MKSAP 18 Sample Pages - Pulmonary and Critical Care Medicine by American College of Physicians

Medical Knowledge Self-Assessment ProgramÂŽ

Pulmonary and Critical Care Medicine 25 AMA PRA Category 1 Creditsâ&#x201E;˘ available until December 31, 2021.

Welcome to the Pulmonary and Critical Care Medicine Section of MKSAP 18! In these pages, you will find updated information on pulmonary diagnostic testing; airways disease; diffuse parenchymal lung disease; occupational lung disease; pleural disease; pulmonary vascular disease; lung tumors; sleep medicine; highaltitude–related illnesses; principles of ventilation in critical care; common ICU conditions such as upper airway emergencies, respiratory failure, sepsis, anaphylaxis, and toxicologic emergencies; and other clinical challenges. All of these topics are uniquely focused on the needs of generalists and subspecialists outside of pulmonary and critical care medicine. The core content of MKSAP 18 has been developed as in previous editions—all essential information that is newly researched and written in 11 topic areas of internal medicine—created by dozens of leading generalists and subspecialists and guided by certification and recertification requirements, emerging knowledge in the field, and user feedback. MKSAP 18 also contains 1200 all-new peer-reviewed, psychometrically validated, multiple-choice questions (MCQs) for self-assessment and study, including 103 in Pulmonary and Critical Care Medicine. MKSAP 18 continues to include High Value Care (HVC) recommendations, based on the concept of balancing clinical benefit with costs and harms, with associated MCQs illustrating these principles and HVC Key Points called out in the text. Internists practicing in the hospital setting can easily find comprehensive Hospitalist-focused content and MCQs, specially designated in blue and with the symbol. If you purchased MKSAP 18 Complete, you also have access to MKSAP 18 Digital, with additional tools allowing you to customize your learning experience. MKSAP Digital includes regular text updates with new, practice-changing information, 200 new self-assessment questions, and enhanced custom-quiz options. MKSAP Complete also includes more than 1200 electronic, adaptive learning–enhanced flashcards for quick review of important concepts, as well as an updated and enhanced version of Virtual Dx, MKSAP’s image-based self-assessment tool. As before, MKSAP 18 Digital is optimized for use on your mobile devices, with iOS- and Android-based apps allowing you to sync between your apps and online account and submit for CME credits and MOC points online. Please visit us at the MKSAP Resource Site (mksap.acponline.org) to find out how we can help you study, earn CME credit and MOC points, and stay up to date. On behalf of the many internists who have offered their time and expertise to create the content for MKSAP 18 and the editorial staff who work to bring this material to you in the best possible way, we are honored that you have chosen to use MKSAP 18 and appreciate any feedback about the program you may have. Please feel free to send any comments to mksap_editors@ acponline.org. Sincerely,

Patrick C. Alguire, MD, FACP Editor-in-Chief Senior Vice President Emeritus Medical Education Division American College of Physicians

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Table of Contents Pulmonary Diagnostic Tests

Diffuse Parenchymal Lung Disease

Pulmonary Function Testing. . . . . . . . . . . . . . . . . . . . . . . . 1 Spirometry. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Bronchial Challenge Testing. . . . . . . . . . . . . . . . . . . . . 1 Lung Volumes and DLCO. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Pulmonary Function Testing Interpretation . . . . . . . 1 6-Minute Walk Test. . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Pulse Oximetry. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Imaging and Bronchoscopy. . . . . . . . . . . . . . . . . . . . . . . . . 3 Imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Bronchoscopy and Endobronchial Ultrasound . . . . . 4

Classification and Epidemiology. . . . . . . . . . . . . . . . . . . . 23 Diagnostic Approach and Evaluation . . . . . . . . . . . . . . . . 23 High-Resolution CT Scanning. . . . . . . . . . . . . . . . . . 25 Serologic Testing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Lung Biopsy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Diffuse Parenchymal Lung Diseases with a Known Cause. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Smoking-Related Diffuse Parenchymal Lung Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 Connective Tissue Diseases . . . . . . . . . . . . . . . . . . . . 26 Hypersensitivity Pneumonitis. . . . . . . . . . . . . . . . . . 27 Drug-induced Diffuse Parenchymal Lung Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 Radiation Pneumonitis. . . . . . . . . . . . . . . . . . . . . . . . 28 Diffuse Parenchymal Lung Diseases with an Unknown Cause. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 Idiopathic Pulmonary Fibrosis . . . . . . . . . . . . . . . . . 29 Nonspecific Interstitial Pneumonia. . . . . . . . . . . . . 30 Cryptogenic Organizing Pneumonia. . . . . . . . . . . . 30 Acute Interstitial Pneumonia. . . . . . . . . . . . . . . . . . . 31 Sarcoidosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

Airways Disease Asthma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Epidemiology and Natural History . . . . . . . . . . . . . . . 4 Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6 Symptoms and Clinical Evaluation. . . . . . . . . . . . . . 6 Asthma Syndromes. . . . . . . . . . . . . . . . . . . . . . . . . . . . 7 Common Comorbidities. . . . . . . . . . . . . . . . . . . . . . . . 8 Management of Chronic Asthma. . . . . . . . . . . . . . . . 9 Management of Asthma Exacerbations . . . . . . . . . . 13 Severe Refractory Asthma . . . . . . . . . . . . . . . . . . . . . 13 Asthma in Pregnancy. . . . . . . . . . . . . . . . . . . . . . . . . 13 Chronic Obstructive Pulmonary Disease. . . . . . . . . . . . . 13 Definition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Epidemiology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 Heterogeneity of COPD. . . . . . . . . . . . . . . . . . . . . . . . 14 Comorbid Conditions. . . . . . . . . . . . . . . . . . . . . . . . . 14 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 Disease Assessment. . . . . . . . . . . . . . . . . . . . . . . . . . 15 Management of COPD . . . . . . . . . . . . . . . . . . . . . . . . 16 Acute Exacerbations. . . . . . . . . . . . . . . . . . . . . . . . . 20 Bronchiectasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Definition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Presentation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Cystic Fibrosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23 Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Occupational Lung Disease When to Suspect an Occupational Lung Disease . . . . . . 32 Key Elements of the Exposure History. . . . . . . . . . . . . . . 33 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Surveillance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33 Asbestos-Related Lung Disease. . . . . . . . . . . . . . . . . . . . . 34 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 Silicosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34

Pleural Disease Pleural Effusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 Pneumothorax. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

Pulmonary Vascular Disease Pulmonary Hypertension. . . . . . . . . . . . . . . . . . . . . . . . . 40 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 ix

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Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 Treatment of Pulmonary Hypertension. . . . . . . . . . 41 Chronic Thromboembolic Pulmonary Hypertension (Group 4). . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Pulmonary Arterial Hypertension. . . . . . . . . . . . . . . . . . 43 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

Lung Tumors

High-Altitudeâ&#x20AC;&#x201C;Related Illnesses Sleep Disturbances and Periodic Breathing. . . . . . . . . . 56 Acute Mountain Sickness. . . . . . . . . . . . . . . . . . . . . . . . . 56 High-Altitude Cerebral Edema . . . . . . . . . . . . . . . . . . . . 56 High-Altitude Pulmonary Edema. . . . . . . . . . . . . . . . . . . 57 Air Travel in Pulmonary Disease. . . . . . . . . . . . . . . . . . . . 57

Critical Care Medicine: ICU Utilization Recognizing the Critically Ill Patient. . . . . . . . . . . . . . . . . 57 Organization of Critical Care. . . . . . . . . . . . . . . . . . . . . . . 58

Pulmonary Nodule Evaluation. . . . . . . . . . . . . . . . . . . . . 44 Solid Indeterminate Nodule Larger Than 8 mm. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 Solid Indeterminate Nodule of 8 mm or Smaller. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Subsolid Nodule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 Lung Cancer. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 Lung Cancer Types. . . . . . . . . . . . . . . . . . . . . . . . . . 46 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Screening. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Diagnosis and Staging. . . . . . . . . . . . . . . . . . . . . . . . . 47 Other Pulmonary Neoplasms . . . . . . . . . . . . . . . . . 48 Mesothelioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Mediastinal Masses. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 Anterior Mediastinum . . . . . . . . . . . . . . . . . . . . . . . 49 Middle Mediastinum. . . . . . . . . . . . . . . . . . . . . . . . . 49 Posterior Mediastinum. . . . . . . . . . . . . . . . . . . . . . . 50

Principles of Critical Care

Sleep Medicine

Common ICU Conditions

Classification of Sleep Disorders. . . . . . . . . . . . . . . . . . . 50 Excessive Daytime Sleepiness . . . . . . . . . . . . . . . . . . . . . 50 Conditions that Disrupt Circadian Rhythm. . . . . . . . . . . 51 Jet Lag. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Shift Work Sleep Disorder . . . . . . . . . . . . . . . . . . . . . 51 Obstructive Sleep Apnea . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Clinical Features and Diagnosis. . . . . . . . . . . . . . . . . 52 Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 52 Central Sleep Apnea Syndromes. . . . . . . . . . . . . . . . . . . . 54 Classification and Pathophysiology. . . . . . . . . . . . . . 54 Risk Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 Symptoms and Diagnosis. . . . . . . . . . . . . . . . . . . . . . 54 Treatment. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 Sleep-Related Hypoventilation Syndromes. . . . . . . . . . . 54 Chronic Obstructive Pulmonary Disease. . . . . . . . . 55 Obesity Hypoventilation Syndrome . . . . . . . . . . . . . 55 Neuromuscular Diseases . . . . . . . . . . . . . . . . . . . . . . 55

Comprehensive Management of Critically Ill Patients. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58 Mechanical Ventilatory Support: General Ventilator Principles. . . . . . . . . . . . . . . . . . 59 Invasive Monitoring. . . . . . . . . . . . . . . . . . . . . . . . . . 61 Intravenous Access . . . . . . . . . . . . . . . . . . . . . . . . . . . 62 Blood Pressure Support . . . . . . . . . . . . . . . . . . . . . . . 62 Sedation and Analgesia. . . . . . . . . . . . . . . . . . . . . . . 63 Nutrition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 64 Early Mobilization. . . . . . . . . . . . . . . . . . . . . . . . . . . 64 ICU Care Bundles . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 High Value Care in the ICU. . . . . . . . . . . . . . . . . . . . 65 ICU Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 ICU-Acquired Weakness. . . . . . . . . . . . . . . . . . . . . . 66 Long-Term Cognitive Impairment. . . . . . . . . . . . . . 66 Post-Intensive Care Syndrome. . . . . . . . . . . . . . . . . 66

Acute Respiratory Failure. . . . . . . . . . . . . . . . . . . . . . . . . 66 Acute Upper Airway Management . . . . . . . . . . . . . 66 Acute Inhalational Injuries. . . . . . . . . . . . . . . . . . . . . 67 Hypoxemic Respiratory Failure. . . . . . . . . . . . . . . . 68 Acute Respiratory Distress Syndrome. . . . . . . . . . . 68 Heart Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Atelectasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Pneumonia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70 Diffuse Parenchymal Lung Disease. . . . . . . . . . . . . . 71 Pulmonary Embolism. . . . . . . . . . . . . . . . . . . . . . . . . 71 Hypercapnic (Ventilatory) Respiratory Failure . . . . . . . . 72 Management of Hypercapnic Respiratory Failure. . . 72 Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Distributive Shock. . . . . . . . . . . . . . . . . . . . . . . . . . . . 75 Hypovolemic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Cardiogenic Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Sepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76 Definition, Pathophysiology, and Clinical Presentation of Sepsis. . . . . . . . . . . . . . . . . . 76

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Epidemiology of Sepsis. . . . . . . . . . . . . . . . . . . . . . . . 77 Management of Sepsis . . . . . . . . . . . . . . . . . . . . . . . . 77

Specific Critical Care Topics Anaphylaxis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78 Hypertensive Emergencies. . . . . . . . . . . . . . . . . . . . . . . . . 79 Hyperthermic Emergencies. . . . . . . . . . . . . . . . . . . . . . . 80 Heat Stroke. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80 Malignant Hyperthermia. . . . . . . . . . . . . . . . . . . . . . 81 Neuroleptic Malignant Syndrome and Serotonin Syndrome. . . . . . . . . . . . . . . . . . . . . . 81 Accidental Hypothermia . . . . . . . . . . . . . . . . . . . . . . . . . . 82 Toxicology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 Alcohol Poisoning. . . . . . . . . . . . . . . . . . . . . . . . . . . . 82 Carbon Monoxide Poisoning. . . . . . . . . . . . . . . . . . . 82

Cyanide Poisoning. . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 Toxicity of Drugs of Abuse. . . . . . . . . . . . . . . . . . . . 84 Overdose of Therapeutic Drugs. . . . . . . . . . . . . . . . 84 Acute Abdominal Surgical Emergencies. . . . . . . . . . . . . . 85 Encephalopathy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 Coma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 Anoxic Brain Injury. . . . . . . . . . . . . . . . . . . . . . . . . . 86

Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88 Self-Assessment Test. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169

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Pulmonary and Critical Care Medicine Pulmonary Diagnostic Tests Pulmonary Function Testing Pulmonary function testing is an essential tool to diagnose obstructive and restrictive pathophysiology and to quantify the severity of the abnormality. Pulmonary function testing can include spirometry, bronchial challenge testing, lung volume testing, and measurement of diffusion capacity of the lung for carbon monoxide (DLCO). These findings are compared to age, sex, height, and race-adjusted population norms and expressed as a percent of the predicted value (Table 1). Values below 80% of the predicted value are considered reduced. Recent American Thoracic Society guidelines alternatively use the lower limit of normal (below the fifth percentile of healthy never-smokers) as a cutoff, but in most cases this is very similar to 80% of the predicted value. Key Point

• Pulmonary function test results below 80% of predicted or below the lower limit of normal are indicative of pulmonary impairment.

Spirometry Measurement of expiratory airflow and volume is an essential diagnostic and management test for patients with lung diseases. Spirometry measures the maximal volume and flow of Table 1. Characterization of Impairment Severity in Pulmonary Function Tests Severity of Impairment

% of Predicted

FEV1 Mild

79-70

Moderate

60-69

Moderately severe

50-59

Severe

35-49

Very severe

<35

Dlco Mild

<LLN but >60

Moderate

40-60

Severe

<40

LLN = lower limit of normal; below the fifth percentile of healthy never-smokers. Reproduced with permission from ©ERS 2018. Pellegrino R, Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi R, et al. Interpretative strategies for lung function tests. Eur Respir J. 2005;26:948-68. [PMID: 16264058] doi: 10.1183/09031936.05.00035205

air during a best-effort, forced exhalation; reported values include the FEV1, the FVC, and the FEV1/FVC ratio. Measurement of maximal expiratory flow by peak flow meter is commonly used at home and in office settings to follow and manage patients with asthma, but is not considered a valid diagnostic tool for airways disease. Spirometry correlates with hand-held peak expiratory flow-meter measurements, but is more reliable, provides more data, and is used in both diagnosis and management of airways disease. Although spirometry is easily performed in the outpatient setting, technical test validation and patient factors—including poor effort, coughing, and failure to exhale for a minimum of 6 seconds—may result in suboptimal test performance and misinterpretation.

Bronchial Challenge Testing Bronchial challenge testing is used to identify bronchial hyperresponsiveness, a diagnostic feature of asthma. This is particularly helpful in patients whose symptoms are suggestive of asthma but for whom other pulmonary function test results are normal. Patients inhale increasing doses of a substance known to induce bronchospasm, such as methacholine or histamine, in a stepwise fashion. This is followed by repeated measurements of FEV1; if FEV1 falls by 20% or more from the baseline value, the test is considered positive. Bronchial challenge testing has a high negative predictive value for diagnosing asthma; however, a positive test can be caused by other conditions including COPD, smoking, upper respiratory infections, allergic rhinitis, bronchiectasis, and cystic fibrosis. Key Point

• Bronchial challenge testing is a helpful diagnostic tool in patients whose symptoms are suggestive of asthma but for whom other pulmonary function test results are normal.

Lung Volumes and DLCO Measures of lung volume include total lung capacity (TLC), vital capacity (VC), and residual volume (RV). DLCO measurement estimates the amount of gas transfer through the alveolar/capillary unit and is proportional to the surface area of functional lung. DLCO is measured by inhalation of a gas mixture containing carbon monoxide and helium; the resulting value is corrected for hemoglobin level.

Pulmonary Function Testing Interpretation The purpose of pulmonary function testing interpretation is to classify abnormal results as an obstructive, a restrictive, or a mixed obstructive/restrictive pattern and to assess the severity of 1

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Pulmonary Diagnostic Tests

CONT.

impairment (Figure 1). The initial step is to review the results of spirometry. An FEV1/FVC ratio below 0.70 is consistent with obstruction, and the severity is determined based on the measured FEV1 as a percent of the predicted value (see Table 1). Reversibility of obstruction is determined by the response to a short-acting inhaled bronchodilator. An increase from baseline in FEV1, FVC, or both of at least 12% and at least 200 mL indicates a positive bronchodilator response (reversibility). The TLC is normal or even increased in pure obstructive disease. Elevation of TLC and residual volume (120% or greater of predicted) can be observed in obstruction and generally is indicative of hyperinflation and air trapping, a common pattern in severe COPD or asthma. If FEV1 or FVC is reduced and the FEV1/FVC ratio is 0.70 or greater, then the pattern may be interpreted as restrictive, but measurement of TLC is needed to confirm this. If the TLC is below 80% of predicted (or the lower limit of normal) a restrictive pattern is present. Some patients may present with coexisting obstructive and restrictive pulmonary disorders, such as a COPD patient who develops an interstitial lung disease. In these cases, a low FEV1/FVC ratio (obstructive pattern) and a low TLC (restrictive pattern) are both present. DLCO is reduced in conditions where functioning alveolar capillary units are destroyed (COPD), infiltrated (interstitial

lung diseases), removed (lung resection), or their function is compromised (pulmonary parenchymal and vascular disorders). Conditions that increase pulmonary capillary blood volume, such as pulmonary alveolar hemorrhage, left-to-right shunt, or asthma, can cause an elevation in DLCO. The flow-volume loop is a graphic representation of maximally forced inspiratory and expiratory flow (on the Y-axis) against volume (on the X-axis). The shape of the spirometric flow-volume loop is also useful in differentiating obstructive from restrictive patterns (Figure 2). Key Points

• The purpose of pulmonary function testing interpretation is to classify abnormal results as either an obstructive or restrictive pattern and to assess the severity of impairment. • The FEV1/FVC ratio is the primary measurement that defines obstructive disease, and total lung capacity is the primary measurement to confirm restrictive disease.

6-Minute Walk Test The 6-minute walk test provides a valid and reliable measurement of exercise capacity in patients with lung disease. Patients walk at their own pace along a course for 6 minutes,

F i g u r e 1 . A simplified algorithm such as this may be used to assess lung function in clinical practice. It presents classic patterns for various pulmonary disorders. As in any such diagram, patients may or may not present with the classic patterns, depending on their illnesses, severity, and lung function prior to the disease onset (for example, did they start with a vital capacity [VC] close to the upper or lower limit of normal [LLN]?). The decisions about how far to follow this diagram are clinical, and will vary depending on the questions being asked and the clinical information available at the time of testing. The FEV1/VC ratio and VC should be considered first. Total lung capacity (TLC) is necessary to confirm or exclude the presence of a restrictive defect when VC is below the LLN. The algorithm also includes DLCO measurement with the predicted value adjusted for hemoglobin. In the mixed defect group, the DLCO patterns are the same as those for restriction and obstruction. This flow chart is not suitable for assessing the severity of upper airway obstruction. CB = chronic bronchitis; CW = chest wall; ILD = interstitial lung diseases; NM = neuromuscular; PV = pulmonary vascular. Reproduced with permission from ©ERS 2018. Pellegrino R, Viegi G, Brusasco V, Crapo RO, Burgos F, Casaburi R, et al. Interpretative strategies for lung function tests. Eur Respir J. 2005;26:948-68. [PMID: 16264058] doi: 10.1183/09031936.05.00035205

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Airways Disease

Table 2. Bronchoscopic Diagnostic Procedures Technique

Description

Examples of Indications

Airway inspection

Visualization of the tracheobronchial tree to the level of segmental airways

Hemoptysis Localized wheeze Persistent atelectasis Diagnosis of tracheobronchomalacia Inhalational injury

Bronchial washings

Samples from large airways

Diagnosis of infections

Bronchoalveolar lavage

Samples from small bronchi and alveoli

Diagnosis of infections Cell counts in diagnosis of parenchymal lung disease Alveolar hemorrhage Cytology for malignancy

Bronchial brushings

Brushings of the endobronchial mucosa for cells

Endobronchial lesions

Endobronchial biopsy

Biopsy within the airway lumen

Endobronchial mass or lesion

Transbronchial lung biopsy

Biopsy of the lung parenchyma or lung nodules/ masses using small forceps; often aided by guidance technology including electromagnetic navigation and radial ultrasound

Diffuse lung disease Persistent infiltrates Lung nodules/masses Posttransplant rejection

Transbronchial needle aspiration

Aspiration of a lymph node or mass adjacent to the airway

Lymphadenopathy Pulmonary mass Mediastinal mass

Endobronchial ultrasound

Use of an ultrasound probe at the distal end of the bronchoscope to guide transbronchial needle aspiration

Lymphadenopathy Pulmonary mass Mediastinal mass

Electromagnetic navigation

Images from a recent CT are “linked” with the bronchoscope. An electromagnetic guidance system at the bronchoscope creates a map of the airways and guides the physician to the area of interest.

Pulmonary mass or nodule

Table 3. Bronchoscopic Therapeutic Procedures Technique

Description

Examples of Indications

Flexible bronchoscopy

Large airway suctioning

Lobar atelectasis from mucus plugs

Basket and forceps

Foreign body

Balloon tamponade of airway

Bleeding

Bronchial thermoplasty

Radiofrequency energy ablation of proximal airway smooth muscle

Severe asthma

Endobronchial stent placement

Bronchoscopic placement of silicon and metal prostheses to expand and support the airways

Malignant obstruction Benign strictures Tracheomalacia or bronchomalacia Anastomotic dehiscence

Airway ablative therapies

Laser therapy

Malignant airway obstruction

Electrocautery

Benign airway obstruction

Argon plasma coagulation

Airway tumor ablation

Cryotherapy Brachytherapy Endobronchial valve placement

Airway placement of one-way valves

Balloon dilation

Targeted endobronchial balloon inflation

Bronchopleural fistula Emphysema Benign or malignant airway stricture

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Airways Disease

CONT.

differs from the finding in asthmatic patients, whose airflow obstruction is fully reversible with bronchodilator therapy. Some patients have bronchial inflammation with features of both asthma and COPD, referred to as asthma-COPD overlap syndrome. A GOLD and the Global Initiative for Asthma (GINA) consensus statement characterizes asthma-COPD overlap syndrome as persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD. Measuring lung volumes and diffusing capacity is not required to diagnose COPD but may help in determining the severity of disease. Clinicians should rule out other causes of chronic respiratory symptoms including heart failure, bronchiectasis, obliterative bronchiolitis, tuberculosis, and diffuse panbronchiolitis. Key Points

HVC

• There is no role for spirometric screening for COPD in asymptomatic individuals. • COPD is defined as a post-bronchodilator FEV1/FVC ratio of less than 0.70.

Disease Assessment After a diagnosis of COPD has been established, the initial assessment focuses on disease severity, which is determined Table 6. Modified Medical Research Council Dyspnea Scale Score

Description of Dyspnea

Severity

I get breathless only with strenuous exercise.

None

I get short of breath when hurrying on level ground or walking up a slight hill.

Mild

On level ground, I walk slower than other people my age because of breathlessness, or I have to stop for breath when walking at my own pace.

Moderate

I stop for breath after walking approximately 100 yards or after a few minutes on level ground.

Severe

I am too breathless to leave the house or breathless when dressing.

Very severe

using a combination of symptoms, degree of airflow obstruction on spirometry, history of acute exacerbations, and presence of comorbid conditions. Several validated tools are available to assess patients’ symptoms, including the COPD Assessment Test (CAT), the Clinical COPD Questionnaire (CCQ), and the mMRC scale (Table 6). The GOLD criteria use the CAT or mMRC scale to determine symptom severity, whereas the BODE index requires the use of the mMRC scale. The CCQ is often used to screen patients for symptoms of COPD. Symptoms are then combined with the results from spirometry (Table 7) to determine disease severity (Table 8). Patients who have had two or more acute exacerbations within the last year, who have an FEV1 of less than 50% of predicted, or who have ever been hospitalized for an acute exacerbation are considered to be at high risk for recurrent acute exacerbations. Clinicians should determine if the patient suffers from any of the common comorbid conditions associated with COPD that indicate a higher morbidity and mortality and treat appropriately. Pulse oximetry at rest and at exertion should be used to determine the need of supplemental oxygen. Arterial blood gases should be measured to assess for underlying hypercapnia in patients with a low FEV1, change in mental status, an acute exacerbation, an elevated level of serum bicarbonate, or oxygen saturation of less than 92% on pulse oximetry. An α1-antitrypsin level should be obtained in patients with COPD under the age of 45 who have a strong family history of COPD or who are without identifiable COPD risk factors. A pattern of basilar emphysema, associated liver disease Table 7. Classification of COPD Severity by Spirometrya Category

Severity

Spirometry

GOLD 1

Mild

FEV1 ≥80% of predicted

GOLD 2

Moderate

50% ≤ FEV1 < 80% of predicted

GOLD 3

Severe

30% ≤ FEV1 < 50% of predicted

GOLD 4

Very severe

FEV1 <30% of predicted

aIn

Used with the permission of the Medical Research Council.

Patients with FEV1/FVC less than 70%.

Reprinted from Vogelmeier CF, Criner GJ, Martinez FJ, Anzueto A, Barnes PJ, Bourbeau J, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 report. GOLD executive summary. Am J Respir Crit Care Med. 2017;195:557-582. [PMID: 28128970] doi:10.1164/ rccm.201701-0218PP

Table 8. GOLD Model for Classifying Severity of Disease in COPDa Patient Category

Characteristics

Exacerbations Per Year

CAT Score

mMRC Score

Low risk, fewer symptoms

≤1

<10

0-1

Low risk, more symptoms

≤1

≥10

≥2

High risk, fewer symptoms

≥2

<10

0-1

High risk, more symptoms

≥2/≥1 with hospital admission

≥10

≥2

CAT = COPD Assessment Test; mMRC = Modified Medical Research Council. aSee

Table 7 for definitions of spirometric classifications.

Data from Vogelmeier CF, Criner GJ, Martinez FJ, Anzueto A, Barnes PJ, Bourbeau J, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 report. GOLD executive summary. Am J Respir Crit Care Med. 2017;195:557-582. [PMID: 28128970] doi:10.1164/rccm.201701-0218PP

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Airways Disease

should be considered in patients who have localized disease with persistent symptoms despite therapy. Key Points

• Identification and treatment of underlying causes of bronchiectasis should be initiated if possible. • Treatment of bronchiectasis focuses on airway clearance, treating infections, and preventing exacerbations.

Treatment of Exacerbations

F i g u r e 4 . Bronchiectasis on chest CT. The airway is larger than its accompanying blood vessel (thick arrow), and the airway fails to taper distally (thin arrows). Key Points

• Bronchiectasis is diagnosed by high-resolution chest CT; diagnostic criteria include airway diameter greater than that of its accompanying vessel, and lack of distal airway tapering. • For every patient diagnosed with bronchiectasis, it should be determined whether there is an underlying cause that can be treated.

Treatment The presence of chronic symptoms of cough and sputum production typically indicates irreversible airway dilation. Therefore, treatment of the underlying cause may not lead to improvement in current symptoms but could prevent further progression. Otherwise, treatment of bronchiectasis focuses on airway clearance, treating infections, and preventing exacerbations. The goal of airway clearance is to improve mucous clearance and thereby prevent chronic or recurrent infections. Bronchodilators, inhaled glucocorticoids, and combination inhalers have been shown to decrease symptoms but have no effect on the decline of lung function or frequency of exacerbations. Studies suggest that long-term use of macrolide antibiotics may prevent future exacerbations due to their anti-inflammatory effects. When deciding whether to use macrolide antibiotics, the risk of future exacerbations should be weighed against the possibility of developing macrolide resistance. Antibiotics may also be used in the management of chronic non–cystic fibrosis bronchiectasis to eradicate organisms such as Pseudomonas aeruginosa or methicillinresistant Staphylococcus aureus. If eradication of bacterial colonization is not successful, there may be some symptomatic benefit from suppressive therapy with inhaled antibiotics. Patients should also be encouraged to exercise, which can improve airway clearance and symptoms. Surgical resection

Exacerbations of bronchiectasis may be difficult to differentiate from baseline symptoms. However, changes in sputum volume, viscosity, or purulence; increased cough; wheezing; shortness of breath; hemoptysis; or declines in lung function are considered evidence of an exacerbation. Therapy for an exacerbation is ideally guided by routine sputum and acid-fast bacilli culture results to identify a possible predominant organism for treatment. Empiric antibiotic therapy is recommended and may be based on previous culture data until the results of the current sputum culture become available. If previous data are not available, a fluoroquinolone can be started to ensure Pseudomonas coverage until sputum culture results are available.

Cystic Fibrosis Cystic fibrosis (CF) is an autosomal recessive disease affecting the CF transmembrane conductance regulator (CFTR) gene. It is diagnosed in approximately 1 of 2000-3000 live births with a predilection for disease in those of European descent. The most common genetic variant resulting in disease is ΔF508, but there are at least 1500 other genetic mutations. The pathogenesis for clinical manifestations of CF remains incompletely understood; however, the abnormal homozygous CFTR genotype results in abnormally thick secretions that are difficult to clear. There is an increased concentration of chloride in sweat gland secretions, and sweat chloride testing is a primary diagnostic tool for CF. The changes in respiratory secretions lead to bacterial colonization of airways and chronic bacterial infection, resulting in chronic inflammation and, ultimately, bronchiectasis. Further tissue destruction results from insufficient lung antiproteases to counteract the effect of elastase released from neutrophils. This ongoing inflammatory process also results in large amounts of free DNA and matrix protein deposition within areas of tissue destruction, which further drives increased viscosity of lung secretions. Thickened secretions in the gastrointestinal tract impair flow of bile and pancreatic secretions, leading to pancreatic exocrine and endocrine deficiency, liver disease, and the development of malabsorption and maldigestion. The secretions increase the risk for bowel obstruction (distal ileal obstructive syndrome, intussusception, and rectal prolapse). Consequently, individuals with CF often present with malnutrition and weight loss.

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Principles of Critical Care

Key Point

• The use of early mobilization strategies decreases length of time in the ICU and hospital stay, improves functional status, and decreases mortality.

ICU Care Bundles An ICU care bundle is a series of evidenced-based interventions that have been shown to improve patient outcomes when used together. Bundles can help clinicians monitor patients and guide appropriate interventions. The Institute for Healthcare Improvement has defined three bundles that apply to critical care (Table 40).

High Value Care in the ICU The cost of health care in the United States is the highest per capita in the world. Critical care is responsible for a large proportion of health care costs. However, the survival and qualityof-life outcomes are not that different from those in other top-economy countries. Societal, organizational, and payment pressures have encouraged a focus on providing high value care, which is defined as care that maximizes benefit relative

Table 40. ICU Care Bundles Prevention of Ventilator-Associated Pneumonia Head of bed elevation at least 30 degrees Daily sedation interruption and assessment of readiness to extubate Stress ulcer prophylaxis Deep vein thrombosis prophylaxis Daily oral care with chlorhexidine Central Line-Associated Bloodstream Infections Hand hygiene

to harms and cost. The ICU is an environment in which high value care can have major effects, as the resources are expensive and the culture favors aggressive resource use. Internal medicine and critical care medical societies have joined the American Board of Internal Medicine (ABIM) Foundation’s Choosing Wisely® campaign to promote cost-effective strategies that improve patient care (Table 41). The focus on resource utilization and cost will remain a central point of health care for the foreseeable future. Key Points

• Don’t order diagnostic tests at regular intervals (such as every day), but rather in response to specific clinical questions.

HVC

• Don’t transfuse erythrocytes in hemodynamically stable, nonbleeding patients in the ICU who have a hemoglobin concentration greater than 7 g/dL (70 g/L).

HVC

• Don’t use parenteral nutrition in adequately nourished critically ill patients within the first 7 days of an ICU stay.

HVC

• Don’t deeply sedate mechanically ventilated patients without a specific indication and without daily attempts to lighten sedation.

HVC

• Don’t continue life support for patients at high risk for death or severely impaired functional recovery without offering patients and their families the alternative of care focused entirely on comfort.

HVC

ICU Complications Critical care illness is no longer viewed as an acute event that ends at the time of discharge from the ICU. ICU complications may be classified as early, which occur during the hospitalization, or late, which persist after the critical care illness. During the last decade, there has been increased recognition of

Maximal barrier precautions Chlorhexidine skin antisepsis Avoid femoral access Daily review of line necessity Sepsis 3-hour bundle Measure lactate level Obtain blood cultures before antibiotics Administer broad-spectrum antibiotics Administer 30 mL/kg crystalloids for hypotension or lactate ≥4 mEq/L (4 mmol/L) 6-hour bundle Use vasopressors if no response to fluids; keep MAP above 65 mm Hg Repeat volume status and tissue perfusion assessment MAP = mean arterial blood pressure, calculated as [(2 × diastolic) + systolic]/3.

Table 41. ICU Choosing Wisely® Top Five Don’t order diagnostic tests at regular intervals (such as every day), but rather in response to specific clinical questions. Don’t transfuse erythrocytes in hemodynamically stable, nonbleeding patients in the ICU who have a hemoglobin concentration greater than 7 g/dL (70 g/L). Don’t use parenteral nutrition in adequately nourished critically ill patients within the first 7 days of an ICU stay. Don’t deeply sedate mechanically ventilated patients without a specific indication and without daily attempts to lighten sedation. Don’t continue life support for patients at high risk for death or severely impaired functional recovery without offering patients and their families the alternative of care focused entirely on comfort. Reprinted with permission of the American Thoracic Society. Copyright © American Thoracic Society. Available at: http://www.choosingwisely.org/wp-content/uploads/ 2015/01/Choosing-Wisely-Recommendations.pdf. Accessed June 20, 2018.

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This self-assessment test contains one-best-answer multiple-choice questions. Please read these directions carefully before answering the questions. Answers, critiques, and bibliographies immediately follow these multiple-choice questions. The American College of Physicians (ACP) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

Self-Assessment Test

Pulmonary and Critical Care Medicine Self-Assessment Test

The American College of Physicians designates MKSAP 18 Pulmonary and Critical Care Medicine for a maximum of 25 AMA PRA Category 1 CreditsTM. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Successful completion of the CME activity, which includes participation in the evaluation component, enables the participant to earn up to 25 medical knowledge MOC points in the American Board of Internal Medicine’s Maintenance of Certification (MOC) program. It is the CME activity provider’s responsibility to submit participant completion information to ACCME for the purpose of granting MOC credit.

Earn Instantaneous CME Credits or MOC Points Online Print subscribers can enter their answers online to earn instantaneous CME credits or MOC points. You can submit your answers using online answer sheets that are provided at mksap.acponline.org, where a record of your MKSAP 18 credits will be available. To earn CME credits or to apply for MOC points, you need to answer all of the questions in a test and earn a score of at least 50% correct (number of correct answers divided by the total number of questions). Please note that if you are applying for MOC points, you must also enter your birth date and ABIM candidate number. Take either of the following approaches: • Use the printed answer sheet at the back of this book to record your answers. Go to mksap.acponline.org,

access the appropriate online answer sheet, transcribe your answers, and submit your test for instantaneous CME credits or MOC points. There is no additional fee for this service. • Go to mksap.acponline.org, access the appropriate online answer sheet, directly enter your answers, and sub-

mit your test for instantaneous CME credits or MOC points. There is no additional fee for this service.

Earn CME Credits or MOC Points by Mail or Fax Pay a $20 processing fee per answer sheet and submit the printed answer sheet at the back of this book by mail or fax, as instructed on the answer sheet. Make sure you calculate your score and enter your birth date and ABIM candidate number, and fax the answer sheet to 215-351-2799 or mail the answer sheet to Member and Customer Service, American College of Physicians, 190 N. Independence Mall West, Philadelphia, PA 19106-1572, using the courtesy envelope provided in your MKSAP 18 slipcase. You will need your 10-digit order number and 8-digit ACP ID number, which are printed on your packing slip. Please allow 4 to 6 weeks for your score report to be emailed back to you. Be sure to include your email address for a response. If you do not have a 10-digit order number and 8-digit ACP ID number, or if you need help creating a username and password to access the MKSAP 18 online answer sheets, go to mksap.acponline.org or email custserv@acponline.org. CME credits and MOC points are available from the publication date of December 31, 2018, until December 31, 2021. You may submit your answer sheet or enter your answers online at any time during this period.

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Each of the numbered items is followed by lettered answers. Select the ONE lettered answer that is BEST in each case.

Item 1 A 52-year-old woman is evaluated in the emergency department for wheezing, dyspnea, and cough productive of clear sputum, which have worsened during the past 3 days despite use of her albuterol inhaler up to four times daily. She has no environmental triggers or recent respiratory infection. She smokes two packs of cigarettes per day and is unable to quit. History is notable for anxiety and a 20-year history of asthma. She has had two exacerbations in the past year and was hospitalized and briefly intubated for one of them. Her prescription for budesonide/formoterol controller inhaler ran out 2 weeks ago, and she has been unable to refill it. Other medications are albuterol, montelukast, and alprazolam. On physical examination, temperature is 37.0 °C (98.6 °F), blood pressure is 140/82 mm Hg, pulse rate is 140/min, and respiration rate is 32/min with increased work of breathing. Oxygen saturation is 89% breathing ambient air. Chest examination demonstrates poor air movement with faint expiratory wheezing. The remainder of the examination is normal. Chest radiograph demonstrates hyperinflation without infiltrates. Albuterol improves her symptoms.

Which of the following is the most appropriate initial management? (A) (B) (C) (D)

24-Hour esophageal pH monitoring Add montelukast Discontinue ibuprofen, begin prednisone Nasal polypectomy

Item 3 A 69-year-old man is evaluated for a 3-year history of dyspnea and chronic productive cough. He was diagnosed with COPD 2 years ago after spirometry confirmed severe airflow obstruction. He discontinued smoking at that time but in the past year he was treated for three COPD exacerbations, one requiring hospitalization. Medications are tiotropium, fluticasone/salmeterol, and albuterol inhalers. On physical examination, vital signs are normal; oxygen saturation is 92% on ambient air. He intermittently coughs during the examination. He has a prolonged expiratory phase. The remainder of the examination is unremarkable. Chest radiograph shows the lungs to be clear. Spirometry demonstrates a postbronchodilator FEV1 of 45% of predicted.

Which of the following is the most appropriate management?

Which of the following long-term treatments is most likely to reduce this patient’s exacerbations of COPD?

(A) Admit patient to the hospital for inpatient management (B) Begin prednisone and schedule outpatient follow-up (C) Refill patient’s prescription for budesonide/formoterol and schedule outpatient follow-up (D) Refill patient’s prescription for budesonide/formoterol, begin prednisone, and schedule outpatient follow-up

(A) Prednisone (B) Roflumilast (C) Theophylline (D) Trimethoprim-sulfamethoxazole

Item 2 A 37-year-old man is evaluated for a 1-month history of worsening cough and wheezing requiring use of rescue therapy several times per week, as well as increasing nasal congestion and rhinorrhea. He has a history of moderate persistent asthma and rhinitis since his early twenties. One month ago the patient underwent repair of a traumatic anterior cruciate ligament tear and has some residual daily knee pain. His medical history is notable for sinusitis. He has no symptoms of gastroesophageal reflux disease. Medications are albuterol, budesonide/formoterol, and ibuprofen. On physical examination, vital signs are normal. Oxygen saturation is 97% breathing ambient air. Examination demonstrates conjunctival injection and nasal polyps in both nostrils. Chest examination reveals wheezing on expiration. The remainder of the examination is noncontributory. Laboratory studies reveal IgE is 265 U/mL (265 kU/L). Complete blood count reveals a leukocyte count of 4000/µL (4 × 109/L) with 10% eosinophils. Office spirometry demonstrates moderate airflow obstruction.

Self-Assessment Test

Directions

Item 4 A 57-year-old man is evaluated for a 6-month history of daytime sleepiness. His wife complains of his loud snoring and has observed breathing pauses; he sometimes awakens with a gasp. He has nocturia twice per night. He takes no medications. On physical examination, vital signs are normal. Oxygen saturation is 96% breathing ambient air. BMI is 33. He has a crowded oropharynx with a low-lying soft palate; his neck is 46 cm (18 in) in circumference; he has trace edema at the ankles. Cardiovascular and neurologic examinations are normal. Which of the following is the most appropriate management? (A) (B) (C) (D)

Auto-adjusting positive airway pressure Home sleep testing Multiple sleep latency testing Overnight pulse oximetry

Item 5 A 72-year-old man is evaluated during a follow-up visit. He was evaluated in the emergency department 2 weeks ago for the sudden onset of chest pain. A CT scan was negative for 93

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Item 1

Answer: A

Educational Objective: Treat an asthma exacerbation in the hospital. This patient should be hospitalized for further management. She has an asthma exacerbation and factors that increase her risk of asthma-related death, including several recent exacerbations, history of intubation for asthma, history of anxiety, and poor compliance with her controller medications. She also has worrisome clinical signs, including tachycardia and diminished oxygen saturation, increased work of breathing and decreased air movement on chest examination. These physical findings suggest a severe degree of airflow obstruction and risk for impending respiratory failure; therefore, the most appropriate site of care is the hospital. Management should include close monitoring of dyspnea, work of breathing, and vital signs; frequent bronchodilator treatment; and systemic glucocorticoids. Pulse oximetry may be falsely reassuring because patients maintain normal oxygen levels despite high work of breathing, and hypoxemia is a late sign of pending respiratory failure. In patients who are at high risk or have lack of symptom resolution with initial therapies, arterial blood gas assessment is vital and should initially reveal hyperventilation with a low arterial Pco2. Normalization of the arterial Pco2 could be an early indicator of respiratory muscle fatigue and impending respiratory arrest. Outpatient treatment with prednisone and the patient’s other medications would not be appropriate for this highrisk patient with severe asthma. Key Point

• Patients with asthma exacerbations who have signs that indicate a severe attack should be hospitalized.

Bibliography Prasad Kerlin M. In the clinic. Asthma. Ann Intern Med. 2014;160:ITC3 2-15; quiz ITC3 16-9. [PMID: 24737276]

Item 2

Answer:

Educational Objective: Recognize the role of NSAIDs in poor control of asthma. Treatment with ibuprofen should be discontinued for this patient, and therapy with prednisone should be started. This patient is presenting with signs of aspirin-exacerbated respiratory disease, triggered by his use of ibuprofen. This condition refers to upper and lower respiratory tract reactions to ingestion of substances inhibiting cyclooxygenase-1, which includes aspirin and many NSAIDs. Also known as aspirin-exacerbated respiratory disease or Samter’s triad, aspirin-sensitive asthma includes severe persistent asthma,

aspirin sensitivity, and hyperplastic eosinophilic sinusitis with nasal polyposis. Asthma is worsened by exposure to aspirin or other NSAIDs, likely because of the inhibition of cyclooxygenase and the resulting increase in leukotriene synthesis. Ingestion of cyclooxygenase-1–inhibiting substances can sometimes cause life-threatening bronchospasm, but patients can also have less severe symptoms, which often cause them to not recognize these substances as a trigger. In addition, the sensitivity to aspirin and other NSAIDs develops over time, generally after the onset of rhinosinusitis. Treatment consists of avoidance of aspirin or other NSAIDs along with typical asthma management. For patients who require aspirin use (such as those with coronary artery disease), an aspirin desensitization procedure can be performed. Successful desensitization down-regulates leukotriene receptors and modifies interleukin sensitivity, which may relieve asthma symptoms in some patients. For this reason, the addition of a leukotriene inhibitor such as montelukast or zafirlukast to an asthma maintenance regimen is helpful for most patients to modify the leukotriene dysregulation thought to contribute to the syndrome; however, addition of a leukotriene inhibitor alone would not be the appropriate next step for this patient. 24-Hour esophageal pH monitoring is helpful to diagnose gastroesophageal reflux disease, but the patient has no symptoms of this; moreover, a trial of empiric proton pump inhibitor therapy would be indicated before invasive testing. A nasal polypectomy may be helpful in the long-term management of this syndrome, but it is not the initial step.

Answers and Critiques

Key Point

• Treatment of aspirin-exacerbated respiratory disease consists of symptom treatment with glucocorticoids and removal of the exposure; treatment can also include a leukotriene receptor antagonist.

Bibliography Ledford DK, Wenzel SE, Lockey RF. Aspirin or other nonsteroidal inflammatory agent exacerbated asthma. J Allergy Clin Immunol Pract. 2014;2:6537. [PMID: 25439353] doi:10.1016/j.jaip.2014.09.009

Item 3

Answer:

Educational Objective: Treat chronic bronchitis and prevent frequent COPD exacerbations with roflumilast. Roflumilast is the most appropriate treatment. It is used primarily as add-on therapy in severe COPD associated with chronic bronchitis and a history of recurrent exacerbations despite other therapies; it has been shown to improve lung function and reduce risk and frequency of exacerbations in these individuals. However, it is not a bronchodilator, is expensive, and has not been shown to be effective in other groups of patients with COPD. Common side effects include 117

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