Study guide
Acute Ischemic Stroke Management & Thrombolysis
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
Acute Ischemic Stroke Management & Thrombolysis
Key Takeaways Explain This Topic AI
Rapidly assess time last known well, disabling deficits, glucose, noncontrast imaging, vascular anatomy, and treatment contraindications.
For eligible adults within 4.5 hours, alteplase 0.9 mg/kg up to 90 mg or tenecteplase 0.25 mg/kg up to 25 mg are supported; use the stroke-specific regimen.
Low NIHSS does not exclude a disabling stroke; selected unknown-onset or later presentations need an established imaging-selection pathway.
After IVT-associated bleeding, urgently assess imaging and hemostasis; cryoprecipitate and selected antifibrinolytic strategies require protocol-based use.
Last updated: October 2026
Acute Ischemic Stroke Management & Thrombolysis
Acute ischemic stroke ( A I S AIS A I S ) is a hyperacute medical emergency where rapid recanalization directly determines neurological salvage and long-term functional independence. Neurocritical care management requires rapid triage, rigorous physiological optimization, and the prompt deployment of intravenous thrombolysis and endovascular therapies.
- Emergency Evaluation & Hyperacute Triage
- The Neurovascular Clock: Time Is Brain
In acute large vessel occlusion ( L V O LVO L V O ), interruption of cerebral arterial blood flow triggers a core of immediate, irreversible necrotic infarction surrounded by an ischemic penumbra—hypoperfused tissue ( C B F between 10 and 20 mL / 100 g / min CBF\text{ between }10\text{ and }20\text{ mL}/100\text{ g}/\text{min} CBF between 10 and 20 mL /100 g / min ) that remains electrically silent but metabolically viable. Quantitatively, the typical patient with an untreated anterior circulation large vessel occlusion loses:
- 1.9 million 1.9\text{ million} 1.9 million neurons every minute
- 14 billion 14\text{ billion} 14 billion synapses every minute
- 12 km 12\text{ km} 12 km ( 7.5 miles 7.5\text{ miles} 7.5 miles ) of myelinated axonal fibers every minute
- An estimated 3.1 weeks of healthy brain life lost for every hour of delayed reperfusion
Note
Hyperacute triage targets a door-to-imaging time ≤ 20 minutes \le 20\text{ minutes} ≤ 20 minutes and a door-to-needle time ≤ 45 minutes \le 45\text{ minutes} ≤ 45 minutes (with best practice goals ≤ 30 minutes \le 30\text{ minutes} ≤ 30 minutes ), reflecting the rapid transition of penumbra into necrotic core.
National Institutes of Health Stroke Scale (NIHSS)
The NIHSS is a validated 15-item neurological impairment scale ranging from 0 to 42. It evaluates level of consciousness, horizontal gaze, visual fields, facial palsy, motor drift, limb ataxia, sensory loss, language/aphasia, dysarthria, and inattention/extinction:
- Minor stroke: 1 – 4 1\text{--}4 1 – 4
- Moderate stroke: 5 – 14 5\text{--}14 5 – 14
- Severe stroke: 15 – 20 15\text{--}20 15 – 20
- Very severe stroke: > 20 > 20 > 20
Clinical Pitfall: The NIHSS is heavily weighted toward left hemispheric anterior circulation deficits (aphasia yields up to 7 points), whereas severe right hemisphere non-dominant strokes (profound neglect, anosognosia) or posterior circulation strokes (vertigo, diplopia, dysmetria, bulbar palsy, isolated hemiataxia) may score deceitfully low (e.g., NIHSS 2–4) despite carrying catastrophic disability or impending basilar thrombosis.
Emergency Neuroimaging & ASPECTS Scoring
Emergent non-contrast head CT ( N C C T NCCT NCCT ) is mandatory to rule out acute intraparenchymal hemorrhage ( I P H IPH I P H ), subdural hematoma, or extensive established infarction. Early ischemic changes ( E I C EIC E I C ) include loss of gray-white matter differentiation at the insular ribbon, lentiform nucleus obscuration, and cortical sulcal effacement.
The Alberta Stroke Program Early CT Score (ASPECTS) is a 10-point quantitative topographic CT assessment of the middle cerebral artery ( M C A MCA MC A ) territory across two axial slices (ganglionic and supraganglionic levels):
Subcortical structures (3 points): Caudate ( C C C ), Lentiform ( L L L ), Internal Capsule posterior limb ( I C IC I C )
Cortical regions (7 points): Insular cortex ( I I I ), M 1 M1 M 1 (anterior inferior MCA), M 2 M2 M 2 (anterior lateral MCA), M 3 M3 M 3 (posterior temporal MCA), M 4 M4 M 4 (anterior superior MCA), M 5 M5 M 5 (lateral MCA above M2), M 6 M6 M 6 (posterior superior MCA above M3)
Normal CT receives 10 / 10 10/10 10/10 ; each defined area demonstrating early hypodensity subtracts 1 point. An ASPECTS ≤ 7 \le 7 ≤ 7 indicates extensive ischemic core, while ASPECTS ≤ 5 \le 5 ≤ 5 historically carried higher hemorrhage risk.
Intravenous Thrombolysis: Pharmacology & Evidence
Intravenous thrombolysis converts plasminogen to active plasmin, which lyses cross-linked fibrin polymers within the thromboembolism. The 2026 AHA/ASA Stroke Guidelines recognize two primary thrombolytic agents.
Parameter Alteplase (rtPA) Tenecteplase (TNK-tPA)
Molecular Structure Recombinant wild-type human tPA Genetically engineered triple mutant ( T 103 N T103N T 103 N , N 117 Q N117Q N 117 Q , K H R R 296 - 299 A A A A KHRR\,296\text{-}299\,AAAA KH RR 296 - 299 AAAA )
Fibrin Specificity Baseline ( 1 × 1\times 1 × ) 14 -fold 14\text{-fold} 14 -fold higher than alteplase
PAI-1 Resistance Sensitive to endogenous inhibition 80 -fold 80\text{-fold} 80 -fold higher resistance to PAI-1
Plasma Half-life ( t 1 / 2 t_{1/2} t 1/2 ) 4 – 8 minutes 4\text{--}8\text{ minutes} 4 – 8 minutes 20 – 24 minutes 20\text{--}24\text{ minutes} 20 – 24 minutes
Dosing Regimen 0.9 mg/kg 0.9\text{ mg/kg} 0.9 mg/kg IV (max 90 mg 90\text{ mg} 90 mg ): 10 % 10\% 10% bolus over 1 min, 90 % 90\% 90% over 60 min 0.25 mg/kg 0.25\text{ mg/kg} 0.25 mg/kg IV single bolus over 5–10 seconds (maximum 25 mg 25\text{ mg} 25 mg )
Key Trial Evidence NINDS rt-PA ( 0 – 3 h 0\text{--}3\text{ h} 0 – 3 h ), ECASS III ( 3 – 4.5 h 3\text{--}4.5\text{ h} 3 – 4.5 h ) AcT, EXTEND-IA TNK (Parts 1 & 2), NOR-TEST 2
Guideline Status Class 1 ( 0 – 4.5 hours 0\text{--}4.5\text{ hours} 0 – 4.5 hours ) Class 1 alternative to alteplase ( 0 – 4.5 hours 0\text{--}4.5\text{ hours} 0 – 4.5 hours )
Tenecteplase Advantages
Tenecteplase's enhanced fibrin specificity preserves circulating fibrinogen and alpha-2-antiplasmin, producing less systemic lytic coagulopathy. In the AcT trial (randomized non-inferiority trial of 1,600 patients), tenecteplase 0.25 mg/kg 0.25\text{ mg/kg} 0.25 mg/kg demonstrated non-inferiority to alteplase with identical rates of 90-day functional independence (mRS 0–1: 36.9 % 36.9\% 36.9% vs 34.8 % 34.8\% 34.8% ) and symptomatic intracranial hemorrhage ( 3.4 % 3.4\% 3.4% vs 3.2 % 3.2\% 3.2% ). In EXTEND-IA TNK , tenecteplase prior to endovascular thrombectomy achieved substantially higher rates of substantial early recanalization than alteplase ( 22 % 22\% 22% vs 10 % 10\% 10% ) and superior 90-day functional recovery. Furthermore, single-bolus administration streamlines inter-facility transfer without requiring infusion pump maintenance.
- Eligibility Criteria, Hemodynamics, and Absolute Contraindications
- Blood Pressure Thresholds
Hypertension dramatically increases the risk of reperfusion-induced intracranial hemorrhage.
Pre-treatment threshold: Blood pressure must be lowered to S B P < 185 mmHg SBP < 185\text{ mmHg} SBP < 185 mmHg and D B P < 110 mmHg DBP < 110\text{ mmHg} D BP < 110 mmHg before initiating thrombolysis.
Post-treatment maintenance: Blood pressure must remain strictly < 180 / 105 mmHg < 180/105\text{ mmHg} < 180/105 mmHg for at least 24 hours post-thrombolysis.
First-line intravenous antihypertensives include:
Nicardipine: Continuous IV infusion at 5 mg/h 5\text{ mg/h} 5 mg/h , titrated by 2.5 mg/h 2.5\text{ mg/h} 2.5 mg/h every 5–15 minutes (maximum 15 mg/h 15\text{ mg/h} 15 mg/h ).
Clevidipine: Rapidly cleared dihydropyridine calcium channel blocker; start at 1 – 2 mg/h 1\text{--}2\text{ mg/h} 1 – 2 mg/h , titrate by doubling every 2–5 minutes until goal achieved (follow the current dosing protocol and lipid-load limits).
Labetalol: 10 – 20 mg 10\text{--}20\text{ mg} 10 – 20 mg IV push over 1–2 minutes, repeatable once or followed by continuous infusion ( 2 – 8 mg/min 2\text{--}8\text{ mg/min} 2 – 8 mg/min ).
Important
If systolic blood pressure cannot be maintained below 185 mmHg 185\text{ mmHg} 185 mmHg or diastolic blood pressure below 110 mmHg 110\text{ mmHg} 110 mmHg with titratable medications, do not administer thrombolysis . Permitting thrombolysis under refractory severe hypertension causes catastrophic intracranial hemorrhage.
Eligibility Is a Structured Risk Decision
Use the complete current stroke protocol rather than a short memorized absolute-contraindication table. Acute intracranial bleeding, active major bleeding, severe relevant coagulopathy, uncontrolled pressure despite treatment, suspected aortic dissection, and suspected infective endocarditis can make IV thrombolysis unsafe. Recent surgery, trauma, anticoagulant exposure, prior hemorrhage, and structural lesions require attention to their specific characteristics and the current guideline.
An incidental unruptured aneurysm or extra-axial neoplasm does not automatically prohibit IVT. An intra-axial tumor has different bleeding considerations. Recent DOAC exposure requires timing, kidney function, drug-specific activity testing when available, and specialist interpretation; a normal INR does not exclude significant DOAC activity. No single universal concentration cutoff or administration of a reversal agent guarantees eligibility. Do not delay an eligible treatment while obtaining laboratory tests that are not clinically required, but investigate suspected coagulopathy promptly.
Within 4.5 hours, treat eligible adults with disabling deficits rapidly regardless of a low NIHSS. For nondisabling deficits, the 2026 guideline favors appropriate dual antiplatelet therapy rather than IVT. Disability is patient-specific: hand weakness or aphasia may prevent a patient's usual work despite few NIHSS points. Selected unknown-onset or 4.5–9-hour patients may qualify through DWI-FLAIR or perfusion mismatch criteria. These pathways require their own imaging and clinical criteria and do not make every late presentation eligible.
Unknown Time of Onset & Wake-Up Strokes (The WAKE-UP Protocol)
T2-FLAIR: Visible signal changes evolve over a variable interval. Absence of marked FLAIR signal can support an established imaging-selection pathway but is not a precise clock for an individual lesion.
In WAKE-UP, administering alteplase to patients with DWI-FLAIR mismatch resulted in a significantly higher proportion of patients with favorable functional outcomes at 90 days ( 53.3 % 53.3\% 53.3% vs 41.8 % 41.8\% 41.8% , p = 0.02 p = 0.02 p = 0.02 ) with an acceptable sICH rate ( 2.0 % 2.0\% 2.0% vs 0.4 % 0.4\% 0.4% ).
Suspected Hemorrhage After IVT
A new headache, vomiting, abrupt hypertension, reduced consciousness, or worsening deficit requires urgent assessment. Stop an alteplase infusion if still running, obtain emergency noncontrast CT and blood tests including CBC, coagulation studies, fibrinogen, and blood bank testing, and involve the stroke, neurocritical, neurosurgical, and transfusion teams. Different studies use different sICH definitions; do not wait for a four-point NIHSS change or a particular hematoma category before investigating deterioration.
The 2026 guidance includes cryoprecipitate 10 units over 10–30 minutes with repeat fibrinogen assessment and replacement to maintain at least 150 mg/dL. Antifibrinolytics such as tranexamic acid or aminocaproic acid may be useful, particularly when blood products are contraindicated or cryoprecipitate is not available promptly. This is not a mandatory identical cryoprecipitate-plus-TXA bundle for every patient. Address any additional coagulopathy separately. PCC is not a specific antidote to fibrinolysis.
Individualize pressure management to bleeding severity, perfusion, intracranial pressure, and the patient's trajectory rather than applying a universal SBP-below-140 rule after all reperfusion complications. Treat hydrocephalus, herniation, airway failure, and systemic instability in parallel. Document serial examinations and imaging, reassess hemostasis, and communicate uncertainty to the family.
Source: 2026 AHA/ASA ischemic stroke guideline .