The Daily Differential — Wednesday, June 24, 2026

Guillain-Barre Syndrome

GBS can look deceptively “stable” until respiratory failure or autonomic collapse appears. The ED job is to recognize the pattern early, measure function objectively, and admit the right patient before the diaphragm quits.

By the Blue Fish Med Desk Jun 24, 2026 · Phoenix

A 36-year-old man sits on the stretcher staring at his own boots, rubbing the tops of his feet against the sheet as if they’ve gone numb under him. He says the “weakness” started as a strange heaviness after a week of diarrhea, then climbed from his toes to his thighs by lunchtime. The nurse notices he’s taking shallow breaths and counting only to seven on one exhale. He can still answer questions clearly, but when you ask him to stand, he grips the rail and waits.

— What’s your move? Read on.

Before you read

What bedside finding tells you the airway may fail before the legs do?
Which patients need ICU, not discharge, even if they can still walk?

When to Think of It

Ascending, symmetric weakness with areflexia, paresthesias, and often recent GI/respiratory infection. Think GBS when weakness is flaccid, reflexes are absent or reduced, cranial nerves may be involved, and the sensory exam is mild relative to the motor deficit.

Sick or Not Sick

The one call that matters: can this patient protect ventilation and swallow safely, or are they headed for respiratory failure/autonomic instability? Bulbar symptoms, neck flexor weakness, rapid progression, poor single-breath count, low FVC/NIF, tachy- or bradyarrhythmias, and labile BP push to ICU.

The First Fifteen Minutes

Weakness with dyspnea, bulbar symptoms, or rapid progression → bedside respiratory mechanics now: serial FVC and negative inspiratory force (NIF), because respiratory decline can precede obvious distress.
Bulbar weakness or unsafe swallow → NPO and aspiration precautions, because dysphagia is an airway threat.
Painful paresthesias or neuropathic pain → gabapentin 300 mg PO, titrate as needed, because neuropathic pain is common and often undertreated.
Confirmed/suspected GBS with significant weakness → IVIG 0.4 g/kg/day IV for 5 days or plasma exchange (typically 4–6 exchanges), because both shorten recovery by interrupting the immune attack.
Autonomic instability with hypotension → IV fluids cautiously, because preload sensitivity and dysautonomia make overcorrection dangerous; use pressors if needed per shock physiology.
Significant pain → acetaminophen 1,000 mg PO/IV or ibuprofen 400–600 mg PO if appropriate, because supportive care matters while immune therapy takes effect.
If intubation becomes necessary → use your standard RSI protocol; avoid assuming the patient will “crash later”, because respiratory arrest can be abrupt.

Definitive Care & Disposition

Admit all suspected GBS patients, and most need ICU or step-down with very close respiratory monitoring if weakness is evolving. Neurology should guide IVIG vs plasma exchange, but in the ED the key is early recognition, objective respiratory trending, and prevention of aspiration. Expect CSF with albuminocytologic dissociation and EMG/NCS later; neither should delay disposition.

How This One Kills

The fatal mistake is sending home or placing on a floor bed a patient with evolving bulbar/respiratory weakness who “still looks okay.” GBS kills by missing the moment when the diaphragm and autonomic system fail.

The Differential — What Else Looks Like This

Spinal cord lesion — sensory level, hyperreflexia/UMN signs, and bladder involvement point away from GBS; confusing them delays decompression or stroke/cord workup.
Myasthenia gravis — fatigable weakness without sensory loss or areflexia; confusing them risks missing the need for ventilatory support and the right antibody-directed workup.
Botulism — descending paralysis, pupils/autonomic findings, and early cranial nerve involvement are clues; confusing them delays antitoxin.
Critical illness myopathy/neuropathy — ICU context and diffuse weakness after critical illness; confusing them with GBS misleads the source and prognosis.

The Second-Day Story

In older adults or patients seen late, the story may be less “ascending paralysis” and more “can’t climb stairs,” “frequent falls,” or “weak voice” after a mild viral syndrome. Pain may dominate early, reflex loss can be subtle, and sensory symptoms may overshadow weakness. The clue is progression over days with symmetric motor decline and a peripheral pattern that doesn’t fit a focal CNS lesion.

Back to Our Patient

Back to our 36-year-old with post-diarrheal leg heaviness and shallow breaths: the pattern is Guillain-Barre Syndrome. He has ascending symmetric weakness with areflexia risk and early respiratory involvement, so the ED priorities are immediate FVC/NIF trending, NPO/aspiration precautions, and ICU-level monitoring. Neurology is consulted for IVIG or plasma exchange, and because his breathing is already trending down, he’s admitted to the ICU rather than the floor.

Patient Presentation to Attending

How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling

“This is a 36-year-old man with progressive bilateral leg weakness and tingling after a diarrheal illness, now with shallow breathing and difficulty standing. He denies back pain, bowel or bladder dysfunction, unilateral symptoms, fever, or trauma. On exam he has symmetric proximal-to-distal weakness, diminished reflexes, and no sensory level or focal cranial nerve deficit yet, but his single-breath count is low and I’m concerned for evolving neuromuscular respiratory failure. I’ve made him NPO, started serial FVC/NIF monitoring, and called neurology and ICU for suspected Guillain-Barre Syndrome with plan for IVIG versus plasma exchange.”

Study Directive

Draw the GBS bedside algorithm from memory: trigger history → exam pattern → FVC/NIF → ICU vs floor.
Practice a 30-second differentiation drill: GBS vs myasthenia vs spinal cord lesion vs botulism.
Memorize the adult IVIG regimen and the key red flags for admission.
Review one case of autonomic instability in GBS and list the monitor findings that would have changed management.

Recent Literature

Review or guideline European Academy of Neurology/Peripheral Nerve Society Guideline on diagnosis and treatment of Guillain-Barré syndrome
van Doorn PA, Van den Bergh PYK, Hadden RDM, et al. · Eur J Neurol, 2023 · PMID 37814552 · cited 196×

Current European guideline covering ED-relevant diagnosis, admission/monitoring decisions, and treatment with IVIG or plasma exchange, including when to anticipate respiratory failure and autonomic complications.

Full text · open access

4 of 4

Altered Mental Status

Altered mental status is not a diagnosis; it is a time-sensitive syndrome with a long list of lethal reversibles. The ED priority is to stabilize, rapidly...

The Case

A 72-year-old man is brought in slumped in a wheelchair, a half-eaten sandwich in his lap and dried coffee at the corner of his mouth. His daughter says he was “just more sleepy” after lunch, then started saying his dead sister was in the hallway, and now he won’t follow commands. His skin is warm, his breath smells faintly sweet, and the monitor keeps flashing a heart rate that seems too fast for the rest of him. No one in the room can say exactly when he was last normal.

Before You Read

What is the first question in AMS that changes everything before you chase the diagnosis?
Which reversible causes must be checked immediately, and in what order?
When is this “altered mental status” actually an airway problem?

Why It Matters

Altered mental status is not a diagnosis; it is a time-sensitive syndrome with a long list of lethal reversibles. The ED priority is to stabilize, rapidly sort structural, metabolic, toxic, infectious, and respiratory causes, and not miss the patient who simply needs glucose, oxygen, naloxone, or a CT now.

When to Think of It

Any acute change in alertness, attention, behavior, cognition, or arousal: confusion, agitation, lethargy, delirium, obtundation, coma, or unexplained “not acting right.” Think broad until proven otherwise, especially if the exam is inconsistent, the history is limited, or the onset is unclear.

Sick or Not Sick

The one call that matters: is this patient protecting oxygenation, ventilation, and airway reflexes? If not, it’s an airway/ICU problem first; if yes, the next fork is unstable structural/toxic/metabolic vs lower-risk delirium.

The First Fifteen Minutes

Hypoglycemia or unknown glucose → dextrose 25 g IV (e.g., D50W 50 mL IV or D10W 250 mL IV), because glucose deprivation is immediately reversible and brain-toxic.
Concern for thiamine deficiency/malnutrition/alcohol use → thiamine 100 mg IV, because glucose without thiamine can worsen Wernicke risk in susceptible patients.
Opioid toxidrome with hypoventilation → naloxone 0.04–0.4 mg IV/IM/IN, titrate to respirations, because reversing respiratory depression is the immediate lifesaving step.
Hypoxia → oxygen by nasal cannula or nonrebreather, escalate to BVM as needed, because the brain is oxygen-sensitive.
Seizure or suspected nonconvulsive status → lorazepam 2 mg IV, then load antiseizure medication per protocol, because ongoing ictal activity can present as AMS.
Fever, sepsis physiology, or meningitis/encephalitis concern → broad-spectrum antibiotics within 1 hour and source-directed therapy (regimen varies by suspected source; verify institutional protocol), because CNS infection is time-critical.
Agitation creating danger → haloperidol 2.5–5 mg IV/IM or olanzapine 5–10 mg IM, because sedation may be necessary to protect the patient and staff; avoid oversedation if airway is tenuous.
If raised ICP or focal deficit suggests structural lesion → head CT now, because hemorrhage/mass effect must be excluded quickly.
If hypercapnia/respiratory depression suspected → ventilatory support rather than more “workup”, because CO2 narcosis is a common miss.

Definitive Care & Disposition

Disposition depends on the cause, but persistent AMS rarely belongs home. Structural lesions, CNS infection, toxicologic coma, recurrent seizures, significant metabolic derangement, or need for airway support require admission and often ICU. Delirium from benign triggers may go to observation or inpatient medicine if the cause is identified and the patient is safe.

How This One Kills

The deadly miss is calling a head-injured, hypoglycemic, hypercapnic, septic, or poisoned patient “just confused.” AMS kills by delayed recognition of a reversible physiologic emergency or a hidden intracranial catastrophe.

The Atypical Presentation

Older adults often present with nonspecific somnolence, falls, reduced appetite, or “just not herself,” and infection or medication effects may be the only clue. Polypharmacy, renal failure, and baseline cognitive impairment blur the exam, so the bedside history from family, med review, fingerstick glucose, vitals, and oxygenation are disproportionately valuable. In partially treated patients, the original syndrome may be masked by fluids, antipyretics, or prehospital meds, so let physiology—not the calm appearance—drive urgency.

Back to Our Patient

Back to our 72-year-old with sleepiness, hallucinations, and unclear last-known-well: this is Altered Mental Status, and the first job is not naming the syndrome but rescuing the reversible causes. He needs immediate fingerstick glucose, oxygenation and ventilation assessment, a toxidrome/medication review, and rapid evaluation for infection, stroke, or hypercapnia; if his airway is not protected, airway management comes first. The warm skin, tachycardia, and sweet odor widen the differential, but his disposition will be driven by physiology and the underlying cause, which at minimum makes him an admission patient and possibly ICU if airway or hemodynamics are unstable.

Patient Presentation to Attending

“This is a 72-year-old man with acute confusion and decreased responsiveness noted after lunch, with hallucinations, poor command following, and an unclear last-known-well. Family denies trauma but says he’s been sleepier than baseline, and on exam he’s tachycardic, warm, and not consistently protecting his airway, without an obvious focal deficit. I’ve checked glucose, started oxygen, reviewed meds for opioid or sedative exposure, and I’m evaluating for sepsis, hypercapnia, and intracranial pathology. He needs a full AMS workup with airway readiness, and I’m planning admission with ICU if his ventilation or mental status worsens.”

Study Directive

Rehearse the AMS first-minute algorithm out loud: glucose, oxygen, ventilation, naloxone, seizure, stroke, infection.
Build a one-page toxidrome grid from memory: opioid, anticholinergic, cholinergic, sympathomimetic, sedative.
Practice a 60-second caregiver collateral script that extracts last-known-well, meds, baseline, and toxin exposure.
Review one AMS case and identify the first abnormal vital sign you would not ignore.

Mechanism Pearl of the Day: When the nervous system fails, it often fails at the interface between signal transmission and perfusion: peripheral demyelination slows motor output in GBS, central demyelination blocks conduction in MS, venous thrombosis raises venous pressure and starves brain tissue in CVT, and AMS is the final common pathway when oxygen, glucose, CO2, or toxin levels derail neuronal function.

Key Medications

Dextrose: D50W 25 g IV (50 mL) or D10W 250 mL IV.
Thiamine: 100 mg IV.
Naloxone: 0.04–0.4 mg IV/IM/IN, titrate; larger doses may be needed in severe overdose.
Lorazepam: 2 mg IV for seizure/status.
Haloperidol: 2.5–5 mg IV/IM for severe agitation; QT and EPS risk.
Olanzapine: 5–10 mg IM for agitation; avoid combining closely with benzodiazepines if respiratory depression risk.
Antibiotics for suspected CNS infection/sepsis: regimen varies by syndrome and local resistance patterns—verify protocol.
Oxygen/BVM/RSI medications: per airway protocol; dosing varies.

High-Yield Pearls

In AMS, airway and ventilation are the diagnosis before the diagnosis—check them first.
A normal glucose does not make AMS benign; it only removes one reversible cause.
Medication review is a neurologic test in older adults with AMS.

The Mimics

Delirium — fluctuating attention with an underlying trigger; confusing it with dementia or psychosis delays treatment of the precipitant.
Stroke/ICH — focal deficits, aphasia, gaze deviation, or sudden onset; confusing them with nonspecific confusion misses reperfusion or hemorrhage care.
Sepsis — fever, tachycardia, hypotension, source clues; confusing it with primary neurologic disease delays antibiotics and fluids.
Toxic ingestion — pupils, respiratory pattern, odor, med list, or toxidrome; confusing it with metabolic encephalopathy misses antidotes.

Board Question

A 68-year-old man is found confused and somnolent with shallow respirations and pinpoint pupils. Fingerstick glucose is 112 mg/dL. Which is the best immediate treatment?

AIV haloperidol
BNaloxone titrated to respiratory effort
CCT head before any intervention
DIV methylprednisolone

Reveal answer

Correct: B

This is an opioid toxidrome with respiratory depression, and naloxone should be given immediately while supporting ventilation. Imaging and other workup can follow once oxygenation and ventilation are addressed.

Recent Literature

Review or guideline Hyperactive Delirium with Severe Agitation
Emerg Med Clin North Am, 2024 · cited 14×

Practical ED-focused review of hyperactive delirium emphasizing immediate safety, rapid search for reversible medical causes of altered mental status, and medication choices for severe agitation.

TheDaily Differential

Guillain-Barre Syndrome

When to Think of It

Sick or Not Sick

The First Fifteen Minutes

Definitive Care & Disposition

How This One Kills

The Second-Day Story

Study Directive

Recent Literature

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Cerebral Venous Thrombosis

Altered Mental Status

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