CONTENTS
- Definition and variants
- Epidemiology
- Signs & symptoms
- Diagnosis
- Treatment
- GBS in COVID-19
- Podcast
- Questions & discussion
- Pitfalls
Guillain Barre Syndrome (GBS) refers to a group of acute, autoimmune polyneuropathies. This chapter is predominantly about AIDP, AMAN, and AMSAN – since these are most often encountered in the ICU. However, the pharyngeal-cervical-brachial variant and facial-diplegia-with-paresthesia variant are also important to be aware of, as they might potentially compromise the airway.
Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
- Epidemiology: Most common cause of GBS in North America and Europe (~90% of patients).
- Pathophysiology: Diffuse demyelination of nerves, with inflammation directed towards the myelin sheaths.
- Clinical presentation: Classic manifestations of GBS.
- Prognosis: Patients often can recover relatively rapidly (over several weeks to months).
Acute motor axonal neuropathy (AMAN)
- Epidemiology: Second most common cause in North America and Europe (<10% of patients). More common in Asia, South America, and Central America.(33002998)
- Pathophysiology: Inflammation directed towards the axons, which is centered at the Nodes of Ranvier (where the axons are more exposed).
- Clinical presentation:
- Prognosis: This often progresses more rapidly than AIDP, with an increased risk of requiring mechanical ventilation. Subsequently, the process of axonal regeneration is slow and often incomplete, so the recovery may be worse.(34618763)
Acute motor and sensory axonal neuropathy (AMSAN)
- Epidemiology: Least common in North America and Europe, but more frequently seen in Asia and South America.
- Pathophysiology: Similar to AMAN, but involves sensory and motor nerves. Axonal degeneration may occur.
- Clinical presentation:
- Prognosis: This form carries the worst prognosis, with the potential for delayed and incomplete recovery.
Pharyngeal-Cervical-Brachial variant
- Basics: May cause
- Oropharyngeal weakness that may involve ptosis, ophthalmoplegia, facial muscles, and/or pharyngeal muscles.
- Neck flexor weakness.
- May spread to involve the arms.
- Epidemiology: Accounts for 3% of cases of Guillain-Barre syndrome.(31279384)
- Clinical presentation:
- Differential diagnosis: May mimic botulism, myasthenia gravis, or a brainstem stroke.
- Diagnostic tests: Electromyography will show acute motor axonal neuropathy.(31279384)
Miller Fisher syndrome
- This is the second most common variant in United States (~10%).
- Its classic clinical triad involves areflexia, external ophthalmoplegia, and cerebellar ataxia.
- Extremity weakness can occur. However, patients usually don't develop respiratory failure. Bulbar dysfunction doesn't occur.(31279384)
- Anti-GQ1b antibodies have been implicated with this disease entity and can be assessed from CSF.
Bickerstaff brainstem encephalitis
- This is extremely rare, possibly representing a variant or subset of Miller Fisher syndrome (both are associated with anti-GQ1b).
- Clinical findings:
- The typical triad consists of ophthalmoplegia, ataxia, and depressed consciousness (which may include coma).
- Hyperreflexia is a feature, unlike other forms of GBS.
- MRI is usually normal, but may show scattered T2 hyperintensities in the brainstem and basal ganglia, with limited enhancement and mild diffusion restriction.(33293366)
Facial diplegia with paresthesia variant
- May cause bilateral facial paralysis and paresthesias.📄
general
- GBS is the most common cause of generalized neuromuscular paralysis.
- Genders are affected roughly equally. The risk may increase somewhat with increased age.
- Specific risk factors include lymphoma, lupus, and HIV.
- A trigger of GBS often occurs 5 days to four weeks before the onset of neurologic symptoms. (Louis 2021)
upstream triggers
- Infection is involved in up to 75% of cases, especially:
- Campylobacter jejuni.
- Mycoplasma pneumoniae, Haemophilus influenzae.(33647239)
- Herpesviruses (CMV, EBV, VZV).
- Hepatitis E virus, Hepatitis A virus.
- HIV – among all these etiologies, HIV is unique in that it will require ongoing treatment.
- Zika virus.
- Influenza A.
- COVID-19.
- Checkpoint inhibitors (may require different treatment 📖).
- Immunizations (extremely rare, and much less common than GBS due to infection).(33647239)
usual presentation
- Sensory disturbance is often the first symptom.
- Paresthesias are common, especially in the fingers and toes.(34618763)
- Pain can result from nerve root inflammation (e.g., in back or extremities, low back pain). Pain may be radicular or neuropathic.(34798967)
- Sensory loss can occur, but this is mild compared to motor dysfunction.
- An exception is the AMAN variant (Acute Motor Axonal Neuropathy), which doesn't involve sensation.
- Ascending flaccid paralysis.
- Relatively symmetric.
- Speed of progression correlates with disease severity.
- The ascending pattern is thought to be due to nerve length, with longer nerves at higher risk of injury.
- 25% of patients develop weakness leading to respiratory failure.(34618763)
- Cranial nerve involvement is common. Occasionally ocular, facial, or oropharyngeal muscles are affected first. (Louis 2021)
- Facial weakness, ophthalmoplegia.
- Difficulty swallowing.
- Dysautonomia:
- Blood pressure may be extremely labile.
- Sympathetic activation can occur (with hypertension, agitation, diaphoresis, tachycardia, vasoconstriction), which may be complicated by:
- Parasympathetic activation can occur (with bradycardia, facial flushing, vasodilation).
- Other features may include constipation, diarrhea, and urinary retention.
signs
- Objective muscle weakness.
- Loss of deep tendon reflexes is a hallmark finding (~90% sensitive).
disease course
- Usually worsens over ~2 weeks (80% will nadir by 2 weeks; 90% of patients will reach nadir by 4 weeks).
- Ongoing disease progression for longer periods suggests an alternative, related disorder: chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).
- Usually GBS is a monophasic illness (with deterioration followed by improvement). However, occasionally patients may improve following therapy and then suffer a subsequent deterioration. This is termed “treatment related fluctuation” and discussed further below.📖
Normal CSF analysis doesn't exclude GBS, especially early in the disease course. To confuse matters further, IVIG therapy may increase CSF protein and white blood cell counts.(33002998)
albuminocytological dissociation
- The classic finding in GBS is albuminocytologic dissociation (elevated protein, despite normal cell count). Protein is usually elevated, up to very high levels (100-1,000 mg/dL)
- Elevated protein has a sensitivity of ~50% during the first week, but this increases over time (to ~80% by 3-4 weeks).
- There is a very broad differential diagnosis of albuminocytologic dissociation, as explored further here: 📖
cell count
- Cell count in GBS is generally normal (<5 cells/uL).
- Cell count of roughly ~10-50/uL is consistent with GBS, but should raise some suspicion for alternative diagnoses.(as listed below).
- Elevated cell count >50 or increased neutrophils in CSF suggest an alternative diagnosis, such as the following:
- Lyme.
- Viruses involving the anterior horn of the spinal cord. (Historically, cell count was used as the main tool to differentiate between polio and GBS.).
- HIV. In the context of HIV, GBS causes a lymphocytic pleocytosis rather than the classic albuminocytological dissociation.(34623100)
- Leptomeningeal carcinomatosis.
- Sarcoidosis.
This is the most sensitive and specific test. Electromyography may initially be normal, but a normal study >1-2 weeks after onset suggests an alternative diagnosis.
AIDP: Demyelination is a predominant feature.
- Earliest findings: (34950409)
- Absent or prolonged F-waves latency (F-wave latency may be the earliest sign).
- Prolonged distal compound muscle action potential latency (CMAP).
- Excessive temporal dispersion of compound muscle action potentials (CMAP).
- Reduced motor nerve conduction velocity.
AMAN (Acute motor axonal neuropathy)
- Decreased compound muscle action potential (CMAP) amplitudes with relatively preserved velocities.
Acute motor and sensory axonal neuropathy (AMSAN)
- Decreased compound muscle action potential (CMAP) amplitudes.
- Decreased sensory nerve action potential (SNAP) amplitudes.
- In cases without cranial nerve involvement, the differential includes spinal cord lesions. MRI may be useful to exclude these.
- Contrast enhancement of spinal nerve roots is sensitive for GBS but nonspecific (for example, it may also be seen in acute flaccid myelitis due to various viral infections).(34618763)
- The role of ganglioside serologies in diagnosis is not well established. Given their long turnaround time, these labs should ideally return after the initiation of treatment. That being said, positive results might help point one of the following conditions:
- AIDP: Ganglioside antibodies are usually absent.(33995011)
- AMAN or AMSAN is associated with antiganglioside antibodies against GM1a, GM1b, GD1a, and GalNAc-GD1a.(33002998, 33995011)
- Miller Fisher syndrome is associated with Anti-GQ1b (often cross-reactive with anti-GT1a) occurs in >80% of patients.
- Cervical brachial variant is associated with anti-GT1a.
- HIV serology – consider obtaining to exclude HIV as a cause of GBS.
Ultimately, the diagnosis of GBS involves a combination of excluding alternative possibilities as well as matching the patient's findings to the diagnosis of GBS. The following criteria may provide a helpful scaffolding to approaching the diagnosis, but aren't necessarily intended for rigid application. They are only relevent for major/paralytic forms of GBS.(33002998)
required and supportive features
- Required features:
- Progressive weakness in more than one limb with relative symmetry (initially only legs may be involved).
- Diminished reflexes in weak limbs (although this may be absent in the acute motor axonal neuropathy variant).
- No other clear explanation for these findings.
- “Supportive” features include the following.
features to consider in GBS diagnosis
- Rate:
- Consistent with GBS:
- Deterioration lasts days to a month (usually <2 weeks).
- Recovery starts 2-4 weeks after deterioration halts (nadir).
- 🚩 Inconsistent with GBS: Maximum weakness reached within <24 hours or >4 weeks.
- Consistent with GBS:
- Symmetry:
- Consistent with GBS: Relatively symmetric.
- 🚩 Inconsistent with GBS: Substantial asymmetry.
- Sensory involvement:
- Consistent with GBS: Mild sensory involvement, often involving pain (can be absent in motor variant).
- 🚩 Inconsistent with GBS:
- Severe sensory signs, with little or no weakness at onset.
- Absence of any sensory symptoms.(35863882)
- Fever:
- Consistent with GBS: No fever at onset.
- 🚩 Inconsistent with GBS: Fever at onset.
- CSF evaluation:
- Consistent with GBS:
- Elevated CSF protein (after one week).
- Cell count <50/mm3 (and usually <10/mm3).
- 🚩 Inconsistent with GBS:
- CSF white cell count >50/mm3.
- Neutrophils elevated.
- Consistent with GBS:
- Localization, regarding spinal cord:
- Consistent with GBS: Cranial nerve involvement (especially bilateral facial palsy).
- 🚩 Inconsistent with GBS:
- Sensory level suggestive of a focal spinal cord lesion.
- Bowel and bladder dysfunction at onset; severe and persistent bowel and bladder dysfunction (this may suggest myelopathy).
- Localization, regarding brain:
- Consistent with GBS: Should lack findings localizing to the brain (except for Miller Fisher syndrome-Bickerstaff brainstem encephalitis spectrum disorders)
- 🚩 Inconsistent with GBS: Other deficits that localize to the brain.
- Miscellaneous other features consistent with GBS:
- Autonomic dysfunction.
- Electrodiagnostic studies consistent with GBS
- Miscellaneous other features inconsistent with GBS:
- 🚩 Severe pulmonary dysfunction with little or no limb weakness at onset (this might suggest myasthenia gravis).
- 🚩 Normal nerve conduction tests after two weeks. (35863882)
These are cornerstone therapies for GBS.
indications
- The exact indications are unclear, but any critically ill or hospitalized patient with new-onset GBS merits treatment.
- Treatment should begin when there is a clinical diagnosis of GBS, rather than awaiting confirmation from lumbar puncture or nerve conduction studies.(30743297)
selection of IVIG or plasma exchange
- Both appear to be equally effective. Importantly, the combination of treatments hasn't been found to be superior to one treatment alone (e.g., plasmapheresis followed by IVIG).(33002998, 33896522)
- IVIG is generally used, since this is safer and easier to perform. The usual dose is 0.4 grams/kg/day for five days. However, among individual patients there may be a contraindication to IVIG, so plasmapheresis could be preferable.
- If there is no improvement after 1-2 weeks, a second repeated course of therapy does not appear to be beneficial. One randomized controlled trial among patients with severe GBS found that a repeat course didn't cause benefit – but did increase the risk of harm due to thromboembolic events.(33743237)
- Broader discussions of:
treatment-related fluctuations
- These occur in up to 10% of patients. Patients stabilize or improve following treatment, but then subsequently deteriorate (within 8 weeks of disease onset).
- There is no evidence regarding management, but consensus is to retreat with the original treatment modality.(33002998, 33647239)
- If more than three relapses occur, or if relapse occurs after 8 weeks of disease onset, this suggests an alternative diagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP).(33647239)
dysautonomia basics
- Dysautonomia is more frequent in patients with severe weakness. It can occur in patients with different types of GBS including demyelination (i.e., Acute Inflammatory Demyelinating Polyneuropathy) or axonal disease (i.e., Acute Motor Axonal Neuropathy).(31996626)
- Some patients may have alternating episodes of sympathetic hyperactivity (e.g., hypertension and tachycardia) and parasympathetic hyperactivity (e.g., bradycardia). This may be very dangerous, as bradyasystole is a potential cause of death in Guillain-Barre Syndrome.
- Some patients experience sustained hypertension. This is easier to manage than patients with hemodynamic fluctuations – hypertension may be treated with a long-acting vasodilator (e.g. with oral isradipine or nifedipine XR 💉).
- Persistent hypertension can cause target organ damage (e.g., Takotsubo cardiomyopathy or posterior reversible encephalopathy syndrome).
hemodynamic management
- General principles:
- (1) Blood pressure swings are often short-lived, so avoid treatment when possible. Aggressive treatment of hemodynamic fluctuations may merely worsen the hemodynamic roller-coaster (e.g., initiation of a vasopressor during a hypotensive episode exacerbates a subsequent episode of hypertension).
- (2) Avoid beta-blockers, as these may increase the risk of bradycardia.
- For persistent or critical hypotension:
- Administer fluid if there is evidence of true hypovolemia (e.g., negative fluid balance, poor PO intake for days).
- May use vasopressor, at the lowest dose possible.
- For persistent or critical hypertension:
- Avoid treatment unless there is target-organ damage or ongoing severe hypertension (e.g., MAP > ~120 mm).
- Avoid beta-blockers (these may aggravate subsequent bradycardia).
- 1st line treatment: Remove the stimulus for hypertension if possible (e.g., ensure that pain and agitation are adequately treated).
- 2nd line treatment: For prolonged and severe hypertension, consider a short-acting vasodilator (e.g., nicardipine 💉 or clevidipine 💉 infusion). If patients respond adequately and are stable for a period of time, this may be transitioned to oral calcium-channel blockers (e.g., nifedipine XR or isradipine 💉).
- For bradycardic episodes:
- Avoid triggers of bradycardia if possible (e.g., endotracheal suctioning).
- Discontinue negative chronotropes (e.g., beta-blockers).
- IV atropine may be useful.
- In severe cases, electrical pacing may be needed.
other autonomic problems
- Urinary retention and incontinence can occur. Depending on the context, either a Foley catheter or frequent bladder scanning with straight catheterization may be needed.
- Gastroparesis 📖 can occur, potentially requiring treatment with pro-motility agents or a post-pyloric feeding tube.
- Small intestinal ileus 📖 and colonic pseudo-obstruction 📖 can occur. This may become a major problem, leading to bowel perforation.
- An aggressive bowel regimen is recommended to avoid obstipation (which may in turn trigger additional autonomic instability).
- For patients receiving opioids, therapies such as oral naloxone or peripheral IV methylnaltrexone may be helpful (along with limitation of the opioid dose as much as possible).
- A rectal tube may be helpful.
- Extreme caution and close monitoring is needed if neostigmine is utilized for treatment of colonic pseudo-obstruction, given its potential for causing autonomic swings (e.g., bradycardia and asystole). Pre-treatment with 0.4 mg glycopyrrolate prior to administration of neostigmine (2 mg over 5 minutes) may reduce the risk of bradycardia. (28893807, 18338263)
- Neuropathic pain is common and potentially debilitating.(33896522) For neuropathic-type pain, gabapentin may be useful.
- Scheduled acetaminophen is often beneficial, especially among intubated patients.
- Opioid may be used, but exercise caution as patients are prone to develop ileus.
Obsessive, repetitive, and uninformed measurement of respiratory mechanics is a common pitfall in the management of GBS. Like many data points in medicine (e.g., troponin), respiratory mechanics can be useful if utilized appropriately.
forced vital capacity (FVC)
- Basics of the FVC:
- FVC is the largest volume of gas that a patient can exhale. Patients are asked to take a full breath in and then exhale maximally, with measurement of the exhaled volume. FVC reflects a global measurement of the patient's ventilatory ability, which takes into account inspiratory and expiratory muscle strength as well as pulmonary compliance.
- FVC is the most reproducible and clinically useful measurement of pulmonary function.
- A normal forced vital capacity is ~60 ml/kg. Values below roughly 30 ml/kg suggest a risk of atelectasis or hypoventilation.
- Absolute values are less valuable than the trend, which may help determine in what direction the patient is going.
- Limitations:
- Excessive performance may cause diaphragmatic fatigue.
- The maneuver is effort dependent.
- Measuring FVC may be impossible in a patient with bulbar weakness, as the patient is unable to close their lips around the mouthpiece.
- There is no high-quality evidence that any particular value has any specific meaning (traditionally utilized cutoff values are not evidence-based).
negative inspiratory force (NIF)
- This is the greatest negative pressure the patient can generate (also known as the minimum inspiratory pressure or MIP). A pressure gauge is used to measure the negative pressure generated by the patient when asked to inhale as hard as they can. This is a measurement of the strength of the inspiratory muscles, primarily the diaphragm.
- Reasons that the NIF should not be used to monitor non-intubated patients with GBS:
- (1) The NIF doesn't add statistically independent or useful information beyond measurement of the forced vital capacity alone. (11405803, 21748507) What this means is that it introduces a source of noise, without adding meaningful information.
- (2) The NIF is more fatiguing and uncomfortable than the forced vital capacity.
use #1 of respiratory mechanics: triage
- Determining which patients require observation in an ICU versus a ward is primarily dependent on history and overall gestalt impression.
- However, pulmonary function testing could play a role in risk-stratification and triage. For example, an FVC under roughly 30 ml/kg might suggest a higher risk of deterioration and the need for closer monitoring.
use #2 of respiratory mechanics: tracking trajectory
- Serial measurement of forced vital capacity (FVC) is often used to determine disease trajectory (e.g., 2-3 times daily during waking hours).
- Serial FVC is only one piece of information to help assess the patient, in addition to numerous others (e.g., subjective impression and strength of other muscle groups).
- No high-quality evidence exists here. Theoretically, respiratory support could prevent exhaustion and the requirement for intubation. However, noninvasive support requires close monitoring for early detection of patients who are frankly failing and require intubation.
- The key is probably early initiation of noninvasive support, before respiratory exhaustion occurs.
- If a patient is completely dependent on BiPAP and entirely unable to breathe without it, then they should simply be intubated. However, nocturnal BiPAP might be useful to off-load respiratory muscles at night, facilitating rest.
- BiPAP or high-flow nasal cannula (HFNC) may be used to support patients with some evidence of respiratory weakness, and who aren't requiring intubation.
- Titration and selection depends largely on patient tolerance.
- BiPAP may be ideally restricted to nocturnal use, possibly with use of high-flow nasal cannula support during the day.
pulmonary function (forced vital capacity)
- As discussed above, this provides only one piece of information.
- The decision to intubate should never be based on respiratory mechanics alone.
- For example, poor patient effort can cause aberrantly low values.
- ⚠️ Several “rules” exist suggesting that specific cutoff values indicate when to intubate (e.g., below 15-20 ml/kg). These rules are not evidence based and should not be blindly followed.🌊
weakness of other muscle groups
- Respiratory weakness tends to track with other types of weakness, especially:
- i) Neck flexion weakness, for example the patient's ability to lift their head off the pillow. (Neck flexion is innervated by the same cervical nerve roots that innervate the diaphragm, correlating with diaphragmatic weakness.)(Torbey, 2019)
- ii) Facial or bulbar weakness.
- iii) Limb weakness (this is unlike myasthenia gravis).(35863882)
- Progressive weakness of multiple muscle groups is concerning.
clinical evaluation of respiratory status and the decision to intubate
- Many criteria for intubation exist, but none are based on high-quality evidence. Ultimately the decision to intubate is a clinical one that should be based on the integration of multiple sources of information. Important parameters to track include the following:
- (1) Evidence of increased work of breathing (e.g., accessory muscle use, subjective dyspnea).
- (2) Difficulty controlling secretions.
- (3) Cough strength.
- (4) Overall course of muscle weakness.
- (5) Trends in forced vital capacity.
intubation procedure
- Intubation procedure carries risk of inducing a vagal episode (prepare push-dose epinephrine ahead of time, but avoid its use if possible). Evaluate for volume status prior to intubation and consider some fluid resuscitation if the patient is grossly volume depleted (as may occur due to bulbar weakness and poor oral intake).
- ⚠️ Succinylcholine is contraindicated (denervation of muscles may lead to excessive potassium release).
mode of ventilation and weaning
- Patients can be ventilated using standard ICU protocols.
- There is no evidence that patients with Guillain Barre syndrome are better managed with SIMV or other modes of ventilation. (Indeed, SIMV is poorly supported by evidence overall and should arguably be avoided.)
weaning from ventilation
- Overall, this may be pursued in the same manner as liberating other patients from the ventilator. Ideally, strength will improve over several days, leading to the ability to extubate.
- One test which may be useful to trend is the patient's voluntary forced vital capacity on the ventilator. This can be assessed during a spontaneous breathing trial by asking the patient to blow out as possible and then to take in a full breath.
- 💡 Diaphragm strength may improve before extremity muscle strength, so it may be possible to extubate patients with persistent extremity weakness.
post-extubation support
- Extubating to BiPAP or high-flow nasal cannula may reduce the work of breathing, reducing the reintubation risk.
tracheostomy
- Many patients will require tracheostomy, due to inability to wean off mechanical ventilation within <1-2 weeks.
- Some predictors of prolonged mechanical ventilation and need for tracheostomy:
- GBS can occur following infection with COVID-19. This generally occurs within two weeks after the initiation of other COVID-19 symptoms (coincident with development of adaptive immunity).(33647239)
- Some patients may lack respiratory symptoms due to COVID upon presentation, presenting instead with weakness or even back pain as a primary complaint.
- Demyelination have been reported most frequently (AIDP), but axonal variants and Miller Fisher variant may also occur.(33647239)
- Weakness is the predominant clinical finding (most often ascending paralysis). Dysautonomia doesn't seem to be a prominent issue.
- Diagnosis can be challenging for patients who are already admitted with COVID pneumonia, since GBS will tend to blend in with other causes of respiratory dysfunction present in these patients (e.g., critical illness neuropathy/myopathy, COVID pneumonia, pulmonary embolism, ventilator acquired pneumonia). In some patients, GBS could be an occult cause of inability to wean from mechanical ventilation.
- Intravenous immune globulin (IVIG) is generally the front-line therapy for Guillain Barre Syndrome (with equal efficacy compared to plasmapheresis and superior tolerability).
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- Over-aggressive treatment of autonomic swings.
- Excessive focus on forced vital capacity and excessive measurement of the forced vital capacity.
- Use of the negative inspiratory force.
- Failure to consider GBS in a patient admitted to ICU with viral illness who develops weakness.
- Assuming that a patient with GBS and respiratory failure has neuromuscular respiratory failure (as opposed to other possible causes of respiratory failure which may occur, such as heart failure).
Acknowledgement: Thanks to Dr. Richard Choi (@rkchoi) for thoughtful comments on this chapter.
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