Study guide
4.2 Diffuse Alveolar Hemorrhage, Interstitial Lung Disease, Pulmonary Vasculitis & Noncardiogenic Edema
ABIM Critical Care Medicine Study Guide Exam
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1 Chapter 1: Exam Orientation: Format, Blueprint & Study Strategy
1.1 ABIM Critical Care Medicine Exam: Format, Blueprint & Study Strategy
2 Chapter 2: Acute Respiratory Failure & ARDS
2.1 ARDS Definition, Pathophysiology & Phenotypes 2.2 Lung-Protective Mechanical Ventilation 2.3 Refractory ARDS: Prone Positioning, Neuromuscular Blockade & VV-ECMO
3 Chapter 3: Obstructive Airways, Pulmonary Vascular & Pleural Emergencies
3.1 Severe Asthma & COPD Exacerbations in the ICU 3.2 Massive & Submassive Pulmonary Embolism 3.3 Pulmonary Hypertension & Right Ventricular Failure in the ICU 3.4 Massive Hemoptysis, Complex Pleural Effusions & Thoracic Drainage
4 Chapter 4: Airway, Parenchymal & Nonthrombotic Pulmonary Emergencies
4.1 Airway Management, Upper-Airway Obstruction & Artificial-Airway Complications 4.2 Diffuse Alveolar Hemorrhage, Interstitial Lung Disease, Pulmonary Vasculitis & Noncardiogenic Edema 4.3 Severe Community-Acquired & Viral Pneumonia 4.4 Nonthrombotic Embolism (Air, Fat, Amniotic Fluid, Tumor, Septic) & Acute Chest Syndrome
5 Chapter 5: Mechanical Ventilation Modes, Dyssynchrony & Liberation
5.1 Mechanical Ventilator Modes & Advanced Breath Delivery 5.2 Patient-Ventilator Dyssynchrony & Waveform Analysis 5.3 Ventilator Liberation, Spontaneous Breathing Trials & Post-Extubation Support
6 Chapter 6: Shock Syndromes & Hemodynamic Principles
6.1 Shock Classification, Cellular Pathophysiology & Biomarkers 6.2 Hemodynamic Monitoring: Arterial Lines, CVP & Pulmonary Artery Catheter 6.3 Dynamic Assessment of Fluid Responsiveness & Resuscitation Targets
7 Chapter 7: Vasoactive Therapies & Mechanical Circulatory Support
7.1 Vasopressors & Inotropes: Pharmacology & Clinical Titration 7.2 Temporary Mechanical Circulatory Support: IABP, Impella & TandemHeart 7.3 Venoarterial ECMO (VA-ECMO) & Differential Hypoxemia 7.4 Post-Cardiac Arrest Care, Targeted Temperature Management & Neuroprognostication
8 Chapter 8: Acute Kidney Injury & Renal Replacement Therapy
8.1 KDIGO AKI Classification, Etiologies & Diagnostic Evaluation 8.2 Continuous Renal Replacement Therapy (CRRT) vs Intermittent Hemodialysis 8.3 Indications & Timing for RRT in Critical Illness: AKIKI & STARRT-AKI
9 Chapter 9: Electrolyte, Acid-Base & Endocrine Emergencies
9.1 Severe Dysnatremias: Hyponatremia, Hypernatremia & Osmotic Demyelination 9.2 Potassium, Calcium, Magnesium & Phosphate Disorders 9.3 Complex & Mixed Acid-Base Disorders: Boston vs Copenhagen vs Stewart 9.4 Endocrine Crises: DKA, HHS, Thyroid Storm, Myxedema Coma & Adrenal Crisis
10 Chapter 10: Glycemic Control, Hyperammonemia, Pituitary & Adrenal Disorders
10.1 ICU Glycemic Control & Severe Hypoglycemia 10.2 Non-Hepatic Hyperammonemia & Metabolic Encephalopathy 10.3 Pituitary Emergencies, Adrenal Excess & Critical Illness-Related Corticosteroid Insufficiency
11 Chapter 11: Acute Coronary Syndromes & Cardiac Arrhythmias
11.1 Acute Coronary Syndromes & Mechanical Complications of Myocardial Infarction 11.2 Critical Tachyarrhythmias: Atrial Fibrillation with RVR, VT & VF 11.3 Critical Bradyarrhythmias, Conduction Blocks & Temporary Cardiac Pacing
12 Chapter 12: Acute Heart Failure, Valvular & Pericardial Emergencies
12.1 Acute Decompensated Heart Failure & Cardiogenic Pulmonary Edema 12.2 Acute Valvular Regurgitation & Prosthetic Valve Emergencies 12.3 Pericardial Tamponade & Acute Aortic Syndromes
13 Chapter 13: Myocardial Disease, Hypertensive & Cardiac Device Emergencies
13.1 Fulminant Myocarditis, Stress & Peripartum Cardiomyopathy, and Hypertrophic Cardiomyopathy 13.2 Hypertensive Emergencies & Ruptured Abdominal Aortic Aneurysm 13.3 Implanted Cardiac Devices, LVAD Emergencies & Electrical Storm
14 Chapter 14: Sepsis & Systemic Infectious Diseases
14.1 Sepsis-3 Definitions & Surviving Sepsis Campaign 2026 Guidelines 14.2 Refractory Septic Shock & Adjunctive Therapies 14.3 Multidrug-Resistant Pathogens & Antimicrobial Stewardship in the ICU
15 Chapter 15: ICU-Acquired & Severe Focal Infections
15.1 Hospital-Acquired & Ventilator-Associated Pneumonia 15.2 Central Line-Associated Bloodstream Infections & Catheter-Associated UTIs 15.3 Intra-Abdominal Sepsis, Necrotizing Soft Tissue Infections & CNS Infections
16 Chapter 16: Focal, Special-Host & Systemic Infections
16.1 CNS Infections Beyond Bacterial Meningitis: Encephalitis, Brain Abscess & Epidural Abscess 16.2 Infections in the Immunocompromised Host, Tropical & Bioterror Infections 16.3 Infective Endocarditis, Device Infections & Other Focal Cardiovascular Infections 16.4 Antimicrobial Pharmacokinetics, Allergy, Toxicity & Infection Prevention 16.5 Gastrointestinal & Hepatobiliary Infections: Fulminant C. difficile, Typhlitis, CMV Colitis & Abscesses
17 Chapter 17: Neurocritical Care & Coma
17.1 Coma, Altered Mental Status & Acute Delirium in the ICU 17.2 Status Epilepticus & Non-Convulsive Status Epilepticus 17.3 Acute Ischemic Stroke & Intracranial Hemorrhage
18 Chapter 18: Cerebrovascular Syndromes, Encephalopathy & Withdrawal States
18.1 Cerebral Venous Sinus Thrombosis, PRES & Reversible Cerebral Vasoconstriction Syndrome 18.2 Alcohol & Sedative Withdrawal, Wernicke Encephalopathy & Drug-Induced Encephalopathy
19 Chapter 19: Intracranial Hypertension & Neuromuscular Weakness
19.1 Intracranial Pressure Monitoring, Cerebral Perfusion & Tiered ICP Management 19.2 Acute Neuromuscular Respiratory Failure, ICU-Acquired Weakness & Brain Death Determination
20 Chapter 20: Traumatic Brain Injury, Spinal Cord Injury & Toxin-Mediated Paralysis
20.1 Traumatic Brain Injury Management & Paroxysmal Sympathetic Hyperactivity 20.2 Acute Spinal Cord Injury, Neurogenic Shock & Autonomic Dysreflexia 20.3 Toxin-Mediated Paralysis & Neuromuscular Crises: Botulism, Tetanus, Tick Paralysis & Myasthenic Crisis
21 Chapter 21: Gastrointestinal, Hepatic & Abdominal Emergencies
21.1 Acute Upper & Lower Gastrointestinal Bleeding in the ICU 21.2 Acute Liver Failure & Severe Acute Pancreatitis 21.3 Abdominal Compartment Syndrome & Acute Mesenteric Ischemia
22 Chapter 22: Luminal GI Emergencies & Complications of Cirrhosis
22.1 Esophageal, Gastric & Bowel Emergencies: Perforation, Obstruction, Ogilvie Syndrome & Colonic Ischemia 22.2 Complications of Cirrhosis: Alcohol-Associated Hepatitis, Hepatorenal Syndrome & Pulmonary Vascular Syndromes
23 Chapter 23: Trauma, Burns & Perioperative Critical Care
23.1 Polytrauma Resuscitation, Damage Control & Massive Transfusion 23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies 23.3 Perioperative Critical Care for High-Risk Surgical Patients
24 Chapter 24: Thoracic Trauma, Environmental Injury & Obstetric Critical Care
24.1 Thoracic Trauma: Flail Chest, Pulmonary Contusion, Great Vessel & Tracheobronchial Injury 24.2 Environmental Injury: Drowning, Diving, Altitude, Heat, Cold, Electrical & Radiation 24.3 Obstetric & Genitourinary Emergencies and the Physiology of Pregnancy
25 Chapter 25: Transplantation, Donor Management & Post-Cardiac Surgery Care
25.1 Solid Organ Transplant Recipients & Deceased Donor Management 25.2 Post-Cardiac Surgery Critical Care: Bleeding, Tamponade, Low Output & Vasoplegia
26 Chapter 26: Hematologic Emergencies, Toxicology, Critical Ultrasound & ICU Liberation
26.1 Hematologic Emergencies in the ICU: HIT, DIC, TMA & Anticoagulant Reversal 26.2 Critical Care Toxicology, Toxidromes & Specific Antidotes 26.3 Critical Care Point-of-Care Ultrasound (POCUS) 26.4 ICU Liberation, Analgosedation, Goals of Care & Critical Care Ethics
27 Chapter 27: Transfusion Medicine, Hematologic & Oncologic Disorders
27.1 Transfusion Medicine: Products, Thresholds, Reactions & Apheresis 27.2 Red and White Cell Disorders, Hemoglobinopathies, Factor Deficiencies & Hypercoagulable States 27.3 Oncologic Emergencies, Hematopoietic Cell Transplant Complications & Cellular Therapy Toxicity
28 Chapter 28: Clinical Pharmacology, Adverse Drug Reactions & Specific Poisonings
28.1 Pharmacokinetic Principles, Dose Adjustment & Drug Interactions in Critical Illness 28.2 Adverse Drug Reactions: Anaphylaxis, Severe Cutaneous Reactions & Hyperthermic Syndromes 28.3 Specific Poisonings: Sodium-Channel Blockers, Lithium, Valproate, Theophylline, Iron, Sulfonylureas & Methemoglobinemia
29 Chapter 29: Ethics, Research Methods, Administration & Abdominal Ultrasound
29.1 Advance Care Planning, Nonbeneficial Treatment, Informed Consent & Confidentiality 29.2 Critical Care Research Methods, Statistics, IRB Oversight & Quality Improvement 29.3 Abdominal, Vascular & Procedural Point-of-Care Ultrasound
4.2 Diffuse Alveolar Hemorrhage, Interstitial Lung Disease, Pulmonary Vasculitis & Noncardiogenic Edema
Key Takeaways Explain This Topic AI
Diffuse alveolar hemorrhage is confirmed when sequential bronchoalveolar lavage aliquots become progressively bloodier; hemoptysis is absent in up to a third of patients.
Anti-GBM disease with alveolar hemorrhage is treated with plasma exchange plus pulse corticosteroids and cyclophosphamide.
In ANCA vasculitis, the PEXIVAS trial (2020) found that plasma exchange did not reduce death or end-stage kidney disease.
In the EXAFIP trial (2020), adding intravenous cyclophosphamide to steroids increased 3-month mortality in acute exacerbation of idiopathic pulmonary fibrosis.
Negative-pressure pulmonary edema follows forceful inspiration against an obstructed upper airway and usually resolves within 24 to 48 hours with supportive care.
Last updated: October 2026
Diffuse Alveolar Hemorrhage (DAH)
DAH is bleeding into the alveolar spaces from injury to the alveolar-capillary membrane. The classic triad is hemoptysis, a falling hemoglobin, and diffuse bilateral infiltrates . Hemoptysis is absent in up to a third of patients, so DAH must be considered in any unexplained diffuse infiltrate with anemia.
Diagnosis : bronchoalveolar lavage (BAL) in one subsegment returns progressively bloodier aliquots . Hemosiderin-laden macrophages appear after about 48 to 72 hours, with more than 20% supporting the diagnosis.
Three histologic patterns :
Pulmonary capillaritis : neutrophilic destruction of the capillaries. Causes include ANCA-associated vasculitis, anti-GBM disease, lupus, antiphospholipid syndrome, and drugs such as propylthiouracil and levamisole-contaminated cocaine.
Bland hemorrhage : anticoagulants or thrombolytics, severe thrombocytopenia, mitral stenosis, and high left atrial pressure.
Diffuse alveolar damage with hemorrhage : hematopoietic cell transplantation, infection, and toxic inhalation.
Workup :
Serology: ANCA (PR3 and MPO), anti-GBM antibody, ANA and anti-dsDNA, complements, and antiphospholipid antibodies.
Kidney screen: creatinine and urinalysis for red cell casts. A pulmonary-renal syndrome strongly suggests vasculitis or anti-GBM disease.
Coagulation studies and a platelet count.
Tissue confirmation from kidney or skin biopsy when it can be obtained.
Treatment
Supportive : lung-protective ventilation with adequate PEEP (which also tamponades bleeding), and correction of coagulopathy and thrombocytopenia. VV-ECMO can be used, with minimal anticoagulation.
Immune capillaritis : pulse methylprednisolone (500 to 1,000 mg IV daily for 3 days), then induction with rituximab or cyclophosphamide for ANCA vasculitis (rituximab was noninferior in RAVE).
Plasma exchange :
Anti-GBM disease : plasma exchange is standard, combined with steroids and cyclophosphamide.
ANCA vasculitis : the PEXIVAS trial (2020) found no reduction in death or end-stage kidney disease with plasma exchange, so its use in alveolar hemorrhage is individualized for the most severe cases.
Pulmonary Vasculitis and Pulmonary-Renal Syndromes
Disease Serology Distinguishing features
Granulomatosis with polyangiitis PR3-ANCA (c-ANCA) Sinusitis, saddle-nose deformity, cavitating nodules, subglottic stenosis, glomerulonephritis
Microscopic polyangiitis MPO-ANCA (p-ANCA) Glomerulonephritis and DAH without granulomas
Eosinophilic granulomatosis with polyangiitis MPO-ANCA in a minority Late-onset asthma, eosinophilia, neuropathy, cardiomyopathy
Anti-GBM disease Anti-GBM IgG (linear deposition on biopsy) Smokers or inhalant exposure; rapid glomerulonephritis
Systemic lupus erythematosus ANA, anti-dsDNA, low complement DAH carries high mortality; also lupus pneumonitis and shrinking lung
Interstitial Lung Disease in the ICU
Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is an acute worsening within about 1 month, with new bilateral ground-glass opacity or consolidation on a background of usual interstitial pneumonia, not fully explained by heart failure or fluid overload. In-hospital mortality is about 50%, and much higher with mechanical ventilation.
Search for triggers: infection, aspiration, pulmonary embolism, pneumothorax, and drug toxicity.
High-dose corticosteroids are commonly given, although the evidence is weak.
In EXAFIP (2020), adding intravenous cyclophosphamide to steroids increased 3-month mortality.
Intubation rarely leads to recovery unless lung transplantation is an option. Have early goals-of-care conversations, and reserve ECMO as a bridge to transplant in listed candidates.
Other ICU-relevant interstitial processes :
Drug-induced pneumonitis :
Amiodarone (with high lung attenuation on CT).
Nitrofurantoin.
Methotrexate.
Bleomycin (worsened by high FiO2).
Immune checkpoint inhibitors. Grade 3 or 4 pneumonitis requires stopping the drug and giving methylprednisolone 1 to 2 mg/kg; infliximab, mycophenolate, or IVIG are options if there is no response in about 48 hours.
Acute interstitial pneumonia : idiopathic diffuse alveolar damage.
Cryptogenic organizing pneumonia : steroid-responsive migratory consolidation.
Hypersensitivity pneumonitis .
Rapidly progressive ILD : for example, anti-MDA5 dermatomyositis.
Noncardiogenic Pulmonary Edema Other Than ARDS
Type Setting and mechanism Course and management
Neurogenic Subarachnoid hemorrhage, traumatic brain injury, seizures; catecholamine surge raises pulmonary capillary pressure and permeability Onset within minutes to hours; usually resolves in 48 to 72 hours; supportive care and treatment of the brain injury
Negative-pressure (post-obstructive) Forceful inspiration against a closed glottis: laryngospasm at extubation, choking, strangulation; young muscular patients Resolves in 24 to 48 hours with oxygen, PEEP or CPAP, and supportive care
Tocolytic-associated Beta-agonists (terbutaline) or magnesium in pregnancy, often with corticosteroids and generous fluids Stop the tocolytic; diuresis and oxygen
High-altitude (HAPE) Exaggerated, uneven hypoxic pulmonary vasoconstriction causes capillary stress failure, usually 2 to 4 days after rapid ascent Descent and oxygen first; nifedipine as adjunct or prophylaxis
Re-expansion Rapid re-expansion of a lung after drainage of a large effusion or pneumothorax Limit drainage volume, stop if chest discomfort or cough develops; supportive
Other Opioid overdose and naloxone reversal, salicylate toxicity, immersion, transfusion-related acute lung injury Treat the cause; supportive ventilation
Atelectasis
Atelectasis has four mechanisms:
Obstructive : mucus plugging or a tumor, causing collapse with volume loss and an ipsilateral shift.
Compressive : effusion, abdominal distension, or obesity.
Adhesive : surfactant loss.
Absorptive : high FiO2 washes out nitrogen.
Prevention and treatment combine mobilization, upright positioning, incentive spirometry, secretion clearance, adequate PEEP, and the lowest FiO2 that meets the oxygen target. Bronchoscopy is reserved for lobar collapse that does not respond to chest physiotherapy, or for a suspected central obstruction.