Keywords

acute inflammatory demyelinating polyneuropathy (AIDP), Guillain-Barre syndrome (GBS), hypokalemia, hypokalemic periodic paralysis (HypoKPP), intravenous human immunoglobulin, plasmapheresis, thyrotoxic hypokalemia periodic paralysis, thyrotoxicosis

 

Authors

  1. Yamamoto, Linda BSN, MBA/HCA, RN, PHN
  2. Texas, Van BSN, RN

Abstract

Guillain-Barre syndrome (GBS), also known as acute inflammatory demyelinating polyneuropathy (AIDP), is a neurologic disorder in which the body's immune system attacks part of the peripheral nervous system. The onset can be sudden and unexpected. Guillain-Barre syndrome is an acute or subacute polyneuropathy that usually follows minor infective illnesses, inoculations, or surgical procedures. Guillain-Barre syndrome is the most common cause of acute flaccid quadriparesis in the United States. It is an acute inflammatory demyelinating polyneuropathy that is primarily characterized by progressive limb weakness and areflexia. Recognition of this disorder is important because early detection of respiratory failure may limit complications and early therapy may limit nerve fiber loss and the extent of ultimate disability. Several disorders, such as acquired hypokalemia, myasthenia gravis, periodic paralysis, and polymyositis, have symptoms similar to those found in GBS, making it difficult to diagnose. Clinical presentation and the diagnostic criteria are critical to assessment and evaluations of treatment regimens. Acute muscle weakness is not an unusual clinical presentation in the emergency department. Potassium imbalance is one of the disturbances in fluid and electrolyte metabolism that can be life threatening. The critical effect of potassium on neuromuscular conduction, particularly cardiac conduction, accounts for the fatalities and near fatalities that accompany hypokalemia. Hypokalemic periodic paralysis (HypoKPP) is one of the many disorders that mimic GBS. It is an occurrence of low serum potassium during attacks of paralysis. It is primarily caused by an enhanced shift of potassium (K+) into cells. Reversal of the paralysis is done by the administration of potassium. In this article, the important features of GBS and HypoKPP, their etiology, risk factors, pathophysiology, clinical manifestations, diagnostic findings, and interventions are discussed. Information on GBS versus HypoKPP and how this comorbidity complicates the neurologic examination is provided. A case study will also be presented.