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Guillain-Barre' Syndrome

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Author:    Donna Thomas (RN, MSN, BSHEd)


Guillain-Barre syndrome (GBS) is a demyelinating disease that is most often seen several weeks after a variety of nonspecific viral or other infectious diseases. It is a rare inflammatory disorder of the peripheral nervous system. The inflammation damages portions of the nerve cell resulting in muscle weakness, paralysis or sensory disturbances. The damage involves loss of the nerve’s myelin sheath (demyelination), which slows the conduction of impulses through the nerve. The damage may also involve destruction of the axon part of the nerve cell (denervation), which blocks conduction through the nerve. The body’s immune system produces antibodies that attack the peripheral nerves. It is often referred to as Acute Idiopathic Polyneuropathy, or Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) (McLeod, ND).

GBS is an inflammation of the peripheral nerve, inflammation ends in the suffix itis and so it is sometimes called neuritis. When many nerves are involved it is referred to as polyneuritis. In GBS it is more specific to the nerve roots (points of attachment of the peripheral nerves to the spinal cord) is termed radiculo. The meaning of diseases with the suffix pathy, which leads to the name polyradiculoneuropathy, is an inflammation of many peripheral nerves and nerve roots. Idiopathic can be applied to the name because idiopathic signifies that the cause of the disease is unknown, as in the case with GBS.

Guillain Barre¢ Syndrome is considered an autoimmune disease. Normally your body’s immune system recognizes the body as “itself” and ignores it, attacking only introduced particles and invading organisms. This mechanism can be disrupted, as seen with GBS. The body’s immune system mistakenly turns against itself, attacking its own tissues; this effect/reaction is known as autoimmune (NINNDS, 2003).

Peripheral nerves transmit signals from the brain and spinal cord to and from the muscles, organs and skin. Depending on their function, the nerves can be classified as motor, sensory and autonomous (involuntary) peripheral nerves.

The immune system is responsible for the production of special proteins, and antibodies or immunoglobulins (IG), as part of the body’s normal defense mechanism. These antibodies are produced in reaction to the presence of antigens, or introduced particles in the body, such as various bacteria and vira. Antibodies match specific antigens, and when the two come in contact, they bind together and a number of destructive reactions occur.


GBS is rare and afflicting about one to two person in 100,000. It is unknown why GBS infects certain people and not others. GBS is neither hereditary nor contagious. It can affect anybody at any age, any race, and can be acquired during any season or geographic area. A definitive cause is unknown, but it is believed to be triggered by a viral or bacterial infection that somehow causes an autoimmune. A humoral etiology is supported because antibody activity is directed toward peripheral nervous system (PNS) tissue, and immunoglobulin deposits have been found along myelin sheaths of the PNS. GBS is preceded in approximately 60% of the cases by a respiratory or GI virus.

The body’s immune system begins to attack the body itself. The macrophages and T-cells attack the healthy myelin in peripheral and cranial nerves, and the central nervous is unaffected. Usually the cells of the immune system attack only foreign material and invading organisms. In Guillain-Barre syndrome, the immune system starts to destroy the myelin sheath that surrounds the axons of many peripheral nerves, or even the axons themselves. Axons are long, thin extensions of the nerve cells that transmit the signals between the nerve cells. Some axons are surrounded by a myelin sheath. Think of it as an electrical cable surrounded by plastic broken up into bead like segments with spaces in between. The spaces between the myelin sheaths are called Ranvier Nodes. The axons are uncovered between these nodes of Ranvier and are vulnerable to attack. The myelin sheath insulates and protects the nerve cells. It also increases both the speed and the distance over which nerve signals can be transmitted.

Listed below are some possible common and uncommon triggers of GBS.


  • Upper respiratory tract infections
  • Gastrointestinal -diarrhea illness due to campylobacter jejuni
  • Cytomegalovirus infection
  • Epstein-barr virus infection
  • Hepatitis A, B, C infection
  • Human immunodeficiency virus infection
  • Borrelia burgdorferi infection
  • Lymphoma
  • Trauma


  • Mycoplasma infection
  • Leptospira icterohaemorrhagiae infection
  • Surgery
  • Salmonellosis
  • Rabies vaccine
  • Tetanus Toxoid
  • Bacilli Calmette-guerin immunization
  • Sarcoidosis
  • Systemic Lupus Erythematous
  • (Shoemaker, Ayers, Grenvik, & Holbrook, 2000)


Clinical Features of Guillain-Barre¢ Syndrome (McLeod, ND)

  • Paresthesias in the hands and feet
  • Back pain in approximately 30% of cases
  • Depressed or absent tendon reflexes
  • Progressive symmetrical weakness of the limbs
  • Cranial nerves are affected (especially the facial nerves) in approximately 50% of cases
  • Progression to peak disability in four weeks

Symptoms of Guillain-Barre¢ can range from mild to extreme. In mild cases, the patient may only have slight weakness in walking, requiring a cane or crutches. In the more extreme cases the weakness may progress to the point where the patient is almost totally paralyzed, possibly requiring mechanical ventilation. Ascending motor weakness can develop over 2-4 weeks, and can be acute or sub acute. This is followed by a gradual recovery period that could last weeks to many months. Most people will have complete recovery from even the most severe cases of GBS, but there are some patients that continue to have some residual weakness.

The main complaint is of weakness that varies widely in severity in different patients and often has a proximal emphasis and symmetric distribution. It usually begins in the legs, spreading to a variable extent but frequently involves the arms and often one or both sides of the face. Back pain is present in approximately 1/3 of GBS cases. The muscles of respiration or deglutition may also be affected. Cranial nerve deficits can be presented either alone or associated with limb weakness. Deep tendon reflexes are usually absent, while pupils and eyelids are often spared.

The paresis, weakness, and pain follow an ascending pathway, ultimately involving the upper extremities and the cranial nerves. Signs and symptoms are symmetrical and may or may not include a sensory component. Paraesthesias are initially described as tingling, prickling, pins-and-needles sensations followed later by needlelike and burning sensations.

Sensory nerves tell us about our surroundings; whether we are hurt; or if something is smooth or rough, hot or cold. Sensory symptoms are less common, but distal paresthesias and dysethesias are common. Neuropathy or radicular pain is present in many patients. The sensory disruptions are thought to be related to ectopic activity from damaged inhibitory neurons. Gradually muscle pain is experienced in the large muscles, such as the thighs, back and shoulders. Stiffness and cramping pain or deep aching muscle pain is common. As the sensory nerves are attacked the patient experiences loss or reduction of the sense of touch, or abnormal sensations such as burning, tingling, pins and needles, ants under the skin sensation or vibrations, and numbness.

Motor nerves control movement and damage to them results in partially or completely blocked signals. The body is affected when the damaged nerve loses its ability to function normally, resulting in reduced movement or coordination. The patient experiences this as a communication breakdown between what he wants to do and his ability to do it.

Autonomic nerves control the inner organs whose function is normally carried out automatically, such as secretion of hormones, heartbeat, urination, breathing, and vision. These functions may be disrupted resulting in arrhythmia, unstable blood pressure, blurred or double vision, dizziness, fainting spells, inability to regulate the body temperature, difficulty breathing, reduced ability to control the functions of the stomach, and digestive system. Loss of weight, vomiting after meals, reduced function of various glands, incontinence, and impotency may be seen. Autonomic disturbances are also common, may be severe, and are sometimes life threatening such as tachycardia, and pulmonary dysfunction. Other symptoms may occur such as sweating, facial flushing and impaired sphincter control. Cardiac dysrhythmias, abnormal hemodynamic response to drugs, and pupil dysfunction are common signs and symptoms of autonomic dysfunction.

Acute ventilatory failure is a common and devastating complication explained by the loss of motor innervation to skeletal muscles of the chest and diaphragm. With decreased inspiratory and expiratory capacities, coughing becomes ineffective, and the airway is compromised, leading to hypoxia, atelectasis, pneumonia, and aspiration. Aspiration occurs as a direct result of weakened laryngeal and glottis musculature. Airway obstruction occurs as a result of tongue and retropharyngeal weakness. Alveolar hypoventilation, along with impaired carbon dioxide levels also may occur. The patient is put at great risk, since the clinical signs of impaired respiratory function, such as hypercarbia, occur well before impaired respiratory function occurs. This is why it is important that serial measurements of respiratory parameters, including respiratory rate and pattern, (observing for paradoxical breathing and frequent changes in muscle use or use of accessory muscles) are completed along with frequent tidal volume, and vital capacity checks (McLeod, ND).

Possible life threatening symptoms of GBS that require close monitoring (McLeod, ND):

  1. Difficulty breathing (dyspnea) or taking deep breaths, breathlessness (SOB)
  2. Drooling, difficulty swallowing (dysphagia)
  3. Fainting spells (syncope)

Etiologies of other rapidly progressive weakness of muscles (McLeod, ND):

  • Transverse myelitis
  • Myasthenia Gravis
  • Poliomyelitis
  • Acquired hypokalemia
  • Periodic paralysis
  • Botulism

Other etiologies of Acute Polyneuritis (McLeod, ND):

  • HIV
  • Acute Intermittent Porphyria
  • Vitamin B deficiencies
  • Heavy metals and other toxins
  • Lymphoma, Carcinoma
  • Lyme disease
  • Vasculitis
  • Diphtheria
  • Diabetes

Diagnostic Tests

Lumbar puncture (spinal tap)

The patient is given a local anesthetic and then a needle is inserted between the third and fourth lumbar vertebrae into the fluid filled area that surrounds the nerve roots, and a sample of Cerebrospinal fluid (CSF) is obtained. CSF surrounds the brain and spinal cord, and acts as a buffer. It is normally clear and colorless. Changes in its color, quantity or composition may be an indication of neurological damage or disease. An elevated level of protein in the fluid is characteristic of GBS.

Electromyogram (EMG)

EMG examines the activity in the muscles for any signs of slowing down or blocking of response to nerve signals. It is used to differentiate between muscle disorders and muscle weakness caused by neurological disorders. When a nerve is stimulated with a brief electrical impulse that feels like a tiny volt, it creates activity in the adjoining muscle. This activity can be measured. A thin electrode is pushed through the patient’s skin, into the muscle to be examined. It is connected to a screen that shows the electrical activity being measured by the electrode. When the patient contracts the muscle, by bending it, the muscle fibers affected by the movement produce electrical activity being measured by the electrode. A muscle that is not in use will not produce electrical impulses, and no signal will be seen on the screen (Anonymous, 2001).

Nerve conduction velocity (NCV)

NCV is a test that investigates how well the nerves function. Nerves with damaged myelin transmit signals slower than undamaged nerve cells, while nerves with destroyed axons cannot transmit signals at all. This test reveals whether the ability of the tested nerves to transmit signals is reduced. This test can in some cases indicate what may have caused the disease. During the test, flat electrodes are placed on the patient’s skin at intervals, above the nerve to be examined for damage. One of the electrodes stimulates the nerve by transmitting a very weak electrical impulse through it. The other electrodes pick up and measure the strength of the impulse that reaches them. The conduction velocity of the nerve is calculated from the distance between the electrodes and the time it takes for the impulse to move between them. The speed of transmission is related to the diameter of the nerve and its myelination. The result is therefore compared with the speed of transmission of an undamaged nerve. The impulse may feel a little like an electric shock, and depending on how strong it is, it will be felt by the patient in varying degrees and may be uncomfortable for some patients. This test is performed along with the EMG; it records the speed at which the signals travel along the nerves (Anonymous, 2001).

Electrocardiogram (EKG)

An EKG records the electrical activity of the heart, and indicates any irregularities in the heart’s rhythm. Electrodes are applied to the chest. Activity of the heart produces small electrical impulses that are picked up and measured by the electrodes, after which the heart rhythm can be seen on the screen (Anonymous, 2001).

Nerve Biopsy

A nerve biopsy may be necessary in rare cases. This requires the removal of a tiny piece of nerve, under local anesthesia. The section is examined under a microscope for signs of damage. Some patients complain of sensory disturbances in the area a long time after the biopsy is completed (Anonymous, 2001).


There is no cure for GBS, but there are some therapies that can help lessen the severity of this illness and speed up recovery. Treatment begins as soon as the diagnosis is verified. Its aim is to reduce symptoms, offer immunotherapy to attempt to shorten the duration of the disease, and maintain the body’s muscles.

The patient should be sent to a hospital immediately if symptoms persist or increase in severity. These symptoms need to be carefully evaluated. If these signs and symptoms start to escalate the patient should be transferred or admitted to an ICU unit for close observation where respiratory therapy and continuous cardiac monitoring are available.

  1. Treat respiratory failure
  2. Cardiac monitoring
  3. Specific treatment therapies
  4. Intragastric or intravenous feedings
  5. General nursing care
  6. Prevent deep vein thrombosis
  7. Psychological support and communication


Treat respiratory failure

Increasing muscular paralysis can temporarily affect the chest muscles, causing shortness of breath. The patient may be required to be put on a ventilator. The ventilator helps to stabilize and assist the patient’s respirations. Most patients may only need to be on a ventilator for 1-2 weeks, while others will need it for longer periods of time. The patients that need mechanical ventilation for increased periods of time may need a tracheostomy. This is a surgical procedure where a small slit is made into the throat and a tracheostomy tube is inserted through the hole into the windpipe/trachea.

Frequent suctioning may be required. This is done through the tracheostomy tube or the endotracheal tube. Suctioning helps to keep the lungs free of secretions that may hinder breathing.

Sedation and pain medications should be used as needed. Many people require light sedation to help prevent them from fighting against the ventilator or pulling at the ventilator tubing. Pain medication is also crucial at this point. Patients still have pain and need to be properly medicated. This may also help reduce anxiety.

Communication is vital while patients are on mechanical ventilator. Effective communication must be established between the patient, family, medical and nursing staff. The patient should be involved in the decision making process regarding their treatment and care. Communication can be sought out by using alphabet boards, pictures, dry erase boards, or pencil and paper. Some patients are only able to shake their head or blink their eyes for yes and no answers.

Cardiac Monitoring

The patent should be monitored for arrhythmias, and changes in blood pressure. These changes can reflect peripheral autonomic nervous system involvement.

Specific Treatment Therapies

Plasmapheresis, also known as plasma exchange, can be thought of as blood cleaning. This treatment involves either removal of the patient’s antibodies or the addition of other antibodies to the patent or a combination of both. Plasmapheresis is done by removing whole blood from the body and processing it so that the red and white blood cells are separated from the plasma. The blood cells are then returned to the patient without the plasma where the body quickly manufactures more plasma to replace what was removed during Plasmapheresis. This process is thought to be effective because the plasma that contained toxic elements that could destroy myelin is processed out of the whole blood.

Immunoglobulin infusion is done via intravenous infusion. Immunoglobulin contains healthy antibodies from blood donors. High doses of intravenous infusions of immunoglobulin are thought to block the antibodies that could damage myelin that contribute to GBS; this process can help lessen the immune attack on the nervous system.

Together these specific treatment therapies help to reduce the severity of the disease. These treatments help reduce destruction which in turn helps to reduce damage. They work together to decrease the time it takes to recover. The patient and family need to be educated about these processes, and that recovery is spontaneous, which makes it impossible to know how many treatments may be needed.

Intragastric or Intravenous Feedings

Patients that can swallow may need assistance with feeding. Swallowing studies maybe necessary to determine the consistency of fluids or foods that are needed to help decrease the risk of aspiration. The head of the bed should be elevated 30-45° to help prevent aspiration. Patients that have difficulty swallowing are given fluids, nourishment and medicine through an intravenous line or nasal gastric tube.

General Nursing Care

Respiratory: Observe for changes in respiratory pattern, shortness of breath, dyspnea, and suction increased secretions.

Cardiac: Look for changes in cardiac rhythms, increased ectopy, and blood pressure. Assess for chest pain or discomfort.

Gastric feeding: The head of the bed should be elevated 30-45° to help decrease the risk of aspiration.

Mouth: The nurse should look for drooping and or drooling from the mouth, and complaints of dysphagia.

Bowels: Bowel movements should be documented. Nausea and/or vomiting could be signs of constipation. Medications should be ordered routine or prn to help prevent constipation.

Bladder: The bladder can temporarily lose its ability to squeeze and empty itself, which can lead to urinary retention. If this happens a foley catheter should be inserted. Daily foley and perineal care should be done routinely to help prevent urinary tract infections.

Skin: The patient’s skin should be inspected every shift for potential breakdown. Patients should be turned and repositioned q 2 hours to decrease the risk of pressure ulcers and promote circulation. Feet and hands should be assessed for foot or wrist drop.

Deep Vein Thrombosis

Bedridden patients are at high risk for developing DVT. Prophylactic anti-thrombolytics should be ordered such as subcutaneous heparin 5,000 units B.I.D.

Physical Therapy

Arrangements for physical therapy should be initiated as soon as possible for the patient to have optimal recovery. Caregivers may need to be taught how to manually move the patient’s arms and legs to help keep the muscles flexible and strong. Whirlpool therapy may help to relieve pain. Once discharged the patient should be sent home with an active exercise routine to help regain muscle strength. Patients should be evaluated for splints, walking aids and rehabilitation.

Psychological Support and Communication

Patients and family members need to be involved in all aspects of care. They need to be informed that the course of the disease is unpredictable, but the majority of patients recover. The patient should be allowed to communicate his or her feelings of frustration, pain, anxiety, isolation, and low self-esteem. Counseling and medication to help deal with these feelings may be necessary for a while for both patient and family.

Guillain-Barre Syndrome Support Groups

There are many support groups for Guillain Barre Syndrome for patients and their families. These support groups can be found on the Internet, in the phone book, or at your local library.

Guillain-Barre Syndrome Foundation International
P.O. box 262
Wynnewood, PA 19096


Anonymous (2001). All about Guillain-Barre Syndrome, Retrieved 7/03 from,,,,,

Anonymous. (ND). Guillain-Barre Syndrome. Retrieved 7/03 from

Bongard, F.S., Sue, D.Y., (1994). Current Critical Care Diagnosis and Treatment. Connecticut: Appleton and Lange (pg. 533).

Health communities Neurology Channel, (2003). Guillain-Barre Syndrome. Retrieved 7/03 from

Kinney, M.R., Dunbar, S.B., Brooks-Brunn, J., Molter, N., Vitello-Cicciu, J. (1998). AACN Clinical Reference for Critical Care Nursing (4th ed.). Missouri: Mosby, Inc (pg. 720-722).

Mayo Foundation for Medical Education and Research (MFMER) (1998-2003). Guillain-Barre Syndrome. Retrieved 7/03 from

McLeod, J. (ND) Reprinted from Modern Medicine of Australia. GBS- a GP’s guide to diagnosis and management. Retrieved 7/03 from

National Institute of Neurological Disorders and Stroke NINNDS, (2003). Gillian Barre Syndrome Fact Sheet. Retrieved 7/03 from

Shoemaker, Ayers, Grenvik, & Holbrook. (2000) Textbook of Critical Care (4th ed.) Pennsylvania: Saunders (pg. 1888-1889).

Tierney, Jr. L.M., McPhee, S.J., Papadakis, M.A. (2000) Current-Medical Diagnosis and Treatment (39th ed.). New York: McGraw-Hill companies (pg. 1006-1007).

Wynngaarden, JB, Smith, LH, Bennet, JC (1996). Cecil Textbook of Medicine, (20th ed.). WB Saunders Company, Retrieved 7/03 from