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Nursing Care & Intervention for the Client with Chronic Neurological Disease
Keith Rischer RN, MA, CEN
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Today’s Objectives… Compare & contrast pathophysiology and clinical manifestations of chronic neurological disorders (MS, Myasthenia Gravis, Guillian-Barre, ALS). Identify the diagnostic tests, nursing priorities, and client education with chronic neurological disorders. Describe the mechanism of action, side effects and nursing responsibilities with pharmacologic management of chronic neurological disorders.
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Multiple Sclerosis Patho Autoimmune disease of myelin sheath T cells
Inflammatory response Destroys myelin sheath in patches Demyelination of nerve fibers Ages 20-40…only 20% have sx in 40-50’s 500,000 currently afflicted w/women slightly more then men Expect to live appx 35 years after onset of sx What is MS? Chronic, progressive degenerative disease that affects the myelin sheath of the brain and spinal cord from viruses, allergies, or an autoimmune response. Myelin sheaths are fatty, segmented wrappings that normally protect and insulate nerve fibers and increase the speed of transmission of nerve impulses T cells which normally move in and out of the CNS remain in the CNS of clients with MS T cells initiate an inflammatory response Inflammatory response destroys myelin leading to axon dysfunction Myelin sheaths of the spinal cord, brain and optic nerve are destroyed in patches, called plaques along the axon Demyelination of nerve fibers slows and distorts conduction of nerve impulses or causes total absence of the impulse Incidence and etiology 500,000 affected Females are affected 1.5 times more than males Incidence is highest among young adults ages yrs. Occurs more in temperate climates including Northern US More prevalent in urban areas and in higher socioeconomic groups Hereditary factor More prevalent among Caucasians
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MS: Classifications Relapsing-remitting most common 85% of cases
Attacks that become increasingly frequent 1-2 weeks relapse 4-8 months to resolve Exacerbations (acute attacks) occurs with either full recovery or partial recovery with disability Classifications of MS – 4 types are common Progressive relapsing…5%...absence of remissions…progressive deterioration Exacerbations secondary due to stress-fatigue, overexertion
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MS: Assessment Fatigue Spinal cord lesions lead to:
Changes in motor and sensory impairments of the trunk and limbs Heaviness or weakness in extremities Numbness or tingling in extremities Bowel or bladder dysfunction Intention tremors Loss of fine motor movement Spasticity Vague and unrelated symptoms often dominate the early period of MS Fatigue affects all clients with MS
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MS: Assessment Brain lesions lead to CNS signs:
Emotional lability – euphoria or depression Irritability Changes in vision and coordination Slurred speech Ataxia Diplopia Nystagmus
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MS: Diagnostic Tests CSF MRI CT scan Elevated protein WBC cells
IgG bands due to the immune response MRI multifocal lesions in the white matter CT scan atrophy and white matter lesions No single test can reliably diagnose MS
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MS: Pharmacologic Management
Corticosteroids Prednisone Solu-medrol (Methylprednisolone) Acute exacerbations Immunosuppressive Antispasmodics Valium Adjunctive Paresthesias Tegretol or Amitriptyline Steroids LT Side Effects HTN Peptic ulcers Skin fragility Impaired immunity Thromboembolism Cushingoid appearance
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MS: Pharmacologic Management
Biologic Response Modifiers delay disability and decrease the number of and severity of relapses Avonex (Interferon Beta 1a) – given IM q week Betaseron (Interferon Beta 1b) – given SQ every other day Copaxone (Glatiramer acetate) – given SQ every day Side Effects Thrombocytopenia Leukopenia Depression injection site reactions
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MS: Nursing Diagnostic Priorities
Fatigue Impaired physical mobility ROM-strengthening exercises Encourage ADL’s but not to excess Urinary Retention Self cath Prevention of UTI Constipation Nursing care varies with the acuity of exacerbations and the presenting problems
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MS: Nursing Diagnostic Priorities
Disturbed Sensory Perception: Visual Cognitive problems Re-orient Speech/swallowing eval Deficient knowledge Medications Bowel/bladder programs Avoid exacerbations Importance of rest Stress reduction Extremes of temperature
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Amyotrophic Lateral Sclerosis (ALS)
Patho Amyotrophy process of muscle atrophy Lateral loss of nerves on each side of the spinal cord Sclerosis hardened scar tissue when nerve cells die Characteristics Loss of motor neurons Flaccid quadriplegia Atrophy extremities Resp. impairment Causes Incidence Approximately 30,000 Americans have the disease Age of onset is between 40 and 70 yrs More prevalent in men Death occurs 2-5 years after the onset Characteristics Progressive loss of motor neurons in both the cerebral cortex and the spinal cord leads to de-enervation with shrinkage of musculature and muscle atrophy until flaccid quadriplegia occurs..eventually death Affects motor neurons in 3 locations…anterior horn cells of the spinal cord, motor nuclei of brain stem Causes Unknown 10% have inherited form of the disease Viral infection creates a disturbance in motor neurons Autoimmune response
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ALS: Assessment Early Late Diagnosis Fatigue Dysphagia/dysarthria
Weakness of extremities Late Muscle atrophy Weakness Flaccid quadriplegia Diaphragm Death if no ventilator Diagnosis CK increased Muscle biopsy
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ALS: Interventions Rilutek Speech therapy Dietician Hospice
Extends survival time only Speech therapy Communication Swallowing eval Dietician Enteral feedings Hospice End of life…living will No specific treatment for the disease exists Rilutek antiglutamate inhibits presynaptic release of glutamic acid in the CNS- protects neurons against excitotoxicity of glutamic acid
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ALS: A Patient’s Perspective
“Having ALS is like walking into a dark room, reaching for the light switch on the wall and it’s not there. You’re in the dark…you ask will life ever be better again? At that point, it dawns on you, the light to get you through these hard times has to come from within. And that flame is fueled by the love and support of everyone around us.”
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Guillain Barre Syndrome
Patho Autoimmune disorder Myelin sheath destroyed Motor, sensory, autonomic involvement Causes Acute illness GI, URI Diseases Hodgkin’s, Lupas, HIV Virus CMV, Epstein-Barr virus, HIV Vaccination Flu, Group A Strep, Rabies PERIPHERAL NERVOUS SYSTEM DISEASE Incidence 1-4 cases per 100,000 Mortality 4-15% 50% in caucasion Higher prevalence >45 years 80-90% ACHIEVE FULL recovery within 6-12 months Pathophysiology Immune system attacks ascending or descending peripheral nerves Myelin sheath surrounding axons is destroyed Motor, sensory and autonomic functions may be involved
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GBS: Assessment of Ascending
Paresthesia lower extremities Weakness progresses upward to trunk, arms and/or cranial nerves Motor deficit mild paresis to total quadriplegia Respiratory compromise 50% prevalence Ascending GBS (most common) PARESTHESIA-is a sensation of tingling, pricking, or numbness of a person's skin with no apparent long-term physical effect. It is more generally known as the feeling of "pins and needles" or of a limb being "asleep" (although this is not directly related to the phenomenon of sleep). The manifestation of paresthesia may be transient or chronic. Abrupt onset of muscle weakness and pain Does not affect LOC Ascending flaccidity or weakness evolves over hours to days
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GBS: Assessment of Descending
Weakness of facial muscles/jaw Ophthalmoplegia Paralysis/weakness of eye muscles Diplopia Dysphagia Difficulty speaking Respiratory compromise
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GBS: Diagnostic Lumbar puncture Moderate leukocytosis EMG MRI/CT
increase in CSF protein level without an increase in cell count Moderate leukocytosis early in illness EMG decreased motor nerve conduction MRI/CT r/o other causes
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GBS: Nursing Diagnostic Priorities
Airway Monitor respiratory status Manage the airway HOB 45 degrees Cardiac Monitor BP, dysrhythmias Acute pain Impaired physical mobility Help prevent muscle atrophy Self-care deficit Risk for aspiration Assess pt’s ability to swallow and chew food
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GBS: Medical Management
Plasmaphoresis Removes circulating antibodies that cause GBS Plasma is separated from whole blood 3 to 4 treatments 1-2 days apart Can reduce recovery up to 50 % IV Immunoglobulin Chills, fever, myalgia Acute renal failure, anaphylaxis
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GBS: Plasmaphoresis Infection Hypovolemia Low K+, Ca++
VS changes Low K+, Ca++ Temporary distal extremity paresthesias Add Ca++ gluconate to exchange fluids
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Myasthenia Gravis Patho Causes
Autoimmune disease of the neuromuscular junction cranial nerves, skeletal and respiratory muscles Antibody attack on the acetylcholine receptors in muscle end plate membranes Nerve impulses not transmitted to muscle Remissions and exacerbations Causes Unknown Overgrowth of thymus gland Incidence 0.5 cases per 100,000 people Affects most people between 20 and 30 yrs old Women are affected three times more than men May be preceded by infection, emotional upset, pregnancy, or anesthesia
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Myasthenia Gravis: Assessment
Early Facial/ocular involvement Incomplete eye closure PEARL Difficulty chewing Dysphagia Late Proximal limb weakness All muscles weak Respiratory Difficulty breathing Diminished breath sounds Respiratory paralysis and failure
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Cholinesterase Inhibiting Drugs
Pyridostigmine (Mestinon) First line management Mechanism Enhance neuromuscular impulse transmission by preventing decrease of Ach by ChE Increases response of muscles to nerve impulses-improves muscle strength Nursing considerations Take w/food 1 hour before meals to prevent aspiration Side effects Cholinergic crisis Cholinergic crisis Acute exacerbation of muscle weakness caused by overmedication Similar to myasthenic crisis
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Myasthenic Crisis Cholinergic Crisis
Assessment HR/BP/RR incr. B/B incontinence Decreased u/o Cyanosis Management Assess resp status closely Monitor VS closely Hold CHI drugs Assessment Hypotension N-V-D Abd cramps Facial twitching Myasthenic crisis…exacerbation of myasthenic sx caused by infection Cholinergic crisis…over medication of CHI
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Myasthenia Gravis: Diagnostic Tests
AChR antibodies 80-90% present Thyroid function tests 5% thyrotoxicosis Tensilon testing Improvement after administration EMG Acetylcholine receptor antibodies Tensilon Cholinesterase inhibitors…inhibits breakdown of Ach which increases availability of Ach for excitation IV injection…improvement within 1” positive but lasts only 5”
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MG: Pharmacologic Treatment
Cholinesterase inhibitors Pyridostigmine (Mestinon) Cholinergic crisis Immunosupression Prednisone Chemotherapy Imuran/Cytotoxan Plasmaphoresis 6 exchanges over 2 weeks Cholinesterase inhibitors First line treatment Enhance neuromuscular impulse transmission by preventing the decrease of Ach by the enzyme cholinesterase This increases response of muscles to nerve impulses and overall muscle strength
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MG: Nursing Diagnostic Priorities
Risk for ineffective breathing pattern Monitor respiratory status Monitor for respiratory failure Monitor speech and swallowing abilities to prevent aspiration Activity intolerance r/t fatigue/muscle weakness….self care deficit Rest Assess abilities…adaptive equipment Deficient knowledge avoid stress, infection, fatigue Medications Need for artificial tears/ointment Nutritional support Deficient knowledge Avoid exacerbations….alcohol, heat, surgery
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