Meningitis and Dementia

Dr. Lubna Dwerij

Meningitis
 Meningitis is an inflammation of the lining around the
brain and spinal cord caused by bacteria or viruses.
 Meningitis can be the primary reason a patient is
hospitalized or can develop during hospitalization and is
classified as septic or aseptic.
 Septic meningitis is caused by bacteria.
 In aseptic meningitis, the cause is viral or secondary to
lymphoma, leukemia, or human immunodeficiency virus
(HIV).
 The bacteria Streptococcus pneumonia and Neisseria
meningitides are responsible for 80% of cases of meningitis
in adults.
Meningitis
 Outbreaks of N. meningitidis infection are most likely to
occur in dense community groups, such as college
campuses and military installations.
 Factors that increase the risk of bacterial meningitis
include tobacco use and viral upper respiratory infection,
because they increase the amount of droplet production.
 Otitis media and mastoiditis increase the risk of bacterial
meningitis, because the bacteria can cross the epithelial
membrane and enter the subarachnoid space.
 People with immune system deficiencies are also at
greater risk for development of bacterial meningitis.
Pathophysiology
 Meningeal infections generally originate in one of two ways:
 Through the bloodstream as a consequence of other
infections
 Or by direct spread, such as might occur after a traumatic
injury to the facial bones or secondary to invasive
procedures.
 N. meningitidis concentrates in the nasopharynx and is
transmitted by secretion or aerosol contamination.
 Once the causative organism enters the bloodstream, it
crosses the blood–brain barrier and proliferates in the
cerebrospinal fluid (CSF).
Pathophysiology
 The host immune response stimulates the release of cell
wall fragments and lipopolysaccharides, facilitating
inflammation of the subarachnoid and pia mater.
 Because the cranial vault contains little room for expansion,
the inflammation may cause increased intracranial pressure
(ICP).
 CSF circulates through the subarachnoid space, where
inflammatory cellular materials from the affected
meningeal tissue enter and accumulate.
 The prognosis for bacterial meningitis depends on the
causative organism, the severity of the infection and illness,
and the timeliness of treatment.
Pathophysiology
 Acute fulminant presentation may include adrenal
damage, circulatory collapse, and widespread
hemorrhages (Waterhouse-Friderichsen syndrome).
 This syndrome is the result of endothelial damage and
vascular necrosis caused by the bacteria.
 Complications include visual impairment, deafness,
seizures, paralysis, hydrocephalus, and septic shock.
Clinical Manifestations
 Headache and fever are frequently the initial symptoms.
 Fever tends to remain high throughout the course of the
illness.
 The headache is usually either steady or throbbing and very
severe as a result of meningeal irritation.
 Meningeal irritation results in a number of other well-
recognized signs common to all types of meningitis:
o Neck mobility: A stiff and painful neck (nuchal rigidity) can
be an early sign and any attempts at flexion of the head are
difficult because of spasms in the muscles of the neck.
Clinical Manifestations

 Positive Kernig’s sign: When the patient is lying with the

thigh flexed on the abdomen, the leg cannot be
completely extended.
Clinical Manifestations

 Positive Brudzinski’s sign: When the patient’s neck

is flexed (after ruling out cervical trauma or
injury), flexion of the knees and hips is produced;
when the lower extremity of one side is passively
flexed, a similar movement is seen in the opposite
extremity.
 Brudzinski’s sign is a more sensitive indicator of
meningeal irritation than Kernig’s sign.
Clinical Manifestations
 Photophobia (extreme sensitivity to light): This finding is
common, although the cause is unclear.
 A rash can be a striking feature of N. meningitidis
infection, occurring in about half of patients with this
type of meningitis.
 Skin lesions develop, ranging from a petechial rash with
purpuric lesions to large areas of ecchymosis.
 Disorientation and memory impairment are common early
in the course of the illness.
 As the illness progresses, lethargy, unresponsiveness, and
coma may develop.
Clinical Manifestations
 Seizures can occur and are the result of areas of irritability
in the brain.
 ICP increases secondary to diffuse brain swelling or
hydrocephalus.
 An acute fulminant infection occurs in about 10% of patients
with meningococcal meningitis, producing signs of
overwhelming Septicemia:
 An abrupt onset of high fever, extensive Purpuric lesions
(over the face and extremities), shock, and signs of
disseminated intravascular coagulation (DIC).
 Death may occur within a few hours after onset of the
infection.
Assessment and Diagnostic Findings
 A computed tomography (CT) scan or magnetic resonance
imaging (MRI) scan is used to detect a shift in brain
contents (which may lead to herniation) prior to a lumbar
puncture.
 Bacterial culture and Gram staining of CSF and blood are
key diagnostic tests.
 CSF studies demonstrate low glucose, high protein levels,
and high white blood cell count.
 Gram staining allows for rapid identification of the
causative bacteria and initiation of appropriate antibiotic
therapy.
Prevention
 People in close contact with patients with
meningococcal meningitis should be treated with
antimicrobial chemoprophylaxis using rifampin (Rifadin),
ciprofloxacin hydrochloride (Cipro), or ceftriaxone
sodium (Rocephin).
 Therapy should be started within 24 hours after
exposure because a delay in the initiation of therapy
limits the effectiveness of the prophylaxis.
 Vaccination should also be considered as an adjunct to
antibiotic chemoprophylaxis for anyone living with a
person who develops meningococcal infection.
Medical Management
 Successful outcomes depend on the early administration
of an antibiotic that crosses the blood–brain barrier into
the subarachnoid space in sufficient concentration to halt
the multiplication of bacteria.
 Vancomycin hydrochloride in combination with one of the
cephalosporins (eg, ceftriaxone sodium, cefotaxime
sodium) is administered intravenously (IV).
 Dexamethasone (Decadron) has been shown to be
beneficial as adjunct therapy in the treatment of acute
bacterial meningitis and in pneumococcal meningitis.
 Dehydration and shock are treated with fluid volume
expanders.
Nursing Management
 The patient with meningitis is critically ill; therefore,
many of the nursing interventions are collaborative with
the physician, respiratory therapist, and other members of
the health care team.
 Neurologic status and vital signs are continually assessed.
 Pulse oximetry and arterial blood gas values are used to
quickly identify the need for respiratory support if
increasing ICP compromises the brain stem.
 Blood pressure (usually monitored using an arterial line) is
assessed for incipient shock, which precedes cardiac or
respiratory failure.
Nursing Management
 Rapid IV fluid replacement may be prescribed, but care is
taken to prevent fluid overload.
 Fever also increases the workload of the heart and
cerebral metabolism.
 Therefore, measures are taken to reduce body
temperature as quickly as possible.
 Other important components of nursing care include the
following measures:
 Protecting the patient from injury secondary to seizure
activity or altered LOC.
Nursing Management
 Monitoring daily body weight; serum electrolytes; and
urine volume, specific gravity, and osmolality.
 Preventing complications associated with immobility, such
as pressure ulcers and pneumonia.
 Instituting infection control precautions until 24 hours
after initiation of antibiotic therapy.
 An important aspect of the nurse’s role is to support the
family and assist them in identifying others who can be
supportive to them during the crisis.
Dementia
 The cognitive, functional, and behavioral changes that
characterize dementia eventually destroy a person’s
ability to function.
 The symptoms are usually subtle in onset and often
progress slowly until they are obvious and devastating.
 The two most common types of dementia are Alzheimer’s
disease (AD), which accounts for 50% to 60% of cases, and
vascular or multi-infarct dementia, which accounts for
10% to 20% of cases.
 Other non-Alzheimer dementias include Parkinson’s
disease, acquired immunodeficiency syndrome (AIDS)-
related dementia, and Pick’s disease; these types of
dementia account for fewer than 15% of cases.
Alzheimer’s Disease
 AD is a progressive, irreversible, degenerative neurologic
disease that begins insidiously and is characterized by
gradual losses of cognitive function and disturbances in
behavior and affect.
 Although AD can occur in people as young as 40 years of
age, it is uncommon before 65 years of age.
 Although the prevalence of AD increases dramatically with
increasing age, affecting as many as half of those 85 years
of age and older, it is important to note that AD is not a
normal part of aging.
Alzheimer’s Disease
 There are numerous theories about the cause of age
related cognitive decline.
 Although the greatest risk factor for AD is increasing age,
many environmental, dietary, and inflammatory factors
also may determine whether a person suffers from this
cognitive disease.
 AD is a complex brain disorder caused by a combination of
various factors that may include genetics,
neurotransmitter changes, vascular abnormalities, stress
hormones, circadian changes, head trauma, and the
presence of seizure disorders.
Clinical Manifestations
 In the early stages of AD, forgetfulness and subtle memory
loss occur.
 Patients may experience small difficulties in work or social
activities but have adequate cognitive function to
compensate for the loss and continue to function
independently.
 With further progression of AD, the deficits can no longer be
concealed.
 Forgetfulness is manifested in many daily actions; patients
may lose their ability to recognize familiar faces, places,
and objects,
Clinical Manifestations
 They may repeat the same stories because they forget
that they have already told them.
 Conversation becomes difficult, and word-finding
difficulties occur.
 The ability to formulate concepts and think abstractly
disappears.
 Patients are often unable to recognize the consequences
of their actions and therefore exhibit impulsive behavior.
 Personality changes are also usually evident. Patients may
become depressed, suspicious, paranoid, hostile, and even
combative.
Clinical Manifestations
 Progression of the disease intensifies the symptoms:
speaking skills deteriorate to nonsense syllables, agitation
and physical activity increase, and patients may wander at
night.
 Eventually, assistance is needed for most ADLs, including
eating and toileting, because dysphagia and incontinence
develop.
 The terminal stage, in which patients are usually immobile
and require total care, may last months or years.
 Death occurs as a result of complications such as
pneumonia, malnutrition, or dehydration.
Assessment and Diagnostic Findings
 AD is a diagnosis of exclusion, and a diagnosis of probable
AD is made when the medical history, physical
examination, and laboratory tests have excluded all
known causes of other dementias (such as other types of
dementia, depression, delirium, alcohol or drug abuse, or
inappropriate drug dosage or drug toxicity).
 The health history—including medical history, family
history, social and cultural history, and medication history.
 Physical examination, including functional and mental
health status, are essential to the diagnosis of probable
AD.
Assessment and Diagnostic Findings
 Diagnostic tests, including complete blood count,
chemistry profile, and vitamin B12 and thyroid hormone
levels, as well as
 screening with electroencephalography, computed
tomography (CT), magnetic resonance imaging (MRI), and
examination of the cerebrospinal fluid may all refute or
support a diagnosis of probable AD.
Assessment and Diagnostic Findings

 Depression can closely mimic early-stage AD and coexists

in many patients. Therefore, assessing the patient for
underlying depression is important to rule this out.
 Infections and physiologic disturbances, such as
hypothyroidism, Parkinson’s disease, and vitamin B12
deficiency, can cause cognitive impairment that may be
misdiagnosed as AD.
Medical Management
 The primary goal is to manage the cognitive and behavioral
symptoms.
 There is no cure and no way to slow the progression of the
disease.
 Four approved medications are available to treat AD
symptoms; however, none of these agents stops the
progression of the disease.
 The cholinesterase inhibitors (CEIs) donepezil
hydrochloride (Aricept), rivastigmine tartrate (Exelon),
galantamine hydrobromide (Razadyne [formerly known as
Reminyl]), and tacrine (Cognex).
Medical Management
 enhance acetylcholine uptake in the brain, thus
maintaining memory skills for a period of time; these
medications are used for mild to moderate symptoms.
 Cognitive ability may improve within 6 to 12 months of
therapy, but cessation of the medications results in
disease progression and cognitive decline.
 Behavioral problems such as agitation and psychosis can
be managed by behavioral and psychosocial therapies.
Nursing Management
 Nurses play an important role in the recognition of
dementia, particularly in hospitalized elderly, by assessing
for signs (eg, repeating or asking the same thing over and
over, getting lost) during the nursing admission
assessment.
 Nursing interventions for dementia are aimed at
promoting patient function and independence for as long
as possible.
Nursing Management
 Other important goals include:
 Promoting the patient’s physical safety.
 Promoting independence in self-care activities.
 Reducing anxiety and agitation.
 Improving communication.
 Providing for socialization and intimacy.
 Promoting adequate nutrition, promoting balanced activity
and rest, and supporting and educating family caregivers.
 These nursing interventions apply to all patients with
dementia, regardless of cause.
Assignment
 Nursing Management for patients with Alzheimer’s Disease (page.
218- 220)
 Vascular Dementia (page. 220)
Parkinson’s Disease
 Parkinson’s disease is a slowly progressing neurologic
movement disorder that eventually leads to disability.
 The disease affects men more often than women.
Symptoms usually first appear in the fifth decade of life;
however, cases have been diagnosed as early as 30 years
of age.
 The degenerative or idiopathic form of Parkinson’s disease
is the most common; there is also a secondary form with a
known or suspected cause.
Parkinson’s Disease
 Although the cause of most cases is unknown, research
suggests several causative factors, including genetics,
atherosclerosis, excessive accumulation of oxygen free
radicals, viral infections, head trauma, chronic use of
antipsychotic medications, and some environmental
exposures.
 Parkinson’s disease is associated with decreased levels of
dopamine resulting from destruction of pigmented
neuronal cells in the substantia nigra in the basal ganglia
region of the brain
Clinical Manifestations
 Parkinson’s disease has a gradual onset, and symptoms
progress slowly over a chronic, prolonged course.
 The cardinal signs are tremor, rigidity, bradykinesia
(abnormally slow movements), and postural instability.
 Tremor
 A slow, unilateral resting tremor is present in the majority
of patients at the time of diagnosis. Resting tremor
characteristically disappears with purposeful movement
but is evident when the extremities are motionless.
Clinical Manifestations
 The tremor may manifest as a rhythmic, slow turning
motion (pronation–supination) of the forearm and the
hand and a motion of the thumb against the fingers as if
rolling a pill between the fingers.
 Tremor is present while the patient is at rest; it increases
when the patient is walking, concentrating, or feeling
anxious.
Clinical Manifestations
 Rigidity
 Resistance to passive limb movement characterizes muscle
rigidity. Passive movement of an extremity may cause the
limb to move in jerky increments.
 Stiffness of the arms, legs, face, and posture are common.
Early in the disease, the patient may complain of shoulder
pain due to rigidity.
Clinical Manifestations
 Bradykinesia
 One of the most common features of Parkinson’s disease is
bradykinesia, which refers to the overall slowing of active
movement.
 Patients may also take longer to complete activities and
have difficulty initiating movement, such as rising from a
sitting position or turning in bed.
 Postural Instability
 The patient commonly develops postural and gait problems.
 A loss of postural reflexes occurs, and the patient stands
with the head bent forward and walks with a propulsive
gait.
Other Manifestations
 The effect of Parkinson’s disease on the basal ganglia often
produces autonomic symptoms that include excessive and
uncontrolled sweating, paroxysmal flushing, orthostatic
hypotension, gastric and urinary retention, and
constipation.
 Psychiatric changes include depression, dementia
(progressive mental deterioration), delirium, and
hallucinations (intellect is not usually affected).
 Hypokinesia (abnormally diminished movement) is also
common and may appear after the tremor.
 As dexterity declines, micrographia (small handwriting)
develops.
Other Manifestations
 The face becomes increasingly masklike and
expressionless, and the frequency of blinking decreases.
 Dysphonia (soft, slurred, low-pitched, and less audible
speech) may occur as a result of weakness and
incoordination of the muscles responsible for speech.
 As the disease progresses, patients are at risk for
respiratory and urinary tract infection, skin breakdown,
and injury from falls.
 The adverse effects of medications used to treat the
symptoms are associated with numerous complications
such as dyskinesia or orthostatic hypotension
Assessment and Diagnostic Findings
 Currently, the disease is diagnosed clinically from the
patient’s history and the presence of two of the four
cardinal manifestations: tremor, rigidity, bradykinesia, and
postural changes.
 Early diagnosis can be difficult because patients rarely are
able to pinpoint when the symptoms started.
 Often, a family member notices a change such as stooped
posture, a stiff arm, a slight limp, tremor, or slow, small
handwriting.
 The medical history, presenting symptoms, neurologic
examination, and response to pharmacologic management
are carefully evaluated when making the diagnosis
Medical Management
 Treatment is directed at controlling symptoms and
maintaining functional independence, because no medical
or surgical approaches in current use prevent disease
progression.
 Care is individualized for each patient based on presenting
symptoms and social, occupational, and emotional needs.
 Pharmacologic management is the mainstay of treatment
Medical Management
 Pharmacologic Therapy
 Levodopa (Larodopa) is the most effective agent and the
mainstay of treatment.
 Levodopa is converted to dopamine in the basal ganglia,
producing symptom relief.
 The beneficial effects of levodopa are most pronounced in
the first few years of treatment.
 Benefits begin to wane and adverse effects become more
severe over time.
 Confusion, hallucinations, depression, and sleep alterations
are associated with prolonged use.
Medical Management
 Within 5 to 10 years, most patients develop a response to
the medication characterized by dyskinesia (abnormal
involuntary movements).
 The patient may experience an on–off syndrome in which
sudden periods of near immobility (“off effect”) are
followed by a sudden return of effectiveness of the
medication (“on effect”).
 Another potential complication of long-term dopaminergic
medication use is neuroleptic malignant syndrome, which
is characterized by severe rigidity, stupor, and
hyperthermia.
Medical Management
 Surgical Management
 In patients with disabling tremor, rigidity, or severe
levodopa-induced dyskinesia, surgery may be considered.
 Although surgery provides symptom relief in selected
patients, it has not been shown to alter the course of the
disease or to produce permanent improvement.
Stereotactic Procedures
 Thalamotomy and pallidotomy are effective in
relieving many of the symptoms of Parkinson’s
disease.
 Patients eligible for these procedures are those
who have had an inadequate response to medical
therapy; they must meet strict criteria to be
eligible.
 The intent of thalamotomy and pallidotomy is to
interrupt the nerve pathways and thereby
alleviate tremor or rigidity.
Stereotactic Procedures
 During thalamotomy, a stereotactic
electrical stimulator destroys part of
the ventrolateral portion of the
thalamus in an attempt to reduce
tremor; the most common
complications are ataxia and
hemiparesis.
 Pallidotomy involves destruction of part
of the ventral aspect of the medial
globus pallidus through electrical
stimulation in patients with advanced
disease.
Stereotactic Procedures
 The procedure is effective in reducing rigidity,
bradykinesia, and dyskinesia, thus improving motor
function and ADLs in the immediate postoperative
course.
 Potential complications include hemiparesis and stroke,
as well as cognitive, speech, swallowing, and visual
changes.
 The desired response of the patient to the electrical
stimulation (ie, a decrease in rigidity) is the basis for the
selection of the area of the brain to be destroyed.
Assignment

 NURSING PROCESS for THE PATIENT WITH PARKINSON’S DISEASE (1989 –

1992)
 Assessment
 Diagnosis
 Planning and goals
 Nursing interventions
 Evaluation
 HOME CARE CHECKLIST The Patient With Parkinson’s Disease
Reference
 Hinkle, J. L., & Cheever, K. H. (2014). Brunner & Suddarth's textbook of
medical-surgical nursing (Edition 13.). Wolters Kluwer Health/Lippincott
Williams & Wilkins.