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Meningitis Final

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Girma., M.

D
Definition of meningitis-

DEFINITION
-Acute &diffuse inflammation of the CNS with
primary
. involvement of the meninges following
infection.
Etiology
During the first 2 mo of life – maternal flora and the environment
Groups B and D streptococci

Gram-negative enteric bacilli (E. coli, Klebsiella )

Listeria monocytogenes

From 2 mo. to 12 Yrs


S. pneumonia

N. meningitides

H. influenzae type b

Listeria persist as important CNS pathogens through the 3rd mo of life


Cont…
Anatomic defects or immune deficits increase the risk of
meningitis from less common pathogens such as;
- Pseudomonas aeruginosa
- Staphylococcus aureus
- Coagulase-negative staphylococci
- Salmonella spp
- L. monocytogenes.
Risk factors

 Immunocompromisation
 Neuroanatomical defects (e.g. dermal sinus,
neurosurgery)
 Parameningeal infection (e.g. sinusitis, mastoiditis)
 Environmental (e.g. day-care centers, household
contact, travel to endemic regions, crowding, poverty)
especially meningococci & H. influenzae
Cont…
 In General
lack of immunity to specific pathogens associated with

young age
recent colonization with pathogenic bacteria,

close contact with individuals having invasive disease

caused by N. meningitidis and H. influenzae type b,


crowding, poverty, black or Native American race, and
male gender.
Absence of breast feeding (especially 2-5 months)
Transmission
 Mode of transmission
Person-to-person contact through respiratory

tract secretions or droplets


Pathogenesis

 Droplet → nasopharynx → URTI → blood


stream invasion → hematogenous seeding of
meninges → meningeal and CNS
inflammation
Cont…

 Meningitis rarely may follow bacterial invasion

from a local focus of infection eg OM,

sinusities,mastodities, orbital celullities

 Meningities may occur after direct introduction

of the bacteria in to subarachinoid space, eg

penetrating cranial trauma.


Pathology and Pathophysiology
 A meningeal purulent exudate distributed around the
cerebral veins, venous sinuses, convexity of the brain,
and cerebellum and in the sulci, basal cisterns, and
spinal cord.
 Cerebral infarction, resulting from vascular occlusion
due to inflammation, vasospasm, and thrombosis
 Inflammation of spinal nerves and roots produces
meningeal signs, and
 inflammation of the cranial nerves produces cranial
neuropathies of optic, oculomotor, facial, and auditory
nerves
Cont…

 Increased intracranial pressure (ICP) also

produces oculomotor nerve palsy due to

the presence of temporal lobe compression

of the nerve during tentorial herniation.


Cont…
 Raised CSF protein levels are due in part to
increased vascular permeability of the BBB and
the loss of albumin-rich fluid from the
capillaries and veins traversing the subdural
space
 Hypoglycorrhachia (reduced CSF glucose
levels) is due to decreased glucose
transport by the cerebral tissue
 Hydrocephalus
Cont…
 Damage to the cerebral cortex may be due to
Focal or diffuse effects of vascular occlusion
(infarction, necrosis, lactic acidosis),
Hypoxia,
Bacterial invasion (cerebritis),
Toxic encephalopathy (bacterial toxins),
Elevated ICP,
Ventriculitis, and
Transudation (subdural effusions).
Clinical manifestations
 Onset of acute meningitis has two predominant
patterns
Sudden onset(rare)

○ meningoccocus
○ rapidly progressive manifestations of shock, purpura, DIC,

and
○ reduced levels of consciousness with progression to coma or

death within 24 hr
Cont…
Subacute onset (more common)
○ Hib , pneumoccocal , meningoccocal

○ Preceded by several days of URTI or GIT

symptoms
○ followed by nonspecific signs of CNS

infection ( lethargy and irritability)


Symptoms & Signs
- Non-specific
 Due to bacteremia

○ Fever(90 – 95 %), ↑PR , ↓BP

○ Anorexia poor feeding

○ Myalgia , arthralgia

○ Other various cutaneous signs – petechial rash, purpura, or an

erythematous macular rash


Symptoms
Cont…
 Specific to CNS inflammation
Signs of meningeal inflammation
Increased ICP manifestations (fever,
headach ,p .vomiting ,photophobia, convulsion ,loss of
consciousness )
Change in mental status
Focal neurologic signs
○ vascular occlusion
○ 10 – 20 % of children
○ Cranial neuropathies of the ocular, oculomotor, abducens,
facial, and auditory nerves may also be due to focal
inflammation
Seizure
○ focal or generalized (tcc)
○ Occur in 20 – 30 %
○ cerebritis, infarction, or electrolyte
disturbances ,hypoglycemia,
photophobia
Meningococcemia - Petechiae
Manifestation of Increased ICP

 Headache and emesis


 Bulging fontanel or diastasis (widening) of the sutures
 Oculomotor ( anisocoria /inequality of pupils > 1mm,
ptosis drooping of the upper eyelid ) or abducens nerve
paralysis
 Hypertension with bradycardia, apnea or
hyperventilation
 Decorticate or decerebrate posturing, stupor, coma, or
 Signs of herniation
History
 The course of illness
 The presence of symptoms consistent with
meningeal inflammation.
 The presence of seizures, an important prognostic
finding.
 The presence of predisposing factors
 Immunization history
 Recent use of antibiotics, which may affect the yield
of blood and/or CSF culture.
 DIAGNOSIS
1) Lumbar puncture
○ Between L3 & L4 or L4 & L5
○ Confirms DX of meningitis
○ CSF
 Pressure …..usually elevated to 100-300 mmH2O ( Nl =50-80 mmH2O )
 Gross appearance……turbid (WBC >200-400 /mm3)
 WBC count (Nl =less than 5 , lymphocyte > 75% or monocytes )
- Usually elevated to >1000/mm3 (100 – 10,000/mm3 or more )
- Neutrophil predominance ( 75- 95% )
- In 20 % of cases WBC < 250/mm3
- Absent pleocytosis …….sever overwhelming sepsis with meningitis
- Pleocytosis with lymphocyte predominance…….during early stages
 Elevated protein …usually 100-500 mg/dl (Nl = 20 - 45 mg/dl )
 Reduced glucose….usually <40 mg/dl (or <50% of serum glucose ) ( Nl
=>50mg/dl or 75 %of serum glucose )
 Gram stain : positive in 70-90 % of cases
 Culture
Contraindications for LP
- Increased ICP
- Sever cardiopulmonary compromise
- Infection of the skin overlying the site of the LP
- Thrombocytopenia( < 20,000/mm3 ) : Relative c/I
Traumatic LP
- Affects CSF WBC & protein concentration
- Does not affect G/S , culture & Glucose level
- Repeat LP after sometime
2) Latex particle agglutination
- Highly sensitive but less specific
3) Blood culture : Positive in 80 -90 % of cases
4) Countercurrent immuno electrophoresis (CIE)
-Rapid & very specific
 DIFFERENTIAL DIAGNOSIS
A) INFECTIONS
1) Generalized infection of the CNS
Bacteria
- M . Tuberculosis (Tb meningitis)
- T . Pallidum (Syphilis 3rd)
Fungi
- Histoplasma ,Candida ,Cryptococcus , Aspergillus
Parasites
- T .godii , Cysticercosis
Viruses
- Enteroviruses , HSV( Viral meningoencephalitis )
2) Focal infections of the CNS
Brain abscess
Para meningeal abscess
- Subdural empyema
- Cranial epidural empyema
- Spinal epidural empyema
B) NON-INFECTIOUS ILLNESSES
-Cause generalized inflammation of the CNS
-Uncommon
- Malignancy
- Collagen vascular syndromes
- Exposure to toxins
 All acute febrile illnesses can be D.DX of acute bacterial meningitis
especially in its early phase.
Principles of management
 Avoidance of delay
 Assurance of adequate ventilation and cardiac perfusion.
 Establishment of venous access.
 Administration of fluids as necessary to treat septic shock,
if present.
 Initiation of Emperical antibiotic treatement following
LP
Supportive treatment
 Treat shock if present
 Antipyretic for fever as cold compression and paracetamol
 IV fluid : ½ -2/3 of maintenance till ICP and SIADH are excluded
(1/3 NS + 10%dextrose)
 Coma care
 Lateral decupitus,
 NG tube feeding,
 Frequent change of position
 UOP monitoring (catheterization)
 Treatment of complications
 Patient follow up ( Neurosign chart)
- Vital signs - Seizure
- Level of conc - Pattern of breathing
- DTR - Pupillary reflex
- Posturing - Motor examination
- Cranial nerves - Head circum ( first 2 yrs)
CONT…….
ANTIBIOTICS
a) Empirical treatment for 10 days
b) Specific ( based on etiologic agent ) in uncomplicated
cases
- N .meningitidis…….5 -7 days
- H .influenzae type b……….7- 10 days
- S .Pneumoniae………..10-14 days
- CSF culture –ve………7- 10 days
- Gram –ve bacilli……03 weeks or 2 weeks after CSF
sterilization
( usually after 2 – 10 days of
treatment )
- Neonates ……..03 weeks
○ Ceftriaxone, 100mg/kg, IV once daily for 10
PRACTICE IN ETHIOPIA
days for all cases
Alternative
○ Cefotaxime, 225-300mg/kg/ day divided
every 6 or 8 hrs
N.B. Antibiotic treatment may be modified
when culture and sensitivity results are
collected.
○ Benzylpenicillin 100,000-150,000 IU/kg every
6 hours
B) Corticosteroids

○ Dexamethasone 0.15 mg/Kg/dose every 6 hrs for 2

days

○ Maximum benefit if given 1-2 hours before antibiotics

are initiated

○ Limit inflammatory mediators that worsen neurologic

injury and CNS symptoms & signs


○Increased ICP

- Elevate head to 30 degree

- Endotracheal intubation & hyperventilation

(To maintain pCO2 at around 25 mmHg)

- Furosemide 1mg/Kg IV…..diuresis & venodilation

- Mannitol 20% 0.5 -1 gm/Kg/dose IV to run in 30 min ,


repeat 6 hourly if needed
○ Seizure control
- IV diazepam 0.1 -0.2 mg/Kg /dose
OR
IV lorazepam 0.05 – 0.1 mg/Kg /dose
- Monitor serum glucose ,Na ,Ca
- Phenytoin 15 -20 mg/Kg loading dose .
- Then 5 mg /Kg /24 hr maintenance dose
OR
- Phenobarbitone 20 mg /Kg IV loading dose
- Then 5 mg/Kg /24 hr maintenance dose
** Phenytoin causes less CNS depression & permits
Complications
 Acute CNS complications :

seizures, increased ICP, cranial nerve palsies, stroke,

cerebral or cerebellar herniation, and thrombosis of the

dural venous sinuses, hydrocephalus.

 Subdural effusion: (10–30%)


Cont…
 SIADH :
resulting in hyponatremia and reduced serum
osmolality
exacerbate cerebral edema or result in hyponatremic
seizures
30-50 % of patients
 Prolonged fever (>10 days) in 10% of patients
due to:
 Intercurrent viral infection.
 Nosocomial or secondary bacterial infection.
 Thrombophlebitis.
 Drug reaction
 Pericarditis or arthritis (reactive or infectious
Cont…
 Hydrocephalus (Obstructive or communicating) :
especially in neonates & infants
 DIC:
○ Thrombocytopenia & hypofibrogenemia.

○ Especially with meningococcal meningitis.

○ Thrombosis may produce peripheral gangrene

(combination of endotoxemia and severe hypotension initiates


the coagulation cascade resulting in thrombosis )
 COMPLICATIONS ( CONT ‘D )
Thrombocytosis

Anemia(Hemolysis ,Bone marrow suppression)

Shock ,DIC

Sensorineural hearing loss

Visual impairment

Behavioral problems

Mental retardation

Delay in acquisition of language


microbi WBC/ Glucos PROTEI Pressure Gross
ology ml e N(mg/ (mmH2O appeara
(mg/dl) dl) ) nce
<5 40-80
sterile ≥ 75% >75% 20-45 50-80 clear Normal CSF
L.cytes of RBG
Gm
↑ 100- ↓ <40
stain & bacterial
10,000 <50% 100-500 ↑ 100-300 cloudy
Culture mng
PMN of RBG
+ve
5-
10,000
Partially
PMN but 100-
± +ve ↓ or N N or ↑ ± clear treated
± 500 bacterial
lymphoc
ytes
AFB ?? 10-500 100-500
opalescen
PCR PMN → <50 ± ↑↑ in Usually ↑ T.B mng
t
cultutre L.cyte obstr.
Rarely >
1000 N or slight
PCR N 20-200 clear viral
PMN → ↑
L.cyte
5-500
Prognosis
 Mortality of bacterial meningitis after the neonatal period is
<10%
 Highest mortality rates in pneumococcal meningitis
 Severe neurodevelopmental sequelae may occur in 10–20% of
patients
 Fifty % minor neurologic sequelae
 The most common neurologic sequelae include:
Sensorineural hearing loss (most common)
- 30% of patients with pneumococcal meningitis,
- 10% with meningococcal, and
- 5–20% of those with H. influenzae type b meningitis
Mental retardation
Recurrent seizures
Delay in acquisition of language
Visual impairment, and
Behavioral problems
POOR PROGNOSTIC FACTORS

○ Pneumococcal meningitis

○ Age < 6 months

○ >106 colony – forming units of bacteria / ml of

CSF
○ Seizure occurring after 4days of therapy

○ Coma or focal neurological signs on

presentation
A. Antibiotic prophylaxis (chemoprophylaxis)
- For N. meningitidis
All close contacts of patients with meningococcal
meningitis regardless of age or immunization status
Penicillin does not eradicate nasopharyngeal carriage;
patients treated with penicillin should receive
prophylaxis before hospital discharge
(Rifampin 10mg/kg/dose every 12 hr
(maximum dose of 600 mg) for 2 days or ceftriaxone single IM
injection or Ciprofloxacin (500 mg orally as a single dose) may be given to
persons ≥18 yr of age )
Cont…
- For Hib
For ALL household contacts, including adults

if any of family members is younger than 4yrs has not


been fully immunized or is immunocompromised.

Rifampin 20 mg/kg/24 hr given once each day for 4 days

- Pneumococcal meningitis
No Chemoprophylaxis needed.
Cont…
B. Vaccination
- For N. menin : A quadrivalent (A,C,Y, W-135)
conjugated vaccine
: Recommended for high-risk
children older than 2 yr
- For Hib : Conjugate vaccine
- For Pneumococcal : Against S. pneumoniae for all children younger
than 2 yr of age with high risk of invasive pneumococcal infections
- Functional or anatomic asplenia and
- Immunocompromised pt
Thank you

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