Study guide
8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8)
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)
8.2 PE, Pneumonia, and Pulmonary Edema (01.N.3, 7–8)
Key Takeaways Explain This Topic AI
Wells PE scoring is a pretest tool: signs of DVT 3, PE most likely 3, HR >100 1.5, immobilization or recent surgery 1.5, prior VTE 1.5, hemoptysis 1, cancer 1; two-level cutoff is PE unlikely ≤4 versus PE likely >4.
Systemic thrombolysis (commonly alteplase 100 mg over 2 hours) is for hypotensive massive PE without a prohibitive bleed risk; anticoagulation treats most other PE, and IVC filters are for anticoagulation contraindications or recurrent PE on adequate anticoagulation, not routine add-ons.
Acute intracranial hemorrhage, an unsecured aneurysm, and recent neurosurgery generally block systemic lytics and often block therapeutic anticoagulation; an IVC filter can bridge until the brain can tolerate anticoagulation.
Ventilator-associated pneumonia is pneumonia after more than 48 hours of mechanical ventilation; aspiration pneumonia follows a witnessed or suspected inoculum into dependent segments and is a different timing and microbiology problem.
Neurogenic pulmonary edema begins minutes to hours after SAH, seizure, or TBI from a sympathetic surge and often improves over 48–72 hours; distinguish it from cardiogenic edema and mixed Takotsubo physiology before aggressive diuresis that threatens CPP.
Last updated: September 2026
Thromboembolism, pneumonia, and pulmonary edema are the three pulmonary processes that most often compete with the brain for blood pressure, oxygenation, and anticoagulation. Neuro ICU patients combine immobility, inflammation, indwelling lines, and — frequently — a contraindication to the very therapy PE usually requires.
Pulmonary embolism: pretest probability and diagnosis
Pulmonary embolism (PE) is venous thrombus in the pulmonary arteries. Risk in the neuro ICU is high: hemiplegia, coma, delayed chemoprophylaxis after hemorrhage, and perioperative neurosurgery. Classic symptoms (pleuritic pain, hemoptysis, isolated dyspnea) are insensitive in intubated patients. Think PE when dead-space ventilation rises, PaCO2 climbs despite a stable or increased minute ventilation, oxygenation slips without new infiltrates, or unexplained hypotension and RV strain appear.
The Wells score is a conceptual pretest tool, not a substitute for imaging in a critically ill patient who already has tachycardia and immobility. Points:
- Criterion Points
- Clinical signs of DVT (leg swelling and deep-vein tenderness) 3
- PE is the most likely diagnosis (or equally likely) 3
- Heart rate > 100 beats/min 1.5
- Immobilization ≥ 3 days or surgery in the prior 4 weeks 1.5
- Previous DVT or PE 1.5
- Hemoptysis 1
- Active cancer (treatment within 6 months or palliative) 1
Two-level interpretation: PE unlikely ≤ 4 , PE likely > 4 . Traditional three-level bands are low < 2, moderate 2–6, and high > 6. In outpatients, PE-unlikely plus a negative D-dimer can stop the workup. In the ICU, D-dimer is almost always positive; go to CT pulmonary angiography (CTPA) when PE is the leading concern and the patient can travel or the scanner can come. V/Q scintigraphy is the usual alternative when iodinated contrast is unsafe and the chest radiograph is relatively clear. Bedside echo does not diagnose PE; it risk-stratifies (RV dilation, septal flattening, McConnell sign) and can justify rescue therapy in a crashing patient who cannot go to CT.
Risk strata used in guidelines:
Label (AHA / ESC language) Bedside meaning Usual first therapy
Massive / high-risk Hypotension (SBP < 90 mm Hg, a ≥40 mm Hg drop, or pressors) from PE Immediate anticoagulation plus reperfusion if bleed risk allows
Submassive / intermediate RV strain or biomarker injury without shock Anticoagulation; lytics only if the patient deteriorates
- Low-risk No shock, no RV injury Anticoagulation, sometimes off the ICU
- Anticoagulation, lytics, and the limited role of the IVC filter
Start parenteral anticoagulation as soon as PE is likely and bleeding risk is acceptable — typically an unfractionated heparin infusion in the neuro ICU because it is titratable and short-acting around EVDs, craniotomy, and angiograms. Direct oral anticoagulants are maintenance drugs, not crash-ICU tools when a trip back to the operating room is plausible.
Systemic thrombolysis is for massive / high-risk PE without a prohibitive bleed risk. The labeled adult regimen is alteplase 100 mg over 2 hours (commonly 10 mg bolus then 90 mg). Cardiac-arrest dosing (for example a 50 mg bolus) appears in resuscitation algorithms but is not a reason to lyse a stable patient. CHEST guidance suggests systemic thrombolysis in hypotensive PE with acceptable bleed risk and recommends against routine lytics in PE without hypotension unless the patient later deteriorates on anticoagulation. Catheter-directed therapy or surgical embolectomy are alternatives when systemic lytics are contraindicated and local expertise exists.
Inferior vena cava (IVC) filters do not treat existing pulmonary clot. CHEST recommends a filter when anticoagulation is contraindicated , and considers one for recurrent PE despite adequate anticoagulation . PREPIC-2 showed no reduction in recurrent PE when a retrievable filter was added to anticoagulation. Filters cause thrombosis of their own; plan retrieval when the contraindication lifts.
Neuro bleed versus PE: the conflict
This is the highest-yield collision on the exam.
Active intracranial hemorrhage, an unsecured ruptured aneurysm, and recent craniotomy or spinal surgery are standard absolute or near-absolute contraindications to systemic thrombolysis .
Therapeutic anticoagulation after ICH, hemorrhagic transformation, or SAH is delayed and individualized. An unsecured aneurysm generally forbids full anticoagulation; once the aneurysm is secured, the question becomes EVD-tract and hematoma risk, not just the original bleed.
Prophylactic subcutaneous heparin after ICH is a different, lower-dose decision (often after 24–48 hours of documented stability in AHA ICH discussions) and does not treat acute PE.
When acute proximal DVT or PE occurs during a hard anticoagulation hold, an IVC filter is a bridge , not a cure. Document a date to start anticoagulation and to retrieve the filter. Catheter-based thrombus removal may be discussed for obstructive PE when lytics are off the table.
Right-ventricular support (norepinephrine to keep CPP and coronary perfusion, cautious volume, inhaled pulmonary vasodilators if hypoxemia and RV failure dominate) can keep the patient alive while the brain and the clot are negotiated.
Worked conflict: a Hunt-Hess 4 SAH patient, aneurysm coiled yesterday, EVD in place, now hypotensive with a CTPA-proven saddle PE and a dilated RV. Systemic alteplase is ordinarily not given. Heparin may still be too early for the EVD tract. An IVC filter, hemodynamic support, and an urgent multidisciplinary decision about catheter therapy is the rational bundle — not “lyse because it is massive.”
VAP versus aspiration pneumonia
Ventilator-associated pneumonia (VAP) is pneumonia that develops after more than 48 hours of mechanical ventilation (hospital-acquired pneumonia is pneumonia after 48 hours in hospital, not necessarily ventilated). Diagnosis is clinical plus radiographic: new or progressive infiltrate plus fever, leukocytosis or leukopenia, purulent secretions, and worsening oxygenation. Quantitative cultures from bronchoalveolar lavage (BAL) or a protected specimen brush help in complex neuro ICU patients on prior antibiotics; endotracheal aspirates are easier but less specific. Empiric coverage follows local ICU ecology and risk for MRSA and Pseudomonas ; de-escalate when cultures return. Prevention is a bundle: head of bed 30–45°, oral care, subglottic suction if a suitable tube is in place, SAT/SBT, and minimizing unnecessary days of ventilation.
Aspiration pneumonia follows inoculation of orogastric contents. In a supine patient the posterior upper lobes and superior lower lobes are the dependent segments; upright aspiration prefers the basal lower lobes, more often on the right. Distinguish:
Entity Timing Mechanism Typical microbiology Immediate therapy
Chemical pneumonitis (Mendelson) Minutes after a large acidic inoculum Chemical injury Sterile at first Supportive; antibiotics not automatic
Aspiration pneumonia Hours to days after witnessed or suspected aspiration Infection of dependent lung Oral streptococci, anaerobes, enteric Gram-negatives Antibiotics that cover oral flora; add hospital pathogens if the patient is already colonized
VAP After > 48 h of ventilation Biofilm and microaspiration around the tube MRSA, Pseudomonas , enteric Gram-negatives depending on unit Empiric ICU pathogens, then de-escalate
A seizure or a depressed GCS at intubation can cause chemical pneumonitis that later becomes infection. Do not label every early infiltrate “VAP,” and do not withhold VAP treatment on day 4 because “it was probably aspiration at the scene.”
Neurogenic versus cardiogenic versus mixed pulmonary edema
Neurogenic pulmonary edema (NPE) is acute alveolar flooding after a CNS insult, classically aneurysmal SAH , convulsive seizure or status epilepticus, TBI, or ICH. Onset is minutes to hours (often within 2–12 hours). A catecholamine surge raises pulmonary capillary hydrostatic pressure and injures the endothelium, so the fluid can be protein-rich. Trigger zones include the hypothalamus, medulla, and insula. Many patients have a normal or near-normal left-ventricular ejection fraction; others overlap with stress (Takotsubo) cardiomyopathy , producing mixed hydrostatic and permeability edema. NPE often improves over 48–72 hours if the neurologic driver is controlled. Incidence after SAH is reported across a wide range (about 2% to over 40% depending on grade and ascertainment) and is associated with worse outcome — mostly because it marks a severe brain injury, not because the lung is independently unsurvivable.
Do not treat NPE as left-ventricular failure by default. Aggressive diuresis can drop CPP in a euvolemic SAH or TBI patient. Echo, ECG, troponin, and BNP separate the phenotypes.
Feature Neurogenic Cardiogenic Mixed (NPE + Takotsubo or volume overload)
Onset Minutes to hours after SAH, seizure, TBI, ICH Tracks ischemia, arrhythmia, or fluid load Hours after CNS insult plus wall-motion or filling-pressure abnormalities
Echo Often preserved EF Reduced EF, high filling pressures, dilated LA Regional or apical ballooning, variable EF
- BNP / NT-proBNP Normal or mildly up Clearly elevated Elevated
- PCWP (if measured) Normal or only transiently high Typically > 18 mm Hg May be high
- Edema character Can be protein-rich; sometimes alveolar hemorrhage Transudative Mixed
Course Often improves in 48–72 h if ICP and catecholamines settle Tracks cardiac recovery Variable; treat both ventricles and the brain
Trap Diurese to “dry lungs” and lose CPP Miss ACS or fluid overload and call everything “neurogenic” Treat only one compartment
Supportive care is lung-protective ventilation, treat the CNS insult (secure the aneurysm, stop seizures, control ICP), modest PEEP for hypoxemia, and euvolemia rather than empiric furosemide. If echo shows a crushed LV or RV, treat that physiology directly. If the picture persists beyond a few days with bilateral infiltrates and a P/F ≤ 300 on PEEP ≥ 5, the patient may have crossed into ARDS and should be ventilated as in Section 8.1.