2. What is meningitis?
Meningitis is an infection of the pia-arachanoid and the CSF fluid
that surrounds the brain. Meningitis is usually caused by an
infection with a virus, with a bacterium or even with fungi.
3. How is Meningitis Caused
■ Colonization of nasopharynx by bacteria or
viruses
■ Is an important way of spreading meningitis
by way of cribriform fossa or viremia or
bacteriaemia and can spread to others by
coughing etc.
4. ■ Hematogenous
■ Many of the bacteria and viruses that cause
meningitis are fairly common and are typically
associated with other routine illnesses.
■ infection of the skin, urinary system,
gastrointestinal or respiratory tract can spread by
the bloodstream
5. ■ Direct infection
■ skull fractures possess abnormal openings to the
sinuses, nasal passages, and middle ears.
Organisms can pass through openings and cause
infection. surgical procedures or who have had
foreign bodies surgically placed within their skulls
(such as tubes to drain abnormal amounts of
accumulated CSF) have an increased risk of
meningitis.
13. Pathogenesis of Meningitis
■ The virus or bacteria replicates in the initial
organ system (ie, respiratory or
gastrointestinal mucosa) and gains access to
the bloodstream. Primary viremia or
bacteremia introduces the virus or bacteria
to the reticuloendothelial organs (liver,
spleen, and lymph nodes.)
14. Pathogenesis of Meningitis
■ If the replication persists despite
immunologic defenses, secondary
bacteremia or viremia occurs, which is
thought to be responsible for seeding of the
CNS. Rapid viral replication likely plays a
major role in overcoming the host defenses.
15. Pathogenesis of Meningitis
■ There occurs local immune response to
bacteria or virus
■ Increased vascular permeability
■ oozing of fluid exudate,inflammatory cells
■ Neutrophils migrate from capillaries and
release toxins
■ TNF-a and IL-B1 produced by activated
macrophages and endothelial cells
17. Pathogenesis of Meningitis
■ cellular damage and loss of cellular homeostasis
and worsen cerebral edema
■ damage to vessels lead to vasculitis and bleed or
thrombose leading to infaraction or haemorrahage
■ exudate formation etc can obstruct CSF flow and
lead to hydrocephalous
■ ICP lead to herniation
18. Pathogenesis of Meningitis
■ exudative pus of dead cells ,fluid,fibrin and
leucocytes (pus) cause thick whitish grey layer
that covers the leptomeninges over the surface of
brain and filling sulci and basal cisterns with
swollen edematous brain.
■ damage to neurons can take place if extending to
brain cells resulting in their degeneration.
19. The white appearance of this calf brain is caused by neutrophils within the
meninges – a condition known as meningitis. This is usually due to a
bacterial infection.
20. This calf brain shows similar pathology. If a glass slide is pressed to the
surface of the brain and stained it would show high numbers of
neutrophils.
21. This brain shows irregular red spots which are areas of hemorrhage
Bov
ain
nd
e necrosis caused by the bacteria, Histophilus somni.
24. Signs & symptoms of Meningitis
◆ Acute (<1 day)- common with S.
pneumoniae and N. meningitides
◆ Subacute (2-3 days)- preceding URI like
symptoms, more common with H. flu and
other pathogens.
25. Signs & symptoms of Meningitis
Non-specific complaints
◆ Fever
◆ Headache
◆ Nausea and vomiting
--Nuchal rigidity
◆ Lethargy
◆ Irritability
◆ Restlessness
◆ Poor feeding
◆ Back pain
◆ Altered mental status (seizure, coma)
26.
27. Signs & symptoms of Meningitis
Febrile
◆ stiff neck causing may causearched position
Opisthotonos
◆ Focal neurologic signs
◆ Petechia/purpura- DIC with N. menigitidis
◆ Positive Kernig’s and Brudniski’s i.e. ,
Meningismus (stiff neck + Brudzinski +
Kernig signs)
Shock
Disseminated intravascular coagulation (DIC)
Cerebral edema
28. Kernig’s Sign
■ Patient placed supine with hips flexed 90
degrees. Examiner attempts to extend the
leg at the knee
■ Positive test elicited when there is
resistance to knee extension, or pain in the
lower back or thigh with knee extension
30. Brudzinski’s Sign
■ Patient placed in supine position and neck is
passively flexed towards the chest
■ Positive test is elicited when flexion of neck
causes flexion at knees and/or hips of the
patient
33. Signs & symptoms of Meningitis
■ Is due to small skin bleed
■ All parts of the body are affeced
■ The rashes do not fade under pressure
■ Pathogenesis:
a. Septicemia
b. wide spread endothelial damage
c. activation of coagulation
d. thrombosis and platelets aggregation
34. Signs & symptoms of Meningitis
■ e. reduction of platelets (cosumption )
f. BLEEDING 1.skin rashes
2.adrenal hemorrhage
Arenal hemorrhage is called Waterhouse-
Friderichsen Syndrome.It cause acute
adrenal insufficiency and is uaually fatal
36. Signs & symptoms of Meningitis
■ May also look like bruises,echymosis .
37. Complications and Outcome of
Meningitis
■ Infection can spreading to
■ Dura – pachymeningitis
■ Leptomeninges - leptomeningitis
■ Brain – encephalitis
■ Spinal cord – myelitis
■ Ventricles - ventriculitis
38. Complications and Outcome of
Meningitis
■ Disseminated intravascular coagulation (DIC)
Cerebral edema
■ Adrenal hemorrhage is called Waterhouse-
Friderichsen Syndrome.It cause acute adrenal
insufficiency and is uaually fatal
■ septicaemia and infection spreading to other
organs
■ motor and neurological deficits
40. Complications and Outcome of
Meningitis
■ risk of adrenal hemorrhage with hypo-
adrenalism (Waterhouse-Friderichsen
syndrome)
■ Serum sodium level may be abnormal
because of dehydration or the rare
occurrence of syndrome of inappropriate
antidiuretic hormone secretion (SIADH).
41. Complications and Outcome of
Meningitis
■ Serum amylase level may be elevated in
cases caused by mumps even in the absence
of parotitis.
■ Focal infarctions/microinfarcts due to
endarteritis oblitrerans
■ Formation of intracranial mass
■ Cranial nerve palsies
42. Complications and Outcome of
Meningitis
■ Tiredness
■ Recurring headaches
■ Memory loss, which may be severe
■ Difficulties in concentration
■ Anger outbursts
■ Clumsiness
43. Differential Diagnosis of
Meningitis
■ Brain abscess
■ Encephalitis
■ Tumor like
ASTROCYTOMAS,OLIGODENDROGLIOMAS
,EPENDYMOMAS
■ MIXED GLIOMAS
■ Metastatic tumor
■ Subdural and epidural empyema
■ subdural
■ subarachnoid
44. Differential Diagnosis of
Meningitis
■ Chemical meningitis: Rupture of tumor
■ intracranial haemorrage like
■ Epidural
■ subdural
■ Subarachnoid
■ intraparenchymal
45. Differential Diagnosis of
Meningitis
■ metabolic encephalopathy
■ hyperglycaemic coma
■ uremia
■ hepatic encephalopathy
■ vit B deficiencies
■ vascular diseases (amyloid angiopathy,
vasculitis, berry aneurysms, A-V
malformations
47. CSF & LUMBER PUNCTURE
■ Indirect measurement of ICP by lumber puncture.
■ The two principal objections to lumbar puncture in
the diagnosis of intracranial hypertension have
been the danger of inducing brain-stem
compression through tentorial or tonsillar
herniation and the contention that spinal fluid
pressure is not always an accurate reflection of
ICP.
48. CSF & LUMBER PUNCTURE
■ Indications
■ 1. Diagnostic aid
■ 2. Therapy for idiopathic intracranial
hypertension
■ 3. Infusion of anaesthetic (“spinal”),
chemotherapy, or contrast agents
(myelography)
49. CSF & LUMBER PUNCTURE
■ Contraindications
■ - INR > 1.4 or other coagulopathy
■ - platelets < 50
■ - infection at desired puncture site
■ - obstructive / non-communicating hydrocephalus
■ - intracranial mass
■ - high intracranial pressure (ICP) / papilloedema
50. Summary of Typical
CSF Findings
Culture
Increased
+TB
+/- Increased
Negative
Increased
Positive
5-40
Negative
Protein
< 30%
Normal
<40%
CSF plasma:
Glucose ratio
Decreased
Normal
Decreased
Glucose
Lymphocytes
Polymorphs
Cells
TB
25-500
+/- increased
Increased
Viral
<1000
Early
Predominate
Bacterial
>1000
Predominate
Late
Normal
0-5
0
5
60-80
66%
51. TREATMENT of MENINGITIS
■ Empiric Antibiotics:
■ Cefotaxime 2g IV q4hrs
■ add Vancomycin 1-2 g IV q8-12 hrs in all patients
(till possibility of Penicillin-resistant Strep
pneumoniae has been ruled out)
■ add Ampicllin 2g IV q4hrs in elderly or
immunocompromised patients (for Listeria
infections)
52. ■ for patients with serious penicillin allergies,
Meropenem 1-2g IV q8hrs as alternative
■ Ceftazidime (2g IV q8hr) + Vancomycin for
neurosurgical patients, those with shunts or CSF
leaks
■ May consider adjunctive Acyclovir (10 mg/kg IV
q8hrs if normal renal function)
53. ■ Therapy can be modified as the results of
Gram stain, cultures, and PCR testing
become available. Patients in unstable
condition need critical care unit admission
for airway protection, neurologic checks,
and prevention of secondary complications.
54. ■ since SIADH has been reported. Fluid
restriction, diuretics, and rarely hypertonic
saline infusion may be used to correct the
hyponatremia
55. ■ Cerebral edema does occur in cases of
severe encephalitis and may require
intracranial pressure control by infusion of
mannitol (1 g/kg initial dose followed by
0.25-0.5 g/kg q6h), IV dexamethasone, or
intubation and mild hyperventilation, with
arterial PCO2 around 28-30 mm Hg
56. ■ Use of adjunctive corticosteroids:
■ - prior to or along with initial antibiotics,
administer Dexamethasone 10 mg IV for
suspected bacterial meningitis (based on cloudy
CSF, CSF WBC counts > 1000 or + Gram stain)
■ - continue 10 mg IV q6hr x 4 days
57. ■ Prognostic Factors:
■ 1. Age
■ 2. Level of Consciousness (50% mortality if
unresponsive or minimally responsive on
admission)
■ 3. Seizures early in course
■ 4. Strep. pneumoniae meningitis
■ 5. CSF results (lower glucose & WBC counts,
higher protein)
