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