Study guide
18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4)
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)
18.3 Toxidromes, ICU Delirium, and Hypertensive Encephalopathy (03.A.2–4)
Key Takeaways Explain This Topic AI
Recognize opioid, anticholinergic, sympathomimetic, serotonin syndrome, neuroleptic malignant syndrome, baclofen withdrawal, and alcohol/benzodiazepine withdrawal by vital signs, pupils, skin, and reflex pattern — not by a urine drug screen alone.
Serotonin syndrome is hyperreflexic with clonus; NMS is lead-pipe rigid and bradyreflexic after dopamine blockade; baclofen (especially intrathecal) withdrawal can mimic sepsis or serotonin syndrome until the pump is restored.
SCCM PADIS 2018: screen delirium with CAM-ICU or ICDSC, prefer light sedation with propofol or dexmedetomidine over benzodiazepines in most ventilated adults, and do not use antipsychotics routinely to prevent or treat ICU delirium.
Hypertensive encephalopathy, PRES, RCVS, and ICH overlap in headache and seizure but split on imaging and BP strategy; do not apply an ICH systolic target of 140 mmHg blindly to every high-BP brain syndrome.
For hypertensive encephalopathy/PRES without ICH, lower MAP by about 20–25% in the first hour with a titratable agent and avoid overshoot hypoperfusion.
Last updated: September 2026
Toxidromes, ICU Delirium, and Hypertensive Encephalopathy
Quick Answer: Match pupils, skin, tone, and reflexes to the toxidrome. Serotonin syndrome = clonus/hyperreflexia; NMS = rigidity/bradyreflexia after dopamine antagonists; intrathecal baclofen withdrawal = fever, spasticity, pruritus until the pump is restored. PADIS : CAM-ICU or ICDSC, light non-benzodiazepine sedation, no routine antipsychotics. Hypertensive encephalopathy / PRES : drop MAP ~ 20–25% in the first hour , not to a random 90/60. RCVS is thunderclap plus vasoconstriction. ICH is blood on CT with its own BP evidence.
Not every unresponsive neuro-ICU patient has a primary brain lesion. Independent ExamFinch teaching in this section covers toxic-metabolic encephalopathies, ICU delirium, and hypertensive encephalopathy as listed among Neurocritical care diseases in the ABPN Content Specifications. This guide is not an ABIM or ABPN product.
Toxidromes that look like primary coma
- Toxidrome Pupils / skin Vitals Neurologic signature Immediate therapy
- Opioid Pinpoint, often diaphoretic or just pale Hypoventilation, bradycardia Coma, low tone Naloxone , airway
Anticholinergic Mydriasis, dry flushed skin, dry mouth, urinary retention Tachycardia, fever Agitated delirium, picking, decreased bowel sounds Physostigmine in selected pure cases; benzos for agitation; never as a “coma cocktail” substitute for glucose
Sympathomimetic (cocaine, amphetamine) Mydriasis, diaphoretic Hypertension, tachycardia, hyperthermia Agitation, seizures, stroke/ICH risk Benzodiazepines, cooling, BP control; avoid pure β-blockade in cocaine
Sedative-hypnotic / alcohol intoxication Midsize or small, not classic pinpoint Hypoventilation Coma, nystagmus Airway; not naloxone unless co-ingestion
Serotonin syndrome Mydriasis, diaphoretic Tachycardia, hyperthermia Hyperreflexia, inducible or spontaneous clonus , especially lower limbs Stop serotonergic drugs; benzos; cyproheptadine ; cooling
NMS Variable Fever, autonomic instability Lead-pipe rigidity , bradyreflexia , slower onset (days) Stop dopamine antagonists; bromocriptine / dantrolene in severe cases; ICU support
Baclofen withdrawal (esp. intrathecal pump failure) Often diaphoretic Fever, hypertension, tachycardia Rebound spasticity , seizures, pruritus; looks like sepsis or serotonin syndrome Restore baclofen (enteral and/or IT); benzos; do not treat as infection alone
Alcohol / benzo withdrawal Mydriasis, diaphoretic Tachycardia, hypertension Tremor, agitation, seizures, delirium tremens Benzodiazepines (or phenobarbital adjunct); thiamine
Hunter criteria for serotonin syndrome (in a patient on a serotonergic agent) include spontaneous clonus; inducible clonus plus agitation or diaphoresis; ocular clonus plus agitation or diaphoresis; tremor plus hyperreflexia; or hypertonia plus temperature >38 °C plus ocular or inducible clonus. That clonus/hyperreflexia split from NMS is the examination discriminator. NMS follows haloperidol , metoclopramide , or antipsychotic exposure (or sudden dopamine-agonist withdrawal in Parkinson disease) over days , with high CK and rigidity without the clonus show.
Intrathecal baclofen withdrawal is a neurocritical care original. A pump that runs dry, a catheter fracture, or a missed refill produces life-threatening hyperthermia and rigidity. Give baclofen back by the route that works and support the airway. Baclofen overdose is the opposite: hypotonic coma, hypothermia, and areflexia — do not reverse a pump for that picture.
Alcohol withdrawal seizures cluster at about 12–48 hours ; delirium tremens at about 48–96 hours (later if benzodiazepines were on board). Benzodiazepines are first-line. Antipsychotics treat hallucinations but do not raise the seizure threshold. Benzodiazepine withdrawal can be delayed days after a long-acting agent stops and can last longer than alcohol withdrawal.
Loading diagram... Hyperthermic rigidity: serotonin syndrome versus NMS versus baclofen withdrawal
ICU delirium: PADIS, not a haloperidol standing order
Delirium is an acute disturbance of attention and awareness that fluctuates. Hypoactive delirium is easy to miss and is associated with worse cognition and longer stays. The 2018 SCCM PADIS guidelines (Pain, Agitation/sedation, Delirium, Immobility, Sleep) tell you to routinely screen with a validated tool: CAM-ICU (Confusion Assessment Method for the ICU) or ICDSC (Intensive Care Delirium Screening Checklist), after a sedation score such as RASS . CAM-ICU requires acute/fluctuating change, inattention , and either disorganized thinking or an altered level of consciousness.
Prevention is the ABCDEF bundle: assess/treat pain, both SAT and SBT, choice of sedation, delirium monitoring, early mobility, family engagement. For most ventilated adults, PADIS suggests light sedation and propofol or dexmedetomidine rather than benzodiazepines . Use dexmedetomidine when agitation is blocking a wean. Do not routinely give typical or atypical antipsychotics to prevent delirium , and PADIS does not support antipsychotics as routine treatment of ICU delirium (they remain reasonable for dangerous agitation after non-drug measures and for specific psychiatric indications). Benzodiazepines stay indicated for alcohol/benzo withdrawal and some seizure indications — that is not a contradiction of “avoid benzos as default sedation.”
Fix the reversible causes: hypoxia, shock, infection, sodium, glucose, urine retention, restraint, sleep disruption, and the medication list (anticholinergics, extra benzos, high-dose opioids). A “new coma” that is actually hypoactive delirium plus residual midazolam is an exam favorite.
Hypertensive encephalopathy, PRES, RCVS, and ICH
These four share headache, seizure, and high blood pressure in some patients. They are not interchangeable.
Hypertensive encephalopathy is acute cerebral hyperperfusion when BP exceeds the upper limit of autoregulation (shifted even higher in chronic hypertension). Papilledema may be present. CT may be near-normal or show edema. Treat as a hypertensive emergency : ICU, arterial-line-level monitoring, titratable nicardipine , clevidipine , or labetalol . Lower MAP by about 20–25% in the first hour , then toward roughly 160/100 mmHg over the next 2–6 hours , then toward baseline over 24–48 hours. Overshoot — a crash from 230 systolic to 110 — causes watershed ischemia in a brain whose autoregulatory floor has moved up. Nitroglycerin is a poor choice when ICP physiology matters because venodilation can raise cerebral blood volume.
Posterior reversible encephalopathy syndrome (PRES) is vasogenic edema, classically parieto-occipital T2/FLAIR hyperintensity with increased ADC (vasogenic, not cytotoxic), though atypical frontal, brainstem, and cerebellar patterns exist. Triggers: abrupt hypertension, eclampsia , calcineurin inhibitors , some chemotherapies, autoimmune disease. Treatment is the cause plus the same controlled BP reduction — not a malignant-MCA craniectomy reflex and not high-dose steroids as if it were ADEM unless an inflammatory mimic is proven.
Reversible cerebral vasoconstriction syndrome (RCVS) presents with thunderclap headache , often recurrent over days, sometimes after vasoconstrictive drugs or postpartum. Angiography shows segmental vasoconstriction that reverses in about 3 months. Convexity SAH, PRES-overlap edema, and rarely infarction occur. Imaging of vessels (CTA/MRA/DSA) is the discriminator from isolated PRES. Nimodipine is commonly used; avoid further vasoconstrictors (triptans, binge sympathomimetics).
Intracerebral hemorrhage is blood on CT . BP care follows ICH evidence ( INTERACT2 , ATACH-2 , AHA/ASA 2022 ICH guidance): uncontrolled hypertension promotes hematoma growth; intensive targets below about 130 mmHg systolic in ATACH-2 increased renal adverse events. For many mild-to-moderate ICH patients with SBP 150–220 mmHg, lowering toward 140 mmHg is a studied range — that is not the same order set as “drop MAP 25%” for encephalopathy without a hematoma, and it is not a license to overshoot to 90 mmHg systolic.
Worked stems
A transplant recipient on tacrolimus has seizures, BP 190/110, and posterior T2 hyperintensity with high ADC. Think PRES ; lower BP in a 25% first-hour fashion and call the transplant team about the calcineurin inhibitor — not hypertonic saline as if this were cytotoxic MCA edema.
A patient with an IT baclofen pump is febrile, rigid, and delirious. Cultures are pending. The first disease-specific move is restore baclofen and inspect the pump, not “culture and wait” as the only plan.
Exam traps
Calling NMS serotonin syndrome because of fever. Using CAM-ICU never and calling all agitation “ICU psychosis” treated with scheduled haloperidol. Dropping SBP from 240 to 90 in hypertensive encephalopathy. Treating RCVS thunderclap as migraine with a triptan. Applying ICH 140 targets to PRES without blood, or ICH patients to 90 mmHg “to protect the brain.” Independent practice at /practice/abim-neurocritical-care should mix these four vascular-looking encephalopathies.