Guillain- Barre Syndrome

Caburian, Kim Adrienne BSN III-A

Guillain-Barre Syndrome
Polyradiculoneuritis Several peripheral nerve roots are affected through an inflammatory process and onset is sudden

 Exact cause is unknown Affected nerves are demyelinated with possible axonal degeneration

 Autoimmune disorder that may be triggered by viral infection, Campylobacter diarrheal illness, immunization, or other precipitating event.

Complications Respiratory failure, Cardiac arrhythmias, and Complications of immobility.

Predisposing Factors

Respiratory Infection Gastrointestinal infection

Viruses:
Cytomegalovirus Epstein Barre Virus Mycoplasma pneumonia Salmonella Typhosa Campylobacter Jejuni (GI bacterial pathogen)

Assessment
Acute onset (hours to weeks) of progressive, usually ascending muscle weakness and fasciculation, possibly leading to paralysis (maximal weakness is reached within 2 weeks). Paresthesia and painful sensations

 Possible hypoventilation due to chest muscle weakness. Difficulty with swallowing, chewing, speech, and gag, indicating fifth (trigeminal) and ninth (glossopharyngeal) cranial nerve movement.

 Reduce or absent deep tendon reflexes, position and vibratory perception.

Autonomic dysfunction with orthostatic hypotension and tachycardia

Diagnostic Evaluation
Lumbar puncture obtains cerebrospinal fluid samples, which reveal low cell count and high protein levels. Abnormal laboratory studies may point to prior infection or illness.

 Nerve conduction studies, which allow decreased conduction velocity of peripheral nerves due to demyelination.

TREATMENT
Muscle and joint pain can be treated with over-the-counter analgesics such as aspirin. If necessary, stronger pain medication (e.g., acetaminophen with hydrocodone) may be prescribed. Muscle spasms can be controlled with relaxants such as diazepam (Valium).

 Unpleasant sensation problems, such as painful tingling, can be treated with tricyclic antidepressants or anticonvulsants such as gabapentin (Neurontin). Plasma exchange (also known as plasmapheresis) and high-dose immunoglobulin therapy.

Nursing Interventions
1. Monitor respiratory status through vital capacity measurements, rate and depth of respirations, and breath sounds.

2. Monitor level of muscle weakness as it ascends toward respiratory muscles. Watch for breathlessness while talking which is a sign of respiratory fatigue.

3.Monitor gag reflex and swallowing ability. 4. Position patient with the head of bed elevated to provide for maximum chest excursion. 5. Monitor the patient for signs of impending respiratory failure.

6. Avoid giving opioids and sedatives that may depress respirations. 7. Position patient correctly and provide range-of-motion exercises.

8. Ensure adequate nutrition

without the risk of aspiration. 9. Encourage physical and occupational therapy exercises to help the patient regain strength during rehabilitation phase.

10. Provide good body alignment, range-of-motion exercises, and change of position to prevent complications such as contractures, pressure sores, and dependent edema.

11. Urge the patient to maintain normal weight because additional weight will further stress monitor function. 12. Instruct patient to wear good supportive and protective shoes while out of bed to prevent injuries due to weakness and paresthesia.

13. Provide assistive devices as

needed (cane or wheelchair) to maximize independence and activity.
14. If verbal communication is possible, discuss the patients fears and concerns.

15. Provide choices in care to give the patient a sense of control . 16. Teach patient about breathing exercises or use of an incentive spirometer to reestablish normal breathing patterns.

17. Instruct patient to check feet routinely for injuries because trauma may go unnoticed due to sensory changes. 18. Encourage scheduled rest periods to avoid fatigue.