Study guide
11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
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)
11.3 Thyrotoxicosis, Myxedema, Adrenal Crisis, and Dysglycemia (01.R.7–9)
Key Takeaways Explain This Topic AI
Thyroid storm is a clinical diagnosis (fever, tachycardia, altered mentation, a precipitant). Give a thionamide before iodine; add a beta blocker and a glucocorticoid. Apathetic hyperthyroidism in older adults can look like depression, weight loss, or atrial fibrillation without a storm.
Myxedema coma presents with hypothermia, hyponatremia, and CO2 narcosis. Treat with intravenous levothyroxine with or without T3, glucocorticoids until adrenal insufficiency is excluded, and supportive ventilation and passive rewarming.
Adrenal crisis is treated immediately with hydrocortisone (100 mg IV, then about 200 mg/day) plus saline. Do not wait for a cosyntropin test in a crashing patient.
SHINE found no 90-day functional benefit from intensive insulin (80–130 mg/dL) versus a standard range (80–179 mg/dL) after ischemic stroke, and more severe hypoglycemia. NICE-SUGAR showed harm from ~81–108 mg/dL in mixed ICU care. Typical neuro-ICU practice is about 140–180 mg/dL.
Hypoglycemia is a neurologic emergency. Treat it at the bedside. Steroid-induced hyperglycemia is expected on dexamethasone; treat with insulin rather than withholding a needed steroid.
Last updated: September 2026
A feverish, delirious patient with a goiter and a heart rate of 160 is a different emergency from a 34 °C, CO2-retaining patient with a sodium of 118 mEq/L and a surgical scar on the neck — and both are different from a day-2 MCA infarct whose glucose is 62 mg/dL after an insulin drip. This section covers thyrotoxicosis and thyroid storm , apathetic hyperthyroidism , myxedema coma , adrenal crisis , and dysglycemia in the neuro ICU, including SHINE-style stroke glucose targets. Independent ExamFinch material here follows topics listed under 01.R.7–9 in the ABPN Content Specifications. It is not an ABIM or ABPN product.
Why glucose and hormones share an examination leaf
The injured brain has little substrate reserve. Hypoglycemia looks like stroke, seizure, or herniation. Hyperglycemia tracks with edema and worse outcome but is not a reason to recreate a medical-ICU insulin drip from 2001. Thyroid and adrenal failures masquerade as "just another ICU encephalopathy." The items test first drugs , sequence , and which glucose band you will actually order .
Thyroid storm versus ordinary thyrotoxicosis
Thyrotoxicosis is excess circulating thyroid hormone. Thyroid storm is that physiology plus decompensation: thermoregulatory failure, CNS dysfunction, and cardiovascular instability, usually after a precipitant (infection, surgery, iodine load, amiodarone, trauma, childbirth, missed thionamide). It is a clinical diagnosis. The Burch–Wartofsky Point Scale is a bedside reminder (≥45 supports storm); do not wait for a magic free-T4 cutoff. TSH is suppressed and free T4/T3 are high, but the same labs occur in compensated thyrotoxicosis.
Storm features to hang a vignette on:
Fever, often high, with sweating.
Sinus tachycardia or atrial fibrillation, wide pulse pressure, high-output heart failure, sometimes shock.
Agitation, delirium, psychosis, or coma.
Diarrhea, vomiting, jaundice (hepatic strain is a severity marker).
Apathetic hyperthyroidism is the other trap, usually in older adults . There is little sympathetic theater: no fever, no tremor, no lid stare. Instead there is weight loss, depression or apathy, atrial fibrillation, and unexplained heart failure . The TSH is still suppressed. Missing this diagnosis is how a "failure to thrive" patient perioperatively goes into storm after a contrast load. Treat the hormone excess; do not file it as dementia.
Storm treatment sequence (order matters)
Supportive care is not optional: airway, cooling with acetaminophen and physical measures (avoid aspirin , which displaces thyroid hormone from binding proteins), volume, and treatment of the precipitant.
Then the hormone-specific bundle, in this order:
Beta blockade for adrenergic drive. Propranolol is traditional because it also reduces peripheral T4-to-T3 conversion at high dose. Use another IV beta blocker if propranolol is unavailable or if reactive airway disease forbids it; then add a conversion blocker later.
Thionamide first. Propylthiouracil (PTU) is often chosen in storm because it blocks peripheral conversion as well as synthesis (load commonly 500–1000 mg , then 200–250 mg every 4 hours ). Methimazole is preferred in most non-storm thyrotoxicosis because of PTU hepatotoxicity. Do not give iodine before a thionamide is in; iodine substrate without a synthesis block can worsen hormone production (jodbasedow).
Iodine (SSKI or Lugol) at least one hour after the thionamide, to block release of preformed hormone (Wolff–Chaikoff).
Glucocorticoid (hydrocortisone 100 mg IV every 8 hours, or equivalent dexamethasone) to block T4-to-T3 conversion and to cover possible coincident adrenal reserve failure.
Cholestyramine can interrupt enterohepatic thyroid-hormone recycling in refractory cases. Plasmapheresis is a last-resort bridge.
Do not give radioiodine in storm. Treat infection. If amiodarone is the precipitant, the pharmacology is messy (type 1 versus type 2 amiodarone thyrotoxicosis); the examination still wants the emergency sequence above plus expert endocrine input, not an unsupervised amiodarone restart.
Myxedema coma
Myxedema coma is decompensated hypothyroidism. It is not defined by non-pitting edema, and many patients are not fully comatose. Think of it in older women with longstanding hypothyroidism, a neck scar, or a forgotten levothyroxine bottle, after an infection, sedative, opioid, or cold exposure.
The neurologic and ICU cluster:
Hypothermia that looks like "the room is cold" until you believe the thermometer. Shivering may be absent.
Hyponatremia from impaired free-water excretion.
Hypoventilation and CO2 narcosis from a low hypoxic drive plus respiratory-muscle weakness. These patients need a CO2 on an arterial blood gas, not just a pulse oximeter that still reads 94% on a little oxygen.
Bradycardia, low-voltage ECG, pericardial effusion, delayed relaxation of reflexes, ileus, and a blunted mental status.
Precipitant: pneumonia, urosepsis, sedatives, lithium, or GI bleed.
TSH is usually very high in primary hypothyroidism; it may be low or inappropriately normal in central hypothyroidism (pituitary disease). Free T4 is low in both. Central disease is another reason the first bag includes glucocorticoid .
Treatment bundle:
Airway and ventilation for hypercapnia. Do not attribute the PCO2 of 80 mm Hg to "just being sleepy."
Intravenous levothyroxine (T4) , commonly a 200–400 mcg loading dose (lower in frail elderly or ischemic heart disease), then about 50–100 mcg daily . Liothyronine (T3) is added in some protocols (often 5–20 mcg , with caution for arrhythmia). The examination language is T4 with or without T3 , not T3 monotherapy as a swagger move.
Glucocorticoids (hydrocortisone in crisis doses) until adrenal insufficiency is excluded. Autoimmune thyroid and adrenal disease can travel together (autoimmune polyglandular syndromes), and T4 without cortisol repeats the apoplexy error in a different costume.
Passive rewarming. Aggressive active external heating can vasodilate a patient who has no thyroid reserve and drop the blood pressure.
Cautious volume; the hyponatremia is not a vaptan case on hour one.
Treat the precipitant. Hold sedatives.
Myxedema is a medical ICU disease that lands in the neuro ICU because of coma, hyponatremia, and CO2 narcosis. The wrong move is a large hypotonic load, an ice-water cooling blanket (that is storm thinking), or PTU.
Adrenal crisis
Adrenal crisis is acute cortisol deficiency with shock that is disproportionately fluid- and catecholamine-resistant until steroid is given. Causes in this unit: abrupt stop of chronic glucocorticoids (including dexamethasone used for tumor edema), pituitary apoplexy and Sheehan syndrome, bilateral adrenal hemorrhage (meningococcus, anticoagulation), etomidate in a borderline patient, and Waterhouse–Friderichsen physiology.
Clues: hypotension, nausea, abdominal pain, fever, hyponatremia , hyperkalemia (more in primary adrenal failure; often absent in secondary/pituitary failure because aldosterone is relatively spared), hypoglycemia, and eosinophilia. Primary failure also has mineralocorticoid loss and often hyperpigmentation if it has been chronic.
Treatment does not wait for the stim test:
Hydrocortisone 100 mg IV , then 50 mg every 6 hours or 200 mg/24 h as an infusion.
Isotonic saline , often a liter or more in the first hour, then as needed. These patients are volume-depleted.
Glucose if hypoglycemic.
Do not delay for cosyntropin. If you still need a diagnostic ACTH-stim later and the patient is not crashing, dexamethasone 4 mg IV does not register in many cortisol assays; in true crisis, hydrocortisone is the better drug because it supplies mineralocorticoid activity at high dose.
Fludrocortisone is unnecessary while hydrocortisone is at stress dose (roughly ≥50 mg/day ).
Relative adrenal insufficiency in septic shock is a separate, contested literature (CORTICUS, ADRENAL, APROCCHSS). For this examination, a patient with known adrenal or pituitary disease plus shock is not a place to withhold steroid while you wait for a research definition.
Worked picture: a 62-year-old on chronic prednisone 10 mg for temporal arteritis is admitted with meningitis, vomits her pills for two days, and has MAP 62 mm Hg, Na 124, K 5.6. Give hydrocortisone and saline now. Ordering a 250 mcg cosyntropin test and a 60-minute wait is the wrong sequence.
Dysglycemia: the injured brain and the insulin drip
Glucose is a neurologic vital sign. Hypoglycemia is a neuro emergency. It produces focal deficits that mimic stroke, seizures, coma, and delayed anoxic injury if it is prolonged. AHA/ASA acute ischemic stroke material treats glucose <60 mg/dL as a must-treat finding. In practice, symptomatic values in the 60s and a falling trend get dextrose without a debate. Give intravenous dextrose (commonly 25 g as D50 in adults, or a D10 infusion if you want a less brutal peak), recheck in 15 minutes, and find the cause (insulin, sulfonylurea, liver failure, adrenal crisis, missed meal on a drip). Do not wait for a laboratory confirmation if a point-of-care glucose is 42 mg/dL and the patient is seizing.
Hyperglycemia after stroke is common and is associated with worse edema, hemorrhagic transformation, and outcome. Association tempted two decades of tight insulin protocols. The trials went the other way.
NICE-SUGAR ( NEJM 2009) compared intensive insulin targeting 81–108 mg/dL with conventional control aiming under 180 mg/dL in a mixed ICU population. Intensive control increased 90-day mortality (27.5% versus 24.9%) and caused more severe hypoglycemia. That is the origin of the teaching to avoid a tight 80–110 mg/dL band in critical illness.
SHINE (Stroke Hyperglycemia Insulin Network Effort; Johnston and colleagues, JAMA 2019) asked the stroke-specific question. Adults with acute ischemic stroke and hyperglycemia were randomized within 12 hours to intensive continuous IV insulin targeting 80–130 mg/dL for up to 72 hours versus standard subcutaneous sliding-scale insulin targeting 80–179 mg/dL . Favorable 90-day modified Rankin Scale rates were 20.5% versus 21.6% — no benefit. Enrollment stopped for futility. Severe hypoglycemia (<40 mg/dL) occurred in 2.6% of the intensive arm and in none of the standard arm. Mean on-treatment glucose was about 118 versus 179 mg/dL , so the intensive arm truly lowered glucose; it just did not help recovery.
AHA/ASA acute ischemic stroke guidance states it is reasonable to treat hyperglycemia to a range of 140–180 mg/dL and to monitor closely to prevent hypoglycemia. That band is the practical neuro-ICU default: treat marked hyperglycemia, do not chase 100 mg/dL, and treat every low glucose as a brain insult. SCCM-style adult ICU practice uses a similar moderate target after NICE-SUGAR. Independent ExamFinch teaching: SHINE-style intensive control is not a stroke outcome tool; hypoglycemia is.
- Strategy Target What the evidence showed
- NICE-SUGAR intensive ~81–108 mg/dL Higher 90-day mortality in mixed ICU
- SHINE intensive 80–130 mg/dL No better 90-day mRS after ischemic stroke; 2.6% severe hypoglycemia
- SHINE standard 80–179 mg/dL Same functional outcome, no severe hypoglycemia in the trial arm
- AHA/ASA-style stroke practice ~140–180 mg/dL Treat hyperglycemia, prevent hypoglycemia
- Steroid-induced hyperglycemia
Dexamethasone for tumor edema, meningitis, spinal cord compression, or anti-emesis, and hydrocortisone for adrenal replacement, raise glucose. The pattern with a morning steroid is often afternoon and evening peaks more than fasting hyperglycemia. Treat with insulin (nutritional plus correction; basal if the steroid will continue). Do not stop a needed steroid to beautify a glucose chart, and do not start a SHINE-style drip to 90 mg/dL because dexamethasone is on the MAR. Watch for the opposite problem too: when the steroid is tapered, yesterday's insulin becomes today's hypoglycemia.
Non-neuro causes still appear: DKA and HHS after a stroke mimic, tube feeds plus glargine in renal failure, octreotide, and propofol infusions. The examination still wants the stroke-specific SHINE lesson, not a 12-step DKA pathway, unless the vignette is clearly ketoacidosis.
Exam traps
Iodine before a thionamide in storm. Aspirin for storm fever. Missing apathetic thyrotoxicosis in an elderly patient with new atrial fibrillation. Treating myxedema with PTU or with aggressive active rewarming. Levothyroxine without glucocorticoid in myxedema. Waiting for cosyntropin in adrenal crisis. An insulin drip to 80–110 mg/dL after SHINE and NICE-SUGAR. Ignoring a glucose of 48 mg/dL because the NIHSS is "just the stroke." Holding dexamethasone for vasogenic edema solely to avoid hyperglycemia.