Study guide
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma
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)
7.1 Emergency Evaluation of Polytrauma, Chest, and Abdominal Trauma
Key Takeaways Explain This Topic AI
ATLS still sequences airway with cervical-spine protection, breathing, and circulation before a head CT; hypoxia and hypotension are the secondary insults that most reliably worsen traumatic brain injury.
Brain Trauma Foundation 4th edition systolic floors are ≥100 mm Hg for ages 50–69 and ≥110 mm Hg for ages 15–49 or over 70; permissive hypotension used for isolated hemorrhage is not appropriate when TBI is present or cannot be excluded.
Tension pneumothorax is a clinical diagnosis. ATLS 10th edition supports adult needle decompression at the fifth intercostal space slightly anterior to the midaxillary line, followed by mandatory tube thoracostomy.
An unstable patient with a positive FAST examination goes to laparotomy, not through the scanner. Massive hemothorax is suggested by ≥1,500 mL immediate chest-tube output or >200 mL/hour for 2–4 hours plus ongoing shock.
After damage-control packing, abdominal compartment syndrome is sustained intra-abdominal pressure >20 mm Hg plus new organ dysfunction and is treated with decompressive laparotomy, not more crystalloid.
Last updated: September 2026
Polytrauma is a competing-priorities problem, not a brain-first problem. On this exam, the expensive mistake is sending an unstable patient to computed tomography (CT) for a possible hematoma while an untreated tension pneumothorax, open-book pelvis, or hemoperitoneum is still collapsing cerebral perfusion pressure (CPP). Advanced Trauma Life Support (ATLS) still sequences Airway with cervical-spine protection, Breathing, Circulation, Disability, then Exposure (ABCDE) . The neurologic examination (Disability) is mandatory, but it does not license skipping hemorrhage control. Hypotension and hypoxia remain the two secondary insults most tightly linked to worse traumatic brain injury (TBI) outcome.
ATLS Sequence Versus Competing Brain Injury
Protect the cervical spine from first contact through imaging clearance: manual in-line stabilization during airway maneuvers, a correctly sized collar, log-roll only, and no neck-extending chin lift. Assume an unstable C-spine in the unconscious polytrauma patient until a high-quality CT (and, when indicated, magnetic resonance imaging for ligamentous injury) says otherwise.
If the Glasgow Coma Scale (GCS) is 8 or less, the airway is unprotected, or obstruction is impending, intubate. Use a hemodynamically gentle induction and have vasopressors drawn—induction is a classic moment of catastrophic cerebral hypoperfusion. Confirm tube position, then immediately recheck blood pressure and oxygenation.
Breathing comes next: inspect, auscultate, and percuss. Needle or finger decompression of suspected tension pneumothorax is a clinical move; do not wait for a chest radiograph. Circulation: stop external bleeding, place a pelvic binder over the greater trochanters for suspected unstable pelvic ring injury, obtain large-bore access, and activate massive transfusion rather than drowning the patient in crystalloid. Disability records GCS, pupils, and lateralizing signs after the ABCs are in motion, not instead of them. Exposure means fully undress, log-roll, and keep the patient warm.
The “competing brain injury” decision is destination, not sequence. An unstable patient with a positive Focused Assessment with Sonography in Trauma (FAST) goes to the operating room, not through the scanner. A patient restored to the Brain Trauma Foundation systolic floors can go to CT to look for a mass lesion. Hyperventilation is a brief bridge for herniation, not a default ventilator setting. Brain Trauma Foundation 4th edition teaching used on this exam: treat intracranial pressure (ICP) at 22 mm Hg, keep CPP about 60–70 mm Hg, and avoid PaCO2 below 25 mm Hg except as a temporizing measure.
Hypotension in TBI Is Catastrophic
Isolated truncal hemorrhage protocols sometimes use permissive hypotension until bleeding is controlled. That strategy is not appropriate when clinically important TBI is present or cannot be excluded. Cerebral autoregulation is often impaired; a single systolic dip can convert a salvageable contusion into a devastated brain. Brain Trauma Foundation 4th edition (Level III) states that maintaining systolic blood pressure (SBP) at ≥100 mm Hg for patients 50–69 years old, or ≥110 mm Hg for patients 15–49 or over 70 years old, may be considered to decrease mortality and improve outcomes. Treat hypotension immediately with blood products and vasopressors while source control proceeds. Do not withhold volume from a hypotensive TBI patient because of a theoretical concern about “popping the clot” in the abdomen—source control and blood-based resuscitation happen together.
Massive Transfusion Concepts
Massive transfusion is no longer defined only as 10 red-cell units in 24 hours. Operational definitions include replacement of an entire blood volume, about 3–4 units in an hour, or any activation of a massive transfusion protocol (MTP) . Give plasma, platelets, and red cells in a balanced ratio approaching 1:1:1 . The PROPPR trial compared 1:1:1 with 1:1:2; 1:1:1 achieved earlier hemostasis without a difference in 24-hour or 30-day mortality and is the usual MTP backbone. Tranexamic acid (TXA) within 3 hours of injury reduced bleeding deaths in CRASH-2; CRASH-3 supported TXA within 3 hours in TBI, particularly outside the most devastated presentations. Reverse hypothermia, acidosis, and hypocalcemia. Excess crystalloid worsens coagulopathy, abdominal hypertension, and cerebral edema.
Immediate Life-Threatening Chest Injuries
Injury Bedside clues First action What the exam expects next
Tension pneumothorax Distress or sudden hypotension, unilateral absent sounds, tracheal shift away, JVD (may be flat if empty) Needle or finger decompression, then chest tube Do not wait for imaging
Massive hemothorax Shock, dullness, absent sounds Blood products + 28–32 Fr tube ≥1,500 mL immediately or >200 mL/h for 2–4 hours → surgical thoracotomy consideration
Open (sucking) pneumothorax Chest-wall hole, bubbling Three-sided occlusive dressing Tube thoracostomy; never a fully sealed dressing without a tube
Flail chest Paradoxical segment, ≥3 contiguous ribs broken in ≥2 places Analgesia, oxygen, pulmonary toilet Underlying pulmonary contusion drives hypoxemia
Cardiac tamponade Shock, muffled sounds, equal breath sounds, pericardial FAST Volume, then window/repair Distinguishes from tension physiology
Blunt aortic injury Deceleration, wide mediastinum, left hemothorax, pulse deficit Anti-impulse control once diagnosed CT angiography; TEVAR for many grade 2–4 injuries
Tension Pneumothorax
Air under pressure collapses the lung, shifts the mediastinum, and obstructs venous return. Treat immediately. ATLS 10th edition supports a large over-the-needle catheter at the fifth intercostal space, slightly anterior to the midaxillary line in adults. The older second-interspace midclavicular site is a recognized alternative but fails more often in thick chests. Finger thoracostomy is used in many trauma bays. Tube thoracostomy is mandatory afterward. On a ventilator, a sudden rise in peak pressure plus hypotension is tension until proven otherwise.
Massive Hemothorax, Flail Chest, and Pulmonary Contusion
Shock plus dullness suggests blood, not air. ATLS treats immediate output of 1,500 mL or more (about one-third of blood volume) or ongoing output greater than 200 mL/hour for 2–4 hours as a reason to involve a surgeon for thoracotomy; the hemodynamic trajectory, not the number alone, drives the knife. Resuscitate with blood and consider autotransfusion.
Flail chest produces a free segment with paradoxical motion. The wall motion is dramatic; the physiology that hypoxemic patients die from is the underlying pulmonary contusion . Chest binders that restrict the wall are outdated. Priorities are multimodal analgesia (including regional catheters), pulmonary toilet, and oxygen. Noninvasive ventilation is reasonable if the airway is safe; intubate for exhaustion, severe hypoxemia, or an operation. Contusion often worsens over 24–48 hours as capillary leak peaks—do not over-resuscitate. Use lung-protective tidal volumes. Selected patients later benefit from surgical rib fixation after the brain and torso are stable.
Blunt Aortic Injury
Rapid deceleration shears the aorta at the ligamentum arteriosum (isthmus) . Clues include a widened mediastinum, left apical cap, first- or second-rib fracture, unexplained left hemothorax, and a pulse deficit. Diagnosis is CT angiography in a resuscitated patient. Anti-impulse control (heart-rate then blood-pressure reduction, typically a short-acting beta blocker before a vasodilator) limits wall stress. Thoracic endovascular aortic repair (TEVAR) is preferred for many grade 2–4 injuries. Delayed repair after other life-threatening bleeding is controlled is often safer than racing a stable intimal injury to the hybrid room while ICP and the pelvis are ignored. Free rupture remains immediately operative.
Pelvis, FAST, Laparotomy, and Compartment After Packing
Pelvic ring disruption can hide liters of retroperitoneal blood. Bind once, do not rock the pelvis repeatedly, and involve interventional radiology or a pelvic packer early. Selected torso or pelvic hemorrhage protocols use resuscitative endovascular balloon occlusion of the aorta (REBOA); it is a hemorrhage adjunct, not a brain therapy, and it still requires a definitive plan.
FAST interrogates Morrison’s pouch, the splenorenal fossa, the pelvis, and the pericardium. Extended FAST (eFAST) adds lung sliding for pneumothorax. Unstable plus positive FAST means laparotomy. Stable plus positive FAST means CT. Unstable plus negative FAST means look for pelvis, retroperitoneum, long-bone, and chest sources—do not declare the abdomen innocent and leave the bay.
Laparotomy indications include peritonitis, evisceration, hemodynamic instability with intraperitoneal blood, free air after blunt trauma, and failed nonoperative management of solid-organ injury. Damage-control packing stops coagulopathic bleeding and defers reconstruction. After packing, watch for abdominal compartment syndrome (ACS) . The World Society of the Abdominal Compartment Syndrome (WSACS) defines ACS as sustained intra-abdominal pressure (IAP) greater than 20 mm Hg (with or without abdominal perfusion pressure below 60 mm Hg) plus new organ dysfunction. Intra-abdominal hypertension is IAP ≥12 mm Hg. Measure bladder pressure with no more than 25 mL of saline, at end-expiration, supine, transducer zeroed at the midaxillary line. Rising ventilator pressures, oliguria, and a tense abdomen after massive resuscitation are the clinical picture. Treatment is decompressive laparotomy and open-abdomen management—not more crystalloid and paralysis as a complete plan.
Keep the collar on through every tube, roll, and trip to CT or the operating room.