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107 Cards in this Set

  • Front
  • Back
Multiple Sclerosis-describe disease and characteristics
• Chronic disease of the central nervous system
• Characterized by relapses, or exacerbations and remissions of neurological symptoms
• Frequently functional disability occurs over time
Multiple Sclerosis Pathology
• Areas of patchy demyelination (destruction or removal of the myelin sheath from a nerve or nerve fiber) and gliosis (scarring) in the brain and spinal cord
Multiple Sclerosis Etiology/Risk Factors
• Variety of Factors:
- Damage to myelin may be initiated by an autoimmune inflammatory response
• May be provoked by a viral infection
• Hormonal changes (Initial MS symptoms often occur in women during the first 6 months postpartum)
• No cause identified for the inflammatory response
Multiple Sclerosis - What happens to the T-cells?
• The inflammatory response is initiated when T -cells migrate into the central nervous system where the T-cells are stimulated to release inflammatory cytokines
Multiple Sclerosis-how is MS related to genetics?
Multiple Sclerosis
• May be influenced by genetics and environmental factors
- Genetics: may play a role in the development of multiple sclerosis
- Environmental factors: exposure to a virus at some point during childhood that potentially has an effect on the development of MS later on in life
Multiple Sclerosis Clinical Presentation
Four Major Courses of the Disease
have been Identified:
• Relapsing-Remitting (most common type and carries the best prognosis results in mild deficits)
• Secondary-Progressive (30-40% of relapsing kind evolve into secondary. People can start in any type and symptoms can worsen without clear periods of remission.
• Primary-Progressive (Marburg Syndrome) -No clear states of remission at all. Explosive exaggerated/acute. Can be some regeneration of myelin sheath. When disease gets down to the Axon-no regineration occurs
• Progressive-Relapsing-Progressive patterns of worsening symptoms
Multiple Sclerosis
• Symptoms of MS
Symptoms of MS frequency and severity
• May be described based on the area of the central nervous system that is involved - Examples: Inflammation of the optic nerve (optic neuritis) can cause retrobulbar pain, color desaturation and visual loss. This is often described as if "looking through a veil or screen."
Multiple Sclerosis
• Examples of possible symptoms.
• Examples:
- Brain stem lesions may produce eye movement changes such as diplopia (double vision) as well as vertigo (dizziness), dysarthria (articulation problems), dysphagia (difficulty swallowing), and facial weakness
- Cerebellar symptoms: ataxia and tremor
- Spinal cord lesions: bowel, bladder and
sexual dysfunction as well as loss of position sense and spastic gait difficulties
• Cerebral lesions, generalized brain atrophy: cognitive disturbances such as short-term memory loss, confusion, difficulty with concentration and multitasking
• Motor symptoms: muscle weakness
• Sensory symptoms: pain, paresthesias, dysethesias (painful feelings such as burning, wetness, itching, electric shock or pins and needles caused by neurological malfunction)
Most common symptom reported by clients with MS is:
• 80% report as most common symptom
• 40% report as the "worst" symptom experienced
• Can be overwhelming and disabling
• Not necessarily related to activity
• Cause of fatigue is unclear but is often the presenting symptom or as a part of presenting symptoms
• Clients express a sense of exhaustion and inability to complete a task
• Often described as worsening as the day progresses
• Restful sleep does not alleviate fatigue
• Clients describe muscle fatigue in large weight-bearing muscle groups in thighs and calves
• Limb "give away" (while walking or going up steps)
Uhthoff's Sign
Lhermitte's Sign
Multiple Sclerosis
• Lhermitte's Sign: sudden, transient, electric-like shocks spreading down the body when the head is flexed forward
• Uhthoff's Sign: Nystagmus (involuntary, rhythmic movements of the eyes)
Multiple Sclerosis Diagnosis
Combination of clinical evidence and laboratory support
• Thorough History of Neurological Events
Separated by time and space
• Neurological Assessment
• MRI (Magnetic Resonance Imaging)
• Cerebrospinal Fluid Analysis
• MRI: MS appears as multiple plaques scattered in the white matter
• Gadolinium enhancement: Identifies active plaques (gadolinium will only enter the CNS if the blood brain barrier has been breached)
MS is the "Great Mimic"
MS is the "Great Mimic"
• Lupus erythematosis
• Sjogren's disease (Congenital condition characterized by ichthyosis (dermatologic condition - dry skin, resembles fish scales), mental deficiency and spastic paralysis)
• CNS Lyme disease, tumors
• Endocrine disturbances
Confirming the Diagnosis of MS
Confirming the Diagnosis
• The clinical diagnosis relies on the following:
- At least 2 attacks in which 2 areas of the CNS were involved (for example, an episode of optic neuritis and an episode of weakness in the legs).
- Neurologic signs (such as optic pallor, spasticity in the legs, cerebellar ataxia) that reflect at least 2 separate areas of CNS involvement.
Multiple Sclerosis
Disease Management Options
Pharmacological Treatment:
- Treatment of Exacerbations
- Disease-Modifying Therapies
- Management of Symptoms
• Non-Pharmacological Measures: - Physical Rehabilitation Efforts
- Effective Energy Expenditure
- Bladder Management
- Psychotherapy
- Hippotherapy
- Cognitive Therapy
Multiple Sclerosis Disease Management Options
• Alternative Therapies:
• Alternative Therapies: -Swank Diet
- Vitamin B12 Supplements
- Cannabinoids
-Bee Venom
• Experimental Therapies: - Stem Cell Transplantation
- IV Gamma Globulin
- Plasmapheresis
Multiple Sclerosis Pharmacological Treatments Treatment of Exacerbations
- Mainstay of the treatment of exacerbations of MS is the use of high-dose methyl prednisone followed by a brief oral prednisone taper
- Steroids are considered to be the gold standard in the treatment of MS exacerbations
- Must determine if presenting symptoms are an exacerbation of MS or if due to another source (ie: fever from infection is known to temporarily worsen symptoms)
Multiple Sclerosis Pharmacological Treatments
• Disease Modifying Treatments
Multiple Sclerosis Pharmacological Treatments
• Disease Modifying Treatments - Immunomodulators
• 1993 FDA approved use of Interferon beta-1b (Betaseron for the treatment of MS
- A Phase III trial demonstrated that Betaseron reduced the relapse rate by approximately 31 %
1996 FDA approved use of Interferon beta-1a (Avonex)
- Research study demonstrated a significant effect on relapse rate and a delay in the progression of disabilities
• 1996 FDA approved use of Glatiramer Acetate (Copaxone)
- Research study demonstrated a reduction in relapse rates with minimal side effects
Multiple Sclerosis Pharmacological Treatments
• Immunosuppressants
- Have been used for 20 years with marginal results
- Reduction in the autoreactive cells should reduce disease activity
• Azathiaprine, methotrexate, cyclophosphamide, cladribine, mitoxantrone
• MITOXANTRONE: shown in clinical trials to reduce exacerbations and progression of multiple sclerosis
Multiple Sclerosis Symptomatic Treatments
Multiple Sclerosis Symptomatic Treatments

• MS is a disease of the CNS therefore the complications of this disease can affect multiple body systems. Most common or troublesome symptoms generally involve bladder and bowel dysfunction, pain, fatigue, and spasticity.

• Bladder Dysfunction:
- Present in the majority of clients with MS
- Infections
- Voiding dysfunctions
- Pharmacological management

• Bowel Dysfunction:
- Most often related to constipation
- Sensitive to many of the treatment regimens used to
treat MS disease
- Decreased mobility and muscle weakness
- Dietary modifications, stool softeners, suppositories,
planned evacuations

• Pain
- Many clients with MS suffer severe and disabling pain
-Identify other sources of pain before assuming cause is MS
- Psychotropic agents (for neuritic pain)
• tricyclic antidepressant drug-Amitriptyline, nortriptyline,

anticonvulsant and mood stabilizing drug: carbamazepine,
gabapentin/Neurontin-for seizures and neuropathic pain

• Fatigue
- Pharmacological agents
- Effective energy management

• Spasticity
- Stretching exercises or physical therapy
- Antispasmodic drugs: baclofen, tizanidine,
diazepam, dantrolene
- Intrathecal infusion of baclofen
- Botulinum Toxin Injections
Multiple Sclerosis Non-Pharmacological Treatments Physical and Occupational Therapy
Multiple Sclerosis Non-Pharmacological Treatments Physical and Occupational Therapy
- Hippotherapy: the action of the horse's
movements strengthens the client's muscles and regain agility. Improves muscular control in the trunk, head, and extremities. Shown to improve the patients' self-esteem, self-image, and interpersonal skills
- Cognitive rehabilitation
• Cognitive problems occur in approximately 50% of clients with MS
• Short-term memory loss, impaired judgment, and multi-tasking difficulties
Multiple Sclerosis
Alternative Treatments
Swank Diet: First published in 1950: Low-fat/Low saturated fat diet based on the eating habits of Norwegian fishermen
• Vitamin B12 deficiency: May correlate to
exacerbations of MS
• Hypnosis: Treating pain
• Herbal Products: St. Johns Wort
• Cannabinoids: Spasticity
• Bee Venom: Clients allow themselves to be stung multiple times, often up to 2,000 times per year (Anti-inflammatory and immune system response)
Multiple Sclerosis Nursing Diagnosis
• Fatigue: Rest and sleep may not result in
• Self-Care Deficit
• Knowledge Deficit
• Body Image Disturbance
Amyotrophic Lateral Sclerosis (ALS)
Lou Gehrig's Disease
• Disorder of the Central Nervous System's motor neurons (both upper and lower motor neurons) Motor neurons affect muscle cells; responsible for the enervation of the muscle
• Fatal disease characterized by progressive muscle weakness resulting in paralysis
• No Cure
Amyotrophic Lateral Sclerosis (ALS)
Neurophysiology of ALS
Neurophysiology of ALS
• ALS clients retain full intellectual capacity and intelligence since motor neurons have little effect on the cognitive aspect of the nervous system
• Connection between muscle and CNS is blocked. Muscle begins to behave as if it is not ennervated and begins to atrophy. Motor neurons shrink- they ennervate less and less

Musculature and the affected muscles atrophy
Amyotrophic Lateral Sclerosis (ALS)
Amyotrophic Lateral Sclerosis (ALS)
• Short answer: Unknown
• Long answer: Multiple theories, most researchers believe that the excess of a neurotransmitter called glutamate builds up in the synapse causing eventual nerve cell death and subsequent muscle atrophy of the muscle attached to that nerve
Amyotrophic Lateral Sclerosis (ALS)
• Hereditary Component
• Hereditary Component
- At least 10% of ALS cases are hereditary, identified as familial ALS (FALS)
- FALS is defined as two or more cases in the same bloodline
- Disease is autosomal dominant: meaning if a parent has ALS, children have a 50% chance of inheriting the defective gene, however not all people with the defective gene will develop the disorder
Amyotrophic Lateral Sclerosis
• Environmental Factors
- Strongly suspected
- Higher incidence of ALS is correlated with
exposure to agricultural chemicals and solvents
Amyotrophic Lateral Sclerosis (ALS)
Who Gets ALS?
• Occurs in all races
• Men are affected more frequently than women (ratio of 2 to 1, after the age of 60 the ratio approaches 1 to 1)
1 to 2 of every 100, 000 people will develop ALS each year, however the incidence in the area of Kii peninsula of Japan, Guam, and western New Guinea is much higher
U.S. approximately 30,000 ALS clients 5,000 new cases per year, 15 per day

• Average age of onset is 53 to 57 years of age (Ethically issues related to passing disease to children unknowingly if symptoms or disease do not occur until well after family is started)
• Approximately 80% of the cases manifest between the ages of 40 to 70 years of age
Amyotrophic Lateral Sclerosis (ALS)
Clinical Manifestations
Clinical Manifestations
• Most ALS clients notice muscle weakness in either the arms or the legs (32% arms, 36% legs) Referred to as limb-onset ALS
• 25% identify difficulty speaking as 1 st symptom. Referred to as bulbar ALS
• 7% identify difficulty with breathing as 1 st symptom
Amyotrophic Lateral Sclerosis (ALS)
what muscles are not effected?
Not all muscles are affected:
Bowel and bladder control remains intact Sexual function remains intact
Heart muscle unaffected
Eye muscles are usually the last affected if at all
Amyotrophic Lateral Sclerosis (ALS)
Disease Progression
• Progression varies considerably from client to client
Common progression:
- Difficulty walking resulting in the use of a cane, walker and finally a wheelchair
- Loss of ability to write, type, feed self
- Difficulty speaking and swallowing (alternative forms
of communication and a feeding tube)
- Decrease in vital lung capacity (once below 50% generally the client has to decide about going on the ventilator)
- Progression may be as quick as 6 months or may take years.
Amyotrophic Lateral Sclerosis (ALS)

• No specific test available
• Diagnosis typically takes weeks or months, process of eliminating other disorders
• EMG: diagnosis abnormal electrical activity of involved skeletal muscles
• Muscle biopsy
Amyotrophic Lateral Sclerosis (ALS)
• Rilutek: slows progression of disease by inhibiting release of glutamic acid in the CNS and protects the neurons
• Rilutek should be taken on an empty stomach at the same time each day.
• Rilutek is expensive, over $600 - $700 for a 30 day supply, but it is covered under most health insurance policies.
• Creatine: A study shows preliminary effectiveness in preventing ALS in mice using creatine.
Amyotrophic Lateral Sclerosis (ALS)
Cause of Death
• Most common cause of death among ALS clients is respiratory failure or cardiac arrhythmias due to insufficient oxygenation.
• Respiratory infection (pneumonia) increases as weakened diaphragm and chest muscles make it difficult to clear lungs of secretions
Amyotrophic Lateral Sclerosis (ALS)
Life Span with ALS
50% of ALS clients die within 18 months of diagnosis
• 20% survive 5 years
• 10% live longer than 10 years
• Ventilator dependent ALS clients may live for many years
Amyotrophic Lateral Sclerosis (ALS)
Symptoms of ALS
Symptoms of ALS
• Tripping
• Stumbling and falling
• Loss of muscle control and strength in
hands and arms
• Difficulty speaking, swallowing, breathing
• Chronic fatigue
• Muscle twitching cramping
Amyotrophic Lateral Sclerosis (ALS)-characteristics of upper and lower motor neuron damage.
ALS is characterized by upper and lower motor neuron damage:
Upper motor neuron damage:
- Stiffness (spasticity), Muscle twitching (fasciculations), Muscle shaking (clonus) Lower motor neuron damage:
- Muscle weakness and Muscle Shrinkage (atrophy)
Amyotrophic Lateral Sclerosis (ALS)
Nursing Diagnosis
Nursing Diagnosis
• Risk for Disuse Syndrome
• Ineffective Breathing Pattern
Huntington's Disease-describe basics of the disease
Results from a genetically programmed degeneration of brain cells (neurons) in certain areas of the brain.
• Characterized by increasing dementia
• Causes uncontrolled movements, loss of intellectual faculties, and emotional disturbance
• First described in medical literature in 1872 by Dr. George Huntington
Huntington's Disease
Hereditary Components Familial disease
- Each child of an HD parent has a 50-50 chance of inheriting the HD gene. If a child does not inherit the HD gene will not develop disease and can-not pass it to subsequent generations
- A person inheriting the HD gene will eventually develop the disease
Huntington's Disease
Cause: Unknown, may be a relationship between a decrease in acetylcholine and increase in dopamine levels related to manifestations of symptoms (excess dopamine causes excessive uncontrolled movements)
Huntington's Disease
Early symptoms:
Early symptoms:
Mood swings Depression Irritability
Difficulty driving or learning new things Remembering facts or making a decision
Outbursts of rage Suicide
Huntington's Disease
ideations Depression
Late symptoms:
• Chorea (severely altered gait)
• Facial grimacing
• Protrusion of tongue Unintelligible speech Eventual dementia Loss of cognitive skills

bradykinesia "slow movement"
Chorea is characterized by brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next.

Dystonia "abnormal muscle tone, a neurological movement disorder involving involuntary, sustained muscle contractions.
Huntington's Disease
Genetic testing: DNA testing for the marker on chromosome 4
Ethical issues related to having children
Huntington's Disease
• Antipsychotics: block dopamine receptors
• Antidepressants
Supportive Care: Client and family - Psychological counseling
- Physical therapy
- Speech therapy
Huntington's Disease
Behavioral Changes
- Slower in thought processes: need more time
- DIFFICULTY WAITING: HD clients with advanced
disease CANNOT wait. Their DEMANDS are driven by areas damaged by the brain
- Swearing and racist remarks: Lack of impulse control and anger resulting from loss of independence will often surface in the form of profanity and racial slurs
Huntington's Disease
Nursing Diagnosis
Risk for Aspiration
Imbalanced Nutrition: Less than Body Requirements
Impaired Skin Integrity
impaired Verbal Communication
Focus of Nursing
Much of the nursing care focuses on teaching about the disease, psychologic support and genetic counseling.
As the S&S become more severe nursing care centers more on problems related to mobility, nutrition and increasing self-care deficits. Teaching methods to cope effectively with the psychosocial and physical changes is an integral part of the nurse's responsibilities.
Teaching ways to prevent injury from falls, methods to avoid malnutrition, measures to assist with incontinence and safety consideration.
Myasthenia Gravis: Describe disease
• An autoimmune disease that affects the transmission of signals from nerves to muscles.
• "Grave Muscle Weakness"
• Most people with Myasthenia Gravis can expect to live a normal Or nearly normal life
Myasthenia Gravis
Hallmark sign
Hallmark sign is muscle weakness that increases during activity and improves after rest
Myasthenia Gravis Signs
Often involves muscles that control eye and eyelid movement, facial expression, chewing, talking and swallowing
• Muscles controlling breathing and neck and limb movement may be affected
Myasthenia Gravis related to acetylcholine
Nerve endings release a substance called acetylcholine that binds or attaches to receptors on the muscle. This leads to muscle contractions. In Myasthenia Gravis the body's own immune system produces antibodies that block this transmission.
Myasthenia Gravis related to the
Thymus Gland
The Thymus Gland is abnormal in most Myasthenia Gravis clients.
Some people with Myasthenia Gravis develop thymomas or tumors on the thymus gland. Generally the thymomas are benign, but can become malignant. Relationship between the thymus gland and Myasthenia Gravis is not fully understood.
Myasthenia Gravis related to women
Bimodal age distribution: early onset ages 20-30 with women effected more often than men; late onset after age 50 with men affected more often than women
If a woman with MG becomes pregnant, the baby may acquire antibiodies from the mother and may have MG symptoms for a few weeks or months after birth.
Myasthenia Gravis
Signs and Symptoms Manifestations of MG correspond to the muscles involved!
Usually first noticeable symptom Is weakness of the eye muscles: ptosis (drooping of one or both eyelids), blurred or double vision (diplopia)
Change in facial expression
Unstable or waddling gait Difficulty in swallowing Shortness of breath
Impaired speech (dysarthria)
Myasthenia Gravis
Diagnosis may be delayed by 1-2 years due to vague symptoms of fatigue and weakness
EMG (electromylogram) Shows fatigue following repeated muscle stimulation
Tensilon test client is injected with edophonium chloride (Tensilon), a short acting anticholinesterase. In patients with MG, there is a significant improvement in muscle strength that lasts approximately 5 minutes.
Tensilon test is used to differentiate between myasthenic crisis (unsufficient medication improvement in symptoms) and cholinergic crisis (overmedication with no improvement in symptoms)
Antibody blood test: a special blood test can detect the antibodies that prevent nerves from signaling to muscles. (Antibodies may not be detected if only eye muscles are affected)
Myasthenia gravis-what can it lead to...
Myasthenia Gravis
MG may cause severe weakness resulting in acute respiratory failure. A rapid deterioration in respiratory and swallowing function necessitates aggressive interventions and management
Myasthenia gravis-treatments
Immunosuppression with glucocorticoids to improve muscle strength (suppresses the production of abnormal antibiodies Thymectomy (improves symptoms in more than 1/2, of the clients)
Plasmapheresis: removes abnormal antibodies from the blood

Treatments follow no specific protocol The client's response in symptoms guide dosage
Anticholinesterases are used to increase levels of acetylcholine at receptor sites to enhance nerve signals to the muscles and thereby increasing muscle strength (Prostigmin, Mestinon, Tensilon, Neostigmine)
Myasthenia Gravis
Myasthenic Crisis:
- Acute rapid exacerbation of the disease usually caused by under-medication, infection, fatigue, stress or surgery
- Usually requires respiratory support or assisted ventilation
Myasthenia Gravis
Cholinergic Crisis:
treatment of Cholinergic Crisis:
- Over-stimulation of the nerves caused by Overmedication with anticholinesterase
• n/v, diarrhea, sweating, increased bronchial secretions
• Treatment: hold anticholinesterase medications and prepare to administer antidote (Atropine) if prescribed
Myasthenia Gravis
Focus of Nursing Care
Focus of Nursing Care Immobility, ineffective breathing Prevention of myasthenic and cholingergic crisis
- Administer meds at the same time every day
- Take medication 30 minutes prior to eating to
enhance swallowing and chewing capabilities - Diet with ample potassium: assists with easing fatigue
Myasthenia Gravis
Nursing Diagnoses
Nursing Diagnoses
Ineffective airway clearance

Impaired swallowing
Bell's Palsy
Describe the disease
Form of facial paralysis resulting from damage to the 7th facial cranial nerve
• Afflicts approximately 40,000 Americans each year
• May strike at any age, however it disproportionately attacks pregnant women, and people with influenza, a cold, or other upper respiratory ailment
Signs of Bell's Palsy
Unilateral paralysis of the facial muscle
• Tearing, drooling, hypersensitivity to sound in the ear on the affected side
• Mask-like face
• Smooth forehead
Face appears asymmetric
• Incomplete eyelid closure on affected side
Bell's Palsy
Causes Common Cold
Herpes Simplex
Local trauma
Bell's Palsy
With or without treatment most clients see improvement in symptoms within 2 weeks, 80% recover completely in 3 months
Treatment Steroids in combination with acyclovir is possibly effective in improving facial function
Protect the affected eye (diminished blink reflex) - May need lubricating drops or ointment
- Eye patch
Bell's Palsy
Nursing Diagnosis
Risk for Altered Nutrition: related to inability to chew
Risk for Injury: related to loss of blink reflex
Body Image Disturbance: related to distorted facial appearance
Trigeminal Neuralgia Describe the disease-what nerve does the disease affect?
Condition that affects the trigeminal nerve (5th cranial nerve)
Trigeminal nerve is responsible for sending impulses of touch, pain, pressure and temperature to the brain from the face, jaw, gums, forehead, and around the eyes
Trigeminal neuralgia is characterized by sudden, severe, electric shock like or stabbing pain felt on one side of the jaw or cheek
Trigeminal Neuralgia
• Attacks
Trigeminal Neuralgia
• Attacks are generally of short duration May occur sporadically and may be initiated when "trigger" zones are stimulated
- Talking, brushing teeth, touching the face, chewing, swallowing
Trigeminal Neuralgia
Local disease, infection
Lesions near the nerve root Demyelination of trigeminal nerve root "Triggers"
Trigeminal Neuralgia
• Anticonvulsants to control pain: Tegretol, Dilantin
• Skeletal muscle relaxants (Baclofen)
• Alcohol injection along the affected portion of the nerve to produce anesthesia of the nerve. May provide up to 16 months of relief.
• Surgery: Severance of the sensory root
Trigeminal Neuralgia
Nursing Diagnosis
Nursing Diagnosis
• Pain
• Risk for Altered Nutrition
what happens when the spinal cord is seriously injured?
- As oxygen circulation is restricted & impaired, the function of the nerves passing through the
injured area is destroyed or injured. Circulation may return to the white area of the spinal cord, while circulation to the gray of the spinal cord is impaired or destroyed.
Any trauma to the spinal cord causing partial or complete disruption of the nerve tracts and neurons.
Spinal cord edema develops and necrosis of the spinal cord can develop as a result of compromised capillary circulation and venous return
Loss of motor function, sensation, reflex activity and loss of bowel and bladder control may result
Define/Describe Spinal shock
Spinal Shock
Temporary loss of reflex function (areflexia) below level of injury
Response may be immediate after a complete transection of the cord or occur later with an incomplete transection: The brain and the spinal cord cease to communicate!
Parasympathetic system dominates in spinal shock: causing bradycardia and hypotension
Usually lasts 1-6 weeks
As spinal shock gradually disappears there is a gradual reappearance of reflexes, hyperreflexia, and muscle spasticity
what does complete Transection of the cord mean?
Complete transection- the spinal cord is completely severed, with total loss of sensation, movement, and reflex below the level of injury
- if the cord had not suffered irreparable damage, early treatment is needed to prevent partial damage from developing into total and permanent damage
what does partial Transection of the cord mean?
- the spinal cord is partially damaged or severed
- the symptoms depend on the extent and location of the damage
Assessment of Spinal Cord Injuries
Depends on the level of the cord injury - the level of spinal cord injury is the lowest spinal cord segment with intact motor and sensory function
Edema extends to 2 cord segments above and below the affected level. Due to edema and tissue damage the level of injury may not be determined for 1 week or more.
Injury identified by vertebral level.
- Paraplegia (45.9%) Injuries in the thoracic, lumbar or sacral vertebrae
- Tetraplegia (51.7%) Injuries to at least one of the 8 cervical segments
Respiratory status
Motor and sensory changes below the level of injury
Loss of reflexes below the level of injury Loss of bowel and bladder control Urinary retention and bladder distention
• Presence of sweat, which does not occur on paralyzed areas
Cervical Injuries
Cervical Injuries
• C2 to C3 injury is usually fatal
• C4 is the major innervation to the diaphragm by the phrenic nerve
• Involvement above C4 causes respiratory difficulty and paralysis of all four extremities
Client may have movement in the shoulder if the injury is at C5 or below
Thoracic Level Injuries
Thoracic Level Injuries
• Loss of movement of the chest, trunk, bowel, bladder and legs, depending on the level of injury
• Leg paralysis (paraplegia)
Lumbar and Sacral Injuries
Lumbar and Sacral Injuries
• Loss of movement and sensation of the lower extremities
• S2 and S3 center on micturation: therefore, below this level, the bladder will contract but not empty (neurogentic bladder)
• Injury above S2 in males allows them to have an erection, but they are unable to ejaculate because of sympathetic nerve damage
• Injury between S2 and S4 damages the sympathetic and parasympathetic response, preventing erection or ejaculation
Emergency Implementation
Spinal cord injuries
• Emergency management is critical because improper handling can cause further damage and loss of neurological function
• Maintain a patent airway
• Always suspect spinal cord injury until this injury is ruled out
• Immobilize client on a spinal backboard with the head in a neutral position to prevent an incomplete injury from becoming complete

• Prevent head flexion, rotation or extension
• During immobilization maintain traction and alignment on the head by placing the hands on either side of the head by the ears
• Maintain an extended position
• Log roll the client
Nursing Care of Spinal Cord Injuries (SCI)
• Respiratory
Nursing Care of Spinal Cord Injuries (SCI)
• Respiratory
- assess because paralysis of the intercostal and abdominal muscles occurs with C4 injuries
- monitor ABG's and maintain mechanical ventilation, if prescribed, to prevent respiratory arrest, especially with cervical injuries
- encourage deep breathing and use of incentive spirometer
- monitor for signs of infection especially pneumonia
Nursing Care of Spinal Cord Injuries (SCI)
• Cardiovascular System
• Cardiovascular System
- monitor for cardiac arrhythmias
- assess for signs of hemorrhage or bleeding
around the fracture site
- assess for signs of shock
- assess lower extremities for DVT
- monitor for orthostatic hypotension when
repositioning the client
Nursing Care of Spinal Cord Injuries (SCI)
• Neuromuscular
Nursing Care of Spinal Cord Injuries (SCI)
• Neuromuscular
- assess motor and sensory status to determine the level of injury
- assess motor ability by testing client's ability to squeeze the hand, spread the fingers, move the toes, turn the feet
- assess sensation by pinching skin or pricking with a pin, starting at the shoulders and working down the extremities
- monitor for signs of autonomic dysreflexia and spinal shock
- immobilize to promote healing and prevent further injury
- assess pain and initiate measure to reduce
- monitor for complication of immobility
- prepare the client for procedures as ordered
- collaborate with therapies to determine
appropriate treatment plan
Nursing Care of Spinal Cord Injuries (SCI)
• Gastrointestinal System
• Gastrointestinal System
- assess for distention and hemorrhage
- monitor bowel sounds and assess for
paralytic ileus
- prevent bowel retention
- initiate a bowel control program as
- maintain adequate nutrition and a high-fiber diet
Nursing Care of Spinal Cord Injuries (SCI)
• Renal System
• Renal System:
- prevent bladder distention
- initiate a bladder training program as
- maintain fluid and electrolyte balance
- maintain adequate intake of 2000+mL daily
- monitor for UTI and calculi
Nursing Care of Spinal Cord Injuries (SCI)
• Integumentary System:
Nursing Care of Spinal Cord Injuries (SCI)
• Integumentary System: - assess skin integrity
- turn client every two hours
Autonomic Dysreflexia Hyperreflexia
Autonomic Dysreflexia Hyperreflexia
• Overactivity of the autonomic nervous system causing an abrupt onset of excessively high blood pressure.
• Usually occurs in clients with injury levels above T-6
• Life-threatening
Autonomic Dysreflexia
Autonomic Dysreflexia
• Occurs when stimuli, such as a full bladder, is unable to ascend the spinal cord, mass reflex stimulation of the sympathetic nerves below the level of the injured cord area occurs, triggering massive vasoconstriction, vagal response and vasodilation above the level of injury.
Autonomic Dysreflexia

Signs and Symptoms
Autonomic Dysreflexia Hyperreflexia
Signs and Symptoms
• Hypertension ( B/P > 200/100
• Pounding Headache
• Flushed face
• Red blotches on the skin above level of injury
• Seating above level of spinal injury
• Bradycardia (secondary to vagal parasympathetic stimulation)
• Piloerection below level of spinal injury
• Cold, clammy skin below level of spinal injury
Autonomic Dysreflexia Hyperreflexia
Autonomic Dysreflexia Hyperreflexia
• Noxious stimuli (irritants which would ordinarily cause pain/discomfort) to areas of the body below the level of spinal injury. - Bladder: over distention or irritation of bladder
wall (UTI, retention, blocked catheter, overfilled collection bag, noncompliance with intermittant catheterization program
- Bowel: over distention or irritation
Autonomic Dysreflexia

signs and symptoms
- Constipation! impaction
- Distention during bowel program
- Hemorrhoids or anal fissures
- Infection or irritation
• Skin-Related Disorders
- Any direct irritant below the level of injury (prolonged
pressure by object in shoe, cut, abrasion, bruise
- Pressure sores
- Ingrown toenails
- Burns
- Tight or restrictive clothing! Sitting on wrinkled
Autonomic Dysreflexia

• Sexual Activity
• Sexual Activity
- Over stimulation during sexual activity that would normally be painful
- Menstrual cramps
- Ejaculation
• Labor and Delivery
Autonomic Dysreflexia

• Identify and remove the offending stimulus (PRIORITY INTERVENTION)
- Bladder: check catheter (kinks, full bag, urine not draining) May need to replace catheter
- Bowel: Assess for fecal impaction, if occurs during digital stimulation STOP
- Skin: loosen clothing, check for sources of irritation
Autonomic Dysreflexia
• Medications:
• Medications:
• Immediate:
- Nitroglycerine 1/150 sublingual or 1/2 inch Nitropaste
- Clonidine
- Hydralazine
• Chronic:
- Minipress
- Catapres
Spinal Cord Injury
Nursing Diagnosis
Nursing Diagnosis
• Impaired Physical Mobility
• Impaired Gas Exchange
• Ineffective Breathing Patterns
• Altered Urinary Elimination and
• Sexual Dysfunction
• Self-Esteem Disturbance
• ETC!!!!
Nursing Care of Spinal Cord Injuries (SCI)
• Psychosocial Integrity:
• Psychosocial Integrity:
- encourage client to express feelings of anger, depression, etc.
- discuss sexual concerns
- promote self-care, setting realistic goals
based on potential functional level
- encourage contact with appropriate community resources
spinal cord injury
• Rehabilitation with a patient with spinal cord injury is an ongoing process from ICU-intermediate care- rehab - home. Nursing interventions are critical throughout the entire process to prevent complications of altered physical mobility and body functions, and teaching aimed to maximize the patient's level of independence with self-care.
New Words!!!
Define Poikilothermia and Tetraplegia:
New Words!!!
• Poikilothermia: Unable to maintain core temperature. Client takes on ambient temperature of the environment.
• Tetraplegia: Replaces quadraplegia (pg 1310 and 1326 L&B 3rd edition)
Spinal Cord Injury Profile
• 250,000 to 400,000 people in U.S. living
with SCI
• 11,000 new cases each year
• Mean age: 16-30 (53%)
• 81% Male
• 59.1 % Caucasian
• MVA 40.9% , followed by Falls, Violence, Sports (diving)
• 62.9 % working when injury occurred
• Post injury employment more promising for paraplegia clients than tetraplegia clients. Post injury year 10:
- 31.8% Paraplegics
-26.4 Tetraplegics
• 88.3% of all clients with SCI's who are discharged alive are sent to private homes
• 53% are single at the time of injury
• LOS:
- Hospital 25 days (1974) 17 days (2001)
- Rehab 115 days (1974) 44 days (2001)
Spinal Cord Injury

Cause of Death:
Spinal Cord Injury

Cause of Death:

• Previously was Renal Failure, however due to dramatic advances in urologic management the leading causes of death for clients experiencing SCI's is Pneumonia, Pulmonary Emboli and Septicemia.
Toxic and Infectious Neurologic Disorders

• Rabies
• Rabies - viral infection of the CNS transmitted by infected saliva that enters the human body through a bite or an open wound.

• Patho - virus spreads to local muscle cells and then invades the peripheral nerves. It eventually travels to the CNS. Final stages of the infection are convulsions, muscle spasms, and periods of apnea. Death occurs 7 days from the onset of the symptoms due to respiratory failure
• Because the disease is always fatal if not treated in time, the best intervention is prevention.
• Nursing care - is provided in an ICU, with the client in a quiet, darkened room to decrease stimulation as much as possible. Standard precautions are essential, because the rabies virus is present in the saliva of the client.
• Client and family teaching focuses on the importance of immunizing pets, providing proper care for wounds and seeking immediate medical attention.
Toxic and Infectious Neurologic Disorders
Tetanus - is a disorder of the nervous system caused by an anaerobic bacillus that lives in the soil. Spores of the bacillus enter the body through open wounds contaminated with dirt, street dust, or feces.
Patho - when the spores enter a wound they germinate and produce a toxin called tetanospasmin. The toxins are absorbed by the peripheral nerves and carried to the spinal cord, where they block the action of inhibitory enzymes thus interfering with transmission of neuromuscular impulses.
The infected person presents with stiffness of the jaw and neck and dysphagia. There is profuse drooling and perspiration. As the infection progresses the person experiences hyperreflexia, spasms of the jaw muscles or facial muscles, and rigidity and spasm of the abdominal, neck and back muscles. The complications of tetanus include urinary retention and airway obstruction from the spasms. Cardiac and respiratory failure are late and life threatening complications.
• Diagnosis is based on clinical manifestations - there is no specific lab or diagnostic test. Immunization of children is thru DPT. All individuals should have a booster dose every 10 years.
• Nursing Care
• Nursing Care - is in the ICU in an area of minimal stimulation. Focus is on assessment and interventions to promote safety, prevent injury, maintain nutrition, and maintain pulmonary and cardiovascular functions.
• Client and family teaching include promoting immunizations for all children and for educating adults about the need for booster shots. The older population is especially at risk for never having been immunized or for letting immunizations lapse. It is also necessary to teach the proper care of wounds.
Toxic and Infectious Neurologic Disorders
• Botulism
• Botulism - is food poisoning caused by ingestion of food contaminated with the bacillus clostridium botulinum. The mortality rate is high if the disease is untreated.
• Patho - the toxins are absorbed by the GI tract and bound to nerve tissues. They block the release of acetylcholine from nerve endings and thus cause respiratory paralysis. First signs are visual disturbances, loss of accommodation, and fixed, dilated pupils. Paralysis of all muscle groups progresses throughout the body, with respiratory paralysis causing death.
• All toxins in the GI system are removed by cathartics, enemas, and gastric lavage. All people who may have eaten the contaminated food must be located and observed.
• Nursing Care - hospitalize with interventions focusing on monitoring for respiratory failure and providing vent assist if necessary. Hydration and nutritional status are monitored.
• Client and family teaching that fatigue may persist up to a year - may need to modify ADLs and take rest periods throughout the day. Education of the public to prevent botulism is important
Toxic and Infectious Neurologic Disorders
• Postpolio Syndrome
• Postpolio Syndrome - is a complication of a previous infection by the polio virus. It was epidemic in the 19405 and 50s but has been largely eradicated through immunizations. It is estimated that almost one half of the people (1.63 million) who have had the disease are re-experiencing manifestations of the acute illness. Manifestations of motor neuron degeneration and weakness may emerge years after the initial infections. These individuals are not infectious. Most are between the ages of 45-65. As the population ages the numbers of postpolio syndrome will Increase. The cause is unknown.
• Patho - is not known. Manifestations include fatigue, muscle and joint weakness, loss of muscle mass, respiratory difficulties and pain. They may also experience cold intolerance, dizziness, headaches, urinary incontinence and sleep disorders.
• Diagnosis is by previous history of polio and the current manifestations.
Postpolio Syndrome
• Nursing Care
• Nursing Care - the client faces the challenge of unexpected physical changes. Respiratory dysfunction requiring oxygen. Muscle weakness may make walking difficult. ADLs, self-care and careers are threatened.
• Client and family teaching is individualized to meet the physical and psychosocial needs of the client and family.