Study guide
24.3 Myasthenic Crisis (03.O.2)
ABIM Neurocritical Care Subspecialty Certification Exam
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1 Introduction & Exam Overview
1.1 Current Exam Facts 1.2 Eligibility, Practice Pathway, and the IM Training Route 1.3 Format, Scoring, Pearson VUE, and Score Reports 1.4 How to Use This Independent Study Guide
2 ICU Neurologic Exam, Cerebral Physiology, and CSF
2.1 Neurological Examination in the ICU 2.2 Cerebral Physiology, ICP, CBF, and Autoregulation 2.3 CSF Physiology
3 Core Neuropharmacology
3.1 Osmotic Agents 3.2 Anti-Seizure Drugs 3.3 Anesthetics, Sedatives, Analgesia, and Paralytics 3.4 Antihypertensives, Vasopressors, and Inotropes
4 Reperfusion Drugs, Airway, and Ventilation
4.1 Thrombolytics, Anticoagulants, and Antiplatelets 4.2 Reversal of Anticoagulation After Acute Hemorrhage 4.3 Airway Management and Tracheostomy 4.4 Mechanical Ventilation
5 Hemodynamics and Shock
5.1 Hemodynamic Monitoring 5.2 IABP, Temporary VADs, LVAD, and ECMO 5.3 Diagnosis and Management of Shock
6 Nutrition, Temperature, and ICU Prophylaxis
6.1 Nutrition (01.J) 6.2 Temperature Control (01.K) 6.3 ICU Prophylaxis, Delirium, and Early Mobility (01.L)
7 General Trauma
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma 7.2 Long-Bone Fractures and Fat Embolism 7.3 Burns, Electrical Injury, and Hanging/Strangulation
8 Pulmonary Critical Care
8.1 Pulmonary Physiology and ARDS (01.N.1–2) 8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8) 8.3 COPD, Asthma, PAH, and Bronchoscopy Basics (01.N.4–6, 9)
9 Cardiovascular Critical Care
9.1 Cardiovascular Physiology, Stress Cardiomyopathy, ACS, and Valves 9.2 Arrhythmias and Pacing 9.3 Acute Aortic Dissection and Cardiac Ultrasound
10 Renal and Infectious Disease
10.1 AKI, RRT, and Renal Drug Dosing 10.2 Acid-Base and Electrolyte Disorders 10.3 Severe Sepsis, Septic Shock, and Infective Endocarditis 10.4 Antimicrobial Use and Infection in the Immunosuppressed
11 Endocrine and Salt-Water Disorders
11.1 Pituitary Apoplexy, DI, and Panhypopituitarism (01.R.1–4) 11.2 SIADH and Cerebral Salt Wasting (01.R.5–6) 11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
12 Gastrointestinal Critical Care
12.1 GI Physiology, Acute Abdomen, Bleed, Ileus, and Perforation (01.S.1–5) 12.2 Mesenteric Ischemia and Abdominal Compartment Syndrome (01.S.6–7) 12.3 Fulminant Liver Failure, Cirrhosis Decompensation, and Hepatic Dosing (01.S.8–10)
13 Hematologic Disorders
13.1 Anemia, Transfusion, Thrombocytopenia, Coagulopathy, and DIC (01.T.1–4) 13.2 VTE in the Neuro ICU (01.T.5) 13.3 Chemo/Immune, SCT, CAR-T, Sickle Cell, and TMA (01.T.6–10)
14 Neuroimaging
14.1 CT of Brain and Spine 14.2 MRI and CT/MR Perfusion 14.3 Noninvasive Angiography and Catheter Angiography
15 EEG, EMG, and CSF Analysis
15.1 EEG, Standard and Processed (02.B) 15.2 Basic EMG Interpretation (02.G) 15.3 CSF Analysis (02.H)
16 ICP, TCD, and Multimodality Monitoring
16.1 ICP Monitoring (02.C) 16.2 Transcranial Doppler (02.D) 16.3 Brain-Tissue Oxygen and Multimodality Monitoring (02.E–F)
17 Brain Death and Bedside Procedures
17.1 Brain Death Prerequisites and Clinical Exam (02.I) 17.2 Apnea Testing and Ancillary Studies (02.I) 17.3 Vascular Access, Thoracic Echo, and Lung Ultrasound (02.J–L)
18 Coma, Anoxia, and Intracranial Hypertension
18.1 Coma and Other States of Altered Consciousness (03.A) 18.2 Global Anoxia-Ischemia and Post-Resuscitation Encephalopathy (03.A.1) 18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4) 18.4 Intracranial Hypertension as a Disease State (03.B)
19 Acute Ischemic Stroke
19.1 IV Reperfusion Therapy (03.C.3) 19.2 Mechanical Thrombectomy Windows and Imaging Selection (03.C.3) 19.3 Malignant Hemispheric Infarction and Basilar Artery Occlusion (03.C.1–2)
20 Intraparenchymal Hemorrhage
20.1 Intracerebral Hematoma (03.D.1) 20.2 Cerebellar Hematoma (03.D.2) 20.3 Intraventricular Hemorrhage (03.D.3)
21 SAH, CVST, and Spinal Cord Infarction
21.1 Aneurysmal Subarachnoid Hemorrhage (03.E.1) 21.2 Non-Aneurysmal SAH (03.E.2) 21.3 Cerebral Venous Sinus Thrombosis (03.F) 21.4 Spinal Cord Infarction (03.G)
22 Vascular Anomalies and Traumatic Brain Injury
22.1 Unruptured Aneurysm, Cavernoma, AVM, and Dural AVF (03.H) 22.2 Diffuse Axonal Injury and Cerebral Contusions (03.I.1–2) 22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7) 22.4 Arterial Dissection and Carotid-Cavernous Fistula (03.I.5–6)
23 Spine, Hydrocephalus, and CNS Infection
23.1 Spinal Cord Injury, Central Cord, and Neurogenic Shock (03.J) 23.2 Unstable Spine Fractures (03.K) 23.3 Hydrocephalus and CSF Diversion (03.L) 23.4 Acute CNS Infections (03.M)
24 Seizures and Neuromuscular Emergencies
24.1 Status Epilepticus and Seizures (03.N) 24.2 Guillain-Barré Syndrome (03.O.1) 24.3 Myasthenic Crisis (03.O.2) 24.4 Motor Neuron Disease, Acute Myopathies, Rhabdomyolysis, and CINM (03.O.3–6)
25 Inflammatory Disease, Neuro-Oncology, and Special Populations
25.1 Fulminant Demyelinating Diseases (03.P) 25.2 Autoimmune Encephalitis and Acute Autonomic Hyperactivity (03.Q–R) 25.3 Neuro-Oncology and Treatment Complications (03.S) 25.4 Pregnancy/Post-Partum, Post-Transplant, and Pediatric Patients (03.T–U)
26 Neurosurgical and Perioperative Complications
26.1 Postoperative Seizures, Hemorrhage, Ischemia, and Hyperperfusion (04.A, C, D, H) 26.2 Infection, CSF Leak, and Pneumocephalus (04.B, E, F) 26.3 Complications of EVD and Lumbar Drain (04.G, I)
27 Ethics, Prognostication, and Organ Donation
27.1 Communication, Decision-Makers, Advance Directives, and DNR (05.A, B, G) 27.2 Uncertainties of Prognostication and the Self-Fulfilling Prophecy (05.C) 27.3 Palliative Care, Withdrawal, Withholding, and Futility (05.D–F) 27.4 Donation After Cardiac Death and Care of the Organ Donor (05.H–I)
24.3 Myasthenic Crisis (03.O.2)
Key Takeaways Explain This Topic AI
Myasthenic crisis is myasthenia gravis with respiratory or bulbar failure requiring ventilatory support; cholinergic crisis adds SLUDGE muscarinic signs and miosis from acetylcholinesterase-inhibitor overdose.
Intubate before respiratory collapse. Pyridostigmine is often held while the patient is ventilated because secretions worsen airway toilet, then restarted before weaning.
Rescue therapy is IVIG or plasma exchange. Corticosteroids help later but can worsen weakness for days after they are started, so begin them in a monitored setting after rescue is underway.
Avoid fluoroquinolones, aminoglycosides, magnesium, and beta blockers. Thymoma imaging is appropriate, but thymectomy is not an ICU day-1 procedure. Ice-pack and edrophonium tests are historical bedside tools, not crisis management.
Last updated: September 2026
Crisis is an airway diagnosis, not a titer
Myasthenia gravis (MG) is an autoimmune attack on the neuromuscular junction, most often acetylcholine-receptor (AChR) antibodies, less often muscle-specific kinase (MuSK) or LRP4. Myasthenic crisis is MG severe enough that ventilatory or bulbar failure threatens life—typically needing intubation or noninvasive ventilation. About 10% of generalized MG patients have a crisis, often in the first 2 years, after infection, surgery, pregnancy, or a new medication. Mortality with modern ICU care is far lower than in the era of the iron lung, but crash intubation of a patient with a weak neck and pooled secretions still kills.
The examination wants you to separate crisis from cholinergic crisis , intubate before the crash, choose IVIG or PLEX , hold pyridostigmine when the patient is ventilated, avoid a short list of drugs, and not send an unstable patient to the operating room for thymectomy on hospital day 1.
Crisis versus cholinergic crisis
Feature Myasthenic crisis Cholinergic crisis
Cause Too little neuromuscular-junction transmission (disease flare, infection, missed doses, offending drugs, steroid initiation) Too much acetylcholinesterase inhibitor (AChEI), historically high-dose pyridostigmine
Nicotinic motor picture Fatigable weakness, ptosis, diplopia, bulbar failure, respiratory failure Weakness as well, plus fasciculations and cramps
Muscarinic picture Not prominent SLUDGE : salivation, lacrimation, urination, diarrhea, gastrointestinal cramping, emesis; plus miosis , bradycardia, bronchorrhea
Pupils Usually mid-position Pinpoint if muscarinic tone is high
Frequency in modern ICUs The usual diagnosis Uncommon at contemporary pyridostigmine doses (crisis is rare below about 120 mg every 3 hours)
Immediate drug move Do not stop pyridostigmine in a still-extubated patient who needs it; do hold it once invasively ventilated Hold AChEI; atropine for muscarinic toxicity
If the picture is mixed and the patient is in extremis, secure the airway first . The historical edrophonium (Tensilon) test can precipitate either worse weakness or a cholinergic storm and is not an ICU procedure. The ice-pack test (ptosis improving after a minute of ice over the eyelid) is a clinic trick for suspected MG, not a crisis tool.
Intubate before the crash
Respiratory failure in MG is fatigable. Morning FVC can look acceptable and evening FVC can be a rapid-sequence emergency. Watch for staccato speech, weak neck flexion (the patient cannot lift the head off the pillow), a weak cough, paradoxical abdominal motion, and pooling of secretions. Arterial blood gas is a late monitor.
Many services use numbers similar to GBS: FVC under 20 mL/kg or a rapidly falling NIF. Some teach a myasthenia-specific 20/20/20 frame (FVC under 20 mL/kg, NIF worse than about −20 cm H2O, rising carbon dioxide). The exact mnemonic matters less than the principle: intubate electively when bulbar function or the trajectory of spirometry is unsafe. Noninvasive ventilation can rescue selected patients without heavy secretion burden or hypercapnic coma; it is not a plan for someone who cannot swallow.
Avoid succinylcholine (unpredictable duration and hyperkalemia risk in some neuromuscular patients). If a paralytic is required, a reduced-dose nondepolarizing agent with neuromuscular monitoring is the usual approach; anticipate prolonged block.
Pyridostigmine when the tube is in
Pyridostigmine should not be stopped in a worsening but still extubated patient—missed doses are a cause of crisis. Once the patient is invasively ventilated , most neurointensivists hold pyridostigmine . The modest benefit on strength is outweighed by bronchorrhea and mucus plugging, and the drug muddies the examination. Restart it before a weaning trial so that junctional transmission is supported when the tube comes out. Intravenous pyridostigmine (about 1 mg IV for 30 mg oral) can cause arrhythmias and is generally avoided.
IVIG or PLEX, then steroids with eyes open
International consensus guidance treats PLEX and IVIG as the short-term treatments for impending or manifest crisis. Expert consensus often favors PLEX when a faster effect is needed ; randomized comparisons suggest similar overall efficacy. IVIG is typically 2 g/kg divided over 2–5 days. PLEX is usually 5 exchanges over 7–14 days. Choose PLEX with caution in sepsis and hemodynamic instability; choose IVIG with caution in hypercoagulability, significant renal failure, or immunoglobulin hypersensitivity.
Corticosteroids are part of bridging to longer-term control, but they can worsen weakness 5–10 days after initiation in a large fraction of patients. Start them in the ICU after rescue therapy is underway, not as the sole emergency drug on the ward. A steroid dip is a reason the patient is still in the unit, not a reason to abandon steroids forever. Steroid-sparing immunosuppressants (azathioprine, mycophenolate, tacrolimus, rituximab—especially in MuSK MG) are not same-day crisis drugs.
MuSK MG is more bulbar, more crisis-prone, and often responds better to PLEX and rituximab than to acetylcholinesterase inhibitors, which may worsen MuSK symptoms.
Drugs that unmask the junction
Build a stop-list into every crisis admission medication review:
- Avoid or use only with no alternative Why it matters
- Fluoroquinolones Well-documented MG exacerbations
- Aminoglycosides Presynaptic impairment of acetylcholine release
- Macrolides , especially telithromycin Telithromycin has caused severe, sometimes fatal flares
Magnesium (infusions, cathartics, tocolysis) Competes at the junction; ICU replacement can tip a fragile patient
- Beta blockers Reduce neuromuscular transmission; labetalol drips are a frequent culprit
- Procainamide, quinidine, some calcium-channel blockers Membrane effects at the junction
- Botulinum toxin, D-penicillamine Obvious junctional toxins
- Iodinated contrast (occasional reports) Not an absolute ban, but do not ignore a temporal association
Infection still needs treatment. Pick a different antibiotic class rather than leaving pneumonia untreated.
Thymoma and thymectomy are not day-1 ICU procedures
A chest CT looking for thymoma belongs in the workup of new MG, and thymoma is over-represented among patients who reach crisis. Thymectomy for thymoma, or for non-thymomatous AChR generalized MG in the indicated age window, is disease-modifying—but it is planned after crisis rescue, when the patient is extubated or at least immunologically pretreated. Sending a crashing myasthenic to the operating room on arrival is the wrong sequence unless there is a separate surgical emergency (for example an obstructing mass with airway compromise that anesthesia and surgery have already planned around).
Examination traps
Performing edrophonium at the bedside of a hypercapnic patient.
Stopping pyridostigmine in a still-extubated patient who was missing doses.
Continuing high-dose pyridostigmine after intubation and then blaming the disease for mucus plugging.
Starting 80 mg of prednisone on the ward without IVIG or PLEX and without an ICU bed.
Prescribing levofloxacin and intravenous magnesium for a COPD flare in known MG.
Booking thymectomy as the 2 a.m. solution to ventilator dependence.