Study guide
22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7)
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)
22.3 Epidural Hematoma, Subdural Hematoma, and Penetrating Injury (03.I.3–4, 7)
Key Takeaways Explain This Topic AI
Epidural hematoma is often arterial (middle meningeal artery), lentiform, and classically preceded by a lucid interval. Evacuate volume of 30 mL or more regardless of GCS, or any EDH with neurologic decline or anisocoria.
Acute subdural hematoma is crescentic. Thickness of 10 mm or more or midline shift of 5 mm or more is a usual evacuation threshold even if the GCS is still fair.
Chronic subdural hematoma is treated with evacuation plus a subdural drain (Santarius: recurrence 9.3% versus 24% without a drain). Middle meningeal artery embolization is an emerging adjunct to cut recurrence.
Do not remove a penetrating object in the emergency department. Obtain vascular imaging along the tract, treat infection risk, and use seizure prophylaxis more readily than in blunt TBI.
Last updated: September 2026
Blueprint items 03.I.3–4 and 03.I.7 are pattern-recognition plus a short list of cubic centimeters and millimeters. An epidural hematoma (EDH) is a skull-and-artery problem until proven otherwise. An acute subdural hematoma (aSDH) is a bridging-vein and high-energy problem. A chronic subdural hematoma (cSDH) is an elderly, atrophic, often anticoagulated problem whose recurrence you can reduce with a drain and, increasingly, middle meningeal artery (MMA) embolization. Penetrating injury adds a foreign body, a vascular tract, and a seizure and infection risk that blunt protocols under-treat.
Numbers below come from the 2006 surgical management of TBI guidelines (Bullock and colleagues), the Santarius drain trial ( NEJM 2009), and 2024 MMA-embolization randomized trials. This is independent ExamFinch teaching, not a BTF handbook reprint.
Epidural hematoma: lucid interval and 30 mL
Classic EDH is a lacerated middle meningeal artery under a temporal or temporoparietal fracture (pterion). Venous EDH occurs at the vertex or in the posterior fossa from a torn sinus and can still kill if the posterior fossa fills. The textbook lucid interval — knocked out, wakes, talks, then collapses as the clot grows — is memorable and incomplete. Many patients never lucid. Many “lucid” patients have a mild concussion rather than a true talk-and-die EDH. Still, a deteriorating patient with a lentiform extra-axial clot is an operative emergency, not a steroid infusion.
CT shape: biconvex (lentiform) , limited by cranial sutures (the dura is tacked at sutures), can cross the midline only if it is a vertex venous EDH that strips the sagittal sinus. Density is homogeneously hyperdense unless the patient is anemic or actively bleeding (swirl sign).
Surgical rules boards still use:
Volume 30 mL or greater: evacuate regardless of GCS.
Also operate for thickness over 15 mm , midline shift over 5 mm , anisocoria , or any neurologic decline referable to the clot.
Nonoperative observation is reserved for under 30 mL , thickness under 15 mm , shift under 5 mm , GCS over 8 , and no focal deficit , in a center that can repeat CT and reach an operating room immediately.
Anisocoria with an EDH is a herniation clock, not a reason to wait for a 30 mL recalculation. Posterior-fossa EDH has a lower volume tolerance because the brainstem is adjacent.
Acute subdural hematoma: crescent and 10 mm / 5 mm
Acute SDH layers over the hemisphere in a crescent , crosses sutures , and stops at the falx and tentorium . It is usually torn bridging veins after high-energy deceleration, or hemorrhagic transformation of a contused surface. The brain underneath is often more injured than the extra-axial millimeters suggest, which is why aSDH mortality exceeds EDH mortality even when the clot looks “smaller.”
Usual evacuation thresholds:
Thickness 10 mm or greater , or midline shift 5 mm or greater , regardless of GCS .
GCS 8 or less with ICP over 20 mm Hg attributable to the SDH.
A drop of 2 or more GCS points between injury and hospital arrival.
Asymmetric pupils or a motor posturing new deficit.
Technique (craniotomy versus decompressive craniectomy, bone flap size) is a neurosurgical call driven by swelling. Your job in the ICU is to reverse anticoagulants, keep the airway safe, treat ICP after the clot is out, and not delay the scanner-to-OR interval for a “complete” spine MRI in a herniating patient. Elderly, anticoagulated aSDH has a grim prognosis; that does not justify skipping reversal or skipping an operation in a previously independent patient who still has a salvageable exam.
Chronic subdural hematoma: drains and MMA embolization
cSDH presents days to weeks after often-minor trauma in older adults with atrophy, alcohol use, or antithrombotic therapy: gait failure, headache, fluctuating cognition, hemiparesis. CT is hypodense or mixed-density with septations. Burr-hole or minicraniotomy evacuation is first-line for symptomatic collections.
Santarius and colleagues ( NEJM 2009) randomized burr-hole evacuation with versus without a subdural drain . Recurrence requiring redrainage was 9.3% with a drain versus 24% without . Six-month mortality was 8.6% versus 18.1% . Leaving a drain is not optional trivia; it is the highest-yield cSDH trial on the exam.
MMA embolization targets the dural blood supply that feeds the inflammatory cSDH membrane. Three 2024 randomized trials (EMBOLISE, MAGIC-MT, STEM) showed fewer recurrences when embolization is added to surgery or, in selected nonsurgical patients, used as primary therapy. Teach it as an emerging adjunct that reduces return-to-OR rates, not as a replacement for evacuating a patient who is already herniating. Antiplatelet or anticoagulant restart after cSDH is individualized once a stability scan is clean; the recurrence cost of staying off stroke-prevention drugs is real.
Penetrating brain injury
Do not remove a knife, arrow, nail, or bone fragment in the trauma bay. The object may be tamponading a vessel or a sinus. Stabilize it, protect the airway without levering the object, give blood products if the patient is in shock, and go to CT/CTA and then the operating room with a cerebrovascular plan.
Vascular imaging (CTA, then catheter angiography when the tract crosses a named artery, cavernous sinus, or dural venous sinus) looks for occlusion, pseudoaneurysm, dissection, and traumatic fistula. Delayed pseudoaneurysm can appear days later, so a negative admission CTA does not close the book on a tract that kissed the middle cerebral artery.
Infection is expected: scalp flora, bone fragments, and sinus violation. Start prompt intravenous antimicrobials; there is no single universally mandated cocktail, but delay is the error. CSF leak and retained organic material raise abscess and meningitis risk. Heroic removal of every deep metallic fragment is not required; remove what is accessible and contaminated, elevate compound depressed fractures, and evacuate mass lesions.
Seizure prophylaxis is more justified than in blunt TBI. Penetrating injury carries a high rate of early and late post-traumatic epilepsy. A time-limited antiseizure medication (often at least 7 days, sometimes longer depending on cortical violation and retained fragments) is reasonable. Blunt TBI prophylaxis stays at the 7-day early-seizure window and is not a license for months of levetiracetam in every concussion.
Extra-axial and penetrating comparison
Feature Acute EDH Acute SDH Chronic SDH Penetrating
Shape Lentiform, suture-limited Crescentic, crosses sutures Crescentic hypodense or mixed Tract, fragments, possible aerocele
Usual vessel MMA (arterial); venous at vertex/PF Bridging veins Dural membrane / MMA supply Whatever the tract hits
Classic story Lucid interval, temporal fracture High-energy, coma, worse brain injury Elderly, minor trauma, waxing exam Impaled object, GSW, stab
Usual operate-now number ≥30 mL or decline / anisocoria ≥10 mm thick or ≥5 mm shift Symptomatic collection Mass lesion, contaminated bone, vascular injury
ICU adjunct Serial CT if observed ICP after craniotomy Drain ; consider MMA embolization Leave object; CTA; antibiotics; ASM
Worked contrast: a 22-year-old talks after a baseball to the temple, then drops his GCS as a 35 mL lentiform temporal clot appears — that is EDH at the 30 mL rule, middle meningeal, tonight. An 80-year-old on apixaban with a 12 mm crescentic aSDH and 6 mm of shift meets thickness and shift criteria even if he still says his name. A 78-year-old who shuffles in 3 weeks after a ground-level fall with a 22 mm hypodense cSDH gets holes and a drain , and you mention MMA embolization to reduce the next admission. A construction worker arrives with a nail gun nail in the orbit pointing at the cavernous sinus: you tape the nail in place, call the endovascular team, and do not pull it in the bay.