Study guide
Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
ABPN Neurocritical Care Study Guide Exam
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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU
Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU
2 Chapter 2: Cerebral Physiology & Intracranial Dynamics
Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes
3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management
Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions
4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management
Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy
5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management
Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury
6 Chapter 6: Neuropharmacology, Analgesia & Sedation
ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU
7 Bleeding, Thrombosis & Hematologic Emergencies
Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine
Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention
9 Systemic Trauma & Environmental Injury
Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging
10 Cardiac Emergencies & Mechanical Support
IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies
11 Kidney Injury, Acid–Base & Renal Replacement
Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement
12 Systemic Infection & Endocrine Emergencies
Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies
13 Gastrointestinal & Hepatic Emergencies
Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects
14 Chapter 9: Neuroimaging in the Neuro-ICU
Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness
15 Chapter 10: Electrophysiology & Neuromonitoring
Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler
16 Angiography, Electrodiagnosis & CSF Analysis
Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage
17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria
Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria
18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies
Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction
19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage
Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH
20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia
Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations
21 Venous, Spinal & Traumatic Vascular Disease
Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury
22 Chapter 15: Traumatic Brain & Spinal Cord Injury
Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes
23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies
Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure
24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis
Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies
25 Neuroinflammation & Neurooncology
Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies
26 Pregnancy, Transplantation & Pediatric Care
Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care
27 Chapter 18: Neurosurgical & Perioperative Emergencies
Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies
28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU
Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor
Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity
Key Takeaways Explain This Topic AI
Acute brain injury transfusion decisions require clinical context; TRAIN and HEMOTION studied different populations and thresholds.
Thrombocytopenia with microangiopathic hemolysis and neurologic abnormalities requires urgent evaluation for TTP and other TMAs.
DIC requires treatment of its cause; blood products address bleeding or procedural needs rather than every abnormal laboratory value.
ICANS after immune effector-cell therapy can include aphasia, seizures, depressed consciousness, and cerebral edema.
Last updated: October 2026
Anemia and Oxygen Delivery
Arterial oxygen content depends mainly on hemoglobin concentration and saturation, with a much smaller dissolved oxygen contribution. A normal saturation therefore does not guarantee adequate oxygen delivery in severe anemia. Assess active bleeding, systemic perfusion, myocardial ischemia, cerebral hypoxia, and the adverse effects of transfusion rather than using saturation alone to decide whether anemia is clinically important.
General restrictive transfusion thresholds cannot be treated as a settled universal rule for all acute brain injuries. TRAIN (2024) compared triggers below 9 versus below 7 g/dL in patients with TBI, aSAH, or ICH and favored the liberal strategy for its neurologic outcome. HEMOTION (2024) compared thresholds of 10 versus 7 g/dL in moderate or severe TBI; its primary comparison did not reach statistical significance. These trials differ in populations, thresholds, and outcome methods. Neither proves that every neuro-ICU patient must be transfused to one fixed value.
During transfusion, watch for circulatory overload, hemolysis, allergic reactions, lung injury, electrolyte abnormalities, and infection-related concerns. Sudden respiratory distress can reflect transfusion-associated circulatory overload or other reactions as well as the original disease. Stop and evaluate a suspected serious reaction according to the transfusion protocol.
Platelets, Coagulation, and DIC
A low platelet count may reflect sepsis, consumption, drugs, marrow disease, immune destruction, or laboratory artifact. The safe threshold depends on the procedure and clinical indication. Intracranial surgery often uses a higher target than low-risk bedside procedures. Do not generalize evidence against platelet transfusion in nonsurgical aspirin-associated ICH to every patient with true thrombocytopenic bleeding.
Disseminated intravascular coagulation (DIC) involves systemic coagulation activation with variable consumption and fibrinolysis. Falling platelets, prolonged clotting times, increased fibrin-degradation markers, and low or declining fibrinogen support the diagnosis in the right setting. Fibrinogen may initially be normal or high as an acute-phase reactant. Treat the cause, such as sepsis, trauma, or malignancy. Give platelets, fibrinogen replacement, or plasma for active bleeding or a defined procedural need as appropriate; chasing every abnormal test can cause unnecessary transfusion.
Heparin-induced thrombocytopenia is a prothrombotic immune disorder, not simply bleeding from a low platelet count. Consider the timing, degree of platelet fall, thrombosis, and alternative causes. A sufficiently concerning presentation requires stopping heparin and arranging an appropriate non-heparin strategy with diagnostic testing and specialist input. Intracranial hemorrhage complicates treatment but does not make the thrombosis risk disappear.
Thrombotic Microangiopathies
Microangiopathic hemolytic anemia features fragmented erythrocytes, increased LDH, reduced haptoglobin, and other hemolysis findings. When accompanied by thrombocytopenia and organ injury, consider a thrombotic microangiopathy (TMA) . TTP, Shiga toxin-associated HUS, complement-mediated TMA, malignant hypertension, pregnancy syndromes, drugs, and transplant-associated disease have overlapping presentations but different treatments.
Syndrome Important clue Immediate implication
Immune TTP Severe ADAMTS13 deficiency, often neurologic involvement Urgent plasma-exchange and immune-directed pathway when strongly suspected
Shiga toxin-associated HUS Relevant diarrheal illness and renal injury Supportive and specialist care; do not assume identical therapy to TTP
Complement-mediated TMA Compatible syndrome after alternative causes assessed Consider complement-directed specialist treatment
DIC Consumptive coagulopathy in a triggering systemic illness Treat cause and manage bleeding or procedural needs
Do not wait for the historic full TTP pentad. Draw ADAMTS13 testing before plasma therapy when feasible, but do not delay urgent treatment of a high-probability case. Therapeutic plasma exchange and corticosteroids form core immune-TTP treatment; rituximab and caplacizumab are selected by the treating team. Routine prophylactic platelet transfusion is generally avoided in TTP, with exceptions for life-threatening bleeding or compelling procedures.
Sickle Cell and Acute Neurologic Deficits
Sickle cell disease can cause ischemic stroke, hemorrhage, venous thrombosis, or other neurologic complications. A new deficit or TIA requires immediate stroke evaluation and urgent hematology involvement. ASH recommends prompt transfusion, preferably within two hours of presentation for an acute event in the applicable window; exchange is often preferred when available, with simple transfusion used in selected circumstances. Avoid excessive viscosity from indiscriminately raising hemoglobin. Obtain imaging and assess other standard stroke therapies without delaying the sickle-specific pathway.
Chemotherapy, Stem-Cell Transplantation, and Immune Effector Cells
Treatment-related encephalopathy can reflect direct chemotherapy toxicity, infection, metabolic disturbance, PRES, vascular disease, or immune effector cell-associated neurotoxicity syndrome (ICANS) . After stem-cell transplantation, also consider transplant-associated TMA and opportunistic infection. Timeline, medication exposure, organ function, imaging, EEG, and targeted CSF assessment guide differentiation.
ICANS can follow CAR-T or related immune effector therapies. Early language or writing changes, inattention, tremor, seizures, and worsening arousal are important. ASTCT grading uses the ICE assessment together with consciousness, seizures, motor findings, and cerebral edema; the ICE score alone is not the whole grade. Exclude hypoglycemia, infection, stroke, medication effects, and other causes. Severe cases need ICU monitoring, EEG, appropriate corticosteroid therapy, and management of seizures or edema under the cellular-therapy protocol.
Cytokine release syndrome (CRS) can coexist and has a distinct treatment pathway. Tocilizumab is used for appropriate CRS but should not be portrayed as adequate sole therapy for isolated ICANS. Discuss treatment with the oncology or cellular-therapy team promptly. Immune checkpoint inhibitors can also cause encephalitis, myositis, neuropathy, and overlapping myasthenia–myositis–myocarditis; respiratory weakness or cardiac abnormalities warrant urgent multisystem evaluation.
Sources checked October 17, 2026: TRAIN , HEMOTION , ISTH TTP statements , ASTCT grading consensus , and ASH cerebrovascular guidance .