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7/28/2019 14-Neurologic Infections and Autoimmune Disorders
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Neurologic Function
Management of Patients with
Neurologic Infections andAutoimmune Disorders
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Meningitis
Inflammation of arachnoid/pia mater of brain,
spinal cord, and CSF
Septic (bacterial) or Aseptic (viral)
Enter CNS indirectly or directly
Resulting inflammatory response can ICP
Exudate may spread to cranial/spinal nervesand cause neurologic deterioration
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Clinical Manifestations
Headache
Fever
Nuchal rigidity
Positive Kernigs sign
Positive Brudinskis sign
Photophobia
Rash with N. meningitidis
Disorientation
Seizures
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Diagnostics
What diagnostics would you
expect to be ordered?
What findings would you expect?
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Prevention
Haemophilus influenzae meningitis is now
rarely seen do to childhood vaccination
College freshmen are targeted for vaccination
against N. meningitidis
Close contacts of patients with meningococcal
meningitis (N. meningitidis) are treated
prophylactically with rifampin (Rifadin),
ciprofloxacin (Cipro) or ceftriaxone (Rocephin)
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Management
Medical
Early administration of
antibiotics
Dexamethasone Fluid volume expanders
Dilantin for seizure control
Nursing
Neurological checks
Monitor VS, SpO2, ABGs
Maintain adequate tissueoxygenation
Monitor arterial BP
Rapid fluid replacement
Prevent ICP Seizure management
Prevent complications
Maintain Infection Control
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Encephalitis
Acute inflammation of brain tissue
Most often viral
Herpes Simplex Virus
Enteroviruses
Arboviruses
Can also be caused by: bacteria, fungi,
paracytes No exudate
Can result in death
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Diagnostics
The specific diagnostics will vary by cause
Common diagnostics include
CSF analysis
Neuroimaging (MRI)
EEG
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Assessment
Use GCS
Clinical manifestations:
fever, n/v, nuchal
rigidity, headache,vertigo
Seizure activity
Cranial nerveinvolvement
Indicators of ICP
What is the GCS?
What does a GCS 15
tell you? A GCS 3?
What signs are
indicative of
increased
intracranial
pressure?
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Treatment
What is the treatment of
encephalitis dependent upon?
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Multiple Sclerosis
Progressive, degenerative disease affecting:
Myelin sheath
Conduction pathways of CNS
Leading cause of neurologic disability in
20 40 year olds
4 patterns Periods of remission and exacerbation
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Pathophysiology
Sensitized T cells cross blood-brain barrier and
remain in the CNS and promote entry of other
agents that damage immune system
Immune system attack leads to inflammation
that destroys myelin and oligodendroglial cells
Damaged myelin is removed by astrocytes and
plaques develop on demyelinated axons
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Pathophysiology
White fiber tracts are affected
Recovery of myelin will occur with remission
Repeated exacerbations will result inpermanent damage caused by degeneration
of the demyelinated axons
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Clinical Manifestations
Fatigue
Depression
Weakness
Numbness
Ataxia
Loss of balance
Pain
Absent abdominal
reflexes
Hyperactive DTRs
Visual disturbances
diplopia
Spasticity
Cognitive changes
Mild to moderate
Emotional lability
Bladder, bowel, and
sexual dysfuntion
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Secondary Complications
UTI
Constipation
Pressure ulcer
Contractures
Dependent pedal
edema
Pneumonia
Reactive depression
Decreased bone density
Increased risk of
osteoporosis
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Gerontologic Considerations
Mrs. S is 60 years old and has had relapsing-remitting MS for35 years. She had just been diagnosed with type 2 diabetes
and her BP is now at a level that requires pharmacotherapy.
With each exacerbation of her MS she seems to have
increased functional deficits. Her functional abilities are alsoimpaired by increasing weakness and a stooped posture. She
has been hospitalized for an acute exacerbation and work-up
that identified the diabetes mellitus. She has recovered to
the point that she can be discharged to home but she is
worried about being a burden.
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Question
As you are planning Mrs. Ss
discharge, what factors must be
considered?
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Assessment and Diagnostic
Findings
MRI identifies multiple plaques in CNS
Electrophoresis of CSF
Evoked potential studies Urodynamic studies
Neuropsychological testing
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Medication
Disease modifying
therapy:
Interferon beta-1a
Interferon beta-1b
Glatiramer acetate
Methylpredinisolone
Mitoxantrone
Symptom management: Baclofen
Benzodiazepines
Zanaflex
Dantrolene
Amantadine
Pemoline
Fluoxetine
Alpha-adrenergic blockers Antispasmotics
Vitamin C
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Nursing Interventions
Promote physical mobiltiy
Prevent injury
Enhance bladder and bowel control Enhance communication & manage
swallowing difficulties
Improve sensory and cognitive function Improve home management
Promote sexual function
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Myasthenia Gravis
Chronic neuromuscular autoimmune disease
Weakness of voluntary muscles
Remissions and exacerbations
Nerve impulse not transmitted to skeletal muscles
Development of specific antibodies to one or more
Ach receptor sites
Degeneration of Ach receptors Thymus gland often abnormal
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Clinical Manifestations
Ocular muscle involvement
Bulbar weakness
Generalized weakness Dysphonia
Describe the clinical presentation of
these manifestations.
What is a major associated risk?
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Assessment/Diagnostics
AchE Inhibitor test: edrophonium (Tensilon) is
injected IV
Identification of Ach receptor antibodies in
serum
Repetitive Nerve Stimulation
MRI
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Medical Management
Medications:
Antichoinesterase Inhibitors (pyridostigmine)
Immunosuppresive agents
Corticosteroids
Cytotoxic agents
Other:
Plasmppheresis
Thymectomy
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Interventions
Identify at least one strategy to:
Assist with activities
Facilitate communication
Provide respiratory support
Provide nutritional support
Provide eye protection
Provide psychosocial support
When is the best time to administer AchIs?
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Serious Complication
Respiratory Failure
Often precipitated by a respiratory infection
Other triggers: medication change, surgery,
pregnancy, medications that exacerbate MG
Discuss why respiratory failure would occur.
What collaborative interventions would be
necessary if respiratory failure occurs?
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Myasthenia Gravis: Crisis
Myasthenia Crisis
Exacerbation of myasthenic symptoms
Undermedication with AchEIs
Cholinergic Crisis
Acute exacerbation of muscle weakness
Overmedication with cholinergic drugs
When is the best time for chest physiotherapy?
What should the nurse offer after CPT?
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Problem Identification
Identify the key Collaborative
Problem and Nursing Diagnosis
associated with Myasthenia Crisis
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Guillian-Barr Syndrome
Autoimmune attack on myelin of PNS
Ascending weakness most typical
Impaired saltatoy conduction Characterized by: dyskinesia, hyporeflexia, and
paresthesia
Antecedent event Most fully recover, but can result in death
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Pathophysiology
Cell mediated and humoral immune attack
Molecular mimicry
Process results in influx of macrophages andother immune mediated agents that attack
myelin
Axon looses ability to conduct impulse
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Clinical Manifestations
Classic presentation: Areflexia and ascending
weakness
Paresthesia
Pain
Blindness
Respiratory compromise Autonomic dysfunction
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Assessment and Diagnostics
No serum test will diagnose
CSF analysis
Evoked potential studies
Discuss what CSF finding is diagnostic of GBS.
What would evoked potential studies show andwhy?
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Medical Management
Baseline respiratory assessment and close
monitoring
Continuous ECG monitoring
Anticipate need for intubation and mechanical
ventilation
Plasmapheresis and IV Immunoglobulin G
(IVIG)
Short acting alpha adrenergic beta blockers
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Nursing Interventions
Identify interventions that will:
Maintain respiratory and cardiovascular
function
Enhance physical mobility
Provide adequate nutrition
Improve communication Decrease fear and anxiety
Monitor and manage potential complications