Predisposing factor Rationale

Age Most cases of viral meningitis occur in children

younger than age 5. Bacterial meningitis is
common in those under age 20. The anatomical
structure of the Auditory tube is different in children
below 2-3 years of age. Children of this age have a
more horizontal auditory tube leading to the
pharynx which increases the likelihood of ear
infection that may lead to meningeal infection.

Underdeveloped immune Infancy is a factor which makes a person more

system susceptible to meningitis and other diseases since
infants don’t have a fully developed immune
sysytem. Removal of your spleen, an important part
of the immune system, also may increase the risk.

Precipitating factor Rationale

Skipping Risk rises for anyone who hasn't completed the
vaccinations.  recommended childhood or adult vaccination
schedule.

Living in a College students living in dormitories, personnel on

community setting military bases, and children in boarding schools and
child care facilities are at greater risk of
meningococcal meningitis. This is probably because
the bacterium is spread through the respiratory route,
and spreads quickly through large groups.

Pregnancy. Pregnancy increases the risk of listeriosis — an

infection caused by listeria bacteria, which may also
cause meningitis. Listeriosis increases the risk of
miscarriage, stillbirth and premature delivery.

Compromised AIDS, alcoholism, diabetes, use of

immune system.  immunosuppressant drugs and other factors that
affect your immune system also make you more
 susceptible to meningitis. Having your spleen
removed also increases your risk, and anyone without
a spleen should get vaccinated to minimize that risk.

Prolonged contact to Meningitis is a communicable disease. Prolonged contact

a patient with may increase the likelihood of cross-contamination.
meningitis

Recent respiratory Meningitis follows invasion of the bloodstream by

and/or ear infection, organisms that live upon mucous surfaces such as the
or sinusitis. nasal cavity and the respiratory tract. Infection in a space
adjacent to the meninges such as the ears may also lead
to meningitis.

Symptomatology

symptoms actual rationale

Nuchal rigidity This is the inability to flex
the neck forward
passively due to
increased neck muscle
tone and stiffness related
to the disease process.

Brudzinski's sign A positive Brudzinski’s

sign signals meningeal
irritation. Passive flexion
of the neck stretches the
nerve roots, causing pain
and involuntary flexion of
the knees and hips.

Kernig's sign Kernig’s sign is hamstring

stiffness and muscle pain
when the examiner
attempts to extend the
knee while the hip and
knee are flexed 90
degrees. Hamstring
muscle resistance results
from stretching the blood
 or exudate-irritated
meninges surrounding the
spinal nerve roots.

Seizure Seizures may result from

increased pressure and
from areas of
inflammation in the brain
tissue.

Decreased level of A decrease in the

consciousness patient’s level of
consciousness usually
results from a neurologic
disorder or infection.
Consciousness is affected
by the reticular activating
system (RAS), an intricate
network of neurons with
axons extending from the
brain stem, thalamus, and
hypothalamus to the
cerebral cortex. A
disturbance in any part of
this system prevents the
intercommunication that
makes consciousness
possible.

Fever Macrophages, white blood

cells, and injured cells
release chemical
substances called
pyrogens that act directly
on the hypothalamus,
causing its thermostat to
be set to a higher
temperature. Also,
immunological reactions
are sped up by
temperature.

Vomiting Vomiting results from an

increased intracranial
 pressure as a response to
the inflammatory process
associated with
meningitis.

Bulging Fontanel This is due to the

inflammatory process
associated with the
disease and the increased
permeability of the blood-
brain barrier. This is only
present in infants up to 6
months of age.

Poor feeding As a response of the

immune system to
infection, interferon is
triggered which initiates a
stress response. The
stress response can elicit
changes in the nervous
and endocrine systems
and, changes in behavior
seen during an infection
acting through the
mediation of
neuropeptides. An effect
of this is anorexia.
Anorexia may be
beneficial in the early
phase of infection
because of the reduction
of nutrients available
which is essential for
microbial growth.

Irritability In meningitis, the infection

of the meninges may also
lead to the inflammation of
the blood vessels,
encountered in acute
infection, which means it
is harder for blood to enter
the brain, and brain cells
 are deprived of oxygen
which may lead to
irritability.

Change in bowel or This is the inability to flex

bladder habits the neck forward
passively due to
increased neck muscle
tone and stiffness related
to the disease process.
 PATHOPHYSIOLOGY

Predisposing Factors Precipitating Factors

 Age
 Underdeveloped immune system  Infection
 Skipping vaccinations
 Compromised immune system
 Pregnancy.
 Prolonged contact to a patient with meningitis
 Recent respiratory and/or ear infection, or
sinusitis.

Bacteria enters into the blood stream

Crosses the blood-brain

barrier

Bacteria proliferates in the CSF

 Irritates and induces inflammatory reaction to the CSF and
meninges

Immune response of astrocytes, microglia and cytokins is

Fever
released

Inflammation of the Meninges

Irritation of the nerve Increase in the number of

Irritability endings WBC

Muscle Vasodila Increased permeability

Nuchal rigidity rigidity tion
Increa
sed Edema
blood
flow

Leaked Increa Irritates

fluid and sed nerve cells of
proteins ICP the brain
move into
inflamed
Purulen
tissue
t
exudate
s
formati
on
IF TREATED:
IF NOT TREATED
Fluid and Electrolyte
Management
Infected CSF and purulent exudates travel throughout
Antibiotic Therapy
the CNS and proliferates in the brain, sheath of cranial
and spinal nerves and to perivascular areas

GOOD PROGNOSIS
Encephalitis
Narrative pathophysiology
The bacteria that commonly cause bacterial meningitis are common
inhabitants of the nasopharynx, but a predisposing factor such as a prior upper
respiratory infection must be present before the bacteria become blood-borne.
Bacterial meningitis also may develop as a consequence of ear, dental, or paraspinal
infections, Impairment in the anatomic barrier from trauma or neurosurgery, and
rarely, when a brain abcess ruptures into the ventricular system or subarachnoid
space. The method of CNS entry is through the choroid plexuses or areas of of
altered blood-brain barrier. Bacteria multiply in the subarachnoid space. The bacteria
or their toxins functions as irritants and induce an inflammatory reaction by the
meninges, the CSF, and the ventricles. The meningeal vessels undergo change,
becoming hyperemic and increasingly permeable. Blood cells migrate into
subarachnoid space, producing an exudate that thickens the CSF and interferes with
normal CSF flow around the brain and spinal cord. The exudate has the potential to
obstruct arachnoid villi and produce hydrocephalus and edema. The amount of
purulent exudate increases rapidly, causing further inflammation. The exudates
extends into the sheaths of the cranial and spinal nerves and into the sheaths of the
cranial and spinal nerves and into the perivascular spaces of the cortex. Meningeal
cells become edematous, the exudate and vasogenic edema increase ICP. The
small and medium-sized subarachnoid arteries, veins, and choroid plexus undergo
inflammatory changes and become endorged, disrupting blood flow and potentially
producing thrombosis. Secondary infection of the brain may occur. The cortical
neurons also show some changes, including an increase in the number of microglia
and astrocytes.

As the microglia and astrocytes are release, the inflammation of the meninges
occurs. The whole process of inflammation takes place. There will be irritation of the
nerve cells thus causing irritability. Muscle rigidity also takes place. This results into
signs such as nuchal rigidity, positive Kerneg’s and Brudzinski’s sign. Blood
examination shows an increase in white blood cells as a result of infection.
Vasodilation and increased permeability also take place where leaked fluids and
other protein accumulate in the inflamed tissue to produce pus. This will also lead to
edema causing increased intracranial pressure. As the CNS is continuously affected,
brain cells are also triggered to produce seizure.
 Lumbar puncture is the best way to diagnose the condition and to detect what
microorganism has infected. Medical management includes prevention of fever and
febrile symptoms, fluid and electrolyte management, antibiotic therapy and
corticosteroids. Dehydration and shock are treated with fluid volume expanders.
Seizures are controlled with phenytoin. Once diagnosed and properly managed,
bacterial meningitis is not fatal and leads to a good prognosis.

However, if no treatment is done, there is a continuous circulation of the

infected cerebrospinal fluid accompanied by the purulent exudates formed. It will
then reach the brain as well as the cranial sheaths. Another infection will occur. As
soon as infection takes place, it can lead to brain damage, decreased cerebral blood
flow and encephalitis among others. Death will soon take place if no treatment is
done.

References

Brunner and Suddarth’s Textbook of Medical Surgical Nursing, 15 th edition; Smeltze,

S.C.; Bare, B.G.; Hinkle, J.L.; Cheever, K.H.; Lippincot, Williams and Wilkins; 2018

Greenlee, J. (2014). Infectious disease. Oxford: Clinical Publishing, An Imprint of

Atlas Medical Publishing Ltd. Retrieved from
https://www.proquest.com/books/infectious-disease/docview/214149956/se-2?
accountid=35028

Hannon, R. (2016). First Canadian Edition Porth Pathophysiology: Concept of

Altered
Houllis, G., & Karachalios, M. (Eds.). (2017). Meningitis : Causes, diagnosis and
treatment : causes, diagnosis, and treatment. Nova Science Publishers,
Incorporated.