Guillain-Barre Syndrome

Guillain-Barre Syndrome (GBS) is also known as acute inflammatory demyelinating polyneuropathy (AIDP). Since the nearly eradication of poliomyelitis, GBS has become the most frequent cause of acute flaccid paralysis. GBS is almost certainly an immune-mediated disoder, it follows some events e.g. respiratory or GI tract infections, surgical procedures, viral exanthems, certain vaccinations and lymphomatous disease.

Clinical Manifestation
   Initially, symptoms often consist of tingling (pins + needles sensations) in the feet and may be associated with dull low-back pain. Within hours or 10 days after the first symptoms, then weakness develops, mostly in the legs but the arms or cranial musculature may be involved, too. Loss of tendon reflexes can be found even in the regions where the strength is retained. Weekness progresses with the nadir reached within 30 days (usually by 14 days). Rapid progression that jeopardize the respiratory function can be presented within a few days or even a few hours.

In the past, the mortality rate was 15%, with the modern technologies nowaday, the mortality rate is only 2%. The early suspicious and prompt + accurate diagnosis is demanded. No lab test is specific, but the increased of spinal fluid protein without pleocytosis is characteristic (usually found after the first week) and the careful electrodiagnostic testing can usually identify the mild abnormalities during the early stages.

Treatment
  
Patient requires hospitalization for observation. VC and ability to swallow is monitored frequently. Prompt airway intervention and respiratory support is available. At the present days, there are 2 treatments.

  1) Plasmapheresis : the exchange of patient's plasma for albumin has been shown to shorten the time to recovery.
  2) Human IvIg : has been proven effective and considered easier than plasmapheresis if the IV access is limited.

The cortcosteroid alone is not beneficial.

Prognosis
  
The prognosis varies with age, severity and the extent to which axonal degeneration exceeds demyelination. Symptoms (including respiratory failure) can be improved (resumes waling) in 3 months with plasmapheresis in the middle-aged patients.

Anesthetic consideration
  -Succinylcholine is contraindicated because of hyperkalemia. The patient is also has increased sensitivity to the nondepolarizing muscle relaxants.
  -There is a possibility of significant hemodynamic variation during induction, the intraarterial monitoring may be of useful.
  -No abnormal responses to anesthetic agents but careful titration with a concerns regarding respiratory function would be suggested.
  -Regional anesthesia is controversial, 2 case reports have cited no ill effects from regional anesthesia while there is one article implicated regional anesthesia as a cause of the disease. Clinical experience has shown that patients are sensitive to local anesthetics.
  -Paturient with GBS, regional anesthesia for labor would be beneficial because the autonomic dysfunction may trigger an exaggerated hemodynamic response to pain.

References
1. Griffin JW. Immune-Mediated Neuropathy in Goldman : Cecil Textbood of Medicine, 21st ed. Copyright© 2000 W. B. Saunders Company
2. Martz DG, Schreibman DL, Matjasko MJ. Neurologic Disease in Benumof JL. Anesthesia & Uncommon Disease, 4th Ed. W.B. Saunders Company 1998