Nursing Refresher for Guillain-Barre Syndrome

• This article will refresh a nurse’s knowledge of Guillain-Barre Syndrome, its pathophysiology, and the two primary types of treatment. 
• Guillain-Barre Syndrome is a rare autoimmune disorder that presents in patients as muscle weakness or sensory disturbances.
• Intravenous Immunoglobulin and Plasmapheresis are the two primary treatments, working to restore proper function to the patient’s antibodies.

Guillain-Barre Syndrome (GBS) is a rare and serious autoimmune disorder named after the French neurologists Georges Guillain, Jean-Alexandre Barre, and Andre Strohl. The syndrome first appeared in a series of case reports in 1916 where the three neurologists observed World War I patients with similar symptoms of muscle weakness, sensory disturbances, and autonomic dysfunction.

First thought to be a bacterial infection, GBS is a distinct collection of neuropathic conditions. The term “Guillain-Barre Syndrome” first appeared in a paper published in 1920 by Guillain, Barre, and Strohl.

Guillain-Barre Syndrome (GBS) has an estimated incidence rate of 0.6 to 4 cases per 100,000 people per year in the general population. However, the incidence rate may vary depending on geographic location and age group.

Overall, the development of GBS is a complex interplay between genetic, environmental, and immunological factors. GBS can affect people of all ages and all genders, but it is more common in adults and older individuals.

Some studies suggest men are slightly more likely to develop GBS than women. The exact cause of GBS is unknown, but factors such as recent viral or bacterial infections, surgeries, and vaccinations may increase the risk of developing GBS. Influenza, Campylobacter jejuni (A leading cause of foodborne illness), and cytomegalovirus may also contribute to the development of GBS.

In rare cases, GBS may develop after receiving certain vaccines, such as the influenza vaccine, tetanus toxoid, or rabies vaccine. GBS may develop after surgery, particularly abdominal or thoracic surgeries. This may be because of the immune system’s response to tissue damage or inflammation.

Other factors that may increase the risk of developing GBS include exposure to chemicals or toxins, such as insecticides or heavy metals, and having a history of autoimmune disorders.

Overall, GBS remains an uncommon condition, but its potential for serious complications and long-term effects underscores the importance of timely diagnosis and treatment.

Pathophysiology of Guillain-Barre Syndrome

The pathophysiology of Guillain-Barre Syndrome (GBS) involves an autoimmune response in which the immune system mistakenly attacks the peripheral nerves, causing inflammation and damage to the myelin sheath and axons.  

This leads to impaired nerve conduction, demyelination, axonal damage, and muscle weakness can lead to nerve conduction abnormalities, which manifest as muscle weakness, sensory disturbances, and autonomic dysfunction. Autonomic dysfunction can also cause cardiovascular and gastrointestinal complications.  

Sometimes, the immune system may also attack the blood-brain barrier (BBB), a selective barrier that separates circulating blood from the brain and spinal cord tissue, causing dysfunction and increased permeability of the barrier. In Guillain-Barre Syndrome (GBS), the BBB plays a critical role in the development and progression of the disease.  

In patients with GBS, studies have shown increased levels of cytokines and other immune factors in the cerebrospinal fluid (CSF), indicating the disorder has affected the central nervous system (CNS). The presence of these immune factors in the CSF suggests a compromised BBB, allowing the entry of immune cells and inflammatory mediators into the CNS and has been associated with more severe disease and poorer outcomes.  

In severe cases of GBS, inflammation and damage to the nerves can progress to involve the respiratory muscles, leading to respiratory failure and the need for mechanical ventilation. Autonomic dysfunction can also cause cardiovascular and gastrointestinal complications. 

Treatment for Fuillain-Barre Syndrome

Intravenous immunoglobulin (IVIG) is a common therapy for GBS and may reduce BBB permeability, suggesting that it may help to restore BBB function and reduce CNS inflammation. Intravenous immunoglobulin (IVIG) involves the administration of high doses of immunoglobulin (antibodies) from pooled human blood products.  

Studies have shown that IVIG can reduce the duration of symptoms and improve outcomes in patients with moderate-to-severe GBS. Risks of IVIG include allergic reactions, thrombotic events, and renal failure.  

Close monitoring and management of potential complications are necessary to optimize outcomes for patients undergoing IVIG treatment for GBS.  

Plasmapheresis can be an effective treatment in GBS because it removes the circulating antibodies that are targeting the peripheral nerves, reducing inflammation, and preventing further damage to the nerves. Treatment teams often reserved plasmapheresis for patients with moderate-to-severe GBS, as it is an invasive and resource-intensive procedure.  

The number of plasmapheresis treatments needed may vary depending on the severity of the patient’s symptoms and the response to treatment. Risks from receiving plasmapheresis include infection, bleeding, and allergic reactions to the donor plasma or plasma substitute.  

Close monitoring and management of potential complications are necessary to optimize outcomes for patients undergoing plasmapheresis for GBS.  

The Bottom Line

The prognosis of Guillain-Barre Syndrome (GBS) varies depending on the severity of the illness and the individual patient’s response to treatment. While many patients recover fully, others may experience significant long-term disability or even death. 

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