GBS, CI, Polio Flashcards

1
Q

Guillain-Barre’ Syndrome characteristics

A
  • Affects CNS and/or PNS
  • Generally Chronic, Usually Progressive
  • Not curable; Treatment can alter course of disease
  • Little known of etiology: Usually considered autoimmune process.
  • Suspected multiple dynamics which may include genetic predisposition, viruses, environmental influences
  • Deterioration of function over time;
  • Requires coping with existing disability & threat of future loss
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2
Q

GBS

A
  • GBS is an acute, demyelinating inflammatory polyradiculoneuropathy.
  • Demyelination
  • Affects nerve roots (brachial plexus)
  • Affects peripheral nerves
  • Leads to motor neuropathy and flaccid paralysis
  • Peripheral nerves
  • Flaccidity
  • Can be caused by reaction to flu shots
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3
Q

GBS Epidemiology: Causation

A
  • Autoimmune disorder
  • Often occurs a few days to weeks after a respiratory (49%) or gastrointestinal viral infection (10%).
  • Bacteria–Campylobacter jejuni (associated w/ undercooked food, esp. poultry)
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4
Q

GBS Epidemiology

A
  • 1 – 2 cases per 100,000 persons
  • All ages
  • Mostly young adults (15-35) and older (50-75).
  • Men slightly more affected
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5
Q

GBS Diagnosis

A
  • Syndrome, not disease
  • Spinal tap: abnormal amounts of protein.
  • NCV: Nerve Conduction Velocity (speed of nerve transmissions).
  • Exclude other relevant disorders.
  • Diagnosis of exclusion
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6
Q

GBS Acute Inflammatory Phase

A
  • Weakness & tingling sensations in legs
  • Rapidly progressing (hours, days or weeks)
  • Symmetrical ascending paralysis
  • Spreads to arms and upper body
  • Intensity increases until almost total paralysis often including respiratory muscles
  • in 30% of cases, respirator necessary.
  • Medical emergency: 5% die.
  • Cranial nerve involvement: eye and facial movement, speaking, chewing, and swallowing.
  • Severe pain in legs, low back.
  • Loss of bladder control.
  • Slow or abnormal heart rate, low or high blood pressure.
  • Symptoms can vary from mild (subclinical) to severe (death)
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7
Q

GBS Plateau Phase

A
  • Stage of greatest weakness/disability
  • 50% of patients reach their full extent of paralysis in 1 week, 70% by 2 weeks, and 90% by three weeks.
  • No change during this phase; can last days, weeks, or (rarely) months
  • Monitored for cardiovascular, respiratory problems, infections, blood clots, bed sores
  • Patient often in ICU & monitored closely
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8
Q

GBS Progressive Recovery Phase

A
  • Recovery most often starts at 2-4 weeks AFTER progression of the symptoms stops.
  • Remyelination and axonal regeneration, lasting a few weeks up to 2 years; average length 12 wks.
  • Recovery begins at head/neck; proceeds distally
  • Stage when therapy oriented to resumption of occupation
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9
Q

GBS Prognosis

A

-Complete return of function in approximately 50% of patients
-Residual weakness that may not resolve (present after 3 years) in 35%
-Significant permanent disability in 15%
3% may suffer relapse many years after initial attack

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10
Q

GBS Medical Management

A
  • Most critical, keep the body functioning while the nervous system recovers.
  • Plasmapheresis: Plasma exchange demonstrates promise as an intervention because of the autoimmune nature of the illness (begun within 2 weeks of onset); reduces severity and duration of symptoms
  • High dose IV immunoglobin: proteins that the body uses naturally to fight invading organisms; slows the body’s immune reaction.
  • High dose steroids (reduce inflammation)
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11
Q

GBS: Acute/ICU OT

A
  • Communication tools matching physical abilities
  • Adapted call button, TV controls, lights, telephone
  • Bed positioning for patients and families
  • Tolerance to upright/ chair positioning. Ensuring head, trunk and UE stability
  • Strategies to reduce anxiety
  • Pain management (modalities, positioning, visual imagery) [what and how]
  • PROM/Stretching to prevent contractures (splinting)
  • Progressive program of passive & active assisted exercise while monitoring for overuse and fatigue.
  • Patient/Family EDUCATION.
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12
Q

GBS: Recovery/Rehabilitation Phase OT

A
  • Occupational performance (ADL, IADL, work)- adaptations, modifications
  • Transfer Training
  • Activities, splinting to preserve limb ROM, particularly wrists, hands, ankles
  • Adapting communication
  • Energy conservation training
  • Progressive activity/exercise
  • Improve hand function by enhancing strength, coordination, sensation
  • Encouraging access to community
  • Recommending adaptive equipment/techniques for home, work
  • Psychosocial support/remediation (coping skills)
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13
Q

GBS: Activity/ Exercise

A
  • In one study if more than 1/3 of motor units remained intact, exercise produced strengthening, if less than 1/3, it damaged muscle tissue.
  • Rule of thumb: exercise will NOT hasten or improve nerve regeneration, nor will it influence the reinnervation rate during the rehabilitation process so be conservative in early stages.
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14
Q

GBS: Exercise/Activity Progression

A
  • Short periods of activity/ exercise appropriate to the patient’s strength
  • Increase this only if the patient improves or if there is no deterioration after 1 week
  • Return to bed rest if a decrease in function or strength occurs
  • Limit fatiguing exercise/ activity for 1 year
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15
Q

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)

A
  • Closely related to GBS; considered chronic counterpoint of that acute disease
  • Caused by damage to myelin sheath of PNS
  • Chronically progressive or relapsing symmetric sensorimotor disorder
  • Autoimmune disorder
  • Weakness occurs over 2 months or more
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16
Q

CIDP Epidemiology

A
  • All ages, races and genders though slightly more common in young adults, men
  • Prevalence: RARE (0.8-3.6 per 100,000)
17
Q

CIDP Causation

A
  • Autoimmune process
  • Respiratory and gastrointestinal infections can precede.
  • Most cases idiopathic
  • Can be associated with other disease processes: HIV, Lupus or Inflammatory bowel disease [all autoimmune]
  • Pregnancy exacerbates the condition.
18
Q

CIDP Initial symptoms

A
  • Weakness of the limbs, both proximal and distal, with proximal muscles affected at least as severely as distal.
  • Sensory symptoms are common, such as tingling and numbness of hands and feet, but usually motor symptoms predominate.
  • Loss of DTR
  • Fatigue
  • Autonomic system dysfunction can occur; patient would complain of orthostatic dizziness, problems with bowel and bladder functions, and cardiac problems.
19
Q

CIDP Progression of symptoms

A
  • Varying levels of chronic paralysis.

- Problems w/breathing, swallowing, mobility, occupational performance.

20
Q

CIDP Disease Course

A
  • Insidious and slow
  • either in a slowly progressive (more than 60% of patients)
  • relapsing manner (approximately one third of patients), with partial or complete recovery between recurrences.
21
Q

CIDP Diagnosis/ Medical Management

A
  • Complete medical and neurological history
  • Spinal tap (proteins in CSF)
  • NCV
  • Rule out other disorders
  • TX: plasmaphoresis, IV immunoglobulin and steroids.
22
Q

CIDP OT Intervention

A
  • Occupational performance modification (task, tools, energy conservation).
  • Mobility adaptation.
  • Strength, stretching, and coordination programs.
  • Psychosocial support (coping, anxiety, depression)
23
Q

Poliomyelitis

A
  • Polio “gray”
  • Myelitis “inflammation of spinal cord”
  • Inflammation of gray matter of spinal cord.
  • Destroyed (nerve cells) in the anterior horns of the spinal cord and the brain stem leads to classic polio manifestation of paralysis
24
Q

Poliomyelitis/Infantile Paralysis

A
  • Poliovirus is an enterovirus: Present in throat & stool of infected person. Enters mouth, spreads to lymphatics then to CNS
  • Only carried by humans
  • Up to 95% of polio infections are asymptomatic (able to spread disease)
  • 4-8% of polio infections consist of minor nonspecific illness (cold, GI disturbance, flu) without CNS involvement
  • Fewer than 1% of infections result in weakness or paralysis, most commonly to the lower extremities.
25
Q

Course of Paralytic Polio

A
  • Paralytic symptoms begin 1-10 days after flu-like symptoms
  • Initial increased DTR, severe muscle aches & spasms in limbs, back
  • Progresses to flaccid paralysis with decreased DTR. Asymmetrical
  • No sensory loss or change in cognition
  • Most people experienced some level of muscle recovery
  • Weakness or paralysis present 1 year after onset is usually permanent.
  • Death rate: 2-5% for children; 15-30% for adults; 25-75% with bulbar involvement
26
Q

Polio history

A
  • Polio first described in 1789; First U.S. outbreak 1843. Polio epidemics occurred in the U.S. and throughout the world primarily in the first half of the 20th century.
  • Polio reached a peak in U.S. in 1952 with 21,000 paralytic cases.
  • Introduction of the Salk (1955) and Sabin (1961) vaccines has eradicated polio in the U.S. and greatly reduced the incidence of polio in the world. Last case of wild-virus polio in U.S. in 1979
  • Concentrated outbreaks of polio continue to occur in developing countries.
27
Q

Polio Recovery

A
  • Surviving motor neurons in the brain stem and spinal cord extend new branches called axonal sprouts… to re-innervate muscle fibers that have lost their motor nerve supply.
  • Muscular function may be partially, or fully regained if this recovery process is extensive enough.
  • These new axonal sprouts end up innervating at least several times the number of muscle fibers that an ordinary motor neuron would normally supply.
28
Q

Post Polio Syndrome

A
  • 1.63 million Americans living with after affects of acute poliomyelitis epidemics occurring in 1900s – 1950s (National Health Interview survey, 1987)
  • As many as 250,000 people in the U.S. may have post-polio syndrome (25-40% of survivors)
29
Q

What is Post-Polio Syndrome

A
  • New condition affecting survivors of paralytic polio 10 to 40 years (usually 15 years or more) after the initial acute infection
  • Symptoms:
  • Gradual onset of progressive and persistent new muscle weakness
  • Generalized Fatigue and/or abnormal muscle fatigability, lack of endurance
  • Muscle and joint pain
  • Muscle atrophy
  • Increasing skeletal deformities such as scoliosis
  • Less commonly, problems with breathing or swallowing
  • Symptoms persist for at least a year
30
Q

What Causes Post Polio Syndrome?

A
  • During initial Polio infection, destruction of muscle nerve cells results in loss of nerve supply to muscles.
  • During recovery, surviving motor nerve cells form new branches (sprouts) which reconnect nerve cell to muscle. Many motor nerve cells end up supplying several times more muscle fibers than normal
  • Suggested that these new sprouts are not stable, but that they can degenerate over time due to an “overexertion” phenomenon resulting once again in muscle fibers that do not contract, new weakness and loss of function
31
Q

Intervention for Post-Polio

A
  • Occupational performance modification (task, tools, energy conservation training)
  • Mobility assessment (use of w/c, scooter, walker, cane, etc.)
  • Bracing/splinting to support weak muscles
  • Management of weakness (strengthening/aerobic exercise)
  • Stretching to decrease/prevent contractures (make sure tightness is not what makes them functional)
  • Assess muscular overuse and redirect patterns as needed.
  • Weight loss
32
Q

Psychological Implications of PPS

A
  • Polio perceived by most as something in the past
  • Difficulty adjusting with the re-emergence of problems associated with polio
  • Diagnosis of PPS may result in depression and need for:
    • Education
    • Support