Updated July 2026 · 9 min read

Guillain-Barré Syndrome: The ICU Nurse's Guide

Part of the ICU Emergencies Hub — browse every related guide in one place.

Guillain-Barré syndrome is the classic "weakness that climbs up the body." A patient who walked into the ED with tingling feet can be intubated a day later. What makes it an ICU disease is not just the paralysis — it is the two ways it kills quietly: the breathing muscles giving out, and an autonomic nervous system that swings the blood pressure and heart rate to dangerous extremes.

What is actually happening

In most cases GBS follows an infection by a week or two — a diarrheal illness (classically Campylobacter), a respiratory virus, or others. The immune system, primed against the bug, cross-reacts with components of the patient's own peripheral nerves. Depending on the variant, the attack strips the myelin (the demyelinating form) or hits the axon directly. Either way, nerve signals slow or fail, and the result is weakness with diminished or absent deep tendon reflexes — that lost-reflex finding is a key clue that separates GBS from many other causes of weakness.

The pattern is usually ascending and symmetric: tingling and weakness start in the feet and hands and climb. Many patients have back and limb pain that is out of proportion to how they look. As it climbs, it can reach the diaphragm and the bulbar muscles that manage the airway — which is where the ICU comes in.

The first killer: respiratory failure

Just like in myasthenic crisis, the failing bellows are a mechanical problem the pulse oximeter hides. The saturation stays fine while the vital capacity quietly falls, and then the patient tires and the CO₂ climbs. So the same bedside tools drive the decisions:

• Forced vital capacity (FVC) — trended serially. A falling FVC, and values dropping toward roughly 15–20 mL/kg, is the classic trigger to prepare for intubation.
• Negative inspiratory force (NIF / MIP) and maximal expiratory pressure — weakening numbers mean a weakening pump and a weakening cough.

A commonly taught memory aid is the "20/30/40 rule": worry as FVC approaches ~20 mL/kg, NIF weakens past about -30 cmH₂O, and MEP falls under ~40 cmH₂O. The trend and the whole picture matter more than any single value. Bulbar weakness — a wet voice, poor swallow, pooling secretions — raises the aspiration risk independently and lowers the threshold to secure the airway. In GBS, intubation is usually a controlled, anticipated decision, and that is exactly the goal.

The second killer: dysautonomia

This is the part that catches people off guard. GBS frequently damages the autonomic nerves too, producing an unstable, unpredictable autonomic nervous system. The patient can swing between extremes:

Because the swings are so labile, the team is cautious with treating any single number aggressively — a big dose of an antihypertensive can be followed minutes later by the pressure crashing on its own. Short-acting, titratable agents and a steady eye on the monitor beat heavy-handed corrections.

Treatment: what helps and what doesn't

The disease-modifying treatments are IVIG or plasma exchange (plasmapheresis) — they are considered roughly equivalent in effect, and they are not combined. The choice is driven by availability, access, and patient factors. A crucial teaching point: corticosteroids do not help in GBS and are not used for it (a deliberate contrast with many other autoimmune neurologic diseases). Everything else is supportive and it is a lot: ventilator management, meticulous DVT prophylaxis and skin care in a paralyzed patient, pain control (the neuropathic pain is real and often undertreated), nutrition, bowel and bladder management, and early involvement of physical and occupational therapy for the long recovery.

What the bedside nurse owns

You own the respiratory trend (serial FVC/NIF, swallow, secretions, cough strength), the autonomic vigilance (continuous monitoring, cautious suctioning, atropine nearby, treating swings gently), and the whole of supportive care that keeps an awake, immobile patient safe: pressure-injury prevention, DVT prophylaxis, eye and mouth care, neuropathic pain, and constant communication with a person who often cannot move but can hear every word. Escalate the falling vital capacity early, and never let succinylcholine near the airway.

Bottom line

Guillain-Barré is ascending, areflexic, autoimmune weakness that becomes an ICU disease through two quiet killers: respiratory pump failure — tracked by serial vital capacity and NIF, not the pulse oximeter — and dysautonomia with dangerous heart-rate and blood-pressure swings, including suction-triggered bradycardia. Treat with IVIG or plasma exchange, never steroids, avoid succinylcholine, and support the awake, paralyzed patient through a usually recoverable, monophasic course. The nurse watching the numbers and the monitor is what makes the difference.

This article is general educational information for licensed clinicians and students, not medical advice or a substitute for your institution's protocols, pharmacy guidance, or a provider's orders. Always follow facility policy and verify doses independently.