14-Neurologic Infections and Autoimmune Disorders

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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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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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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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

14-Neurologic Infections and Autoimmune Disorders

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