bones and meninges,
Through medical procedures such as spinal taps, or by traveling via axonal transport in peripheral neurons in the CNS.
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http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
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3. CNS Infections
• Most common cause of fever associated with
signs and symptoms of CNS disease
• Viral > bacterial > fungal and parasitic
infections
• Regardless of etiology, most patients with CNS
infection have similar clinical manifestations
3
6. Acute Bacterial Meningitis
• Definition-Inflammation of the leptominges
surrounding the brain and spinal cord: pia,
arachnoid and subarachnoid matter
• Occurs at all ages but is commonest during infancy
(greatest risk 6-12 months)
6
7. Con…...
• Bacterial meningitis is one of the most potentially
serious infections occurring in infants and older
children.
• This infection is associated with a high rate of acute
complications and risk of long-term morbidity.
• The incidence of bacterial meningitis is sufficiently
high in febrile infants that it should be included in
the differential diagnosis of those with altered
mental status and other evidence of neurologic
dysfunction
12. EPIDEMIOLOGY
Predisposing Factors
Major risk –Lack of immunity to specific pathogens associated
with young age
Additional risk factors
• Recent colonization with pathogenic bacteria
• Close contact with patients having invasive disease caused
by N. meningitidis and H. influenzae type b,
• Crowding
• Poverty
• Male sex
Person to person contact through respiratory secretions or
droplets.
12
13. Risk factors …
Congenital or acquired CSF leak
Middle ear or inner ear fistulas
Basal skull fracture into the cribriform plate or increased risk
of pneumococcal meningitis.
• Lumbosacral dermal sinus and meningomyelocele:
staphylococcal and gram-negative enteric meningitis.
13
14. Streptococcus pneumonia
• Commonly occurs during the first 2yrs of life
• Peak 6-12 months
• Highest in children with
• HIV- infection
• Anatomic or functional asplenia
• Other risk factors include
• Otitis media
• Sinusitis
• Pneumonia
• CSF otorrhea or rhinorrhea
14
15. Neisseria Meningitides
Occurs
• Sporadically or as epidemics
• Serogroups A,B,C,Y, W-135,X are responsible
• Contact infection
• Epidemics is defined as the occurrence of 3
cases in 3 months time with attack rate of 10
cases per 100,000 population in the same
community
• Epidemics is usually caused by serogrup A
15
16. Haemophilus influenza type B
• Primarily occurs in infants 2month to 2 yrs
• 50% of cases occur in the 1st year of life
• Peak at 6-9 months of age
• Risk increased
among family or day care center contacts of
patients with HIB disease.
unvaccinated and
those with blunted immunologic responses to
vaccine
( HIV- Infection)
16
17.
18. Pathogenesis
Routes of infection
• Hematogenous dissemination of micro-organisms
from a distant site of infection-Most common route.
• Direct invasion of the CNS from
contiguous focus of infection: otitis media,
mastoditis, sinusitis,osteomyelitis (cranial,vertebral)
through anatomic abnormalities
head trauma
neurosurgical procedures
18
19. Pathogenesis
• Bacterial colonization of the nasopharynx
• Hematogenous dissemination
• Bacteremia
• Prior or concurrent viral upper respiratory tract
infection may enhance the pathogenicity of bacteria
producing meningitis
20. Pathogenesis…..
• Bacteria gain entry to the CSF
• Multiply rapidly and incite local inflammatory
response, with polymorphonuclear cell
infiltration.
• Marked inflammatory response with local
production of TNF, IL-1, and other cytokines
• Inflammatory response in characterized by
– Neutrophilic infiltration
– Altered BBB
– Increased vascular permeability
– Vascular thrombosis and vasculitis
• Inflammation of spinal nerves and roots
produces meningeal signs
• Inflammation of the cranial nerves produces
cranial neuropathies
20
21. Nasopharyngeal colonization
Local invasion
Bacteremia
Meningeal invasion
Bacterial replication in the subarachnoid space
Release of bacterial components (cell wall, LOS)
Cerebral microvascular endothelium Macrophages, neutrophils, other CNS Cells
Cytokines
Subarachnoid space inflammation
Cerebral
vasculitis
Increased CSF outflow resistance
Hydrocephalus
Interstitial edema
Increased intracranial pressure
Decreased cerebral blood flow and loss of cerebrovascular autoregulation
Cytotoxic edema
Cerebral
infarction
Increased BBB
permeability
Vasogenic
edema
21
23. Clinical manifestations…..
Older children
• Classic signs are preceded upper respiratory
or GIT symptoms
• Fever
• Headache
• Projectile Vomiting
• Poor feeding
• Seizures are common-20-30% of patients
before or during the first 3 days after
diagnosis
23
25. • Alterations of mental status
– Irritability, lethargy to coma may be due to:
• Increased ICP
• Cerebritis
• Hypotension
• Factors that lead to Death or Brain Damage in
Meningitis
– SIADH secretion With resultant Hyponatremia
– Brain edema → Acute Brainstem Compression
– Subdural Effusion/Empyema/Brain Abscess
– Seizures
25
27. Diagnosis
Lumbar Puncture- CSF analysis
• Leukocyte count (>1000/mm3
) with neutrophilic
predominance (75–95%).
• Turbid CSF when WBC count is >200–400/mm3
.
– <250/mm3
in as many as 20% of patients
– pleocytosis may be absent in severe overwhelming
sepsis and meningitis and is a poor prognostic sign
– lymphocyte predominance may be present during the
early stage
• Elevated protein
Gram stain-positive in 70–90% of untreated patients
• Culture
27
28. Conditions Pressure
(mmH2O)
Leukocyte
(mm3)
Protein
(mg/dl)
Glucose
(mg/dl)
Normal 50-80 <5, ≥75%
Lymphocytes
20-45 >50 (or 75%
Serum
Glucose)
Acute
Bacterial
Usually
elevated
(100 -300)
>100-10,000 ;
usually 300-2,000;
PMNs
Usually
100-500
usually <40
(or <50%
serum
glucose)
Partially
Rxed Bact.
Normal or
elevated
5-10,000; PMNs
early/Mon
dominate most of
the course
Usually
100-500
Normal or
decreased
Viral Normal/slight
ly (80-150)
Rarely >1,000,
Mon predominate
Usually 50-
200
Generally
normal; but
mumps
Tuberculou
s
Usually
elevated
10–500;lymp
predominate
through most of the
100-3,000;
may be
higher
<50 in most
cases
28
29. Diagnosis……
• CBC- Leukocytosis, with polymorph
predominance
• Blood culture- reveals organisms in
~80-90% of cases
» CXR if pneumonia or TB is suspected
29
30. Contra-indications for Lumbar Puncture
• Elevated ICP and focal Neurologic deficit
• Severe cardio respiratory compromise – postpone
LP
• Infection of the overlying skin
• Thrombocytopenia ( relative)
30
32. Management
I. Supportive Measures
Vital Signs _ 15-30 min.
Frequent Neurologic assessment -Follow patient with
neurosign chart
– Level of consciousness(GCS)
– Pupillary size and reactivity
– Pattern of breathing
– Posture
– Occulocephalic reflex
– Seizure
– Cranial nerve palsies or focal Neurologic deficits
– Daily HC measurement –for children<18 months
32
33. Management…..
Strict input/output recording
Serum electrolytes
Body weight
Antipyretics ,Cold sponging
• Fluid restriction to 2/3rd maintenance for fear of syndrome
of inappropriate ADH secretion
- fluid restriction should be avoided in the presence of
hypotension
• Coma care- bowel, bladder, skin, air way
• Seizure control
– Active SZ –arrest with diazepam 0.1 -0.3
mg/kg/IV or PR
– Prevention of recurrence of seizure
» Phenytoin- 20mg/kg loading then 5mg/kg/ 24
hrs – bid
– Phenobarbitone can be added for refractory SZ
33
35. Antibiotic therapy
Empirical treatment
• Cyst.pencillin plus
• Chloramphenicol or
• Ceftriaxone 100mg/kg/24hrs Bid
• Vancomycin – penicillin/ceftriaxone resistant
S.pneumoniae
• According to culture and sensitivity result
35
36. Antibiotics
• Duration of therapy
– 5-7 days for meningococcal meningitis
– 7-10 days for H. influenzae meningitis
– 10-14 days for pneumococcal meningitis
– Gram-negative meningitis should be treated
for 3 wk or for at least 2 wk after CSF
sterilization
36
37. Corticosteroids
• Corticosteroid:
– decrease ICP by decreasing meningeal
inflammation and brain water content
– modulate the production Of cytokines, lessens the
meningeal inflammatory response
– decrease incidence of sensorineural hearing loss
or other neurologic complications
• Dexamthasone
• 0.15 mg/kg/dose Qid for 2 days before the 1st
dose of antibiotic for those older than 6wks
37
38. Complications
Increased Intracranial pressure(ICP)-
• Common acute complication
1. Increase ICP is due to:-
– Cytotoxic cerebral edema- due to cell swelling→cell
death
– Vasogenic cerebral edema- due to cytokine induced
increased capillary vascular permeability
– Interstitial cerebral edema- increased hydrostatic
pressure after impaired reabsorption or obstruction of
CSF flow (Hydrocephalus)
38
39. Management of Increased ICP
– Elevating head by 300
– 20%Manitol 0.5-1g/kg/dose over 30min, Q6hrs or
Frusemide 1mg/kg or hypertonic saline(3% Saline)
– Dexamethasone 0.25 -0.5mg/kg QID
– Endotracheal intubation and hyperventilation (Pco2
25-30mmHG)
– Treat fever aggressively
39
40. 2 .Hydrocephalus
• Communicating
– Ocurrs most commonly
– due to adhesive thickening of arachnoid villi
around the cisterns - impaired CSF
reabsorption
• Obstructive
– Less often
– due to fibrosis and gliosis of the aqueduct of
sylvius
40
41. 3 .Subdural effusion
• 10-30% of cases
• Highest in infants ,and H.influenzae
meningitis(45% of cases)
• 85-90% are asymptomatic
• C/Fs
o bulging fontanel
o diastasis of sutures
o enlarging HC
o Persistence /recurrence of emesis
o Persistent/focal seizures
o persistence of fever
• Symptomatic - subdural tap
41
42. Complications…..
4 . Cranial nerve palsies
– Inflammation of cranial nerves results cranial
neuropathies of Optic ,Oculomotor, Facial ,Auditory
Nerves
– Increased ICP Produces oculomotor and abducens
nerve palsies
5. Seizure
– focal or generalized
– 20–30% of patients
– occurs due to cerebritis, infarction, or
electrolyte disturbances
_ on presentation or within the 1st 4 days of
onset is usually of no prognostic significance
42
45. Prognosis
Poor prognostic factors
1. Infants <6 months
2. Delayed/Late presentation
3. >106
CFU/ml of CSF
4. Seizure that persist after 4 days of illness and
difficult to treat/control
5. Coma or focal Neurologic signs at
presentation.
6. Delayed sterilization of CSF
45
47. Prevention…
H. Influenza
– Rifampin 20mg/kg/daily for 4 day for all close
contacts
if any close family member younger than
48 mo has not been fully immunized or if an
immunocompromised person, of any age,
resides in the household
– HIB vaccine - Prevents development of HIB
Infection – If given for all < 2yrs
Pneumococcal
• Conjugate vaccine against S.pneumoniae ( PCV10) for
all younger than 2 yrs.
47
Most infections of children are acquired from a contact in a daycare facility, a colonized adult family member, or an ill patient with meningococcal disease.
BBB (arachnoid membrane, choroid plexus epithelium, and cerebral microvascular endothelium)
A household contact is one who lives in the residence of the index case or who has spent a minimum of 4 hr with the index case for at least 5 of the 7 days preceding the patient&apos;s hospitalization