Nursing 4 Lecture 13 Guillain-Barre Syndrome

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  1. Guillain-Barre Syndrome: Pathophysiology
    • -Acute, rapidly progressive, potentially fatal syndrome (aspiration and can die because of respiratory problems)
    • -Affects middle aged men mostly between 30 and 50

    Demyelination causing destruction of the myelin sheath causing inflammation and degenerative changes in both sensory and motor nerve roots; so signs of sensory and motor impairment occur simultaneously

    • Symptoms tend to occur in the legs first then moving up to the arms and upper body aka ascending paralysis
    • -Paralysis can increase in intensity until the muscles cannot be used at all and the patient is almost totally immobile (causing patients to require ventilation)
    • -Paralysis of the internal and external intercostal muscles leads to a reductionin functional breathing
    • -Vagus nerve paralysis causes loss of protective mechanism that respond to brachial irritation and foreign bodies as well as a diminished or absent gag reflex
  2. Factors associated with the development of Guillain-Barre:
    • Acute illness
    • Gastrointestinal illness
    • Campylobacter jejuni bacteria
    • HIV infection
    • Mycoplasma pneumonia
    • Surgery
    • Upper respiratory infection

    • Virus:
    • -Cytomegalovirus
    • -Group A streptococcus
    • -Rabies

    • Drugs:
    • -Captopril
    • -Danazol
    • -Penicillamine

    • Systemic lupus
    • Hodgkins disease
  3. Cause:
    The exact cause remains unclear but it is thought to be an immunologic attack of peripheral nerves in response to a virus; this reaction causes the immune system to start to destroy the myelin sheath

    Segmental demyelination (destruction of myelin between the nodes of ranvier) is a major pathological finding in GBS

    Prevents normal transmission of electrical impulses along the sensiormotor nerve roots which causes inflammation, swelling and path demyelination which impairs impulse transmission among the dorsal and ventral nerve roots
  4. Acute Stage:
    aka initial period

    • -Lasts 1 to 4 weeks
    • -Begins with the onset of the first sx and ends when no further deterioration occurs
  5. Plateau Stage:
    Several days to two weeks
  6. Recovery Stage:
    4 to 6 months maybe up to 2 years

    -Believed to coincide with remyelination and axonal regrowth; some patients do not completely recover and ave permanent neurological deficits
  7. Assessment:
    • -Presence of pain is common if the patient has parathesias (unpleasant sensation such as burning, stinging, and prickling feeling)
    • -Most patients report a sudden onset of muscle weakness and pain
    • -Typically does not affect levol of consciousness, cerebral function, or pupillary constriction or dilation

    -Cranial nerve involvement most often affects the facial nerve (VII); Assess the patients ability to smile, frown, whistle, or drink from a straw

    -Inability to gag, cough, or swallow results from the involvement of nerves IX and X

    -Assess the patient closely for varying BP, bradycardia, heart block, and possibly asystole

    -Assess cranial nerve XI (accessory) by asking the patient to shrug the shoulders

    -Assess cranial nerve XII (hypoglossal) for the ability to stick the tongue straight out
  8. Assessment: Coping
    Not unusual for depression or for the feeling of powerlessness
  9. Assessment: Labs
    Although NO clinical or lab finding confirms the diagnosis, you may perform a lumbar puncture which will show a normal WBC count, and increase in CSF protein level with an increase in cell count is common

    High protien levels may not occur until after 1 to 2 weeks of illness reaching a peak in 4 to 5 weeks
  10. Electrophysiologic Studies:
    Demonstrate demyelinating neuropathy and may reveal marked slowing of nerve conduction velocities

    Changes appear only after denervation of muscle has been present for 4 weeks or longer
  11. Interventions: Plasmapheresis
    -Removes circulating antibodies thought to be responsible for the disease

    • Nursing interventions:
    • -Providing information and reassurance
    • -Weighing before and after the procedure
    • -Administering proper care to the shunt if used (checking for patency, assessing for bruits ever 2 to 4 hours, keeping double bull dog clamps at the bedside, and observing the puncture site for bleeding or echymosis)
  12. Interventions: IVIG
    -Shown to be as effective as plasmapheresis and is safer and immediatley available

    • Side effects:
    • -Chills
    • -Mild fever
    • -Myalgia
    • -Headache
    • -Anaphylaxis
    • -Aseptic meningitis
    • -Retinal necrosis
    • -Acute renal failure
  13. Interventions: Respiratory Status

    *Look for restlessness and anxiety

    • -Assess for dyspnea, adventitious breath sounds, decreased O2 sat, and cyanosis
    • -Assess rate, rhythm, and depth ever 1 to 2 hours
    • -Assess LOC, and the ability to swallow and cough
  14. Interventions: Cardiac dysfunction
    • -Risk of dysrhythmias
    • -Monitor VS closely
    • -May need to treat HTN with a beta blocker or nitropress
    • -Hypotension is treated with IV fluids and supine position

  15. Interventions: Immobility
    • -Assess motor function, safety, position changes and active or passive ROM exercises
    • -Collaborate with nutritionalist due to a possibity of malnutrition (gastric motility, dysphagia, depression) may need a feeding tube
    • -Weigh patient 3x a week
    • -Monitor prealbumin

  16. Interventions: Pain
    May have paresthesia or hyperesthesia (extreme sensitivity to touch)

    May help to lie in cool, dark, quiet place

    Deep muscle aches and muscle stiffness
  17. Interventions: Communication
    May need to develop a communication system

    • *eye blinking
    • *flash cards
  18. Interventions: Support
    Assess for powerlessness, anxiety, fear, grieving, and lifestyle changes that need to be made
  19. Community Based Care:
    Depends on the extent of the residual deficits; self help and support groups for chronic illness are common
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Nursing 4 Lecture 13 Guillain-Barre Syndrome
Nursing 4 Lecture 13 Guillain-Barre Syndrome
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