Nursing Diagnosis for Guillain-Barré Syndrome (GBS): A Comprehensive Guide for Nurses

Introduction

Guillain-Barré Syndrome (GBS) stands as the most prevalent cause of acute, flaccid, neuromuscular paralysis in the United States, demanding critical attention from healthcare professionals. Since its initial discovery over a century ago, significant strides have been made in understanding GBS. These advancements encompass the exploration of its immune-mediated pathophysiology, the identification of diverse clinical presentations, progress in diagnostic methods, the development of prognostic models, and the execution of randomized treatment trials aimed at enhancing patient outcomes. Given the potential for significant morbidity if left unaddressed, a thorough understanding of this rare yet critical condition is essential for all clinicians and nurses. This article aims to provide a comprehensive overview of GBS, with a specific focus on relevant nursing diagnoses and patient care strategies.

Nursing Diagnoses for GBS Patients

Effective nursing care for patients with Guillain-Barré Syndrome hinges on accurate and timely nursing diagnoses. These diagnoses guide the nursing care plan and ensure holistic patient management. Key nursing diagnoses pertinent to GBS patients include:

• Impaired Respiratory Function related to rapid and progressive muscle weakness and the risk of respiratory failure.
• Impaired Physical Mobility related to paralysis.
• Imbalanced Nutrition: Less Than Body Requirements related to swallowing difficulties.
• Impaired Verbal Communication related to cranial nerve dysfunction.
• Acute Pain related to neurological changes and immobility.
• Anxiety and Fear related to the sudden onset of paralysis and potential life-threatening nature of the condition.

Etiology of Guillain-Barré Syndrome

Guillain-Barré syndrome and its variants are recognized as post-infectious, immune-mediated neuropathies. Molecular mimicry is believed to play a crucial role, as supported by animal model studies. Campylobacter jejuni gastrointestinal infections, for instance, contain a lipooligosaccharide in their outer membrane that bears resemblance to gangliosides, which are integral components of peripheral nerves. Consequently, the immune response initiated to combat the infection can inadvertently trigger a cross-reaction against the host’s nerves.

Numerous infections have been associated with GBS, predominantly gastrointestinal or respiratory illnesses. Notably, up to 70% of GBS patients report experiencing an antecedent illness within the 1 to 6 weeks preceding the onset of GBS symptoms. The Zika virus outbreak also saw a surge in reported GBS cases. Furthermore, case reports have linked various other factors to GBS etiology, including certain medications and surgical procedures.

In 1976, influenza vaccination against the influenza A/H1N1 antigen was linked to a notable increase in GBS incidence. However, subsequent surveillance of flu vaccinations in later years has indicated a much lower risk, with approximately one additional GBS case per 1 million vaccines administered. It’s also estimated that the likelihood of developing GBS after a flu infection is up to seven times greater than after flu vaccination.

Risk Factors for Guillain-Barré Syndrome

While Guillain-Barré syndrome is considered a rare condition, with an incidence rate of 0.4 to 2 cases per 100,000 individuals, its impact on healthcare systems is substantial. The economic burden of medical care for a single GBS patient can reach up to $318,966, and the overall annual cost of treating GBS patients is estimated at $1.7 billion. Males are slightly more prone to GBS than females. Globally, it is estimated that around 100,000 individuals contract GBS each year.

Assessment and Clinical Manifestations of GBS

Patients with Guillain-Barré syndrome typically present with a rapidly progressing course of symptoms, characterized by ascending weakness and sensory symptoms that are not length-dependent. The condition usually reaches its most severe point (nadir) within four weeks. Symmetrical weakness is a hallmark feature of GBS. Typically, GBS follows a monophasic course, and a relapsing or remitting pattern at onset is considered atypical. Recurrent GBS is also uncommon, occurring in less than 5% of cases. If symptom progression extends beyond eight weeks, alternative diagnoses should be considered.

Onset of GBS often occurs within 1 to 6 weeks following an antecedent illness in up to 70% of patients. Other preceding events linked to GBS include vaccinations (particularly the 1976 swine flu vaccine strain), surgery, trauma, and other infections.

Classic GBS presentation involves proximal and distal flaccid weakness, which can be profound in hospitalized patients. Significant neck flexion weakness may be present, indicating a potential need for intubation. Areflexia or hyporeflexia is typically observed, although rare cases without hypo/areflexia have been reported, mainly in the Acute Motor Axonal Neuropathy (AMAN) variant of GBS.

Besides weakness and areflexia, patients experience sensory symptoms that are non-length-dependent. Unlike common chronic neuropathies like diabetic neuropathy, dysesthesias may begin in the hands before the feet. Facial diplegia can develop due to involvement of both facial cranial nerves, and dysphagia may arise from the involvement of the glossopharyngeal, vagus, and hypoglossal cranial nerves. Autonomic nerve involvement can lead to significant complications, necessitating monitoring in an intermediate or intensive care unit for cardiac arrhythmias or blood pressure instability. Dysautonomia is a primary contributor to GBS-related morbidity and mortality. Furthermore, involvement of lower cranial nerves (glossopharyngeal, vagus, and hypoglossal) or respiratory muscle nerves may necessitate mechanical ventilation. Respiratory failure occurs in up to 30% of patients, often resulting in prolonged hospitalization and recovery.

Variants of GBS beyond the classic presentation include AMAN, characterized by pure motor involvement and more common in Asian populations. Rarely, AMAN patients may have normal reflexes. The pharyngeal-cervical-brachial variant primarily affects pharyngeal, neck, and upper extremity muscles. Some variants, like Bickerstaff Encephalitis, involve the central nervous system. A paraparetic variant also exists. Miller Fisher syndrome, perhaps the most recognized variant, is classically defined by a triad of ophthalmoplegia, areflexia, and ataxia, though other cranial nerves may also be involved.

Evaluation and Diagnostic Procedures for GBS

Diagnosis of Guillain-Barré syndrome is primarily clinical, often achievable at the bedside. However, ancillary testing can be valuable for atypical cases or less common subtypes.

Electromyography and nerve conduction studies are useful in differentiating GBS from mimicking conditions. Nerve conduction studies (NCS) help distinguish between demyelinating and axonal neuropathy types. Needle electromyography can assess the chronicity of symptoms. These studies can also aid in evaluating other differential diagnoses like neuromuscular junction disorders or diabetic neuropathy. Ideally, electrodiagnostic studies should be conducted 10 to 14 days post-symptom onset to allow for Wallerian degeneration of nerve fibers. However, studies show that early, nonspecific findings can assist in diagnosing GBS as early as 3 to 7 days after symptom onset.

Early electrodiagnostic findings in GBS commonly include absent or prolonged H-reflexes and/or F-wave latencies. The sural sparing pattern, indicating an intact sural sensory response with abnormal upper extremity sensory responses, is considered specific to GBS compared to other polyneuropathies. Findings vary based on the GBS variant. Acute inflammatory demyelinating polyneuropathy (AIDP) is likely to show partial motor conduction block, temporal dispersion, slow conduction velocities, prolonged/absent F-wave latencies, and prolonged distal latencies. AMAN typically presents with low compound muscle action potential amplitudes or inexcitable motor nerves, although partial or complete conduction block can occur due to “reversible conduction failure.” Complement deposition at nodes of Ranvier and paranodal regions explains this phenomenon, where nerves can either undergo Wallerian degeneration or recover, termed conduction failure. This explains the rapid recovery seen in some severely weak AMAN patients. Sensory nerves are typically spared clinically and electrodiagnostically in AMAN. Acute motor and sensory axonal neuropathy (AMSAN) shows low amplitude motor and sensory potentials. Miller Fisher syndrome often presents with reduced or absent sensory nerve action potentials.

Cerebrospinal fluid (CSF) analysis classically reveals albuminocytologic dissociation, characterized by normal white blood cell count and elevated CSF protein. However, this pattern is present in only 80% of patients at 2 weeks after symptom onset. Therefore, its absence does not rule out GBS. Elevated white blood cell count should prompt consideration of GBS mimics like HIV seroconversion.

Ganglioside antibodies, including anti-GM1, anti-GD1A, anti-GT1A, and anti-GQ1B, are associated with GBS. Sensitivity ranges from up to 60% for anti-GM1 antibodies in AMAN to over 90% for anti-GQ1B antibodies in Miller Fisher syndrome. However, these tests take time to process and may not be immediately helpful for admission decisions.

Spinal magnetic resonance imaging (MRI) may show nerve root enhancement, indicating blood-nerve barrier breakdown due to GBS inflammation. MRI is most valuable for excluding other causes of quadriparesis or facial diplegia, such as transverse myelitis or intracranial disease.

Negative inspiratory force (NIF) measurement is crucial in suspected GBS patients, with serial NIFs monitored in those at high respiratory risk. Patients unable to achieve a NIF of -20 to -30 cm H2O are at very high risk of respiratory compromise.

Medical Management of Guillain-Barré Syndrome

Currently, two standard treatments for Guillain-Barré syndrome, supported by randomized controlled trials, are intravenous immunoglobulin (IVIG) and plasma exchange. IVIG is believed to modulate the immune system, though the exact mechanism is not fully understood. IVIG is administered at 2 grams/kilogram over 5 days. Plasma exchange is thought to remove pathogenic antibodies, humoral mediators, and complement proteins implicated in GBS pathogenesis, but its precise mechanism also remains unconfirmed. Plasma exchange typically involves a volume exchange over five sessions. IVIG and plasma exchange have demonstrated comparable efficacy. Treatment is most effective when initiated within 4 weeks of symptom onset, with potentially greater benefit within the first two weeks. Notably, corticosteroids, whether oral prednisone or intravenous methylprednisolone, have not shown benefit over placebo or in combination with IVIG or plasma exchange. Overall, treatment aims to shorten GBS recovery time. Studies indicate that treated patients achieved independent ambulation approximately 32 days faster than untreated patients.

While most GBS patients recover well, with up to 85% regaining independent ambulation, a significant proportion (20%) experience residual morbidity. Further research into combined therapies like plasma exchange followed by IVIG, or IVIG concurrently with steroids, has not shown significant improvement. Ongoing trials are investigating double courses of IVIG and complement inhibitors for refractory GBS.

Nursing Management and Interventions for GBS

Nursing management is critical in addressing the nursing diagnoses identified for GBS patients. Key interventions include:

1. Impaired Respiratory Function:

   • Closely monitor vital signs for changes in respiratory rate, breathing quality, and decreasing vital capacity.
   • Assess for signs of ascending paralysis and impending respiratory failure, such as shallow, irregular breathing, use of accessory muscles, and difficulty clearing secretions.
   • For intubated patients, collaborate with physicians and respiratory therapists for comprehensive mechanical ventilation management.
   • Continuously assess and monitor for respiratory infections, including pneumonia.

2. Impaired Physical Mobility:

Alt Text: Nurse assisting Guillain-Barre Syndrome patient with leg exercises during physical therapy for mobility improvement.

-   Address immobility-related issues arising from muscle weakness and paralysis.
-   Support and position paralyzed extremities in functional alignment.
-   Perform passive range of motion (ROM) exercises at least twice daily.
-   Ensure position changes every two hours and utilize pressure-relieving support surfaces (foam, air, water, or gel beds).
-   Conduct regular skin assessments for breakdown.
-   Monitor bowel function, including bowel sounds and frequency of movements.
-   Apply anti-embolism stockings and compression boots to prevent deep vein thrombosis (DVT) and pulmonary embolism (PE).
-   Maintain adequate hydration to minimize pressure ulcer risks.

3. Imbalanced Nutrition:

   • Collaborate to maintain optimal nutrition.
   • Assess patients with swallowing difficulties for aspiration risk.
   • Manage gastrostomy tube feedings, intravenous (IV) fluid administration, or parenteral nutrition as needed to ensure adequate nutrient intake.

4. Impaired Verbal Communication:

   • Implement communication strategies for patients unable to communicate verbally due to paralysis.
   • Utilize methods like eye blinks, picture boards, or computer-based communication aids.
   • Involve family members and friends in communication strategies.
   • Refer to speech therapy for addressing communication impairments.

5. Acute Pain:

   • Thoroughly assess pain related to muscle changes from GBS.
   • Employ pain assessment tools like picture scales or pain management scales for non-verbal patients.
   • Observe non-verbal pain indicators such as restlessness or facial grimacing.
   • Provide effective pain management, especially during acute GBS stages.

6. Anxiety and Fear:

   • Assess and manage potential psychological distress.
   • Recognize anxiety, fear, and helplessness stemming from sudden loss of control during a life-threatening illness.
   • Address patient and family uncertainty, helplessness, and isolation.
   • Acknowledge the impact of GBS on family dynamics, particularly if the patient is a primary caregiver or breadwinner.
   • Provide education about GBS, treatments, and equipment to patients and families to reduce fear and enhance coping.
   • Offer patient education materials, support group referrals, and social worker or psychologist consultations to improve coping mechanisms.

Interprofessional Team Collaboration

Effective GBS management necessitates an interprofessional team approach to collaborative patient care. Nurses play a pivotal role in monitoring patients for complications. Changes in respiratory function, indicated by decreased vital capacity, require immediate physician notification. Complications such as cardiac dysrhythmias, hypo- or hypertension, DVT, PE, urinary retention, or swallowing difficulties also warrant physician consultation. Pharmacist consultation is essential for managing issues related to IVIG or corticosteroid use. Respiratory therapists collaborate in managing mechanical ventilation. Expressions of fear, anxiety, or hopelessness from patients or families should prompt referrals to social workers, psychologists, or other mental health professionals within the team.

Expected Patient Outcomes

Desired outcomes for GBS patients include:

1. Restoration of normal respiratory function, demonstrated by normal respiratory rate, vital capacity, effective airway clearance, and oxygen saturation levels.
2. Improved mobility without contractures or muscle weakness, regaining the ability to ambulate and functional use of extremities.
3. Restoration of swallowing ability and maintenance of adequate nutrition and hydration through oral diet.
4. Recovery of verbal communication skills.
5. Pain resolution or effective pain management via medication or non-pharmacological strategies like exercise, relaxation, and stress management.
6. Reduction or elimination of psychological distress, including fear, anxiety, uncertainty, helplessness, loss of control, and loneliness.
7. Prevention and resolution of complications such as pressure ulcers, DVT, and bowel or bladder dysfunction.

Essential Monitoring Parameters

Nurses must vigilantly monitor GBS patients for:

1. Respiratory impairment: Assess vital signs, measure vital capacity, and observe for accessory muscle use and secretion clearance difficulties.
2. Cardiac dysrhythmias related to autonomic dysfunction: Monitor blood pressure for hypo- or hypertension and use cardiac monitoring for heart rate and arrhythmia detection.
3. Extremity weakness and paralysis: Check for absent lower extremity tendon reflexes and assess the patient’s ability to ambulate and use extremities.
4. Skin changes due to immobility: Monitor for erythema and early signs of skin breakdown or pressure ulcers.
5. Fluid and electrolyte imbalances: Monitor IV fluids, parenteral nutrition, and intake and output.
6. Bowel and bladder dysfunction: Monitor urinary output (via catheter if necessary) and bowel movement frequency.
7. Pain: Conduct frequent pain assessments using numeric or picture scales.
8. Psychological distress: Monitor for symptoms of fear, anxiety, or depression.

Coordination of Interdisciplinary Care

Care for GBS patients requires seamless collaboration among all healthcare team members. Nurses are central to care coordination in the acute phase, focusing on complication prevention, including pressure ulcers and infections. Pharmacists are crucial for managing medication-related adverse effects. Respiratory therapists prevent aspiration pneumonia. Physical and occupational therapists are essential for rehabilitation, focusing on muscle strengthening, gait training, ROM exercises, assistive device training, and activities of daily living. Psychological support is coordinated with social workers and mental health professionals. Hospital-based clinical care managers facilitate acute phase care coordination. Rehabilitation potential is assessed by a rehabilitation team, including physicians, physiatrists, speech therapists, social workers, and rehabilitation nurses and care managers. Post-recovery, support groups through the GBS Foundation are beneficial. Patient and family education is coordinated by nurses throughout the illness, in collaboration with health educators.

Health Education and Health Promotion

Health education is paramount throughout the GBS journey. In the acute phase, nurses educate patients and families about GBS symptoms, disease progression, medical management (IVIG, plasmapheresis), risks, autonomic dysfunction monitoring, and potential morbidity and mortality. ICU patients and families need education about ICU equipment and monitoring.

In the recovery phase, education focuses on rehabilitation expectations and activities led by the interprofessional team. This includes physical, occupational, speech, and nutritional therapy. Family education includes training on adaptive devices (canes, walkers, wheelchairs, etc.) and home safety modifications. Health promotion education covers optimal nutrition, exercise, sleep, social interaction, and routine health screenings (mammograms, colorectal and skin cancer screening).

Risk Management in GBS Nursing Care

Nursing liability risks in GBS care include medication errors, inadequate respiratory monitoring leading to respiratory arrest, failure to detect cardiac dysrhythmias causing cardiac arrest, inadequate fluid and electrolyte imbalance management, improper positioning and ROM exercises resulting in contractures and pressure ulcers, inadequate IV and parenteral nutrition line management, feeding tube mismanagement leading to aspiration pneumonia, insufficient psychological assessment and referrals causing depression, and inadequate ambulation monitoring leading to falls.

Discharge Planning for GBS Patients

Discharge planning begins at hospital admission, focusing on transitioning patients to acute rehabilitation, long-term care, or home care. The interprofessional team tailors discharge plans to individual needs, aiming for optimal recovery. Transition from the ICU involves weaning from mechanical ventilation, re-introducing oral feeding, initiating sitting and standing, and ambulation. Discharge plans include specific recommendations from therapists, such as physical therapy for muscle strength and occupational therapy for ADLs. Nurses coordinate care and provide health education to ensure a smooth transition from acute illness to recovery.

Evidence-Based Considerations

Evidence-based issues in GBS include:

1. Limitations in evidence for definitively linking infections and immunizations to GBS causality.
2. Lack of conclusive evidence supporting the superiority of IVIG or plasmapheresis as GBS treatments.

Nursing Pearls for Interprofessional GBS Care

Nurses are vital, often underestimated, in GBS patient management. An interprofessional team approach is essential for addressing the complexities of GBS care.

Review Questions

(Review questions are omitted as per instructions)

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(References are included as in the original article)

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Disclosure: Thy Nguyen declares no relevant financial relationships with ineligible companies.

Disclosure: Roger Taylor declares no relevant financial relationships with ineligible companies.

Disclosure: Andrea Renwanz Boyle declares no relevant financial relationships with ineligible companies.