INTRODUCTION: (LESTI)
EXPLANATION:
• Guillain-Barré Syndrome (GBS) is described as an acute infectious neuronitis affecting cranial
and peripheral nerves.
• The immune system mistakenly attacks and destroys the myelin sheath, which insulates nerve
fibers.
• GBS often follows a mild upper respiratory infection or gastroenteritis.
• The recovery process can be lengthy, potentially taking years.
• The primary concern in GBS is respiratory difficulty, necessitating close monitoring of
respiratory status.
PATHOPHYSIOLOGY: (LESTI)
EXPLANATION:
The pathophysiology of GBS involves several key mechanisms:
1. Triggering Event:
- Infection or Other Trigger: GBS is often preceded by an infection, typically a respiratory or
gastrointestinal infection. Common pathogens associated with GBS include Campylobacter jejuni,
cytomegalovirus (CMV), Epstein-Barr virus (EBV), and Mycoplasma pneumoniae. Less commonly,
vaccinations or surgical procedures can act as triggers.
2. Immune Response:
- Molecular Mimicry: The immune system, activated by the preceding infection, mistakenly
targets the body's own peripheral nerves due to similarities between microbial antigens and nerve
cell components (molecular mimicry). This cross-reactivity leads to an autoimmune response.
- Antibody Production: The body produces antibodies against the pathogens, but these
antibodies also attack components of the nerve cells, particularly the myelin sheath and sometimes
the axon itself.
3. Inflammatory Response:
- Inflammation: The binding of these autoantibodies to nerve components activates the
complement system and recruits immune cells, such as macrophages and lymphocytes, to the site
of injury.
- Demyelination: Macrophages strip the myelin sheath from the nerve fibers. The myelin sheath
is essential for the rapid transmission of nerve impulses. Its loss disrupts the conduction of electrical
signals along the nerve.
- Axonal Damage: In some severe cases, the axons (nerve fibers) themselves may be
damaged. This is more common in specific subtypes of GBS, such as the acute motor axonal
neuropathy (AMAN) variant.
4. Nerve Conduction Impairment:
- Slowed Conduction: The loss of myelin slows down the nerve conduction velocity, leading to
the primary symptoms of GBS, such as muscle weakness and paralysis.
- Conduction Block: In some instances, the nerve impulse may be completely blocked,
exacerbating the severity of muscle weakness.
5. Clinical Manifestations:
- Ascending Paralysis: The characteristic symptom of GBS is progressive, symmetrical muscle
weakness that typically begins in the lower limbs and ascends to the upper limbs and face.
- Sensory Disturbances: Patients often experience sensory symptoms like tingling, numbness, or
pain.
- Autonomic Dysfunction: GBS can affect the autonomic nervous system, leading to fluctuations in
blood pressure, heart rate variability, and other autonomic symptoms.
- Respiratory Compromise: In severe cases, the muscles involved in breathing can be affected,
necessitating mechanical ventilation.
*In summary, GBS is an autoimmune disorder where the body's immune system attacks the
peripheral nerves, leading to demyelination and axonal damage. This results in impaired nerve
conduction, causing the clinical symptoms of muscle weakness, sensory disturbances, and
autonomic dysfunction. With timely treatment and supportive care, many patients can recover,
though the process may be prolonged and vary in completeness.
RISK FACTORS: (DIVINE)
EXPLANATION:
• AGING – As people age, their immune system undergoes changes, including a decline in
immune function and a tendency towards chronic low-level inflammation. These changes can
make older adults more susceptible to autoimmune conditions like GBS. Also, aging is often
associated with comorbid conditions such as diabetes or cardiovascular diseases, which might
complicate or trigger an immune response.
• DIARRHEA OR RESPIRATORY ILLNESSES - Diarrhea or respiratory illnesses often involve
infections by pathogens such as Campylobacter jejuni, cytomegalovirus (CMV), Epstein-Barr
virus (EBV), and Mycoplasma pneumoniae. These pathogens can trigger an autoimmune
response through molecular mimicry, where the immune system produces antibodies to fight
the infection, but these antibodies also attack the body's own nerve cells because of structural
similarities between the pathogen and nerve cell components.
• VIRAL INFECTIONS - Viral infections can directly stimulate the immune system to produce a
robust response, including the generation of antibodies and activation of immune cells. If these
immune components cross-react with nerve tissues, they can cause the demyelination
characteristic of GBS. After the viral infection resolves, the immune system may remain
activated and misdirected, continuing to attack the peripheral nerves. This is particularly noted
in infections by viruses like Zika, which have been associated with GBS outbreaks.
• VACCINES – Vaccines are designed to stimulate the immune system to recognize and combat
specific pathogens. In rare cases, this immune activation can lead to an autoimmune response
where the immune system mistakenly attacks the myelin sheath of peripheral nerves.
• MEN - There are known differences in immune system function and response between genders.
Men and women may have different susceptibilities to autoimmune diseases, and hormonal
differences might influence immune regulation. Epidemiological data have shown a slightly
higher incidence of GBS in men compared to women, though the exact reasons for this
difference are not fully understood.
• SURGERY - Surgery is a significant physical stressor and can lead to an altered immune
response. The stress of surgery might precipitate an autoimmune reaction in some individuals.
Post-surgical infections, including those acquired in healthcare settings, can trigger GBS through
mechanisms similar to those of other infections. Moreover, the inflammatory response
associated with surgery and the subsequent healing process might activate the immune system
in a way that predisposes some individuals to autoimmune reactions.
SIGNS AND SYMPTOMS: (KATRINA)
EXPLANATION:
1. Paresthesias: Patients with GBS often experience abnormal sensations such as tingling,
numbness, or burning in their extremities. This occurs due to damage to the peripheral nerves,
leading to altered sensory perceptions. The rationale behind this symptom is the disruption of
nerve function caused by the immune system's attack.
2. Pain and/or hypersensitivity: GBS can cause heightened sensitivity to touch or pressure,
leading to pain or discomfort even with light stimuli such as the weight of bed sheets or
clothing. This sensitivity arises from nerve damage, which can amplify sensory signals, causing
pain or discomfort. The immune system's attack on the nerves disrupts their normal functioning,
making them more sensitive to stimuli.
3. Gradual progressive weakness of the upper extremities: Weakness in the upper
extremities, such as arms and hands, typically starts subtly and gradually worsens over time.
This weakness occurs due to the immune system damaging the nerves responsible for muscle
movement, leading to impaired muscle function. As the disease progresses, muscle weakness
becomes more noticeable.
4. Weakness of the lower extremities: Similar to the weakness in the upper extremities,
weakness in the lower extremities (legs and feet) is a common symptom of GBS. It results from
damage to the nerves controlling leg muscles, leading to difficulty walking, standing, or
performing other motor activities.
5. Possible progression to respiratory failure: In severe cases of GBS, muscle weakness can
extend to the muscles involved in breathing, leading to respiratory failure. This occurs due to
paralysis of the respiratory muscles, which can compromise the ability to breathe adequately.
It's a life-threatening complication of GBS and requires immediate medical intervention, often
including mechanical ventilation.
6. Cardiac dysrhythmias: GBS can affect the autonomic nervous system, which regulates heart
function. As a result, patients may experience irregular heartbeats or cardiac dysrhythmias. This
occurs due to the disruption of nerve signals controlling the heart's rhythm and may manifest as
palpitations, dizziness, or fainting.
7. CSF that reveals an elevated protein level: Cerebrospinal fluid (CSF) analysis in GBS
typically shows elevated protein levels without an increase in white blood cells. This finding,
known as albuminocytologic dissociation, is a hallmark of GBS and reflects the immune-
mediated damage to the peripheral nerves. The rationale behind this is the leakage of proteins
from damaged nerves into the CSF.
8. Abnormal electroencephalogram (EEG): Although GBS primarily affects the peripheral
nervous system, some patients may exhibit abnormal brainwave patterns on EEG. This
abnormality can result from secondary effects of GBS, such as metabolic disturbances or
seizures. However, EEG findings are not a primary diagnostic criterion for GBS but may be
performed to rule out other neurological conditions or complications.
MEDICAL MANAGEMENT: (KATRINA)
EXPLANATION:
1. Mechanical Ventilation: In severe cases of GBS, muscle weakness can progress to the point
where the patient is unable to breathe adequately on their own, leading to respiratory failure.
Mechanical ventilation is often necessary to support breathing until the patient's respiratory
muscles recover. By providing mechanical assistance to the lungs, ventilation ensures sufficient
oxygenation and removal of carbon dioxide from the body, preventing complications associated
with respiratory insufficiency or failure.
2. Plasmapheresis: Plasmapheresis, also known as plasma exchange, is a treatment method
aimed at removing harmful antibodies from the bloodstream. In GBS, the immune system
produces antibodies that attack the peripheral nerves, contributing to nerve damage and
symptoms of the disease. Plasmapheresis involves removing a portion of the patient's blood,
separating the plasma (which contains antibodies) from the blood cells, and then replacing the
plasma with a substitute such as albumin or saline. This process helps reduce the levels of
harmful antibodies in the bloodstream, potentially slowing down the progression of nerve
damage and promoting faster recovery.
3. Continuous ECG Monitoring: Guillain-Barré Syndrome can affect the autonomic nervous
system, leading to cardiac dysrhythmias or irregular heartbeats. Continuous electrocardiogram
(ECG) monitoring is essential for detecting and managing any cardiac complications that may
arise during the course of the disease. By continuously monitoring the heart's electrical activity,
healthcare providers can promptly identify and treat cardiac dysrhythmias, minimizing the risk of
serious cardiovascular complications.
4. Propranolol: Propranolol is a medication classified as a beta-blocker, commonly used to
manage symptoms of autonomic dysfunction in GBS patients. It helps control heart rate and
blood pressure by blocking the effects of adrenaline on the heart and blood vessels. In GBS,
propranolol may be prescribed to stabilize heart rate and blood pressure, especially in patients
experiencing cardiac dysrhythmias or other autonomic disturbances. By reducing the workload
on the heart and controlling abnormal heart rhythms, propranolol can help prevent
cardiovascular complications associated with GBS.
5. Atropine Sulfate (Atropine SO4): Atropine sulfate is a medication that acts as an
anticholinergic agent, blocking the activity of the parasympathetic nervous system. It is
commonly used to treat bradycardia and other cardiac conduction abnormalities, which may
occur as a result of autonomic dysfunction in GBS patients. By blocking the effects of
acetylcholine on the heart, atropine sulfate can increase heart rate and improve cardiac output,
helping to maintain adequate blood flow to vital organs.
NURSING INTERVENTIONS: (LESLYN)
EXPLANATION:
1. Maintain patent airway & adequate ventilation: Ensuring a clear airway and proper
ventilation is crucial, especially as respiratory muscle weakness can lead to ventilatory
insufficiency and respiratory failure. Regular monitoring of respiratory rate, depth, and vital
capacity helps detect early signs of respiratory compromise, while keeping the airway clear of
secretions reduces the risk of pneumonia.
2. Check individual muscle groups every 2 hrs in acute phase: Monitoring muscle strength
and function helps assess the progression of weakness, allowing for timely interventions and
adjustments in care.
3. Assess cranial nerve function: Evaluating cranial nerve function, including the gag reflex,
swallowing ability, and vocal function, helps identify any impairments that may affect airway
protection, swallowing, or communication.
4. Monitor vital signs, input and output, neurocheck, ECG, and signs of autonomic
dysfunction: Regular monitoring helps detect changes in the patient's condition, including
cardiac arrhythmias, fluctuations in blood pressure, and signs of autonomic dysfunction, which
are common in GBS.
5. Maintain side rails to prevent injury related to fall: Muscle weakness and impaired
mobility increase the risk of falls, so maintaining side rails provides support and reduces the risk
of injury.
6. Prevent complications of immobility: Turning the patient every 2 hours helps prevent
pressure ulcers and other complications associated with prolonged immobility.
7. Assist in passive ROM exercise: Passive range of motion exercises help prevent contractures
and maintain joint flexibility in immobilized patients.
8. Promote comfort (especially in clients with sensory changes): Providing comfort
measures such as foot cradles, sheepskin, and relaxation techniques helps alleviate discomfort,
particularly in patients with sensory changes.
9. Promote optimum nutrition: Assessing swallowing ability and starting with pureed foods
helps prevent aspiration, while considering NGT feeding for patients unable to swallow ensures
adequate nutrition and hydration.
10. Administer medications as ordered: Corticosteroids help suppress the immune response,
while anti-cholinergic and antiarrhythmic agents manage autonomic dysfunction and cardiac
complications.
11. Assist in plasmapheresis: Plasmapheresis removes autoimmune antibodies from the blood,
reducing the immune-mediated damage to peripheral nerves.
12. Prevent complications: Vigilant monitoring and prompt intervention help prevent cardiac
arrhythmias and respiratory muscle paralysis, reducing the risk of respiratory arrest.
13. Provide psychological support & encouragement: GBS can be emotionally challenging for
patients and their families, so providing support and encouragement helps alleviate anxiety and
promote coping.
14. Refer for rehabilitation: Rehabilitation helps regain strength and address any residual
deficits, improving the patient's functional outcomes and quality of life.
By implementing these nursing interventions, healthcare providers can effectively manage the
complex needs of patients with Guillain-Barré Syndrome, minimize complications, and promote
recovery.
