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Guillain Barre syndrome

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• Patient Care & Health Information
• Diseases & Conditions
• Guillain-Barre syndrome

• Nerve and damaged myelin sheath

The demyelinating form of Guillain-Barre syndrome destroys the protective covering of the peripheral nerves (myelin sheath), preventing the nerves from transmitting signals to the brain.

Guillain-Barre (gee-YAH-buh-RAY) syndrome is a rare disorder in which your body's immune system attacks your nerves. Weakness and tingling in your hands and feet are usually the first symptoms.

These sensations can quickly spread, eventually paralyzing your whole body. In its most severe form Guillain-Barre syndrome is a medical emergency. Most people with the condition must be hospitalized to receive treatment.

The exact cause of Guillain-Barre syndrome is unknown. But two-thirds of patients report symptoms of an infection in the six weeks preceding. These include a COVID-19 , respiratory or a gastrointestinal infection or Zika virus.

There's no known cure for Guillain-Barre syndrome, but several treatments can ease symptoms and reduce the duration of the illness. Although most people recover completely from Guillain-Barre syndrome, some severe cases can be fatal. While recovery may take up to several years, most people are able to walk again six months after symptoms first started. Some people may have lasting effects from it, such as weakness, numbness or fatigue.

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Guillain-Barre syndrome often begins with tingling and weakness starting in your feet and legs and spreading to your upper body and arms. Some people notice the first symptoms in the arms or face. As Guillain-Barre syndrome progresses, muscle weakness can turn into paralysis.

Signs and symptoms of Guillain-Barre syndrome may include:

• A pins and needles sensation in your fingers, toes, ankles or wrists
• Weakness in your legs that spreads to your upper body
• Unsteady walking or inability to walk or climb stairs
• Difficulty with facial movements, including speaking, chewing or swallowing
• Double vision or inability to move the eyes
• Severe pain that may feel achy, shooting or cramplike and may be worse at night
• Difficulty with bladder control or bowel function
• Rapid heart rate
• Low or high blood pressure
• Difficulty breathing

People with Guillain-Barre syndrome usually experience their most significant weakness within two weeks after symptoms begin.

Guillain-Barre syndrome has several forms. The main types are:

• Acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the most common form in North America and Europe. The most common sign of AIDP is muscle weakness that starts in the lower part of your body and spreads upward.
• Miller Fisher syndrome (MFS), in which paralysis starts in the eyes. MFS is also associated with unsteady gait. MFS is less common in the U.S. but more common in Asia.
• Acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) are less common in the U.S. But AMAN and AMSAN are more frequent in China, Japan and Mexico.

When to see a doctor

Call your doctor or health care provider if you have mild tingling in your toes or fingers that doesn't seem to be spreading or getting worse. Seek emergency medical help if you have any of these severe signs or symptoms:

• Tingling that started in your feet or toes and is now moving up your body
• Tingling or weakness that's spreading rapidly
• Difficulty catching your breath or shortness of breath when lying flat
• Choking on saliva

Guillain-Barre syndrome is a serious condition that requires immediate hospitalization because it can worsen rapidly. The sooner appropriate treatment is started, the better the chance of a good outcome.

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The exact cause of Guillain-Barre syndrome isn't known. The disorder usually appears days or weeks after a respiratory or digestive tract infection. Rarely, recent surgery or vaccination can trigger Guillain-Barre syndrome. There have been cases reported following infection with the Zika virus. Guillain-Barre syndrome may occur after infection with the COVID-19 virus. It's also a rare reaction in those who receive the Johnson & Johnson or AstraZeneca COVID-19 vaccine.

In Guillain-Barre syndrome, your immune system — which usually attacks only invading organisms — begins attacking the nerves. In AIDP , the nerves' protective covering (myelin sheath) is damaged. The damage prevents nerves from transmitting signals to your brain, causing weakness, numbness or paralysis.

Risk factors

Guillain-Barre syndrome can affect all age groups, but your risk increases as you age. It's also slightly more common in males than females.

Guillain-Barre syndrome may be triggered by:

• Most commonly, infection with campylobacter, a type of bacteria often found in undercooked poultry
• Influenza virus
• Cytomegalovirus
• Epstein-Barr virus
• Hepatitis A, B, C and E
• HIV , the virus that causes AIDS
• Mycoplasma pneumonia
• Hodgkin's lymphoma
• Rarely, influenza vaccinations or childhood vaccinations
• COVID-19 virus
• COVID-19 Johnson & Johnson and AstraZeneca vaccine

Complications

Guillain-Barre syndrome affects your nerves. Because nerves control your movements and body functions, people with Guillain-Barre may experience:

• Breathing difficulties. The weakness or paralysis can spread to the muscles that control your breathing, a potentially fatal complication. Up to 22% of people with Guillain-Barre syndrome need temporary help from a machine to breathe within the first week when they're hospitalized for treatment.
• Residual numbness or other sensations. Most people with Guillain-Barre syndrome recover completely or have only minor, residual weakness, numbness or tingling.
• Heart and blood pressure problems. Blood pressure fluctuations and irregular heart rhythms (cardiac arrhythmias) are common side effects of Guillain-Barre syndrome.
• Pain. One-third of people with Guillain-Barre syndrome experience severe nerve pain, which may be eased with medication.
• Bowel and bladder function problems. Sluggish bowel function and urine retention may result from Guillain-Barre syndrome.
• Blood clots. People who are immobile due to Guillain-Barre syndrome are at risk of developing blood clots. Until you're able to walk independently, taking blood thinners and wearing support stockings may be recommended.
• Pressure sores. Being immobile also puts you at risk of developing bedsores (pressure sores). Frequent repositioning may help avoid this problem.
• Relapse. A small percentage of people with Guillain-Barre syndrome have a relapse, experiencing muscle weakness even years after the symptoms ended.

Severe, early symptoms of Guillain-Barre syndrome significantly increase the risk of serious long-term complications. Rarely, death may occur from complications such as respiratory distress syndrome and heart attacks.

Guillain-Barre syndrome care at Mayo Clinic

• Wijdicks EFM, et al. Guillain-Barre syndrome. Mayo Clinic Proceedings. 2017; doi:10.1016/j.mayocp.2016.12.002.
• Willison HJ, et al. Guillain-Barre syndrome. The Lancet. 2016; doi:10.1016/S0140-6736(16)00339-1.
• Guillain-Barre syndrome fact sheet. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Guillain-Barr%C3%A9-Syndrome-Fact-Sheet. Accessed April 21, 2022.
• Chandrashekhar S, et al. Guillain-Barre syndrome in adults: Pathogenesis, clinical features, and diagnosis. https://www.uptodate.com/contents/home. Accessed April 21, 2022.
• Edwards KM, et al. COVID-19 : Vaccines. https://www.uptodate.com/contents/search. Accessed April 21, 2022.
• Ferri FF. Guillain-Barre syndrome. In: Ferri's Clinical Advisor 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed April 21, 2022.
• Muley SA. Guillain-Barre syndrome in adults: Treatment and prognosis. https://www.uptodate.com/contents/search. Accessed April 21, 2022.
• Ryan MM. Guillain-Barre syndrome in children: Treatment and prognosis. https://www.uptodate.com/contents/search. Accessed April 21, 2022.
• Braswell-Pickering EA. Allscripts EPSi. Mayo Clinic. Jan. 28, 2022.
• Leonhard SE, et al. Diagnosis and management of Guillain-Barre syndrome in ten steps. Nature Reviews Neurology. 2019; doi:10.1038/s41582-019-0250-9.
• Elkind MSV, et al. COVID-19 : Neurologic complications and management of neurologic conditions. https://www.uptodate.com/contents/search. Accessed April 21, 2022.
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Guillain-barre syndrome (nursing).

Thy P. Nguyen ; Roger S. Taylor ; Andrea G. Renwanz Boyle .

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Last Update: February 7, 2023 .

• Learning Outcome

At the conclusion of this article the reader be able to:

• Identify and discuss nursing diagnoses relevant to the care of the Gullain-Barre Syndrome (GBS) patient
• Identify the etiology of GBS 
• Identify potential causes and risk factors of GBS
• Discuss the assessment and evaluation of GBS 
• Describe key components of medical management of GBS
• Identify key components of nursing management and monitoring of GBS
• Identify members of the interprofessional team available for assistance 
• Discuss selected outcomes for the GBS patient
• Discuss selected elements of interdisciplinary care of the GBS patient
• Discuss important elements of health education and health promotion for the GBS patient and family members
• Identify selected risk management concerns for nurses caring for GBS patients
• Identify selected important elements of discharge planning for the GBS patient in the acute and recovery phases of the illness
• Describe evidence-based issues related to GBS
• Identify nursing pearls related to interprofessional practice in the care of the GBS patient
• Introduction

Guillain-Barre syndrome (GBS) is the most common cause of acute, flaccid, neuromuscular paralysis in the United States. Guillain-Barre syndrome was first discovered more than a century ago. Advances in the past century include investigating the immune-mediated pathophysiology of the disease, recognizing the spectrum of presentations, advancing diagnostic modalities, prognostic models, and performing randomized trials of treatments to improve outcome. Given the morbidity that can occur without treatment, all clinicians and nurses should have a knowledge of this rare disease. [1] [2] [3] [4]

• Nursing Diagnosis
• Impaired respiratory function related to rapid and progressive weakness and impending respiratory failure
• Immobility related to paralysis
• Nutritional imbalance related to swallowing difficulties 
• Impairments to verbal communication related to cranial nerve dysfunction
• Pain 
• Psychological problems 

The Guillain-Barre syndrome (GBS) and its variants are considered post-infectious, immune-mediated neuropathies. Evidence from animal models suggests a key role of molecular mimicry. In Campylobacter jejuni gastrointestinal infections, a lipooligosaccharide present in the outer membrane of the bacteria is similar to gangliosides that are components of the peripheral nerves. [5] Therefore, an immune response triggered to fight infection can lead to a cross-reaction on host nerves.

Many infections have been linked with GBS. The most common are gastrointestinal or respiratory illnesses. Up to 70% of patients have reported an antecedent illness in the 1 to 6 weeks before the presentation of GBS. [6]  During the Zika virus outbreak, many GBS cases were described. [7] Case reports detail many other possible etiologies linked to GBS including medications and surgeries. (Evidence level III)

In 1976, flu vaccination against the influenza A/H1N1 antigen led to a well-documented, increased incidence of cases of GBS; however, further surveillance data of flu vaccinations in subsequent years have described only one additional case of GBS for every 1 million vaccines. Subsequent studies estimate that developing GBS after a flu infection is up to 7 times more likely than developing GBS after a vaccination. [8] [9] [10] [11] [12]  (Evidence level IV)

• Risk Factors

Although rare, with an incidence of 0.4 to 2 per 100,000, Guillain-Barre syndrome (GBS) has major effects on the health care system. The cost of medical care for a patient with GBS has been estimated at up to $318,966. Overall, the cost of treating patients with GBS has been estimated at $1.7 billion dollars per year. Males are affected at a slightly higher incidence than females. Each year, it is estimated 100,000 patients worldwide would contract GBS. [13] [14]  (Evidence level III)

Guillain-Barre syndrome (GBS) patients describe a fulminant course of symptoms that usually include ascending weakness and non-length dependent sensory symptoms. By definition, the nadir is usually reached within 4 weeks. Symmetric involvement is a key feature of GBS. [6]  GBS is usually considered monophasic; therefore, a relapsing or remitting course at presentation would be considered atypical. [15]  Additionally, a prior GBS event (recurrent GBS) is also unusual, occurring in < 10% of all patients. [16]  If the patient reports progression beyond 8 weeks, other diagnoses should be considered.

GBS often presents (up to 70% of patients) within 1 to 6 weeks of antecedent illness. [17]  Other antecedent events that have been linked with GBS include vaccinations (specifically a 1976 strain of swine flu vaccine), surgery, trauma, or other infections. [17] [11]  

Classically, patients with GBS will have a pattern of proximal and distal weakness, which is flaccid and often profound if hospitalized. Significant neck flexion weakness may be present and can portend the need for intubation. Areflexia or hyporeflexia is usually present. (Rare cases without hypo/areflexia have been described, mostly in the AMAN variant of GBS). [18]  Besides the flaccid weakness and areflexia, patients experience non-length-dependent sensory symptoms; therefore, unlike more common chronic neuropathies such as diabetic neuropathy, patients may report dysesthesias in the hands followed by the feet. Patients can develop facial diplegia due to the involvement of both facial cranial nerves. They can also develop dysphagia due to the involvement of the glossopharyngeal, vagus, and hypoglossal cranial nerves. [6] Autonomic nerves can lead to significant morbidity; therefore, most physicians recommend monitoring in an intermediate or intensive care unit for cardiac arrhythmias or blood pressure lability. Dysautonomia is a primary etiology of the morbidity and mortality attributable to GBS. Additionally, the involvement of the lower cranial nerves (glossopharyngeal, vagus, and hypoglossal nerves) or involvement of the nerves to the muscles of respiration may lead to the need for artificial ventilation. Respiratory failure can occur in up to 30% of patients, usually leading to prolonged hospitalization and recovery. [19]

Besides the classic GBS presentation described above, many variants of GBS have been described. There is a variant with pure motor involvement called "AMAN (acute motor axonal neuropathy)" that is more common in Asian countries. [20] Rarely,  these patients can have normal reflexes. [18]  There is also a regional variant involving primarily the pharyngeal, neck, and upper extremity muscles called the "pharyngeal-cervical-brachial" variant). [21] Some variants can involve the central nervous system, termed "Bickerstaff Encephalitis." [22] There is also a variant that presents with paraparesis. [23] Arguably, the most famous variant is the Miller Fisher syndrome. [24] [25] This is classically described as a triad of ophthalmoplegia, areflexia, and ataxia; however, other cranial nerves besides the oculomotor nerves have been reported in this variant. [25]

Guillain-Barre syndrome (GBS) is considered a clinical diagnosis; therefore, a diagnosis can be made with confidence at the bedside in most cases. For atypical cases or unusual subtypes, ancillary testing can be useful. [15]

Electromyography and nerve conduction studies may be helpful in distinguishing GBS from its mimics. Nerve conduction studies (NCS) utilize technology to help distinguish between demyelinating and axonal forms of neuropathy. Needle electromyography may help to determine the acuity of a patient’s symptoms. In some cases, these studies may be helpful in evaluating for other considerations in the differential diagnosis such as neuromuscular junction disorders or diabetic neuropathy. Classically, electrodiagnostic studies should be undertaken at 10 to 14 days after symptom onset due to the time for Wallerian degeneration of sensory and motor nerve fibers; however, there have been many studies that reveal that early, nonspecific findings may be helpful in diagnosing GBS as early as 3 to 7 days after symptom onset. [26] [27]  

The more common early electrodiagnostic findings in GBS include absent or prolonged H-reflexes and/or F-wave latencies. [28] [27]  The sural sparing pattern is considered specific for GBS as compared to other polyneuropathies. [29] This pattern would show an intact sural sensory response with abnormal upper extremity sensory responses. Other findings would depend on the variant of GBS. Acute inflammatory demyelinating polyneuropathy would be more likely to have partial motor conduction block, temporal dispersion, slow conduction velocities, prolonged/absent F-wave latencies, and prolonged distal latencies. [30] [20]  AMAN would usually show a pattern of low, compound muscle action potential amplitudes or even inexcitable motor nerves; however, partial motor conduction block or complete conduction block can be seen in AMAN nerve conduction study (NCS). This phenomenon is explained by “reversible conduction failure.” [31]  Complement is deposited in nodes of Ranvier and paranodal regions on peripheral nerves. Subsequently, the nerves can undergo Wallerian degeneration leading to significant and prolonged axonal damage or can reverse, deemed conduction failure. [32] [33] This phenomenon explains the relatively rapid recovery of some severely weak patients with AMAN. Sensory nerves would be spared both clinically and electrodiagnostically in AMAN. Acute motor and sensory axonal neuropathy (AMSAN) would show low amplitude motor and sensory potentials. Miller Fisher syndrome is more often described with reduced or absent sensory nerve action potentials. [34]  

Cerebrospinal fluid (CSF) shows a classic pattern of albuminocytologic dissociation. This term means that spinal fluid shows a normal amount of white blood cells and an elevated CSF protein level. [4] [15] However, this pattern is only present in 80% of patients at 2 weeks following symptom onset. Therefore, the absence of this classic finding does not exclude the diagnosis. If the white blood cell count is elevated, this should prompt consideration of other infectious GBS mimics, such as HIV seroconversion. [6]  

A number of ganglioside antibodies have been associated with GBS. Antibodies include anti-GM1, anti-GD1A, anti-GT1A, and anti-GQ1B. These range in sensitivity from up to 60% (anti-GM1 antibodies in acute motor axonal neuropathy) to up to more than 90% (anti-GQ1B antibodies in Miller Fisher syndrome). However, these laboratory studies usually require some time to obtain results and, therefore, may not be as helpful in decision making at the time of a patient admission. [35] [36] [37]

Imaging studies such as magnetic resonance imaging (MRI) spine may show enhancement of the nerve roots, indicating a breakdown of the blood-nerve barrier due to inflammation in GBS. However, MRI utility in GBS is most useful to rule out other etiologies of quadriparesis or facial diplegia such as transverse myelitis or intracranial disease. [38] [39]

A negative inspiratory force (NIF) should be performed on patients with suspected GBS.  Serial NIFs should be followed in patients with a high risk of respiratory compromise.  Patients that are unable to perform a NIF of -20 to -30 cm H2O should be considered at very high risk.  

• Medical Management

In randomized controlled trials, there are two treatment options currently considered the standard of care in Guillain-Barre syndrome (GBS). These include either intravenous immunoglobulin (IVIG) or plasma exchange. IVIG is thought to act by its immune-modulating action; however, the exact mechanism remains to be elucidated. IVIG is given 2 grams/kilogram divided over 5 days. (Evidence level I) [40] ) Plasma exchange is thought to act by removing pathogenic antibodies, humoral mediators, and complement proteins involved in the pathogenesis of GBS. Similar to IVIG, its exact mechanism of action in the treatment of GBS has not been proven. Plasma exchange is generally given as a volume of an exchange over five sessions. Plasma exchange and IVIG have been shown to be equally efficacious. (Evidence level I) [41]  The effect is present if either treatment is given within 4 weeks, but the stronger effect may be present if treatment is administered within two weeks. (Evidence level II) [42] [43] [44] [42]  Surprisingly, corticosteroids (both oral prednisone and intravenous methylprednisolone) have not shown benefit over placebo or in combination with IVIG and plasma exchange over either modality alone. Overall, treatment is generally considered to shorten the course of recovery of GBS. Treated patients in one study achieved independent ambulation 32 days faster than untreated patients. (Evidence level I) [45] [46] [43] [41] [47] [48]

 Overall, most patients with GBS do well, with up to 85% of patients achieving independent ambulation with recovery; however, there is a significant proportion of patients (20%) with morbidity. (Evidence level III) Further studies of plasma exchange followed by IVIG and IVIG concurrent with steroids have not shown significant improvement. (Evidence level I) [49] [50]  An ongoing trial of 2 courses of IVIG should have results within the next year. (Evidence level III)  [51] There are also ongoing trials of complement inhibitors in patients with refractory GBS. (Evidence level II) [52] [53] [54]

• Nursing Management

Nursing management for identified nursing diagnoses includes:

1. Impaired respiratory function

The nurse will need to carefully monitor vital signs for changes in respiratory rate, quality of respirations, and decreasing vital capacity. Respiratory assessment for ascending paralysis and impending respiratory failure due to weakness of intercostal muscles and diaphragm along with shallow and irregular breathing, the use of accessory muscles, and difficulty in clearing secretions. If the patient is intubated, the nurse will need to work with the physician and respiratory therapist to manage all aspects of mechanical ventilation. During the course of GBS, the nurse will need to assess and monitor the patient for respiratory infections including pneumonia.

2. Immobility

The nurse will need to assess for problems associated with immobility related to muscle weakness and paralysis. The nurse should support and maintain paralyzed extremities in function positions, perform passive ROM exercises at least twice daily, ensure that the patient has position changes every two hours or ensure the patient is positioned on a foam, air, water, or gel support surface bed. Skin assessment for skin breakdown, assessment of bowel function through monitoring of bowel sounds and frequency of bowel movements, use of anti-embolism stockings and compression boots to prevent DVT and  PE, and maintenance of adequate hydration to decrease the risks of pressure ulcers are important nursing management considerations for the immobility related to GBS.

3. Nutritional imbalance

The nurse will need to carefully work to assist in the maintenance of optimal nutrition in the patient with GBS. The patient with impaired swallowing due to muscle weakness should be carefully assessed for aspiration. The nurse will need to manage gastrostomy tube feedings, IV fluid administration, or the administration of parenteral nutrition as needed to ensure that the patient receives necessary nutrients. 

4. Communication impairments

The nurse will need to provide strategies for adequate communication with the patient who is unable to verbally communicate due to paralysis associated with GBS. Management of adequate patient communication may include the use of strategies such as eye blinks, use of pictures, or the use of computer graphics. The nurse should also consider discussing the use of communication strategies with family members and friends. Referrals to a speech therapist may also assist to address communication impairments due to GBS.

5. Pain 

The nurse will need to carefully assess the patient for pain related to GBS related muscle changes. If the patient is unable to communicate verbally, the nurse should use assessment strategies including pictures or pain management scales to obtain an adequate understanding of the patient's pain level. Non-verbal signs of pain including restlessness, facial grimaces, or restlessness should also be noted in this assessment. Adequate pain management is essential, especially in the acute stages of GBS. 

6. Psychological problems

The nurse will need to carefully assess and manage the GBS patient for potential psychological problems. The sudden onset of loss of control in the acute phase of a potentially life-threatening illness may result in anxiety, fear, and feelings of helplessness. Patients and family members may also confront uncertainty, helplessness, and loneliness when dealing with GBS. The impact of GBS on family members may be influenced by the role of the patient in the family. Social and economic issues may be exacerbated if the patient is the primary breadwinner or major source of family support. Patients and family members may experience fear and helplessness, especially within the ICU or acute care setting. The nurse will need to educate the patient and family members, providing information about GBS and the equipment, medications, and therapies used to treat GBS. The nurse may also suggest patient education materials, referrals to support groups, social workers, or psychologists as strategies to improve patient and family coping with GBS. 

• When To Seek Help

Management of GBS requires that the nurse participates in an interprofessional team dedicated to collaborative patient care delivery. The nurse should plan to assess and monitor the patient with GBS for potential complications. Changes in respiratory function with decreased vital capacity require the nurse to contact the MD. Complications including cardiac dysrhythmias, hypertension, hypotension, DVT, PE, urinary retention, or alterations in swallowing are findings that require the nurse to contact the MD. The nurse should contact the pharmacist for problems associated with IVIG or corticosteroids frequently used in the management of acute GBS. Monitoring of patients and determination of appropriate mechanical ventilation settings should occur with assistance from the MD and respiratory therapist. Expressions of fear, anxiety, hopelessness, and helplessness by the patient or family members should prompt the nurse to contact the social worker. psychologist, or other mental health providers in the interprofessional team. 

• Outcome Identification

Expected patient outcomes include the following:

1. Normal respiratory function with normal respiratory rate, normal vital capacity, effective respiratory functioning and airway clearance, and O2 levels within normal limits

2. Increased mobility with no contractures or muscle weakness, ability to ambulate and regain function in all extremities

3. Ability to swallow, maintain diet that provides adequate nutrition and hydration

4. Maintain adequate verbal communication with recovery of speech

5. Pain is resolved or adequately controlled through oral pain medications or other pain management strategies such as exercise, relaxation exercises, and stress managment

6. Reduction or elimination of psychological problems including fear, anxiety, uncertaintly, helplessness, loss of control, and lonliness

7. Reduction or elimination of complications including decubitus ulcers, DVT, bowel or bladder dysfucntion

The nurse will need to carefully monitor the GBS patient for:

1. Respiratory impairment- monitoring includes assessment of vs, measurement of vital capacity, observation for use of accessory muscles and difficulty clearing secretions 

2. Cadiac dysrhythmias associated with autonomic dysfunction- monitoring includes measurement of blood pressure for hyper or hypotension, use of cardiac monitoring devices to measure heart rate and presence of dysrhythmias

3. Weakness and paralysis  in extremities- monitoring includes checking for the absence of lower extremity tendon reflexes and the patient's ability to walk,  and use extremities for lifting or movement

4. Changes in skin due to immobility- monitoring for erythema or early signs of skin breakdown and decubiti 

5. Fluid and electrolyte imbalance- monitoring of IVs, parenteral nutrition, and intake and output

6. Changes in bladder and bowel function due to autonomic dysfunction, immobility, or use of pain medications- monitoring of output through use of indwelling catheter and monitoring of bowel movement frequency

7. Pain- monitor by freequent patient assessment using numeric or picture pain scales

8. Psychological problems- monitor the patient for symptions of fear, anxiety, or depresion 

• Coordination of Care

The care of the patient with Guillain-Barre syndrome (GBS) requires collaboration by all members of the healthcare team. Nurses are integral in coordinating care services in the acute phase of GBS and in recognizing and preventing GBS complications, including decubitus ulcers, and infection prevention. Pharmacists should be well-versed in the adverse effects that may occur with the administration of medications including IVIG as well as pain and cardiac medications. Respiratory therapists should assist in preventing problems such as aspiration pneumonia. Physical and occupational therapists are crucial in assisting with muscle strengthening exercises, gait training, ROM exercises, use of assistive devices such as walkers, canes, and wheelchairs as well as activities to improve functional status and activities of daily living (eating, grooming, bathing, etc). Psychological support should be coordinated with social workers, psychologists, or psychiatrists. GBS patients should have care coordinated in the acute phase of the illness by a hospital-based clinical care manager. Patients should be assessed for rehabilitation and care coordination with an assessment of rehabilitation potential by members of the rehabilitation team including MDs, physiatrists, speech therapists, social workers, and rehabilitation care managers and nurses.  Following GBS recovery, patients often find it helpful to enlist in support groups available through the GBS foundation. Education of the GBS patient and family members should be coordinated by the nurse throughout the course of the illness in collaboration with health educators. 

• Health Teaching and Health Promotion

Health education is critical throughout the course of GBS. In the initial acute phase of GBS, the nurse should educate both the patient and family members about GBS including the symptoms of GBS, disease progression, medical management of the disease, current treatments for GBS including IVIG and plasmapheresis, risks associated with GBS, required monitoring of autonomic dysfunction including cardiac and respiratory monitoring, and morbidity and mortality associated with GBS. Patients admitted to the ICU and their family members will need to be educated about the equipment and monitoring routinely performed in this setting.  

Health education in the continuing or recovery phase of GBS should focus on rehabilitation efforts by the members of continuing care interprofessional teams. Team members educate both the patient and family members on rehabilitation expectations, and activities designed to return the patient to functional status. Education is focused on the preparation of the patient and family members to assume activities in acute rehabilitation, long-term care, outpatient or home settings with an emphasis on specific activities such as physical therapy, occupational therapy, speech therapy, and nutritional therapy. Education for family members caring for the recovering GBS patient should also include training in the use of adaptive devices such as canes, walkers, wheelchairs, bedside commodes, bathtub or shower benches, and safety measures such as ramps for easy home access. Health education during the recovery phase of GBS should also include information about health promotion and health maintenance including education about optimal nutrition, exercise, adequate sleep, and the importance of social interactions with friends, co-workers, and family members. Health education about routine health maintenance screenings such as mammograms and screening for colorectal cancer and skin cancer should be provided to both patients and family members. 

• Risk Management

Specific nursing liability risks in the acute and recovery phases of GBS include medication errors, inadequate monitoring of respiratory function resulting in respiratory arrest, inadequate assessment of risks such as cardiac dysrhythmias resulting in cardiac arrest, inadequate reporting of fluid  and electrolyte imbalance,  inadequate positioning and  failure to perform ROM exercises resulting in contractures and development of decubiti, inadequate monitoring of IVs, and lines for parenteral nutrition, inadequate positioning and monitoring of feeding tube resulting in aspiration pneumonia, inadequate assessment and referrals for psychological problems including fear and anxiety resulting in psychological problems such as depression and inadequate monitoring of ambulation resulting in falls and possible fractures. 

• Discharge Planning

Discharge planning for the GBS patient should begin at the point of hospital admission for the acute phase of GBS with an emphasis on providing continuing care for the patient in acute rehabilitation, long-term care, or home care settings. Discharge planning is coordinated by members of the interprofessional care team and specific discharge plans determined for each individual patient. The focus of discharge planning should be on how best to return the patient to complete recovery. As the GBS patient begins the recovery process from the acute phase of GBS, plans should focus on transitioning the patient from the ICU. This may require plans to wean the patient from mechanical ventilation, the introduction of food following use and removal of IVs, parenteral nutrition or feeding tube, the introduction of sitting and standing activities, and introduction of ambulation. Discharge planning should also include specific recommendations from individual team members. For example, the physical therapist should recommend specific plans to promote muscle strength in extremities and assistance in ambulation. The occupational therapist should recommend specific plans to promote activities of daily living including feeding, bathing, and dressing. The nurse should plan to provide care coordination and health education for patients and family members to ensure that the patient makes as smooth a transition from acute illness to recovery as possible.  

• Evidence-Based Issues

Evidence-based issues are related to:

1. limitations of evidence to identify and describe possible causal relationships of GBS to infections and immunizations   [55]

2. lack of definitive evidence in support of either IVIG or plasmapheresis as effective treatments for GBS  [56] [57] [58] [59]

• Pearls and Other issues

The nurse serves an important and sometimes overlooked role in the management of the patient with GBS. It is also important to note the relevance of an interprofessional team in care delivery to manage the complex issues connected to GBS.

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Guillain–Barre syndrome of acute motor axonal neuropathy (AMAN) type associated with herpes zoster: a case report

• Leonard Wanninayake 1 ,
• Dilani Rajapaksha 2 ,
• Narmada Nair 2 ,
• Kamal Gunarathne 3 &
• Udaya Ranawaka 4  

BMC Neurology volume  24 , Article number:  109 ( 2024 ) Cite this article

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Guillain Barre syndrome (GBS) following Varicella zoster is a rare presentation and has only been reported in a few cases around the world. Of the reported cases, the type of GBS is not specified in the majority, and where specified is of the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) type. We report a case of acute motor axonal neuropathy (AMAN) type GBS following herpes zoster in a 27-year-old male who presented with bilateral lower limb weakness and left sided lower motor neuron type facial nerve palsy a week after herpes zoster infection.

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Introduction

Guillain–Barre syndrome (GBS) is a relatively rare disorder with an incidence of 1–2 per 100,000 cases [ 1 ]. It is an acute peripheral neuropathy with several subtypes described based on clinical and electrophysiological features: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN), acute sensory neuropathy, acute pandysautonomia and overlap syndrome [ 2 ]. The prevalence of different types of GBS varies with geographic location [ 2 ].

Several infectious triggers have been implicated in the pathogenesis of GBS. Of them, the most common is Campylobacter jejuni infection which is commonly associated with AMAN type GBS [ 3 ]. Several other infectious agents such as Epstein Barr virus, Mycoplasma pneumoniae , Cytomegalovirus and HIV have been implicated as common aetiologies. GBS can rarely manifest following some vaccines such as measles, rabies, influenza, measles and MMR [ 2 ]. More recently, GBS has been reported following SARS-CoV-2 infection and COVID-19 vaccination [ 4 , 5 ]

Acute varicella infection (chicken pox) is a rare trigger for GBS [ 3 ], and GBS following varicella infection is usually of the AIDP type [ 6 , 7 , 8 , 9 ]. A recent review identified 88% of the GBS cases following varicella infections to be of the AIDP type, and 13% axonal type [ 6 , 7 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ]. Herpes zoster is a clinical syndrome due to reactivation of dormant varicella virus in sensory ganglia several years after initial varicella infection [ 10 ]. GBS following herpes zoster is a rare association described only in a few case reports [ 6 , 7 , 8 , 10 , 29 , 30 , 31 , 32 , 33 , 34 ]; where reported, it has always been of the AIDP variety [ 6 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ]. We were unable to identify any reports of zoster-associated AMAN type GBS on a literature survey of several electronic databases although a few cases of AMAN type GBS after chicken pox have been reported. We report a case of AMAN type GBS associated with herpes zoster.

Case report

A 27-year-old previously healthy man initially presented with a painful vesicular skin rash over the maxillary and mandibular distributions of the right trigeminal nerve (as shown in Fig.  1 ), which was clinically diagnosed as herpes zoster and treated at the local hospital outpatient clinic with oral acyclovir. Two days following the onset of the rash, he developed progressive bilateral lower limb weakness with predominant difficulty in standing up from a seated position. Six days later, he developed progressive bilateral upper limb weakness, difficulty with left eyelid closure and deviation of the mouth to the right side. There was no associated incoordination, or difficulty in speech or swallowing. He was admitted to a Sri Lankan tertiary care hospital on the 7th day of the illness. He was an unmarried driver, who was independent in his daily activities prior to the onset of the current illness. There was no history of smoking, alcohol use or substance abuse.

Herpes zoster rash over the right face

On admission, there was no fever, pallor, jaundice or lymphadenopathy. No evidence of muscle wasting or fasciculations was noted. Lower limb neurological examination revealed bilateral hypotonia and predominant proximal weakness, with MRC grade 3 power in hip flexors and extensors, and MRC grade 4- power in the flexors and extensors at the knee and ankle. Bilateral knee and ankle tendon reflexes were diminished (grade 1/4) with flexor plantar responses. Upper limb neurological examination showed normal tone bilaterally with MRC grade 4 + power in all muscle groups at shoulder, elbow and wrist, and normal biceps and triceps tendon reflexes. Cranial nerve examination revealed a left sided lower motor neuron type facial nerve palsy. No other cranial nerve abnormalities or cerebellar signs were noted. Sensory examination of the face, lower limbs and upper limbs was normal for pain, temperature, touch and proprioception.

Routine investigations including full blood count, electrolytes, creatinine, ESR, CRP, liver function tests, TSH and fasting blood sugar were normal. Retroviral screening was negative. MRI scan of the lumbosacral spine was normal. Nerve conduction studies (NCS) and EMG revealed AMAN type GBS (Table  1 ). CSF analysis showed elevated protein of 78 mg/dL, with 12 lymphocytes/mm3 and no neutrophils. CSF glucose was 76.5 mg/dl with a simultaneous blood glucose of 100 mg/dl. CSF testing for ADA, TB Gene expert and TB culture were negative. Serology for varicella zoster IgG antibodies was positive after 2 weeks from presentation, whereas varicella IgM antibodies were equivocal.

Given the close temporal relationship to herpes zoster infection, a diagnosis of GBS secondary to herpes zoster was made. He was treated with intravenous immunoglobulin [IVIg] 2 g/kg divided over 5 days duration and regular physiotherapy. Limb and facial weakness gradually improved after one week of hospital stay and he was discharged with plans for outpatient rehabilitation. At the time of discharge, he had MRC grade 4 + power in all four limbs. On three months review, he had normal limb power in all muscle groups (MRC 5) and normal facial muscle strength.

Herpes zoster and varicella zoster manifests with several sensory and motor manifestations. Transverse myelitis, varicella associated segmental motor weakness, Ramsey hunt syndrome, GBS are some of many motor manifestations of herpes zoster [ 37 ]. We report a case of GBS following herpes zoster, which adds to the limited number of cases in published literature. The neurophysiological subtype of GBS has not been reported in most published cases of zoster-related GBS. Where specified, it had been of the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) type [ 6 , 7 , 8 , 9 ]. Our patient had GBS of the acute motor axonal neuropathy (AMAN) type. To the best of our knowledge, this is the first case of AMAN type GBS confirmed with electrodiagnosis, associated with herpes zoster.

Herpes zoster is known to be associated with several motor and sensory neurological manifestations such as post herpetic neuralgia, meningoencephalitis, myelitis, poly-cranial neuritis, motor dysfunction and GBS. The pathophysiology of zoster-related GBS is not very well understood. The postulated hypotheses are molecular mimicry or the deranged immune system in the host, particularly of the lymphocyte subtypes. Although molecular mimicry with C. jejuni has been demonstrated, molecular mimicry with varicella zoster and peripheral nerves has not been confirmed [ 38 , 39 ].

In the majority of reported cases, the diagnosis had been based on clinical grounds with the chronological relationship between the rash and neurological symptoms [ 33 , 34 ]. There had been a few case reports with positive varicella serology in CSF and serum but with negative varicella PCR [ 22 , 29 ]. Some reports have considered reduced CD 8 lymphocyte response as an evidence of varicella zoster infection [ 10 ]. Our patient had positive IgG varicella serology but equivocal IgM results. This is likely to be the result of delayed testing for serology as the hospital laboratory was being primarily utilized for COVID 19 testing during this time.

The delay to the onset of GBS symptoms following the zoster rash has varied from 3 to 42 days in previous cases [ 6 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ]. Our patient developed neurological manifestations 2 days after the rash. A majority of the reported cases of zoster related GBS (71%) had cranial nerve abnormalities, with the facial nerve involvement being the most common [ 6 , 22 , 33 ]. Our patient had lower motor neurone type facial nerve palsy, but no other cranial nerve abnormalities were noted. Some of the patients with zoster-related GBS had developed complications such as respiratory failure, and some case fatalities have been reported [ 6 ]. Mechanical ventilation was required in a few cases [ 6 , 36 ]. However, our patient did not require intensive care or respiratory support and made a good recovery with treatment.

We report a case of AMAN type GBS following herpes zoster. We believe our report adds to the growing literature on the diverse neurological complications following herpes zoster. Although rare, herpes zoster should be considered as an important underlying aetiological cause of GBS.

Availability of data and materials

All data and the materials of the patient are available with the corresponding author.

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UR conceptualize the case report. LW and UR prepared the manuscript. DR, NN and KG contributed in the management of the patient and in editing the manuscript. All authors agreed on the final manuscript..

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Wanninayake, L., Rajapaksha, D., Nair, N. et al. Guillain–Barre syndrome of acute motor axonal neuropathy (AMAN) type associated with herpes zoster: a case report. BMC Neurol 24 , 109 (2024). https://doi.org/10.1186/s12883-024-03607-1

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Le Syndrome Guillain-Barré

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Le Syndrome Guillain-Barré. Auteurs: Adina Honoria Budea Tabita-Ligia Dume médecins résidentes épidémiologistes. La définition.

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Le Syndrome Guillain-Barré Auteurs: Adina Honoria Budea Tabita-Ligia Dume médecins résidentes épidémiologistes

La définition Le syndrome de Guillain-Barré (SGB) ousyndrome de Guillain-Barré-Strohlestunemaladie auto-immuneinflammatoire du systèmenerveuxpériphérique. C'estunemaladieacquise. On l'appelleégalementpolynévropathieaiguëinflammatoiredémyélinisante, polyradiculonévriteaiguëidiopathique, polynévriteaiguëidiopathiqueouparalysieascendante de Landry. Il se caractérise principalement par une faiblesse, par l’apparition d’une paralysie et s'accompagne souvent de sensations anormales.

L’histoire de la maladie En 1859, le médecin français Jean Ladry a décrit pour la première fois ce syndrome. En 1916, George Guillain, Jean Alexandre Barré et André Strohl ont diagnostiqué deux soldats d’une paralysie généralisée transitoire qui avaient dans la liquide céphalo-rachidien la concentration augmentée des protéines, avec un tissu cellulaire normal. Cette découverte a été la clef du diagnostic de ce syndrome. Jean Landry Jean-Alexandre Barré George Charles Guillain André Strohl

L’épidemiologie Le SGB représente le tableau clinique le plus fréquente caractérisé par l’apparition des paralysies avec une évolution rapide (jours ou semaines); la moitié des cas surviennent quelques jours, voire quelques semaines après une infection virale. l’incidence de la maladie est de 1 - 2 cas aux 100.000 d’habitants pour une année. L’incidence est plus diminuée pendant la grossesse, mais elle augmente rapidement dans les premières deux semaines après la naissance. La maladie peut apparaître aux personnes de tous âges (l’enfance y compris), ayant peut-être deux pointes d’incidence: pendant l’adolescence et comme jeune adulte (15-35 ans) et aux personnes âgées (55-75ans) aussi. Il n’y a pas une prédisposition raciale ou de genre, les femmes et les hommes ayant la même chance de se rendre malade par SGB.

L’étiologie L'origine du SGB n'est pas connue. Ce syndrome reste toujours exceptionnel vis-à-vis des différents facteurs causals suspectés, faisant émettre l'hypothèse d'une susceptibilité particulière de certains individus. La possibilité d'une prédisposition génétique unique est assez peu probable, car le SGB ne se manifeste pas au sein d'une même famille. Un certain nombre de manifestations semblent déclencher la maladie. La moitié des cas surviennent après quelques jours, ils apparaissent quelques semaines après une infection virale..

La pathogénie Les nerfs du patient atteint du SGB semble être attaqués par son propre système immunitaire. • La sensibilisation des lymphocytes périphériques à un composant protéique de la myéline (après une agression la plus fréquente virale), suivie de la destruction de la myéline par la migration des lymphocytes sensibilisés au niveau du système nerveux périphérique. • L’agent pathogène peut léser les cellules Schwann, avec la délivrance secondaire des antigènes qui par un mécanisme immun vont vers la démyélinisation segmentaire. La source: www. mayoclinic.com

Des causes hypothétiques: • des infections bactériennes: - Campylobacter jejuni - (1 à 2000 infections), à cause du mimétisme moléculaire apparententre les antigenes de C. jejuni et les ganglions neurolonales; - Mycoplasma  pneumoniae;  - Borrelia burgdorferi. • des infections virales: grippal, Epstein-Barr, enterovirus, cytomégalovirus, les virus hépatitiques primaires etc. La source:www.cdc.gov

les vaccins: - contre la grippe (AH1N1 y compris) - contre le méningocoque - contre la rage - contre la fièvre jaune • rarement - porphyrie • exceptionnellement - après des traumatismes - abus des médicaments - à ceux qui ont des maladies auto-immunes (2,5% de cas)

Le tableau clinique On décrit plusieurs types du Syndrome Guillain-Barré: • la polyneuropathie démyélinisante inflammatoire aiguë – (PDIA) (avec des cellules Schwann) • la neurophathie axonale motrice aiguë(AMAN) (axoplasma du nerf périphérique) • début rapide progressif • déficit moteur ou sensitif-moteur ascendant • affectations des nerfs crâniens • insuffisance respiratoire • la neurophathie axonale sensitive motrice aiguë (AMSAN) (axoplasma du nerf périphérique) - maigreur musculaire distaux - sans l’affectation des nerfs crâniens

le syndrome Miller-Fischer - 5% des cas (on affecte l’oeil) -la diplopie  - l’ataxie  - l’hipporéflexion  - l’affection de la musculature extraoculaire • la neurophathie sensorielle aiguë • la neurophathie autonome aiguë– fréquent encéphalophathie et des arythmies cardiaques

Le diagnostic A cause de la rareté, dans le cas du Syndrome Guillain-Barré est presque difficile de poser un diagnostic aux étapes initiales. On met le diagnostic sur: • - l’anamnèse • - des investigations cliniques- de maigreur musculaire avec une évolution progressive qui affecte les mains, les membres inférieurs bilatéraux, - l’absence des réflexes • - des investigations paracliniques: - l’analyse de la liquide céphalo-rachidien: l’augmentation du niveau des protéines, sans l’augmentation des leucocytes; (les protéines de la liquide céphalo-rachidien augmentent après une semaine ou plus encore dès le début de la maladie); La source http://en.wikipedia.org/wiki/Guillain Barre_syndrome

l’électrocardiogramme montre des disfonctionnalités au niveau cardiaque; • l’électromyogramme teste l’activité électrique des muscles (elle indique la déficience de réponse des nerfs aux stimulus); - le test de la vitesse des impulsions nerveusemontre le ralentissement ou le blocage de l’activité électrique au long des nerfs. La source: www. mayoclinic.com

Le diagnostic différentiel • a. Affections médullaires: la myélite transverse, des processus médullaires de remplacement d’espace (des tumeurs, des abcès, des malformations vasculaires) • b. Botulisme • c. Maladies des cellules dans les cornillons antérieurs médullaires (la poliomyélite antérieure aiguë ou la poliomyélite à la vaccination et autres infections avec des virus neurotropes) • d. La myosite ou la dermatomyosite • e. La paralysie diskaliemica  • f. Autres causes: des maladies infectieuses qui associent des neuropathies aiguës périphériques ( la diphtérie); des neuropathies aiguës toxiques (des métaux lourds,la piqûre des insectes – la maladie Lyme, la morsure des serpents); quelques médicaments; des neuropathies aiguës dans le cadre des maladies métaboliques (la porphyrie).

Le traitement – on ne connaît pas aucun traitement étiologique Le traitement peut être: • a. Symptomatique: la plasmaphérèse, la thérapie avec des immunoglobulines dans une concentration aiguë • b. des complications: des anticoagulants pour la prévention de trombe-embolie; l’assistance respiratoire ou l’intubation; des anti-inflammatoires et des stupéfiants pour le traitement de la douleur; le sondage gastrique ou la surveillance de la position du corps au temps qu’on nourrit, si tant que les muscles de la mâchoire sont affaiblis • c. récupérateur: la mobilisation du malade pour maintenir en bon état le tonus musculaire et la prévention des escarres; physiothérapie; psychothérapie

Pronostic • Le quart des patients requiert une ventilation assistée en raison de la faiblesse des muscles respiratoires. • La mortalité est d'un peu moins de 10%. Elle est essentiellement secondaire à des troubles du rythme cardiaque, une infection ou à une embolie pulmonaire. Pour les formes graves (troubles de la déglutition et paralysie des muscles respiratoires nécessitant une ventilation mécanique), elle atteint 20%. • Il existe un risque de séquelles à long terme : de 5 à 15 % des patients demeureront invalides à plus ou moins long terme. 35 % environ se plaignent d'anomalies légères à long terme comme des étourdissements.

La prophylaxie et le contrôle • prévenir l’exposition aux infections bactériennes et virales; • la surveillance / le suivi des personnes vaccinées; • éviter tout traumatisme, l’abus de médicaments. Il n‘y pas à l'heure actuelle des méthodes éprouvées pour la prévention du SGB. Toutefois, la meilleure façon de rester en santé est d'inclure dans ses habitudes quotidiennes la pratique régulière d'activités physiques et de suivre un régime alimentaire équilibré.

Références • Sîrbu Carmen – Adela, L’abordage moderne desneurophathiepériphériques (Abordarea modernă a neuropatiilor periferice), Stetoscop, Nr. 19, 2003, pag.2-3. • Mihancea Petru – Boli neurologice eredodegenerative, Editura Universităţii din Oradea, 2005pag.43-45. • Guirado A, De Juan Frigola J. Boletín de Neurología. Síndrome de Guillain-Barré. Bol Pediatr.Es. 2006 2010; • http://en.wikipedia.org/wiki/Guillain Barre_syndrome • http://www.mayoclinic.com/health/guillain-barre-syndrome • http://www.cdc.gov

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