Management of Patients With Neurologic Infections, Autoimmune Disorders & Neuropathies
Transcript of Management of Patients With Neurologic Infections, Autoimmune Disorders & Neuropathies
Management of Patient’s with
Neurologic Infections,
Autoimmune Disorders &
NeuropathiesBy Esperancita A. Ferrer RN MD
Infectious Neurologic Disorders
Meningitis Is an inflammation of the pia
mater, the arachnoid & the cerebrospinal fluid.
Classification: Septic – Bacteria (N.
meningitidis & S. pneumoniae) Aseptic – Virus MC or lymphoma(nonpolio enterovirus)
Clinical Manifestations High grade fever Headache Nuchal rigidity – early sign
Attempt to flex the head is difficult because of spasm in the ms
Kernig’s sign – Thigh flexed on abdomen, leg
cannot be completely extended
Brudzinski’s sign – When neck is flexed, flexion of
the knees & hips is produced Sensitive indicator of
meningeal irritation
Petechial rash w/ purpuric lesions
Photophobia Disorientation Lethargy Seizures ↑ ICP – sec.
accumulation of purulent exudate
Diagnostic Evaluation Bacterial Culture & Gram Staining of CSF
Prevention Vaccination Antimicrobial Prophylaxis rifampin,
ciprofloxacin hcl, ceftriaxone Na (24h) For close contact
Medical ManagementAntibiotics that cross the BBB Penicillin antibiotics (Ampicillin,
Piperacillin) Cephalosphorins (ceftriaxone Na,
cefotaxime Na) Vancomycin & Rifampin resistant cases
Nursing Management Assessment & management of meningitis
should be a collaborative effort Institute infection control precautions until
24h after initiation of antibiotic therapy (oral & nasal discharge is considered infectious)
Cooling measures, antipyretics Rapid IV fluid tx prescribed caution fluid
overload Observe for ↑ ICP
Quiet calm environment Darken room Assist on position of comfort Administer Antibiotics on time &
Analgesics as prescribed
Encephalitis Inflammation of Cerebral tissue, typically
accompanied by meningeal inflammation Heres Simplex Virus (HSV) MC
HSV-1 children & adults HSV-2 neonates
Clinical Manifestations High grade fever Headache Disorientation Neurologic deficits Seizure Motor weakness hemiparesis ↑ DTR & extensor plantar response Visual field defects, aphasia, dysphagia,
ataxia & paresthesia
Diagnostic Evaluation EEG CSF Examination MRI
Medical Management Acyclovir (Zovirax) x 3 wks IV
Nursing Management Assessment & management of encephalitis
should be a collaborative effort Cooling measures, antipyretics Observe for ↑ ICP Quiet calm environment Darken room Assist on position of comfort Administer Antiviral agent on time &
Analgesics as prescribed Reorient
Autoimmune Nervous System
Disorders
Multiple Sclerosis An auto-immune
mediated progressive demyelinating disease of the CNS
Causes impaired transmission of nerve impulses from the brain to the peripheral nervous system.
Destruction of myelin in optic nerve, brain & SC
Cause: Unkown Possibly related to autoimmune
dysfunction, genetic susceptibility, or an infectious process
Multiple factors viral infection environmental factors geographic location and genetic predisposition
Common in WOMEN ages 20-40
PathophysiologySensitized T cells
Enters and remains in CNS
Inflammation
Destroys myelin and oligodendroglial cells
Plaques of sclerotic tissue
Interruption of impulse transmission
s/s depending on nerve affected
Promotes infiltration of other agents
Damage to immune system
Relapsing Remitting MS Mild infrequent sensory exacerbations with full
recovery. Lack of disease progression
Primary Progressive MS Episodes of exacerbations and remissions during
which not all symptoms resolve completely. The patient may be left with permanent disability which may vary in severity. relapses are often more severe than in the previous group. Relapses also become more severe with time.
Secondary Chronic Progressive Condition of patients with relapsing/remitting
disease begins to gradually worsen over time with resulting accumulation of neurologic signs and symptoms. In this form of the disease, relapses become more severe while remissions are less complete, shorter in duration, and eventually non-existent. The course of MS becomes steadily progressive.
Progressive Relapsing Progression of neurologic deficits. But w/ clear
acute relapses w/ or w/o recovery. Problems appear and gradually worsen over time. Common problems include spastic paraparesis, cerebellar ataxia, urinary incontinence.
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Clinical Manifestations Symptoms reflect area of demyelination Visual Disturbances- blurring of vision,
double vision (diplopia), patchy blindness (scotoma), & total blindness; Retrobulbar Optic Neuritis
Visual Disturbances
Clinical ManifestationsFRONTAL LOBE MOTOR CORTEX Spasticity of extremities & loss of abdominal reflexes (motor
pathway, corticospinal tract) Bladder bowel & sexual dysfunction(corticospinal tract) Fatigue (most disabling) WeaknessFRONTAL LOBE Cognitive (memory) psychsocial problem, Depression
(frontal/parietal lobe)PARIETAL LOBE Paresthesia, loss of proprioception (sensory pathway, posterior
column Pain (lesions on sensory pathways) CEREBELLAR Signs Ataxia & tremor Difficulty in coordination Loss of balance
Diagnostic Evaluation MRI
Sclerotic plaques throughout white matter Evoked potential studies
Slowed conduction CSF electropheresis
IgG Ab
Pharmacologic TherapyInterferon A- B –C
AVonex (beta 1a Interferon)
Decreases T-cell proliferation
IM, once a week
Betaseron (Interferon beta 1b) Decreases frequency of
relapse Decreases appearance of
new lesions SQ, every other day
Copaxone (Glatiramer Acetate)
Decreases number of lesions Decreases relapse rate SQ, once a day
Avonex & Betaseron – rapidly progressive
Copaxone –immunomodulator, relapsing-remitting disease
Corticosteroids Methylprednisolone
IV 1g x 3d tapered w/ prednisone po
Shortens duration of relapse Tx acute relapse Relieves Sx acute attack
Novantrone mitoxantrone Chemotherapeutic
agent Iv infusion q3m Reduces frequency of
clinical relapse in px w/ secondary progressive % relapsing – remitting MS
Baclofen, BZD, Dantrolene (centrally acting ms relaxant) spasticity
amantadine Symmetrel, fluoexetine Prozac Fatigue
Beta adrenergic blockers, anti-siezure medication, BZD Ataxia
Anticholinergics, alpha adrenergic blockers, antispasmodics, Bladder & bowel
problems Ascorbic acid
UTI
Nursing Interventions
Promote Physical Mobility Exercise
walking improves gait Stretching (stretch-hold-relax)
Apply ice packs before stretching Progressive weight bearing
Schedule activity and rest periods Warm packs over the spastic area Swimming and cycling are very
useful
Prevent injuries Wide stance walking Use of walking aids Wheelchair, motorizes scooters If with loss of position sense,
walk while watching feet
Enhance bladder and bowel control
Set a voiding schedule q 1.5 – 2hr initially
Intermittent bladder catheterization Use of condom catheter Adequate fluids, dietary fibers and
bowel training program
Manage speech and swallowing difficulties
Careful feeding, proper positioning, suction machine availability Speech therapist
Improve Sensory and Cognitive function
VISION use eye patch on one eye for diplopia Obtain large printed reading
materialsCOGNITION & EMOTIONAL RESPONSES Offer emotional support Involve the family in the care
Build general resistance to infection
Avoid Fatigue Extremes of temperature Exposure to infection
Myasthenia Gravis A chronic autoimmune d/o effecting
the neuromuscular transmission of impulses in the voluntary ms. of the body
It is due to an antibody mediated attack against Ach receptors at the NMJ
Loss of Ach receptors leads to a defect in neuromuscular transmission.
Release of Ach from vesicles(Myoneural
junction)↓
Ach attaches to receptor sites(Motor end plate)
↓
Muscle contraction
Continuous binding of Achto receptor site necessaryfor ms contraction to besustained
When the nerve impulse reaches the presynaptic terminal at the NMJ, Synaptic vesicles discharge Ach into the synaptic cleft
PathophysiologyAntibodies attack
receptor sites↓
Ach attaches to receptor sites (Motor end plate)
↓Transmission of nerve
impulse impaired↓
Poor Muscle contraction↓
Voluntary ms weakness
Pathophysiology
Follows an unpredictable course of periodic exacerbations and remissions
Purely motor, no effect on sensation and coordination
EtiologyAutoimmuneThymoma
Women suffer at an earlier age and are more affected
MYASTHENIA GRAVIS Clinical Manisfestations:
Gradually progressive skeletal muscle weakness and fatigue; partially reversed by rest
Weakness that worsens during the day; muscles are stronger in the morning
Ptosis (CN III), diplopia and weak eye closure Blank, mask-like facies Difficulty chewing, swallowing, talking Respiratory difficulty Dysphonia(nasal voice)
Diagnostic Tests EMG
decremental response to repetetive nerve stimulation
Serum anti- Ach Receptor antibodies CT scan/MRI
enlarged thymus gland Acetylcholinesterase Inhibitor Test:
TENSILON TEST (Edrophonium)
TENSILON TEST (Edrophonium) Tensilon IV (2mg at a time, total of 10
mg) 30 sec after injection, facial weakness
and ptosis should resolve for 5 min Atropine sulfate should be available to
counteract side effects Bradycardia Sweating cramping
Medical Management
BASIS OF DRUG TREATMENT IS TO INACTIVATE ACETYLCHOLINESTERASE
ANTICHOLINESTERASE
DOC: Pyridostigmine bromide (Mestinon) Neostigmine bromide (Prostigmin)
Inhibit breakdown of Ach ↑ conc. of available acetylcholine at NMJ Dose is gradually increased Should be administered on time AE:
Abdominal pain Diarrhea Fasciculations Increase oropharyngeal secretions
Immunomodulating DrugsCorticosteriods
Suppress immune response thus decreasing the amount of Ab production
Eg. PrednisoneImmunosuppresant
Inhibits T lymphocytes & ↓ Ach receptor Ab levels Azathioprine (Imuran)
Plasmapheresis Plasma exchange Patient’s plasma and
plasma components are removed through a centrally placed large-bore double lumen
Blood cells and antibody-containing plasma are separated
Cells and plasma substitute are reinfused
Effects is temporary
Surgical Management Thymectomy
Myasthenic Vs Cholinergic Crisis
Myasthenic Cholinergic
Cause Disease exarcerbationPrecipitating events
Anticholinergic overmedication
S/S Generalized muscle weaknessSudden inability to swallow, speak or maintain a patent airway( needs artificial ventilation)
Generalized muscle weakness
Myasthenic Cholinergic
Response to Tensilon Test
Improvement DeteriorationNo improvement
Treatment Neostigmine methylsulfateIV, IM
D/C all anticholinergicAtropine sulfate
DANGER:•Respiratory muscle weakness•Bulbar muscle weakness•Inadequate cough and gag
Bulbar muscle weakness Weakness of palatal muscles can result in a nasal
twang to the voice and nasal regurgitation of food and especially liquids.
Chewing may become difficult. Severe jaw weakness may cause the jaw to hang
open (the patient may sit with a hand on the chin for support).
Swallowing may become difficult and aspiration may occur with fluids, giving rise to coughing or choking while drinking.
Weakness of neck muscles is common and neck flexors usually are affected more severely than neck extensors.
Respiratory muscle weakness
May produce acute respiratory failure. True neuromuscular emergency, immediate intubation may be necessary. Weakness of the intercostal muscles and the diaphragm may result in carbon dioxide retention due to hypoventilation.
Weak pharyngeal muscles may collapse the upper airway. Careful monitoring of respiratory status is necessary in the acute phase of MG. Negative inspiratory force (NIF), vital capacity (VC), and tidal
volume must be monitored carefully. Relying on pulse oximetry to monitor respiratory status can
be dangerous. During the initial phase of neuromuscular hypoventilation,
carbon dioxide is retained but arterial blood oxygenation is maintained.
Nursing Interventions
Administer prescribed medication as scheduled
Prevent problems with chewing and swallowing Administer Medications 30-45 ac; sit up right
w/ neck slightly flexed Soft food; pureed food Suction standby Rest before mealtimes Prevention of aspiration Mealtimes should coincide with peak effects of
anticholinesterase
Prepare for complications like myasthenic crisis and cholinergic crisis
Prevent problems associated with impaired vision resulting from ptosis of eyelids Tape eyes Artificial tears Eye patching
Promote respiratory function Encourage adjustments in lifestyle to prevent
fatigue Maximize functional abilities
Guillain – Barre Syndrome
Polyradiculoneuritis
Definition An auto-immune attack of the peripheral
nerve myelin
Acute, rapid segmental demyelination of peripheral nerves and some cranial nerves
Rapidly progressive ascending inflammatory demyelinating polyneuropathy of the peripheral sensory & motor nerves & nerve roots
Antecedent Events: Viral Infection (C. pneumoniae, CMV, EBV,
H. Influenzae) Influenza Vaccination Infectious Diarrheal Illness
(Campylobacter)
Schwann cells-produce myelin
Myelin- fatlike subs, that sheaths around certain nerve fibers Insulation Axons conduct impulses
rapidly Demyelination-
degeneration of myelin Dysfunction in conduction of
impulses Axons- impulses away
from the cell Dendrites- impulses
toward the cell body
The dorsal root are sensory and transmit sensory impulses from specific areas of the body known as dermatomes
Sensory fibers may be: Somatic – carrying
information about pain, temperature, touch, position sense (proprioception) from tendons, joints, and body surfaces
Visceral – carrying information from the internal organs
The ventral roots are motor and transmit impulses from the spinal cord to the body.
Either: Somatic Visceral – includes
autonomic fibers that control the cardiac muscles and glandular secretions
Infectious organism contains amino acid that mimics the peripheral nerve
Pathophysiology
Antibody cannot distinguish between the 2 proteins
Antibody attacks peripheral nerve myelin
Inflammation and destruction of peripheral nerve myelin
Axon unable to support nerve conduction
Causes inflammation & Degenerative changes inpost. & ant. nerve roots, MOTOR and SENSORYLosses occur SIMULTANEOUSLY!
Clinical Manifestations: Symmetric ms weakness beginning in the
LE ascending to involve the trunk, UE & facial ms. Paralysis may develop
Hyporeflexia → Areflexia Paresthesia Dyskinesia Pain Blindness Difficulty w/ swallowing, speech, chewing Autonomic Dysfunction (↓or↑ BP, HR) Decreased Vital Capacity, depth of respirations
& breath sounds
Diagnostic Tests: Lumbar Puncture - CSF protein level
is INCREASED but the WBC remains normal in the CSF
Electrophysiologic Studies - nerve conduction velocity ↓ conduction
Medical Management: Plasmapharesis Intravenous Ig
Reduction of circulating Ab ECG monitoring
Short acting alpha adrenergic blocking agents
Intubation & Mechanical ventilation Analgesics & muscle relaxants
Anticoagulant Thigh-high elastic compression stockings
Sequential Compression Boots
Mechanical Ventilator
Nursing Interventions
Chest physiotherapy Incentive spirometry Elevate HOB Monitor for signs of respiratory
failure: Tachycardia, Tachypnea Monitor for Respiratory Fatigue:
Breathlessness when talking, ↓ VC, PaO2 <70 mmHg, Bulbar weakness
Mechanical ventilator Suction
Maintain respiratory function
Paralyzed extremities functional positions
PROM 2x/d Prevent DVT & PE
ROM, position changes, anticoagulation, thigh high elastic compression stockings, adequate hydration
Prevent Pressure Ulcers Padding over bony prominences,
turning q2h
Enhance physical mobility
Problem: Paralytic Ileus insufficient parasympathetic activity
Auscultate BS- hold feeding if absent to prevent gastric distention
Assess CN V & IX IVF & Parenteral nutrition Gastrostomy Tube
Provide adequate nutrition
Improve communication Use other means of communication,
picture cards, eye blink system Px call system. Standard call lights
cannot be activated by the severely weak GBS px. Constant monitoring & surveillance.
Patient Education & Health Maintenance
Acute phase 1-4wks, afterwards pax stabilizes, rehabilitation can begin
Instruct: Breathing exercises, incentive spirometer
Wear good supportive & protective shoes while out of bed
Check feet routinely Scheduled rest periods
Respiratory Failure- major cause ofMortality
DVT Urinary retention Pulmonary embolism Respiratory failure
Monitor and manage complications
Cranial Nerve Disorders:
Trigeminal Neuralgia A.k.a Tic
Douloureux Condition of the
fifth cranial nerve Characterized by
paroxysms of pain in the area innervated by any of the three branches of trigeminal nerve
Cause: Not certain May be due to
chronic compression or irritation of the trigeminal nerve
Unilateral, shooting/stabbing pain Starts and end abruptly May last for 1 – 15 minutes
Associated symptom: Involuntary contraction of the facial
muscle
Clinical Manifestations:
Stimuli that can trigger pain:
Washing of face Shaving Brushing of the teeth Eating Drinking Draft of cold air Direct pressure on the nerve
Medical Management Antiseizure agents
CARBAMAZEPINE (Tegretol) Relieves pain by decreasing the
transmission of impulses at certain nerve terminals
Should be taken with meals Side effects:
Nausea Dizziness Drowsiness Aplastic anemia
Mgt Pain Gabapentin (Neurontin), Baclofen,
phenytoin (Dilantin)
Surgical Management Microvascular Decompression of the
Trigeminal Nerve Intracranial approach Relieve contact between cerebral
vessel & trigeminal nerve root Relieves pain while preserving normal
sensation Radio frequency thermal
coagulation Thermal lesion on trigeminal nerve Dysesthesia of the face & loss of
corneal reflex occurs
Percutaneous Balloon Microcompression Balloon compresses the nerve root for
1 minute Microvascular compression Masseter ms weakness & facial
dysesthesia results
Nursing Interventions: Prevent pain
Help recognize precipitating/aggravating factors
Chew on the unaffected side Ingest soft foods
Provide emotional support Encourage to express feelings Provide adequate nutrition in small frequent
meals at room temperature Post-op
Assess for motor and sensory deficit in the trigeminal nerve
BELL’S PALSY Dysfunction of the facial
nerve Due to unilateral
inflammation of the 7th cranial nerve
Cause: unknown May be related to
Vascular ischemia Viral disease Autoimmune disease Combination of the
these factors
PathophysiologyInflammation
Compression of the nerve
Damage
“Bell’s smile”
Clinical Manifestations: Unilateral facial weakness Mouth drooping Distorted taste perception Smooth forehead Inability to close eyelid on the affected side Incomplete eye closure Excessive tearing when attempting to close the
eyes Inability to raise eyebrows, puff out the cheek Painful sensation in the face, behind the ear and in
the eye
Medical ManagementRecovery 3-5 wks
Prednisone To decrease inflammation and edema To decrease vascular compression To permit restoration of blood
circulation Artificial Tears Analgesics TENS
Nursing Intervention Apply moist heat to reduce pain Massage the face to maintain muscle
tone Give frequent mouth care Protect the eye with an eye patch. Eyelid
can be taped at night Instruct to chew on unaffected side