BAC T E R IA L

MEN IN G ITIS
NSG128 - SECTIO
NB
GROUP 5
 ÍNDICE

01 02 03
MUNDER MAUNTOL MATUAN
- Bacterial Meningitis - Pathophysiology: - Diagnostic Procedures
- Anatomy and a. Disease proocess - Diagnostic Findings
Physiology b. Complications
- Predisposing and c. Alterations on the
Percipitating Factors bbbLaboratory findings
04 05
MAULANA MALAQUE
- Nursing Managements - Medical Management
a. Pharmacologic
b. Nonpharmacologic
 MENINGITIS
Meningitis is inflammation of the meninges, which cover and
protect the brain and spinal cord. The two main types of
meningitis are bacterial, viral, and fungal.

Meningitis is classified as septic or aseptic.

1. Septic meningitis is caused by bacteria.
2. In aseptic meningitis, the cause is viral or secondary to
cancer or having a weakened immune system, such as in
human immunodeficiency virus (HIV). The most common
causative agents are the enteroviruses.
 MENINGITIS
Bacterial meningitis is an inflammation of the leptomeninges,
usually causing bacterial infection. It is a serious and life-
threatening condition that requires prompt diagnosis and
treatment. It may present acutely (symptoms evolving rapidly
over 1-24 hours), sub-acutely (symptoms evolving over 1-7 days),
or chronically (symptoms evolving over more than 1 week). It is
caused by these etiological agents:
Streptococcus pneumoniae, Neisseria meningitides, Haemophilus
influenza, Staphylococcus aureus, and Mycobacterium
tuberculosis.
MENINGES & CEREBROSPINAL FLUID
The connective tissue membranes that
cover the brain and spinal cord are called
meninges.
The thick outermost layer, made of
fibrous connective tissue, is the dura
mater, which lines the skull and vertebral
canal.
The middle arachnoid membrane is
made of web-like strands of connective
tissue.
The innermost pia mater is a very thin
membrane on the surface of the spinal
cord and brain.
Between the arachnoid and the pia mater
is the subarachnoid space, which
contains cerebrospinal fluid (CSF), the
tissue fluid of the central nervous system.
MENINGES & CEREBROSPINAL FLUID
The connective tissue membranes that
cover the brain and spinal cord are called
meninges.
The thick outermost layer, made of
fibrous connective tissue, is the dura
mater, which lines the skull and vertebral
canal.
The middle arachnoid membrane is
made of web-like strands of connective
tissue.
The innermost pia mater is a very thin
membrane on the surface of the spinal
cord and brain.
Between the arachnoid and the pia mater
is the subarachnoid space, which
contains cerebrospinal fluid (CSF), the
tissue fluid of the central nervous system.
The ventricles (cavities) of the brain: two lateral
ventricles, the third ventricle, and the fourth
ventricle. Each contains a choroid plexus, a capillary
network that forms cerebrospinal fluid from blood
plasma. This is a continuous process, and the
cerebrospinal fluid then circulates in and around the
central nervous system.
From the lateral and third ventricles, cerebrospinal
fluid flows through the fourth ventricle, then to the
central canal of the spinal cord, and to the cranial
and spinal subarachnoid spaces. As more
cerebrospinal fluid is formed, you might expect that
some must be reabsorbed, and that is just what
happens. From the cranial subarachnoid space,
cerebrospinal fluid is reabsorbed through arachnoid
villi into the blood in cranial venous sinuses. The
cerebrospinal fluid becomes blood plasma again,
and the rate of reabsorption normally equals the rate
of production.
 Predisposing Factors:
1.Age:

01
Infants (under 1 year of age) &
Adolescents to Young
Adulthood (16 to 21)

2.Genetics

FACTORS
Predisposing and Precipiating
 Precipitating Factors:
1. Head injury

01
2. Tobacco use
3. Craniotomy
4. Upper respiratory infection
5. Otitis media and mastoiditis
6. Impaired renal function
7. People with immune system
xxdeficiencies (AIDS, alcohol use
FACTORS xxdisorder, diabetes, use of
xximmunosuppressant drugs)
Predisposing and Precipiating
8. Living in crowded conditions
9. Exposures: Travel to endemic
xxareas
10. Skipping vaccinations
 LEGEND:
- Pathophysiology
- Predisposing and

02
Percipitating Factors & -
- Causative Agents
- Clnical Manifestation
- Complication
PATHOPHYSIOLOGY
 PATHOPHYSIOLOGY
PREDISPOSING FACTORS PRECIPITATING
(NON-MODIFIABLE) Prolonged close contact (MODIFIABLE)
with infected patients.

S.peumonia, Group B Streptococcus

S.peumonia, N.meningitidis, Listeria E.coli, Klebsiella, Pseudomonas
N.meningitidis, (vaginal), E.coli, Listeria
monocytogenes, Staphylococcus aureus (for rarer causes of meningitis
H.influenza (for adults monocytogenes(for
(for the immunocomprimised or elderly) from neurosurgical precedures)
and children) neonates)

Inhalation of airborne droplets Bacteria gains entry into the body Spread from parameningeal focus (otitis
containing causative organism. through other mechanisms media, sinusitis, etc.
Airflow and lung anatomy favors
Penetrating head trauma
deposition of bacili in the midlung zone.
Infected macrophages
Alveolar macrophages engulf enhaled travel to the thoracic Anatomic defects in the meninges
bacili via the process of phagocytosis. lymph nodes via the
lymphatic system. Previous neurosurgical procedures
Bacili evades intracellular destruction
via complex mechanisms. Immune cells
proliferation within the
Macrophages infected are activated and thoracic nodes.
relase inflammatory cytokines.
Bacili activates macrophages,
Pro-inflammatory cytokines further activate neutrophils, and dendritic cell
and recruit neutrophils, t-lymphocytes and death programs.
monocytes to the site of respiratory infection.
Infection induces a systematic Bacili are released and enters the lymphatic and circulatory system - hematogenous spread. Meningococcus also infects
inflammatory response blood vessel endothelium in
Bacili then spreads to other regions of the body. the lower limbs

Inflammatio Predisposes infection and colonization by bacteria that can cause meningitis Results to the immune
n increases response creating a
the body’s Inflammation near In a susceptible host, bacteria enters the nervous system and colonizes the meninges vasculitis
basal brain parenchyma Local clotting abnormalities
metabolic interferes with the
Stimulates dural Meningeal irritation
rate normal function of Petechial or Purpuric rash
nociceptors
the central nervous (especially on the lower
Fever system. Cranial Nerves exiting the limbs)
Central Nervous System
Tachycardia Altered mental through the inflamed meninges Detected by certain physical maneuver: Limb Ischemia
status: GCS < 14 can be irritated themselves
Visual (Lethary, stupor, Hip flexion while Passive neck flexion
pathways confusion,delirium, Cranial Nerve Palsies the patient is supine
become coma) Stretches lumbar or
sensitized to CN 3, 4, 6,& 7 are Stretches lumbar or sacral meninges
light, and Around the brain most often affected sacral meninges
pain due to Irritation and
inflamed Headache Irritation and excitation of the
meninges excitation of the nerve roots
Around the brainstem (neck) nerve roots innervating hip and
around the
CN2 is innervating knee knee flexor
Stiff neck (pain worsens flexor
worsened
when neck is flexed These muscles
wiith CN2
Hamstrings contracts contracts
stimulation Around the spinal cord
by light Decrease in knee extension Spontaneous hip or
Sore back
knee flexion
Photophobia Kernig’s Sign
Brudzinski’s Sign
 SIGNS AND SYMPTOMS
1. Fever
2. Tachycardia
3. Altered GCS
- Photophobia
1. Headache
2. Stiff neck
3. Sore back
4. Cranial Nerve Palsies
5. Kernig’s Sign
6. Brudzinki’s Sign
 SIGNS AND SYMPTOMS
1. Fever
2. Tachycardia
3. Altered GCS
- Photophobia
1. Headache
2. Stiff neck
3. Sore back
4. Cranial Nerve Palsies
5. Kernig’s Sign
6. Brudzinki’s Sign
Inflammation of the meninges, Infection of cerebral arteries by bacteria causing the meningitis Bacteria can enter
release of the inflammarory general circulation
cytokines or other mediator Vasculitis of intra-cerebral arteries Bacteria gain
entry into brain Sepsis
Damaged Weakens the
Irritates Irritated arachnoid parenchyma Massive, systemic release of inflammatory
vessell blood vessel
adjacent granulation blocks endothelium cytokines causes blood clotting abnormalities
wall Brain Abscess
cerebral the cerebrospinal more prone to
cortex, fluid drainage thrombosis High blood Post-inflammatory production of
Disseminated
causing pressure antibodies against invading bacteria
The cerebrospinal Intravascular
hypersyn Decreases the more easily
fluid accumulates Coagulation Antibodies form immune
chronous blood flow to cause the
in the ventricles of (DIC) complexes that cross-react to joint
neuronal the brain fragile
the brain and pericardial tissue
activity parenchyma vessels to Abnormal
The intracranial rupture perfusion of Arthritis Joint Effusions
Seizures pressure increases Ischemic
organs
Stroke Hemorrhagic Sterile Pericardial
There is an increased Non-obstructive Stroke Organ Failure
permeability of the (Communicating)
blood-brain barrier Hydrocephalus
causing fluid Obtun- Then
extravasation Hemiplegia the
dation
(Short Hemiparesis pituitary
Subdural Effusion, is
Cerebral Edema term) Seizure involved
Edema in superior Mental SIADH
aspects of the brain Retardation
pushes down on the (Long term)
brain
Squeezes uncus of
the temporal lobe
through the tentorial
notch
Trans-tentorial
herniation (uncal
herniation)
 - Non-Specific Blood Test

02.5
- Cerebrospinal Fluid
xGram Stain Findings
- Cerebrospinal Fluid
xAnalysis

ALTERATION ON
LABORATORY
FINDINGS
ALTERATION ON LABORATORY FINDINGS
NON SPECIFIC BLOOD TESTSV
• Decreased hemoglobin
Complete
• Decreased hematocrit
blood count CEREBROSPINAL FLUID GRAM STAIN
• Elevated CRP
• Elevated or decreased leukocyte count(severe FINDINGS
infection) with a left shift CSF GRAM STAIN CAUSATIVE
CULTURE MEDIUM
• To detect meningococcal septicemia, routine FINDING ORGANISM
assessment of the neutrophil counts must be Gram positive Streptococcus
White blood Blood agar plate
considered, as follows: diplococcus Pneumonia
cell count Gram Neisseria Blood agar plate and
- Absolute Neutrophil Count (ANC): ≤1000/mm or
≥10,000/mm negative diplococcus Meningitides chocolate agar plate
- Immature Neutrophil Count (INC): ≥500/mm Gram Listeria
Immature-to-Total Neutrophil Ratio (ITR): ≥0.20 positive coccobacillu Monocytogene Brain heart infusion
• Hypoglycemia s s
• Elevated creatinine Small pleomorphic g Chocolate agar plate
Haemophilus
• Elevated ALT, AST ram - negative enriched with NAD and
Biochemistry Influenzae
• Possible hyponatremia coccobacilli hematin
• Acidosis: High lactate;
• Low bicarbonate (shock)
• Thrombocytopenia-poor prognosis
Coagulation • Increased D-Dimers,
• Increased PT/APTT-DIC
• Positive in 50 to 90 percent of patients
Blood culture • Two sets of blood cultures needed before
antimicrobials
ALTERATION ON LABORATORY FINDINGS
CEREBROSPINAL FLUID ANALYSIS
V

CEREBROSPINAL FLUID LEVEL NORMAL LEVEL BACTERIAL MENINGITIS

Cells/ul <5 >300

Cells Lymphos:Monos 7:3 Gran. > Lymph
Total protein (mg/dl) 45-60 Typically 100-500

Glucose ratio
> 0.5 < 0.3
(CSF/plasma)

Lactate (mmols/l) < 2.1 > 2.1

CSF gram stain, CSF culture,
Others ICP:6-12 (cm H2O)
CSF bacterial antigen
 Diagnostic procedure and

03
Findings on each.

CT Scan
MRI
Spinal Tap
DIAGNOSTIC Blood Tests
PROCEDURE
 Brain Imaging
CT scan
• usually obtained before lumbar
puncture to exclude a mass lesion
or other signs of elevated
intracranial pressure.
• The meninges may show contrast
enhancement, suggesting
inflammation. However,
meningeal enhancement alone is
not specific for meningitis.

Subtle meningeal enhancement was

noted on contrast-enhanced CT scan.
 Brain Imaging
MRI
• is the most sensitive
imaging modality
because the presence
and extent of
inflammatory changes
in the meninges can be
detected.

Acute bacterial meningitis. This contrast-enhanced, axial T1-weighted

magnetic resonance image shows leptomeningeal enhancement.
 Spinal Tap
• the only test that can confirm a diagnosis of meningitis
• The patient will either lie on his side with his legs bent toward his
body in a fetal position (C position) or he will sit up with his upper
body bent over slightly. Then, the healthcare provider will sterilize an
area of skin on his lower back and insert a hollow needle into the
subarachnoid space between the third and fourth or fourth and
fifth lumbar vertebrae to allow CSF to be extracted. The fluid is sent
to a laboratory for examination.
• Indicator of possible meningitis:
ü low glucose
ü high protein levels
ü high white blood cell count
 Blood Tests
• Complete Blood Count test is done to check for elevated white blood
cells which indicates a presence of infection.

• Procalcitonin blood test measures the level of procalcitonin in the

blood and help determine if a meningitis infection is more likely
bacterial or viral. Normally, there are very low levels of procalcitonin in
the blood. A high level of procalcitonin in the blood may be a sign of
infection.

• Blood culture may be done if a bacterial infection is suspected. A

sample of blood is examined for the growth of bacteria under a
microscope.
 - Observe isolation precaution.
- Do handwashing and don on PPE.
- Ens ure patient’s env i r o n m e n t i s
cleaned and disinfected regularly.

04
- Clean and disinfect equipment used to
the patient thoroughly.
- Properly dispose contaminated
materials.
- Regularly monitor patient’s vital signs
and neurologic status.
- Monitor I&O and assess for signs of
dehydration or fluid overload.
NURSING - Maintain a patent IV line for
medication administration and fluid
MANAGEMENT replacement.
- Elevate HOB.
- Monitor respiratory status. Provide
supplemental oxygen if necessary.
 Pharmacologic:

- Penicillin antibiotics (e.g.

05
ampicillin, piperacillin)
- Cephalosporins (e.g.
ceftriaxone sodium,
cefotaxime sodium)
- Vancomycin
MEDICAL hydrochloride (or with
MANAGEMENT Rifampin) Cortecosteroid
 NONpharmacologic:

- Intravenous fluids

05
- Oxygen Therapy
- Treatment of
concomitant infections
- Treatment of specific
complications (e.g.
MEDICAL surgical drainage for
MANAGEMENT subdural empyema)