Approach to internal medicine 2016

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Approach to Internal Medicine

Approach to Internal Medicine

A Resource Book for Clinical Practice

Fourth Edition

Edited by

David Hui, MD, MSc Alexander A Leung, MD, MPH, FRCPC, MRCP(UK), FACP

Raj Padwal, MD, MSc, FRCPC

With Assistance from

Christopher Ma, MD

ISBN 978-3-319-11820-8 ISBN 978-3-319-11821-5 (eBook)

DOI 10.1007/978-3-319-11821-5

Library of Congress Control Number: 2015952117

Springer Cham Heidelberg New York Dordrecht London

© Springer International Publishing Switzerland 2016

This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recita-tion, broadcasting, reproduction on microfi lms or in any other physical way, and transmission or infor-mation storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed

The use of general descriptive names, registered names, trademarks, service marks, etc in this tion does not imply, even in the absence of a specifi c statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use

The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein

or for any errors or omissions that may have been made

Printed on acid-free paper

Springer International Publishing AG Switzerland is part of Springer Science+Business Media

Editors: David Hui, Alexander A Leung, Raj Padwal

Assistant Editor: Christopher Ma

First edition, first printing, April 2006

Second edition, first printing, August 2007

Second edition, second printing, November 2007

Second edition, third printing, March 2008

Second edition, fourth printing, July 2008

Second edition, fifth printing, November 2008

Second edition, sixth printing, June 2009

Third edition, first printing, January 2011

Fourth edition, first printing, September 2015

Approach to Internal Medicine: A Resource Book for Clinical Practice

Additional material to this book can be downloaded from http://extras.springer.com

To Ella, Rupert and Nancy

Discl aimer

Approach to Internal Medicine is meant to be a practical field guide

Dos-ages of medications are provided for quick reference only Readers should consult other resources before applying information in this manual for

direct patient care The author, editors, and publisher of Approach to

Inter-nal Medicine cannot be held responsible for any harm, direct or indirect,

caused as a result of application of information contained within this manual

Pref ace

Practice is science touched with emotion

Confessio Medici, Stephen Paget, 1909

In this fourth edition of Approach to Internal Medicine, we have substantially updated the content to

provide practicing clinicians and trainees with a practical, evidence-based, and concise resource for

everyday clinical use, bedside teaching and examination preparation Approach to Internal Medicine

consists of over 250 internal medicine topics classified under 17 subspecialties

Under each topic, the sections on differential diagnoses, investigations, and treatments are designed for the rapid retrieval of high-yield clinical information and can be particularly useful when one is all

alone assessing a patient at 3 o’clock in the morning Unique to Approach to Internal Medicine, we have

included multiple comparison tables aimed at highlighting the distinguishing features between various

System (SI) units, this edition also provides US customary units [in square brackets] for quick reference For this new edition, we are very fortunate to have recruited a new assistant editor, Dr Christopher Ma,

who brings with him a wealth of knowledge and the perspective of a chief medicine resident The JAMA

Rationale Examination Series has now been updated with new data We are most grateful to our section

editors and contributors for their meticulous review of each subspecialty, providing expert input on the most up-to-date information We also would like to thank the editorial and production teams at Springer for their expert guidance and support throughout this mammoth project Finally, we would like to thank all previous and current users of this manual for their support and feedback

While every effort has been made to ensure the accuracy of information in this manual, the author, editors, and publisher are not responsible for omissions, errors, or any consequences that result from application of the information contained herein Verification of the information in this manual remains the professional responsibility of the practitioner Readers are strongly urged to consult other appropri-ate clinical resources prior to applying information in this manual for direct patient care This is particu-larly important since patterns of practice and clinical evidence evolve constantly We welcome any constructive feedback to help make this manual a more accurate, practical, comprehensive, and user- friendly resource

Bryan Jonathan Har , MD, MPH, FRCPC

Clinical Assistant Professor

Department of Cardiac Sciences

Divisions of Critical Care Medicine

and Infectious Diseases

Michael H Kroll , MD, FACP

Department of Benign Hematology

The University of Texas MD Anderson

Cancer Center

Houston, TX, USA

ONCOLOGY

Ahmed Eid , MD, MEd

Department of General Oncology The University of Texas MD Anderson Cancer Center Houston, TX, USA

David Ramirez , MD

Department of General Oncology The University of Texas MD Anderson Cancer Center Houston, TX, USA

Caren L Hughes , PharmD, BCOP

Division of Pharmacy The University of Texas MD Anderson Cancer Center Houston, TX, USA

INFECTIOUS DISEASES

Stephanie W Smith , MD, MSc, FRCPC

Division of Infectious Diseases Department of Medicine University of Alberta Edmonton, AB, Canada

RHEUMATOLOGY

Steven J Katz , MD, FRCPC

Division of Rheumatology Department of Medicine University of Alberta Edmonton, AB, Canada

NEUROLOGY

Michael M C Yeung , MD, FRCPC

Department of Clinical Neurosciences Cumming School of Medicine University of Calgary Calgary, AB, Canada

Ronak K Kapadia , MD, BSc

Department of Clinical Neurosciences

Cumming School of Medicine

Susan Y Chon , MD, FAAD

Division of Internal Medicine

Department of Dermatology

The University of Texas MD

Anderson Cancer Center

Department of Palliative Care

and Rehabilitation Medicine

Department of General Oncology

Division of Cancer Medicine

The University of Texas MD

Anderson Cancer Center

Kari McKnight , RD

WholeSUM Nutrition Consulting Inc

Edmonton, AB, Canada

GENERAL INTERNAL MEDICINE

Peter Hamilton , MBBCh, FRCPC

Division of General Internal Medicine Department of Medicine

University of Alberta Edmonton, AB, Canada

Christopher Ma , MD

Department of Medicine University of Alberta Edmonton, AB, Canada

Contents

1 Pulmonary Medicine 1

Asthma Exacerbation 1

COPD Exacerbation 4

Pneumonia 7

Pulmonary Embolism 10

Pleural Effusion 12

Chronic Cough 14

Hemoptysis 15

Solitary Pulmonary Nodule 16

Pulmonary Hypertension 17

Interstitial Lung Disease 18

Obstructive Sleep Apnea 20

Respiratory Acidosis: Hypoventilation 22

Respiratory Alkalosis: Hyperventilation 22

Hypoxemia 23

Ventilation Issues 23

Approach to Chest Imaging 23

Approach to Pulmonary Function Tests 25

2 Cardiology 27

Aortic Dissection 27

Acute Coronary Syndrome 28

Pericardial Diseases: Pericarditis and Tamponade 35

Heart Failure 37

Digoxin Intoxication 43

Atrial Fibrillation 45

Syncope 49

Cardiac Examination 49

Aortic Stenosis 54

Aortic Regurgitation 56

Mitral Stenosis 57

Mitral Regurgitation 59

Endocarditis 60

Peripheral Vascular Disease 62

Hypertension 65

Hyperlipidemia 70

Smoking Issues 73

Approach to ECG 73

3 Nephrology 77

Acute Renal Failure: Pre-renal 77

Acute Renal Failure: Renal 78

Acute Renal Failure: Post-renal 80

Glomerulopathies 80

Chronic Kidney Disease 83

Proteinuria 85

Hematuria 85

Cystic Kidney Diseases 86

Metabolic Acidosis 87

Metabolic Alkalosis 89

Hyponatremia 90

Hypernatremia 92

Hypokalemia 92

Hyperkalemia 93

Hypomagnesemia 94

Hypophosphatemia 94

Ureteral Calculi 95

Hypertension 96

Approach to Dialysis 96

4 Critical Care 99

Intensive Care Issues 99

Hypoxemia 102

Acute Respiratory Distress Syndrome 104

Ventilation Issues 105

Shock 108

Sepsis and Septic Shock 111

Lactic Acidosis 112

Rhabdomyolysis 113

Toxicology 114

Alcohol Withdrawal and Complications of Alcoholism 117

Hypothermia 120

Smoke Inhalation 121

Anaphylaxis 122

5 Gastroenterology 123

Nausea and Vomiting 123

Dysphagia 124

Dyspepsia 125

Acute Abdominal Pain 128

Upper GI Bleed 131

Lower GI Bleed 134

Inflammatory Bowel Disease Exacerbation 135

Acute Diarrhea 137

Chronic Diarrhea 138

Malabsorption Syndromes 140

Constipation 141

Acute Liver Failure 143

Hepatitis B 145

Hepatitis C 147

Chronic Liver Disease: Cirrhosis 149

Hepatic Encephalopathy 152

Ascites 153

Jaundice 155

Acute Pancreatitis 156

6 Hematology 159

Polycythemia 159

Microcytic Anemia 160

Normocytic Anemia 161

Macrocytic Anemia 162

Sickle Cell Disease 163

Neutropenia 164

Eosinophilia 165

Thrombocytosis 166

Thrombocytopenia 167

Pancytopenia 170

Bleeding Diathesis 170

Hypercoagulable States 173

Deep Vein Thrombosis 176

Approach to Anticoagulation Therapies 178

Transfusion Reactions 180

Approach to the Peripheral Blood Smear 182

Splenomegaly 182

Myeloproliferative Disorders 184

Acute Myelogenous Leukemia 185

Acute Lymphoblastic Leukemia 188

Chronic Lymphocytic Leukemia 189

Hodgkin’s Lymphoma 191

Non-Hodgkin’s Lymphoma 193

Multiple Myeloma 198

Febrile Neutropenia 201

Hematopoietic Stem Cell Transplant 201

7 Oncology 203

Lung Cancer 203

Mesothelioma 206

Thymoma and Thymic Carcinoma 207

Breast Cancer 208

Esophageal Cancer 215

Gastric Cancer 217

Colorectal Cancer 219

Carcinoid Tumors 221

Gastrointestinal Stromal Tumor 223

Anal Cancer 224

Cancer of the Exocrine Pancreas 225

Hepatocellular Carcinoma 227

Renal Cancer 228

Bladder Cancer 230

Prostate Cancer 231

Testicular Cancer 234

Brain Tumors 237

Cancer of Unknown Origin 237

Tumor Markers 239

Cancer Screening 240

Hereditary Cancer Syndromes 243

Antineoplastic Agents 246

Oncologic Emergencies 253

Febrile Neutropenia 254

Chemotherapy-Induced Nausea and Vomiting 254

Oral Mucositis 256

Chemotherapy-Induced Diarrhea 257

8 Infectious Diseases 259

Fever of Unknown Origin 259

Fever and Rash 260

Fever and Joint Pain 262

Sepsis 262

Febrile Neutropenia 263

Fever with Travel History 265

Pneumonia 268

Endocarditis 268

Meningitis 269

Urinary Tract Infections and Sexually Transmitted Infections 272

Soft Tissue Infections 275

Osteomyelitis 277

Septic Arthritis 279

Tuberculosis: Pulmonary 279

Approach to Gram Stain, Culture, and Sensitivity 282

Approach to Empiric Antibiotics 289

Hepatitis B 290

Hepatitis C 290

Herpes Simplex Virus Infection 290

Human Immunodeficiency Virus 291

Influenza 295

Antiviral Agents 297

Fungal Infections 298

Antifungal Agents 302

Infection Control 304

Immunization for Adults 305

9 Rheumatology 309

Septic Arthritis 309

Gout 311

Polyarticular Joint Pain and Fever 312

Rheumatoid Arthritis 314

Systemic Lupus Erythematosus 316

Seronegative Spondyloarthropathies 319

Back Pain 322

Osteoarthritis 324

Fibromyalgia 325

Vasculitis 326

Approach to Serologies 331

Joint Examination 333

10 Neurology 335

Brain Tumors 335

Acute Stroke Syndromes 337

Cranial Nerve Examination 344

Diplopia 347

Bell’s Palsy 347

Multiple Sclerosis 349

Dementia 350

Delirium 350

Seizures 350

Syncope 353

Migraine Headaches 355

Meningitis 356

Dizziness and Vertigo 357

Hearing Impairment 359

Myasthenia Gravis 360

Ataxia 361

Subacute Combined Degeneration 362

Parkinson’s Disease 362

Radiculopathy 366

Peripheral Neuropathy 371

Muscle Weakness 377

Approach to Neuroimaging 378

11 Endocrinology 381

Diabetes Mellitus 381

Principles of Insulin Use 387

Hypoglycemia 389

Hypothyroidism 390

Hyperthyroidism 391

Solitary Thyroid Nodule 393

Pituitary Tumors 394

Polyuria 396

Adrenal Incidentaloma 396

Adrenal Insufficiency 398

Cushing’s Syndrome 399

Hypocalcemia 401

Hypercalcemia 402

Osteoporosis 403

Hypertension 406

Hyperlipidemia 406

Amenorrhea 406

Hirsutism 407

12 Dermatology 409

Eczema 409

Psoriasis Vulgaris 410

Acne Vulgaris 412

Exanthematous Lesions 413

Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis 414

Ulcers 416

Melanoma and Skin Tumors 418

Cutaneous Lupus Erythematosus 421

Drug Eruptions 422

Erythema Nodosum 424

Clubbing 425

Dupuytren’s Contracture 426

13 Geriatrics 427

Geriatric-Specific Issues 427

Dementia and Cognitive Impairment 429

Delirium 432

Falls 434

Osteoporosis 435

Urinary Incontinence 435

Hearing Impairment 436

Pharmacological Issues in the Elderly 436

14 Palliative Care 439

Palliative Care-Specific Issues 439

Principles of Pain Control 442

Delirium 445

Cancer-Related Fatigue 446

Dyspnea in the Palliative Setting 446

Nausea and Vomiting in the Palliative Setting 448

Constipation in the Palliative Setting 448

Anorexia–Cachexia 449

Communication Issues 451

Prognostication in Far Advanced Cancer Patients 453

Management of Other Distressing Symptoms 454

15 Nutrition 457

Obesity 457

Malabsorption Syndromes 459

Anorexia–Cachexia 459

Vitamin B12 Deficiency 459

Diet and Supplemental Nutrition 460

16 Obstetric Medicine 465

Physiologic Changes in Pregnancy 465

Preeclampsia/Eclampsia/HELLP Syndrome 467

Pulmonary Diseases in Pregnancy 469

Cardiac Diseases in Pregnancy 470

Hepatic Diseases in Pregnancy 471

Infectious Diseases in Pregnancy 472

Diabetes in Pregnancy 474

Thyroid Diseases in Pregnancy 475

Other Disorders in Pregnancy 476

17 General Internal Medicine 479

Approach to Diagnostic Tests and Clinical Trials 479

Smoking Cessation 480

Multisystem Disorders 482

Perioperative Assessment for Non-cardiopulmonary Surgery and Postoperative Complications 484

Medical Fitness to Drive 490

Obtaining Consent for Medical Procedures 492

Biomedical Ethics Issues 492

Hospital Admission and Discharge Issues 494

Appendix A Advanced Cardiac Life Support 495

Appendix B List of Common Abbreviations 497

Appendix C Common Laboratory Values and Unit Conversion 503

Appendix D History Template 509

Selected Internal Medicine Topics 511

Index 513

D Hui et al (eds.), Approach to Internal Medicine: A Resource Book for Clinical Practice,

PATHOPHYSIOLOGY

EXACERBATORS OF ASTHMA

· OUTDOORS—respirable particulates, ozone,

sulfur dioxide, cold air, humidity, smoke

· INDOORS—smoke, dust mites, air conditioners,

humidity, perfumes, scents, mold, animal dander

· NON - ADHERENCE

CLINICAL FEATURES

HISTORY —history of asthma and any

visits/hospital admissions in the last 6 months

(or  ever), any ICU admissions, previous

predni-sone use, triggers for attacks, usual peak

expiratory flow rate, change in peak flow rates,

wheezing, cough, dyspnea, decreased function,

exercise limitation, nocturnal symptoms,

absenteeism from work/school, postnasal drip,

medication history, psychosocial issues, tional and work environment, home environment (pets, heating source, filter changes)

PHYSICAL —HR ↑, RR ↑, pulsus paradoxus, O 2 requirement, moderate-severe dyspnea, barrel chest, cyanosis, hyperresonance, decreased breath sounds, wheezing, forced expiratory time

TYPES OF WHEEZING —inspiratory wheeze and

expiratory wheeze are classically associated with extrathoracic and intrathoracic airway obstruc-tion, respectively However, they are neither sensitive nor specific and cannot help to narrow differential diagnosis

Asthma Exacerbation

1

PULMONARY MEDICINE

Ashley-Mae   Gillson

DIFFERENTIAL DIAGNOSIS OF WHEEZING

EXTRATHORACIC AIRWAY OBSTRUCTION

retropha-ryngeal abscess, obesity, post-nasal drip

· LARYNX —laryngeal edema, laryngostenosis,

laryngocele, epiglottitis, anaphylaxis, severe

laryngopharyngeal reflux, laryngospasm

· VOCAL CORDS —vocal cord dysfunction,

paraly-sis, hematoma, tumor, cricoarytenoid arthritis

INTRATHORACIC AIRWAY OBSTRUCTION

tracheomalacia, tracheobronchitis (herpetic,

fungal), malignancy, benign tumor,

aspira-tion, foreign body

· TRACHEAL COMPRESSION —goiter, right-sided

aortic arch

· LOWER AIRWAY OBSTRUCTION —asthma, COPD,

bronchiolitis, bronchiectasis, carcinoid

tumor, aspiration, malignancy

· PARENCHYMA —pulmonary edema

· VASCULAR —pulmonary embolism

INVESTIGATIONS

BASIC

· MICROBIOLOGY—sputum Gram stain/AFB/C&S, nasopharyngeal swab for viral studies

· IMAGING —CXR

SPECIAL

· PEAK FLOW METER —need to compare bedside reading to patient’s baseline

· SPIROMETRY / PFT (non-acute setting)—

↑ FEV1 >12% and an absolute ↑ by 200 mL post-bronchodilator suggests asthma

· METHACHOLINE CHALLENGE (non-acute setting)—if diagnosis of asthma not confirmed by spirometry alone A decrease

of FEV1 >20% after methacholine challenge suggests asthma Sens 95%

· SPUTUM EOSINOPHIL COUNTS (non-acute setting) — performed in specialized centres for monitoring of asthma control in patients with moderate to severe asthma

Can Resp J 2012 19:2

CLINICAL FEATURES CONT’D

ACUTE MANAGEMENT

ABC — O 2 to keep sat >92%, IV

BRONCHODILATORS — salbutamol 100 μg MDI

MDI 2 puffs q6h ATC (frequency stated is only a guide,

may increase or decrease on a case by case basis)

STEROID — prednisone 0.5–1  mg/kg PO

daily × 7–14 days (may be shorter depending on

response) or methylprednisolone 0.4–0.8 mg/kg

IV daily (until conversion to prednisone)

OTHERS —if refractory case and life-threatening,

consider IV epinephrine, IV salbutamol,

MECHANICAL VENTILATION — BiPAP , intubation

LONGTERM MANAGEMENT

EDUCATION — smoking cessation (see p.  480)

Asthma action plan Puffer technique

educa-tion and review

ENVIRONMENTAL CONTROL — avoidance of

out-door/indoor allergens, irritants, and infections; home

environment cleanliness (e.g steam cleaning)

VACCINATIONS —influenza vaccine annually

and pneumococcal vaccine every 5 years

FIRST LINE — SABA ( salbutamol 100 μg MDI 2

puffs PRN) Proceed to second line if using more

than 2×/week or 1×/day for exercise-induced

symptoms, symptoms >2×/week, any nocturnal

symptoms, activity limitation or PEF <80%

SECOND LINE —low-dose ICS plus short-acting

β2-agonist PRN

THIRD LINE —moderate-dose ICS , combined ICS

should never be used alone in asthma), or

leuko-triene receptor antagonist (most effective in

asthma complicated with sinus disease and

exercise- induced asthma) May also consider using

single inhaler budesonide/formoterol combination

therapy as both a controller and an acute reliever

FOURTH LINE — anti-IgE therapy (omalizumab)

for refractory allergic asthma, administered

subcutaneously q2–4 weeks, dosed by IgE level

and body weight, for add-on therapy or

inade-quately controlled moderate-to-severe allergic

asthma despite use of high doses of inhaled

corticosteroid therapy

NEJM 2009 360:10 Can Resp J 2012 19:2

TREATMENT ISSUES

COMMON INHALED MEDICATIONS

· SHORT - ACTING ANTICHOLINERGICS — ipratropium

· LONG - ACTING β - AGONISTS (LABA) — formoterol

puff BID

· LONG - ACTING ANTICHOLINERGICS — tiotropium

· INHALED CORTICOSTEROIDS — beclomethasone

asthma at this time, not COPD), mometasone

twisthaler 100–400 μg INH BID

Absence from work or school due to asthma

None

best

difference between the highest and lowest PEF divided by the highest PEF multiplied

by 100 for morning and night (determined over a 2 week period)

SPECIFIC ENTITIES

EXERCISEINDUCED ASTHMA

symp-toms only during exercise due to

bronchocon-striction as a result of cooling of airways

associated with heat and water loss

· DIAGNOSIS —spirometry Exercise or

methacho-line challenge may help in diagnosis

· TREATMENTS —prophylaxis with salbutamol 2

puffs MDI, given 5–10  min before exercise

Consider leukotriene antagonists or

inhaled  glucocorticoids if frequent use of

prophylaxis

TRIAD ASTHMA (Samter’s syndrome)—triad of

asthma, aspirin/NSAIDs sensitivity, and nasal

symptoms Management include ASA/NSAIDs

avoidance and leukotriene antagonists

(montelukast)

A L L E R G I C B R O N C H O P U L M O N A RY ASPERGILLOSIS (ABPA)

and cystic fibrosis Due to colonization of the

airways by Aspergillus fumigatus , leading to an

intense, immediate hypersensitivity-type reaction in the airways

· CLINICAL FEATURES —history of asthma, rent episodes of fever, dyspnea, and productive cough (brownish sputum) Peripheral eosino-philia CXR findings of patchy infiltrates and central bronchiectasis, CT chest findings of central bronchiectasis, “finger-in-glove” appearance (i.e mucous-filled dilated bronchi)

recur-· DIAGNOSIS—above clinical features plus

Aspergillus extract skin test, serum IgE level, sputum for Aspergillus and/or serologic tests (IgE and IgG against Aspergillus )

· TREATMENTS —systemic glucocorticoids, itraconazole

ADMISSION CRITERIA

DISCHARGE CRITERIA —consider discharging patient if peak flow >70% of usual (or predicted)

value for at least 1 h after bronchodilator

OXYGEN DELIVERY DEVICES

SPECIFIC ENTITIES CONT’D

TREATMENT ISSUES CONT’D

[cigarette smoke, dust, pollutants, cold air]),

non-adherence, pulmonary embolism,

pulmo-nary edema, pneumothorax, progression of

COPD

CLINICAL FEATURES

DIFFERENTIAL DIAGNOSIS OF ACUTE DYSPNEA

RESPIRATORY

exacerbation, acute bronchitis, infectious

exacerbation of bronchiectasis, foreign body

obstruction

· PARENCHYMA —pneumonia, cryptogenic

organizing pneumonia (COP), ARDS, acute

exacerbation of interstitial lung disease

· VASCULAR—pulmonary embolism,

· VALVULAR—aortic stenosis, acute aortic

regurgitation, mitral stenosis, endocarditis

· PERICARDIAL —pericardial effusion,

tamponade

SYSTEMIC —sepsis, metabolic acidosis, anemia

OTHERS —neuromuscular, psychogenic,

anxiety

RATIONAL CLINICAL EXAMINATION SERIES:

DOES THE CLINICAL EXAMINATION

PREDICT AIRFLOW LIMITATION?

Clinical Judgement

Overall Clinical Prediction

of Moderate-Severe Disease

Overall Clinical Prediction  

of Mild Disease

APPROACH —“no single item or

combina-tion of items from the clinical examinacombina-tion rules out airflow limitation The best findings associated with increased likelihood of air-flow limitation are objective wheezing, FEV1

>9 s, positive match test, barrel chest, resonance and subxyphoid cardiac impulse Three findings predict the likelihood of air-flow limitation in men: years of cigarette smoking, subjective wheezing and either objective wheezing or peak expiratory flow rate”

JAMA 1995 273:4

UPDATE —multivariate ‘Rule In’ Obstructive

Disease Model (history of obstructive airways disease, smoking >40 pack-years, age ≥45, and laryngeal height ≤4 cm) has posterior odds of disease of 220 Multivariate ‘Rule Out’ Obstructive Disease Model (smoking <30 years,

no wheezing symptoms, and no auscultated wheezing) has posterior odds of disease of 0.02

The Rational Clinical Examination

McGraw- Hill, 2009

CLINICAL FEATURES CONT’D

PROGNOSTIC ISSUES

PROGNOSIS OF PATIENTS WITH ACUTE

EXACERBATION OF COPD —in-hospital

mortal-ity 5–10%

GOLD CLASSIFICATION 2007 —all have FEV1/

FVC <0.7

· STAGE I ( MILD ) —FEV1 ≥ 80% predicted

· STAGE II ( MODERATE ) —FEV1 50–79% predicted

· STAGE III ( SEVERE ) —FEV1 30–49% predicted

· STAGE IV ( VERY SEVERE ) —FEV1 < 30% predicted,

or <50% predicted + cor pulmonale

BODE INDEX

· OBSTRUCTION (post-bronchodilator FEV1)—0

points = ≥65% predicted, 1 point = 50–64%,

2 points = 36–49%, 3 points = ≤35%

· DISTANCE WALKED IN 6 MIN —0 points = ≥350 m,

1 point = 250–349 m, 2 points = 150–249 m, 3

points = ≤149 m

· EXERCISE MMRC DYSPNEA SCALE —0 points = 0–1,

1 point = 2, 2 points = 3, 3 points = 4

· SCORING —total BODE score calculated as sum

of all points Relative risk for death (any cause)

is increased by 34% per one-point increase

in  BODE score Relative risk for death (from

respiratory failure, pneumonia, or pulmonary

embolism) is increased by 62% per one-point

increase in BODE score

NEJM 2004 350:10

ACUTE MANAGEMENT

ABC — O 2 to keep sat >90%, or 88–92% if CO 2 retainer, IV

BRONCHODILATORS — salbutamol 100 μg MDI

STEROIDS — prednisone 40–60  mg PO daily × 5–14 days (tapering dose not always

necessary) or methylprednisolone 60–125 mg IV

q6-12 h (inpatient)

ANTIBIOTICS —give if any two of the following

the need for non-invasive mechanical ventilation and “at risk” for poor outcome (substantial comor-bidities, severe COPD, frequent exacerbations >3/year, recent antibiotics within 3 months); choices

500  mg PO daily × 7–10 days [or 750  mg PO

100  mg PO BID × 7–10 days, amoxicillin 500  mg

BID × 10 days, or azithromycin 500 mg PO × 1 day

then 250 mg PO daily × 4 days)

MECHANICAL VENTILATION — BiPAP , intubation OTHERS —DVT prophylaxis ( unfractionated heparin 5000 U SC q8-12 h, enoxaparin 40 mg SC

q24h, dalteparin 5000 U SC q24h), physiotherapy

NEJM 2002 346:13

LONGTERM MANAGEMENT

EDUCATION — smoking cessation (see p.  480)

Disease-specific self-management program

Puffer technique education and review

VACCINATIONS —influenza vaccine annually

and pneumococcal vaccine booster every 5 years

REHABILITATION — education and exercise training (increases quality of life and exercise

tolerance); pulmonary rehabilitation associated

with moderate to very severe COPD and recent AECOPD (<4 weeks)

FIRST LINE — SABA or short-acting

anticholiner-gic on an as-needed basis

SECOND LINE — LABA or long-acting

anticho-linergic ( tiotropium 1 puff [18 μg/puff] INH daily) plus SABA PRN. Consider early initiation of long- acting agents if requiring regular PRN short- acting agents as long-acting agents are superior

INVESTIGATIONS

BASIC

· MICROBIOLOGY—sputum Gram stain/AFB/

C&S/fungal, nasopharyngeal swab for viral

studies

· IMAGING —CXR

fibrilla-tion, sinus tachycardia

· SPIROMETRY / PFT —FEV1/FVC <0.7, may be

partially reversible Severity based on FEV1

SPECIAL

· ECHOCARDIOGRAM

THIRD LINE — LABA plus long-acting

anticho-linergic , with SABA PRN

FOURTH LINE — long-acting anticholinergic

plus LABA/ICS (e.g Advair, Symbicort) No role for

ICS monotherapy Consider

4 inhibitor ( roflumilast 500 μg PO daily) as

adju-vant maintenance therapy in moderate to severe

COPD with ≥1 exacerbation in previous year

375–750 mg PO TID) if ≥2 exacerbations in

previ-ous 2 years Chronic antibiotic therapy generally

not recommended

FIFTH LINE —fourth line plus theophylline

400  mg PO daily × 3  days, then 400–600  mg PO

SIXTH LINE— fifth line plus home O 2

SEVENTH LINE — lung volume reduction

sur-gery (may be beneficial if upper lobe involvement

and poor functional capacity) or lung transplant

Canadian Thoracic Society COPD

Guidelines 2007 American College of Chest

Physicians (CHEST) and Canadian Thoracic Society (CTS) Joint

Guidelines 2014

TREATMENT ISSUES

FACTORS FOR IMPENDING INTUBATION —

cardiac or respiratory failure, hemodynamic

instability, markedly elevated respiratory rate

(>35/min), fatigue and labored respiration, use of

accessory muscles, worsening hypercapnia,

acidosis (especially lactic), stridor (impending

upper airway obstruction), agonal breathing

(impending respiratory arrest)

LIFEPROLONGING MEASURES FOR COPD —

INDICATIONS FOR SUPPLEMENTAL HOME

O 2 —ABG done at room air PaO 2 <55 mmHg alone

ankle edema, cor pulmonale, or hematocrit >56%

SPECIFIC ENTITIES

α 1-ANTITRYPSIN DEFICIENCY

protease inhibitor (homozygous ZZ) with

impaired transport out of the liver Serum level is

activity leads to emphysema and cirrhosis (10%)

· DIAGNOSIS — α 1-antitrypsin levels; targeted

testing should be considered in patients with

COPD diagnosed before 65 years of age or with

· TREATMENTS—similar to COPD, α 1-antitrypsin

replacement

BRONCHIOLITIS OBLITERANS

differ-ent from bronchiolitis obliterans organizing pneumonia (BOOP)/cryptogenic organizing pneumonia (COP), a parenchymal lung disorder

· CAUSES —infection (viral, mycoplasma), matory (ulcerative colitis, rheumatoid arthritis), transplant (bone marrow, lung), toxic fumes, idiopathic

inflam-· TREATMENTS —bronchiolitis obliterans (with an organizing intraluminal exudate and prolifera-tive granulation tissue polyp) is usually steroid responsive Constrictive bronchiolitis (late, fibrotic, concentric) is not responsive to glucocorticoids

BRONCHIECTASIS

types of bronchiectasis include

· CYLINDRICAL OR TUBULAR BRONCHIECTASIS —dilated airways alone, sometimes repre-sents residual effect of pneumonia and may resolve

· VARICOSE BRONCHIECTASIS —focal constrictive areas along the dilated airways

· SACCULAR OR CYSTIC BRONCHIECTASIS —most severe form Progressive dilatation of the airways, resulting in large cysts or saccules

· CAUSES

· FOCAL —broncholith, post-infectious, tumor, extrinsic lymph node compression, post-lobar resection, recurrent aspiration

· DIFFUSE

· POST - INFECTIOUS —bacterial ( Pseudomonas,

viral (adenovirus, measles, influenza, HIV)

· IMMUNODEFICIENCY —cancer, apy, hypogammaglobulinemia, immuno-suppression, sequelae of toxic inhalation

chemother-or aspiration of fchemother-oreign body

· INTERSTITIAL LUNG DISEASE —traction bronchiectasis

· INFLAMMATORY—RA, SLE, Sjogren’s syndrome, relapsing polychondritis, IBD

· INHERITED — α 1-antitrypsin deficiency,

cys-LONGTERM MANAGEMENT CONT’D SPECIFIC ENTITIES CONT’D

(Kartagener’s syndrome, Young’s

(Mounier–Kuhn syndrome), cartilage

defi-ciency (Williams–Campbell syndrome),

Marfan’s syndrome

· DIAGNOSIS—high-resolution CT chest (signet

ring sign), PFT (obstruction ± reversibility)

· TREATMENTS—exercises, chest physiotherapy,

and bronchodilators similar to COPD; however,

if reversible, inhaled corticosteroids should be

given early Ensure adequate systemic tion Effective treatment of exacerbations

PATHOPHYSIOLOGY

COMPLICATIONS OF PNEUMONIA

formation, parapneumonic effusion/empyema, pleuritis ± hemorrhage

· EXTRAPULMONARY —purulent pericarditis, natremia (from SIADH), sepsis

CLINICAL FEATURES

TYPES OF PNEUMONIA

COMMUNITYACQUIRED PNEUMONIA

Staphylococcus aureus , Haemophilus, Moraxella

· ATYPICAL — Mycoplasma , Chlamydia ,

Legionella , TB, community-acquired MRSA

· VIRAL —influenza, parainfluenza,

metapneu-movirus, RSV, adenovirus

· FUNGAL —blastomycosis, cryptococcus,

histoplasmosis

ASPIRATION PNEUMONIA

Bacte-roides , Peptostreptococcus , Fusobacterium

species and other Gram-positive bacilli

· CHEMICAL PNEUMONITIS

COMPROMISED (see p. 291)

NOSOCOMIAL PNEUMONIA —begins in

non-intubated patient within 48 hours of admission

coli , Serratia ), Haemophilus , Acinetobacter

· VIRAL —influenza

VENTILATORASSOCIATED PNEUMONIA —

begins >48 hours after the patient is intubated

(see p. 107)

HEALTHCARE ASSOCIATED PNEUMONIA —

pneumonia that (A) occurs within 90 days of

hospitalization of 2 days or more, a stay at

nurs-ing home, or a visit to an oral puncture care

facility, hospital-based clinic or hemodialysis

facility; or (B) occurs within 3 days of receiving

antibiotics, chemotherapy, or any type of

wound care

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE COMMUNITY ACQUIRED PNEUMONIA?

PREDICTION RULE—Diehr model

(rhinor-rhea = −2 points, sore throat = −1 point, night sweats = +1 point, myalgias = +1 point, sputum all day = +1 point, RR >25 = +2 points, temp

≥37.8  °C [≥100  °F] = +2 points If score ≥3, LR 14; if ≥1, LR 5.0; if < −1 LR 0.22)

SURFACE LUNG MARKINGS

at the mid-clavicular line, level of 8th rib at the

mid-axillary line, and level of 10th rib at the

mid-scapular line

· OBLIQUE ( MAJOR ) FISSURES —draw a line

diago-nally from T3 vertebral body posteriorly to the

6th rib anteriorly

· HORIZONTAL ( MINOR ) FISSURE —draw a

horizon-tal line at the level of right anterior 4th rib

DIAGNOSTIC AND PROGNOSTIC ISSUES

PNEUMONIA SEVERITY OF ILLNESS (PSI) SCORE

(+10), cancer (+30), liver disease (+20), heart failure (+10), CVA (+10), renal failure (+10), altered mental status (+20), RR >30 (+20), SBP

room air (+10), pleural effusion (+10)

· UTILITY —originally developed as a prognostic tool Consider admission if PSI score >90 Clinical judgment more important than PSI in determining admission

treat-ment issues for an approach to selecting the appropriate regimen (remember to adjust for renal function)

· TETRACYCLINE — doxycycline 100  mg PO BID × 10 days

· MACROLIDES — azithromycin 500  mg PO first day, then 250 mg PO daily × 4 days; clarithro-

mycin 250–500 mg PO BID × 10 days

· FLUOROQUINOLONES — levofloxacin 500  mg

PO daily × 7–10 days (or 750  mg × 5  days),

avoid if exposed to fluoroquinolone within last 3–6 months

· ANTI - PSEUDOMONAL —ceftazidime, cefepime, meropenem, ciprofloxacin, aminoglycosides, piperacillin–tazobactam (do not use same class of agent when double covering for

Pseudomonas )

APPROACH —“individual or combinations of

symptoms and signs have inadequate test

char-acteristics to rule in or rule out the diagnosis of

pneumonia Decision rules that use the

pres-ence or abspres-ence of several symptoms and signs

to modify the probability of pneumonia are

available, the simplest of which requires the

absence of any vital sign abnormalities to

exclude the diagnosis If diagnostic certainty is

required in the management of a patient with

suspected pneumonia, then chest radiography

(gold standard) should be performed”

AST, ALT, ALP, bilirubin, urinalysis

· MICROBIOLOGY—blood C&S, sputum Gram

stain/AFB/C&S/fungal, urine C&S

· IMAGING —CXR ± CT chest

deciding on possible hospitalization

SPECIAL

· NASOPHARYNGEAL SWAB—if suspect viral

infection, check for influenza A/B,

parainflu-enza, human metapneumovirus, RSV,

· FURTHER G RAM - NEGATIVE COVERAGE —

cipro-floxacin 500 mg PO BID, gentamicin 6 mg/kg

IV q24h, tobramycin 6 mg/kg IV q24h (follow

levels to adjust dosing)

· ANAEROBIC COVERAGE —if suspect aspiration,

replace gentamicin with clindamycin 150–

450  mg PO q6h or 600–900  mg IV q8h or

add metronidazole 500 mg PO BID

· ANTIBIOTIC COURSE—7–8 days for most,

14–21 days for Pseudomonas , Staphylococcus

aureus , Stenotrophomonas , and Acinetobacter

· ASPIRATION PNEUMONIA — clindamycin 600 mg IV

BID, switch to 300 mg PO QID when stable May

add cefotaxime or ceftriaxone for Gram-

positive and Gram-negative coverage

· TUBERCULOSIS PNEUMONIA —see p. 279

NONPHARMACOLOGIC TREATMENTS

pneumococcal vaccine booster every 5 years

· CHEST PHYSIOTHERAPY

TREATMENT ISSUES

IMPORTANT NOTE —avoid using the same

anti-biotic class if given within 3 months Consider

vancomycin or linezolid if MRSA suspected;

emer-gence of community-acquired MRSA associated

with serious necrotizing infections

OUTPATIENT ANTIBIOTICS CHOICE

clarithromycin, or doxycycline) Other

antibi-otic choices include fluoroquinolone,

macro-lide plus amoxicillin ± clavulanate

· COMORBIDITIES (COPD, diabetes, renal failure, HF,

INPATIENT ANTIBIOTIC CHOICE

respi-ratory fluoroquinolone

ICU ANTIBIOTICS CHOICE

β-lactam or fluoroquinolone plus β-lactam

ALLERGY—fluoroquinolone with or without

clindamycin

agents that are effective against Pseudomonas

(different classes)

aztreonam plus levofloxacin or aztreonam plus moxifloxacin, with or without aminoglycoside

NURSING HOME ANTIBIOTICS CHOICE

or macrolide plus amoxicillin–clavulanate

· IN HOSPITAL —same as inpatient

DISCHARGE DECISION —clinical stabilization

usually takes 2–3 days When symptoms have significantly improved, vital signs are normalized, and patient has defervesced, patients at low risk may be safely discharged on the day of switching

to oral therapy without adverse consequences Time to radiographic resolution is variable, with

up to 5 months for pneumococcal pneumonia associated with bacteremia

IDSA Guidelines 2003

SPECIFIC ENTITIES

CAUSES OF NONRESOLVING PNEUMONIA —

bron-choalveolar carcinoma or lymphoma, cryptogenic

bacterial (viral, fungal), immunocompromised host, antibiotic resistance , pneumonia com- plications (abscess, empyema, ARDS) CAUSES OF RECURRENT PNEUMONIA

S uppressants (steroids, chemotherapy,

D ecreased nutrition, I mmunoglobulin

(renal, liver, splenectomy), T umors

· PULMONARY—bronchiectasis, COPD, cystic fibrosis, abnormal anatomy

LUNG ABSCESS

Gram positive ( S milleri , microaerophilic

Nocardia and actinomycosis can rarely cause lung abscess

· TREATMENTS —clindamycin until radiographic improvement and stabilization (usually sev-eral weeks to months, can be completed with oral antibiotics once patient is stable) No need for percutaneous drainage If compli-cated abscess, consider lobectomy or pneumonectomy

· ENDOTHELIAL OR VESSEL WALL INJURY —fracture of

pelvis, femur, or tibia

· HYPERCOAGUABILITY —obesity, pregnancy,

estrogen, smoking, cancer (high suspicion of

occult malignancy in patients who develop

pulmonary embolism while on

phospholipid antibody syndrome, lupus

anticoagulant, IBD), genetics (history of DVT/

PE, factor V Leiden, antithrombin III deficiency,

protein C/S deficiency, prothrombin G20210A

mutation, hyperhomocysteinemia)

· STASIS —surgery requiring >30 min of

anesthe-sia, prolonged immobilization, CVA, HF

CLINICAL FEATURES

HISTORY —dyspnea (sudden onset), pleuritic

chest pain, cough, hemoptysis, pre/syncope,

uni-lateral leg swelling/pain, past medical history

(previous DVT/PE, active cancer, immobilization

or surgery in last 4 weeks, miscarriages),

medica-tions (birth control pill, anticoagulation)

PHYSICAL —vitals (tachycardia, tachypnea,

hypotension, fever, hypoxemia), respiratory

examination (pulmonary hypertension if chronic

PE), cardiac examination (right heart strain), leg

swelling

DIAGNOSTIC ISSUES

CXR FINDINGS IN PULMONARY EMBOLISM —

normal, atelectasis, unilateral small pleural effusion, enlarged central pulmonary artery, elevated hemidiaphragm, Westermark’s sign (abrupt truncation of pulmonary vessel), Hampton’s hump (wedge infarct)

DDIMER (sens 85–96%, spc 45–68%, LR+ 1.7–

2.7, LR–0.09–0.22)—can rule out PE if low cal suspicion

V/Q SCAN (sens high, spc high)—result often

not definitive (intermediate probability) because

of other intraparenchymal abnormalities

CT PE PROTOCOL (sens 57–100%, spc

78–100%)—can be very helpful as it provides clues to other potential diagnoses/pathologies as well

RATIONAL CLINICAL EXAMINATION SERIES:

DOES THIS PATIENT HAVE PULMONARY

EMBOLISM?

PREDICTION RULES —Wells, PISA-PED,

Geneva rule

APPROACH —combining the pretest

probabil-ity with results of D-dimer testing reduces the

need for further investigations in patients with

low (<15%) to moderate (15–35%) clinical

pre-test probability A patient with low to moderate

clinical probability of PE with a normal D-dimer

has a LR of 0 (95% CI 0–0.06) for PE. When there

is a discrepancy between clinical gestalt and

clinical prediction rule, consider placing the

patient into the higher pretest probability

troponin/CK × 3, D-dimer (if low probability for PE or outpatient), βhCG in women of reproductive age

· IMAGING —CXR, duplex US of legs, V/Q scan,

CT chest (PE protocol)

common), sinus tachycardia (most common abnormality), atrial fibrillation, right ventric-ular strain (T wave inversion in anterior pre-cordial leads), non-specific ST-T wave changes, right axis deviation, right bundle

lead I, Q wave and inverted T wave in lead III)

SPECIAL

strain (dilated RV and elevated RVSP) Particularly important if hemodynamic changes

· PULMONARY ANGIOGRAM —gold standard

· THROMBOPHILIA WORKUP —factor V Leiden, thrombin G20210A, anticardiolipin antibody, lupus anticoagulant, protein C, protein S, anti-thrombin III, fibrinogen; consider homocyste-ine level and workup for paroxysmal nocturnal hemoglobinuria and antiphospholipid syn-drome in cases of combined arterial–venous thrombosis Routine testing for hypercoagu-lable disorders is NOT warranted

LEG VEIN DOPPLER (sens 50%, spc moderate)—

serial dopplers may be used for diagnosis of DVT

if CT or V/Q scan failed to demonstrate PE but

clinical suspicion still high

WELL’S CRITERIA FOR PULMONARY

EMBOLISM

alter-native diagnosis less likely (+3), HR >100

(+1.5), immobilization or surgery in last 4

weeks (+1.5), previous DVT/PE (+1.5),

hemop-tysis (+1), active cancer (+1)

· LOW SUSPICION (sum 0–1, <10%

· INTERMEDIATE SUSPICION (sum 2–6, 30%

but still suspicious, pulmonary angiogram

· HIGH SUSPICION (sum >6, >70% chance)—CT or

pulmo-nary angiogram

NEJM 2003 349:13

MANAGEMENT

ACUTE —ABC, O 2 to keep sat >94%, IV, consider

thrombolysis (must be done in ICU) for massive PE

(hemodynamic instability, right ventricular strain)

ANTICOAGULATION —if moderate to high risk

of developing PE, consider initiating

1,000 U/h and adjust to 1.5–2.5× normal PTT; use

UFH if considering thrombolysis), LMWH (

tinzaparin 175 U/kg SC daily), or fondaparinux

5  mg SC daily (<50  kg), 7.5  mg SC daily (50–

100 kg), or 10 mg SC daily (>100 kg) Start

heparin/LMWH/fondaparinux for at least 5 days

and until INR is between 2 and 3 for at least 48 h

Factor Xa inhibitors (rivaroxaban, apixaban) and

direct thrombin inhibitors (dabigatran) not

rec-ommended for initial treatment of

hemodynami-cally unstable PE; may consider in stable patients

under supervision of physician familiar with novel anticoagulant therapy

THROMBOLYTICS —controversial as increased

risk of intracranial bleed and multiple cations (see below) Consider only if hemody-namically unstable or life-threatening pulmonary

contraindi-embolism TPA 100 mg IV over 2 h, or streptokinase

250,000  IU over 30  min, the 100,000  IU/h over 12–24 h or 1.5 million IU over 2 h Unfractionated heparin may be used concurrently

SURGICAL —embolectomy Consider if

throm-bolysis failed or contraindicated or if namically unstable

IVC FILTER —if anticoagulation contraindicated

TREATMENT ISSUES

CONTRAINDICATIONS TO THROMBOLYTIC THERAPY

hem-orrhagic stroke or stroke of unknown origin, ischemic stroke in previous 3 months, malig-nant intracranial neoplasm, suspected aortic dissection, active bleeding, major trauma in previous 2 months, intracranial surgery or head injury within 3 weeks

· RELATIVE CONTRAINDICATIONS—TIA within 6 months, oral anticoagulation, pregnancy or within 1 week postpartum, non-compressible puncture sites, traumatic/prolonged (>10 min) CPR, uncontrolled hypertension (SBP

>185 mmHg, DBP >110 mmHg), recent ing (<2–4 weeks), current use of anticoagu-lants, advanced liver disease, infective endocarditis, active peptic ulcer, thrombocytopenia

ANTICOAGULATION DURATION

TIME - LIMITED RISK FACTOR —anticoagulation for

at least 3 months

· UNPROVOKED PE —at least 3 months of

treat-ment If no obvious risk factors for bleeding, consider indefinite anticoagulation

LMWH better than oral warfarin Treatment should be continued until eradication of cancer

as long as there are no significant tions to anticoagulation

outpatient treatment Total duration of therapy should be 6 months unless patient has risk fac-tors for hypercoagulable state

Pulmonary Embolism in Pregnancy (p. 469)

SPECIFIC ENTITIES

FAT EMBOLISM

to fatty acids leading to inflammatory response

Commonly caused by closed fractures of long

bones, but may also occur with pelvic fractures,

orthopedic procedures, bone marrow harvest,

bone tumor lysis, osteomyelitis, liposuction,

fatty liver, pancreatitis, and sickle cell disease

· CLINICAL FEATURES—triad of dyspnea,

neurological abnormalities (confusion), and

petechial rash (head and neck, chest, axilla) May also have fever, thrombocytopenia, and DIC

· DIAGNOSIS —clinical diagnosis (rash is gnomonic) Investigations may include CXR, V/Q scan, CT chest, and MRI head

patho-· TREATMENTS —supportive care as most patients will fully recover Mortality is 10% Primary prophylaxis includes early mobilization Consider trial of systemic steroids

CLINICAL FEATURES

HISTORY —dyspnea, cough, hemoptysis, chest

pain, weight loss, fever, trauma, occupational exposures, past medical history (pneumonia, liver disease, kidney disease, thyroid disease, cancer,

HF, thromboembolic disease, connective tissue disease, smoking), medications

PHYSICAL —vitals, cyanosis, clubbing, tracheal

deviation away from side of effusion (if no collapse or trapped lung), peripheral lymphade-nopathy, Horner’s syndrome, respiratory examina-tion (decreased breath sounds and tactile fremitus, stony dullness to percussion), cardiac examination, leg swelling (HF or DVT)

DIFFERENTIAL DIAGNOSIS

EXUDATIVE —malignancy, infections,

connec-tive tissue disease, hypothyroidism, pulmonary

embolism, hemothorax, pancreatitis,

chylotho-rax, trapped lung

TRANSUDATIVE —HF, hypoalbuminemia

(GI losing enteropathy, cirrhosis, nephrotic

syn-drome, malnutrition), SVC obstruction,

hepato-hydrothorax, urinothorax, atelectasis, trapped

lung, peritoneal dialysis, hypothyroidism,

pul-monary embolism

NOTE: pulmonary embolism, malignancy,

hypothyroidism, trapped lung, SVC

obstruc-tion, and sarcoidosis are usually exudative, but

can occasionally be transudative HF following

diuresis may become “pseudo-exudative”

SPECIFIC ENTITIES CONT’D

RATIONAL CLINICAL EXAMINATION SERIES: DOES THE PATIENT HAVE PLEURAL EFFUSION?

AUSCULTATORY PERCUSSION —auscultate with the diaphragm of the stethoscope over the

poste-rior chest wall while gently tapping over the manubrium with the distal phalanx of one finger Diminished resonance suggests effusion

APPROACH —“dullness to percussion and tactile fremitus are the most useful findings for pleural

effusion Dull chest percussion makes the probability of a pleural effusion much more likely but still requires a CXR to confirm the diagnosis When the pretest probability of pleural effusion is low, the absence of reduced tactile fremitus makes pleural effusion less likely so that a CXR might not be neces-sary depending on the overall clinical situation”

DIAGNOSTIC ISSUES

OVERALL APPROACH —generally, if the

effu-sion is >1/4 of hemithorax, enough fluid is

pres-ent for diagnostic thoracpres-entesis US-guided

thoracentesis is standard of care If only a small

amount of fluid is present (<10  mm [<0.4  in.])

and/or HF suspected, start with diuresis for 2–3

days If no improvement, perform thoracentesis

to distinguish between transudative and

exuda-tive causes

LIGHT’S CRITERIA FOR EXUDATIVE EFFUSION

—any one of the following criteria would suggest

exudative effusion: fluid/serum total protein ratio

>0.5, fluid/serum LDH ratio >0.6, fluid LDH >2/3

upper limit of normal serum level

THORACENTESIS PROCEDURE —see NEJM

PLEURAL FLUID ANALYSIS

para-pneumonic, TB, paragonimiasis, malignancy, rheumatoid arthritis, SLE, hemothorax, esoph-ageal rupture

· FLUID GLUCOSE (<3.3 mmol/L pneumonic, TB, paragonimiasis, malignancy, rheumatoid arthritis, Churg–Strauss, hemothorax

[<60 mg/dL])—para-· FLUID EOSINOPHILIA (>10%)—paragonimiasis, malignancy, Churg–Strauss, asbestos, drug reaction, pulmonary embolism, hemothorax, pneumothorax, idiopathic (20%)

· CYTOLOGY FOR MALIGNANCY —the yield for nosis with single attempt is 60%, two attempts is 85%, three attempts is 90–95%; obtain as much fluid as possible to increase diagnostic yield

diag-· FLUID FOR AFB—obtain as much fluid as possible and ask laboratory to centrifuge collection and to culture sediment to increase diagnostic yield

MANAGEMENT

SYMPTOM CONTROL — O 2 , diuresis mide), drainage (thoracentesis, pigtail catheter,

slurry or poudrage), surgery (talc slurry,

pleuro-peritoneal shunt, pleural abrasion, pleurectomy)

TREAT UNDERLYING CAUSE

SPECIFIC ENTITIES

PARAPNEUMONIC EFFUSION

resolves with resolution of pneumonia Generally disappears with antibiotics alone

DIAGNOSTIC ISSUES CONT’D

INVESTIGATIONS

BASIC

protein, AST, ALT, ALP, bilirubin, INR, PTT,

albumin

· IMAGING —CXR (PA, lateral, decubitus), CT chest

· THORACENTESIS —send pleural fluid for cell

count and differential, Gram stain, C&S,

AFB and fungal cultures, LDH, total protein,

pH, and cytology Under special

circum-stances, also consider amylase, glucose,

cholesterol, adenosine deaminase (for TB),

albumin

SPECIAL

thoracoscopy, bronchoscopy, surgical biopsy

(video-assisted thoracic surgery)

RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN EXUDATIVE PLEURAL EFFUSION?

APPROACH —effusions meeting none of Light’s criteria are most likely transudative However, if the

effusion meets Light’s criteria or if the effusion has a pleural cholesterol >55  mg/dL, pleural LDH

>200 U/L, or ratio of pleural cholesterol to serum cholesterol >0.3, the effusion is likely exudative

JAMA 2014 311:23

CLINICAL FEATURES CONT’D

· COMPLICATED—persistent bacterial invasion

and fluid collection Characterized by pleural

fluid acidosis but sterile fluid Pleural

locula-tion may occur as fibrin gets deposited from

inflammation Treated the same as

empyema

· EMPYEMA —presence of bacteria in Gram stain

or pus in drainage (culture not necessary) pH

often <7.2 For unloculated fluid, chest tube/

small-bore catheter drainage usually adequate

For loculated effusions, intrapleural

thrombo-lytics (streptokinase or TPA) and DNase could

be considered Thoracoscopy represents an

alternative to fibrinolytics Open decortication

is the last resort

TRAPPED LUNG —stable chronic effusion,

espe-cially with history of pneumonia, pneumothorax, thoracic surgery or hemothorax Diagnosis is established by measuring negative change in intrapleural pressure during thoracentesis Depending on chronicity, treat by lung re- expansion Thoracotomy with decortication sometimes required in infectious cases

HEPATOHYDROTHORAX —suspect if cirrhosis and

portal hypertension, even in the absence of ascites Pleural effusion results from passage of peritoneal fluid into pleura because of negative intrathoracic pressures and diaphragmatic defects Do not insert chest tube Treat with diuresis, salt restriction, and consider liver transplantation/TIPS procedure

Chronic Cough

PATHOPHYSIOLOGY

DEFINITION OF CHRONIC COUGH — > 3 weeks

exhaustion, insomnia, anxiety, headaches,

dizzi-ness, hoarsedizzi-ness, musculoskeletal pain, urinary

incontinence, abdominal hernias

COUGH REFLEX

cough receptors in the epithelium of the upper

and lower respiratory tracts, pericardium,

nerves (vagus, glossopharyngeal, trigeminal,

· EFFERENT—cough center with cortical

MANAGEMENT

SYMPTOM CONTROL — codeine 20  mg PO q4h

PRN, dextromethorphan 20 mg PO q4h PRN

TREAT UNDERLYING CAUSE —switch to ARB if

ACE inhibitor suspected as cause of chronic cough

CHEST 2006 129:1 Suppl

SPECIFIC ENTITIES

POSTNASAL DRIP/UPPER AIRWAY COUGH SYNDROME

air-way stimulate cough receptors within the ryngeal or laryngeal mucosa

pha-· CAUSES —allergic, perennial non-allergic tis, vasomotor rhinitis, acute nasopharyngitis, sinusitis

DIFFERENTIAL DIAGNOSIS

NONPULMONARY —GERD, ACE inhibitors,

occult congestive heart failure

PULMONARY

cough syndrome, asthma, chronic

bronchi-tis, non-asthmatic eosinophilic bronchibronchi-tis,

bronchiectasis, neoplasm, foreign body,

post-viral

· PARENCHYMA —occult infection, occult

aspi-ration, interstitial lung disease, lung abscess

· VASCULAR —early pulmonary hypertension

· DIAGNOSIS—non-specific findings; consider

sinus imaging

· TREATMENTS—reduce irritant exposure,

( diphenhydramine 25–50  mg PO q4–6  h PRN,

0.03% 2 sprays/nostril BID–TID, nasal steroids, nasal saline rinses BID), surgical cor-rection for anatomical abnormalities

Hemoptysis

PATHOPHYSIOLOGY

MASSIVE HEMOPTYSIS —100–600 mL blood in

24 h Patients may die of asphyxiation (rather than

exsanguination)

CLINICAL FEATURES

HISTORY —characterize hemoptysis (amount,

frequency, previous history), cough (productive),

dyspnea, chest pain, epistaxis, hematemesis,

weight loss, fever, night sweats, exposure, travel,

joint inflammation, rash, visual changes, past

medical history (smoking, lung cancer, TB,

throm-boembolic disease, cardiac disease), medications

(warfarin, ASA, NSAIDs, natural supplements)

PHYSICAL —vitals, weight loss, clubbing,

cyano-sis, lymphadenopathy, Horner’s syndrome,

respi-ratory and cardiac examination, leg swelling (HF

or DVT), joint examination, skin examination

MANAGEMENT

ACUTE —ABC, O 2 , IV , intubation to protect airway if significant hemoptysis (with double lumen tube if available), position patient in lateral decubitus position with affected lung on bottom (to preserve non-affected lung on top)

SYMPTOM CONTROL —cough suppressants,

saline, topical epinephrine, cautery, airway blocker, double lumen endotracheal tube)

Angiographic arterial embolization Lung

resection TREAT UNDERLYING CAUSE — correct coagu-

lopathy ( vitamin K 10 mg SC/IV × 1 dose or FFP);

antibiotics ; radiation for tumors; diuresis for HF; immunosuppression for vasculitis

SPECIFIC ENTITIES CONT’D SPECIFIC ENTITIES CONT’D

DIFFERENTIAL DIAGNOSIS

N O N  C A R D I O P U L M O N A RY — epistaxis,

upper GI bleed, coagulopathy

CARDIAC —HF, mitral stenosis

PULMONARY

bronchiectasis, malignancy, foreign body,

trauma

· PARENCHYMA

· MALIGNANCY —lung cancer, metastasis

· INFECTIONS —necrotizing pneumonia

( Staphylococcus, Pseudomonas ), abscess,

septic emboli, TB, fungal

· ALVEOLAR HEMORRHAGE —granulomatosis

with polyangiitis (Wegener's), Churg–

Strauss, Goodpasture disease, pulmonary

capillaritis, connective tissue disease

· VASCULAR—pulmonary embolism,

pulmo-nary hypertension, AVM, iatrogenic

· BRONCHOSCOPY —warranted in most patients unless obvious explanation

SPECIAL

(myelo-peroxidase MPO antibodies), c-ANCA

antibody, rheumatologic screen (extractable nuclear antigens)

SPECIFIC ENTITIES

GOODPASTURE DISEASE

and renal basement membrane

· CLINICAL FEATURES —hemoptysis and ria, with respiratory and renal failure if severe

hematu-· DIAGNOSIS —lung/kidney biopsy

· TREATMENTS —steroids, cyclophosphamide, plasmapheresis

CLINICAL FEATURES

HISTORY —dyspnea, cough, hemoptysis,

wheez-ing, chest pain, weight loss, fever, night sweats,

rheumatologic screen, past travel history,

occupa-tional exposures, medical history (smoking, lung

cancer or other malignancies, TB, infections,

rheu-matoid arthritis), medications

PHYSICAL —vitals, weight loss, clubbing,

cyano-sis, Horner’s syndrome, SVC syndrome,

lymphade-nopathy, respiratory examination, abdominal

examination (hepatomegaly), bony tenderness

TIMING —if malignant, usually able to detect an

increase in size of SPN between 30 days and 2 years Unlikely to be malignant if significant change in <30 days or no change in 2 years

medium probability , bronchoscopy with biopsy/

brush or transthoracic (CT/US-guided) biopsy If

high probability , thoracotomy with resection or

video-assisted thoracoscopy (for patients who cannot tolerate thoracotomy medically and physiologically)

SPECIFIC ENTITIES

PANCOAST TUMOR

(mostly squamous cell carcinoma) invading and compressing the paravertebral sympa-thetic chain and brachial plexus

· CLINICAL FEATURES—shoulder and arm pain

(C8,  T1, T2 distribution), Horner’s syndrome

(upper lid ptosis, lower lid inverse ptosis, miosis, anhydrosis, enophthalmos, loss of

symptoms in the arm (intrinsic muscles weakness and atrophy, pain and paresthesia

of  4th and 5th digit) Other associated findings  include clubbing, lymphadenopathy, phrenic or recurrent laryngeal nerve palsy, and superior vena cava syndrome

SPECIFIC ENTITIES CONT’D

DIFFERENTIAL DIAGNOSIS

MALIGNANT —bronchogenic, carcinoid,

met-astatic cancer

BENIGN —healed infectious granuloma,

benign tumors (hamartoma), AVM, rheumatoid

nodule, granulomatosis with polyangiitis (GPA),

hydatid cyst, round atelectasis, intra- pulmonary

lymph nodes, pseudotumor

INVESTIGATIONS

BASIC

ALP, bilirubin, INR, PTT

· IMAGING —old films (2 years ago for

compari-son), CXR, CT chest

SPECIAL

· SCREENING FOR INFLAMMATORY DISORDERS —

ESR, CRP, ANA, ANCA

· BIOPSY —bronchoscopy or CT guided

of lung cancer

DIAGNOSTIC ISSUES CONT’D

· DIAGNOSIS —CXR, CT chest, percutaneous core

biopsy

· TREATMENTS —concurrent chemoradiotherapy

THORACIC OUTLET OBSTRUCTION

neuro-vascular bundle supplying the arm at the

superior aperture of the thorax Common

structures affected include the brachial plexus

(C8/T1 > C5/C6/C7, 95%), subclavian vein (4%),

and subclavian artery (1%)

· CAUSES — anatomic (cervical ribs, congenital

bands, subclavicular artery aneurysm),

repetitive hyperabduction/trauma

neo-plasm (supraclavicular lymphadenopathy)

· CLINICAL FEATURES —triad of numbness,

swell-ing and weakness of the affected upper limb,

particularly when carrying heavy objects

Brittle finger nails, Raynaud’s, thenar wasting

and weakness, sensory loss, decreased radial

and brachial pulses, pallor of limb with

elevation, upper limb atrophy, drooping

shoulders, supraclavicular and infraclavicular

lymphadenopathy Specific maneuvers include

fists with arms abducted and externally

(Valsalva maneuver with the neck fully extended, affected arm elevated, and the chin

turned away from the involved side),

costocla-vicular maneuver (shoulders thrust backward

and downward), hyperabduction maneuver

(raise hands above head with elbows flexed and extending out laterally from the body),

brachial plexus in supraclavicular fossa reproduces symptoms)

· DIAGNOSIS —cervical spine films, CXR, MRI

· TREATMENTS —conservative (keep arms down at night, avoiding hyperabduction), surgery

SPECIFIC ENTITIES CONT’D SPECIFIC ENTITIES CONT’D

RELATED TOPICS

Lung Cancer (p. 203) SVC Syndrome (p. 253)

WHO CLASSIFICATION OF PULMONARY

HYPERTENSION

GROUP I.  PULMONARY ARTERIAL

HYPERTENSION

· FAMILIAL AND RELATED DISORDERS —collagen

vascular disease, congenital systemic-to-

pulmonary shunts, portal hypertension, HIV,

drugs and toxins, thyroid disorders,

glyco-gen storage disease, Gaucher’s disease,

hereditary hemorrhagic telangiectasia,

hemoglobinopathies, myeloproliferative

dis-orders, splenectomy

· ASSOCIATED WITH SIGNIFICANT VENOUS OR CAP

-ILLARY INVOLVEMENT —pulmonary veno-

occlusive disease, pulmonary–capillary

hemangiomatosis

· PERSISTENT PULMONARY HYPERTENSION OF

NEWBORN

HYPERTENSION —left-sided atrial or ventricular

heart disease, left-sided valvular heart disease

GROUP III.  PULMONARY HYPERTENSION ASSOCIATED WITH HYPOXEMIA —COPD, interstitial lung disease, sleep-disordered breathing, alveolar hypoventilation disorders, chronic exposure to high altitude, developmen-tal abnormalities

GROUP IV.  PULMONARY HYPERTENSION DUE TO CHRONIC THROMBOTIC DISEASE, EMBOLIC DISEASE, OR BOTH —thromboem-

bolic obstruction of proximal pulmonary ies, thromboembolic obstruction of distal pulmonary arteries, pulmonary embolism (tumor, parasites, foreign material)

GROUP V.  MISCELLANEOUS —sarcoidosis,

pulmonary Langerhans cell histiocytosis, lymphangiomatosis, compression of pulmo-nary vessels (adenopathy, tumor, fibrosing mediastinitis)

WHO CLASSIFICATION OF PULMONARY HYPERTENSION CONT’D

PATHOPHYSIOLOGY

D E F I N I T I O N O F P U L M O N A RY

HYPERTENSION —mean pulmonary arterial

pressure (PAP) >25  mmHg at rest or mean PAP

>30  mmHg with exercise measured with right

heart catheterization

CLINICAL FEATURES

HISTORY —unexplained dyspnea on exertion,

cough, chest pain, hemoptysis, dizziness,

syn-cope, hoarseness, past medical history (cardiac

and respiratory diseases, thromboembolic

dis-eases, HIV, cirrhosis, autoimmune and

rheumato-logic disorders), medications (amphetamine, diet

pill such as dexfenfluramine)

PHYSICAL —vitals (tachypnea, tachycardia, atrial

fibrillation, hypoxemia), peripheral cyanosis, small

pulse volume, elevated JVP (prominent a wave or

absent if atrial fibrillation, large v wave), right

ven-tricular heave, loud or palpable P2, right-sided S4,

tri-cuspid regurgitation murmur, Graham Steell murmur

(high-pitched, decrescendo diastolic rumble over

LUSB), crackles, congestive liver, ascites, ankle edema

MANAGEMENT

SYMPTOM CONTROL — diuretics , O 2 ,

antico-agulation , calcium channel blockers if positive

vasoreactivity test (in high doses), endothelin

receptor antagonists (bosentan), terase type-5 inhibitors (sildenafil), prostanoids,

phosphodies-soluble guanylate cyclase stimulant

TREAT UNDERLYING CAUSE ATRIAL SEPTOSTOMY LUNG TRANSPLANT

Chest 2014 146:2

SPECIFIC ENTITIES

EISENMENGER SYNDROME —left-to-right

shunt leading to pulmonary hypertension and eventually right-to-left shunt

Interstitial Lung Disease

CLINICAL FEATURES

HISTORY —dyspnea (duration, progression),

cough, hemoptysis, wheezes, chest pain, impaired exercise tolerance, occupational history (details of all previous jobs, exposure to gases or chemicals particularly important), environmental exposure (home setting, air-conditioning, pets, hobbies),

INVESTIGATIONS

BASIC

bilirubin, INR, albumin, ANA, RF, anti-CCP,

anti-Scl-70, anticentromere antibody, ESR,

PRIMARY (idiopathic)—usual interstitial

pneu-monia (UIP), respiratory bronchiolitis- associated

interstitial lung disease (RBILD), desquamative

interstitial pneumonia (DIP), acute interstitial

pneumonia (AIP), non-specific interstitial

pneu-monia (NSIP), lymphoid interstitial pneupneu-monia

(LIP), cryptogenic organizing pneumonia (COP)

SECONDARY ★DICE★

penicillin, sulfonylurea, gold, penicillamine,

phenytoin, amiodarone, nitrofurantoin

sarcoidosis

coccidioidomycosis

scleroderma, ankylosing spondylitis, myositis

(asbestos, silica, beryllium, coal worker’s pneumoconiosis)

INFILTRATES —allergic bronchopulmonary aspergillosis (ABPA), parasitic, drugs

pulmonary hemosiderosis, myomatosis, radiation

lymphangioleio-DIFFERENTIAL DIAGNOSIS CONT’D

rash, joint swelling, past medical history

(smok-ing), medications, family history

PHYSICAL —vitals (tachypnea, hypoxemia),

cya-nosis, clubbing (idiopathic pulmonary fibrosis,

asbestosis, rheumatoid lung, fibrosing NSIP),

decreased chest expansion, crackles (fine),

wheezes, cor pulmonale Note that sarcoidosis

and silicosis may have a normal lung

examination

DIAGNOSTIC ISSUES

CHARACTERISTIC CXR PATTERNS FOR

INTERSTITIAL LUNG DISEASE

hyper-sensitivity pneumonitis, pneumoconiosis,

sili-cosis, histiocytosis X, PJP, ankylosing

spondylitis, ABPA, TB

· LOWER LOBE PREDOMINANCE —idiopathic

pulmo-nary fibrosis, asbestosis, rheumatoid arthritis,

scleroderma, drugs

· BILATERAL HILAR / MEDIASTINAL ADENOPATHY WITH

INTERSTITIAL INFILTRATES —sarcoidosis,

beryllio-sis, lymphangitic carcinomatoberyllio-sis, TB, fungal,

lymphoma

· EGGSHELL CALCIFICATION OF HILAR / MEDIASTINAL

LYMPH NODES—silicosis (other

pneumoconio-sis), TB, fungal

· CALCIFIED PLEURAL PLAQUES —asbestos

· PLEURAL EFFUSIONS WITH INTERSTITIAL INFIL

-TRATES—HF, lymphangitic carcinomatosis, rheumatoid arthritis, SLE

MANAGEMENT

TREAT UNDERLYING CAUSE — sarcoidosis

(if ≥ stage II or symptomatic, give steroids for at least 6 months, even with improvement of symp-toms See p. 482 for details)

LUNG TRANSPLANT

SPECIFIC ENTITIES

IDIOPATHIC PULMONARY FIBROSIS (IPF)

than inflammatory process; associated with histopathological and/or radiological pattern

of usual interstitial pneumonia (UIP)

· DIAGNOSIS—CT chest (honeycombing, lobular septal thickening, traction bronchiecta-sis, peripheral, sub-pleural, lack of ground glass pattern), bronchoscopy (to rule out other causes, mostly infectious); consider open lung biopsy if CT is not consistent with above

inter-· TREATMENTS —referral for lung transplantation should be done early; consider pirfenidone or nintedanib for mild to moderate disease Systemic steroids ineffective

CMAJ 2004 171:2

Am J Respir Crit Care Med 2011 183:6

NEJM 2014 370:22 HYPERSENSITIVITY PNEUMONITIS

or chronic granulomatous pneumonia

· DIAGNOSIS — major criteria (compatible

symp-toms, antigen exposure, imaging findings, lavage lymphocytosis, histologic findings (poorly formed granulomas), reexposure trig-

major and minor criteria will help raise cion of hypersensitivity pneumonitis Serology may be helpful

suspi-· TREATMENTS —cessation of exposure, steroids

CRYPTOGENIC ORGANIZING PNEUMONIA (COP)—previously known as bronchiolitis obliter-

ans organizing pneumonia (BOOP)

· CAUSES — idiopathic (80%), post-infectious

(CMV, influenza, adenovirus, Chlamydia),

drugs (amiodarone, bleomycin, gold, zine, cephalosporin, cocaine), connective tis-

sulfasala-sue disease (RA, SLE, scleroderma, Sjogren’s,

Scl-70, anticentromere antibody,

anti-Jo-1 antibody

· IMAGING —CXR, CT chest (high resolution),

echocardiogram (if suspect pulmonary

hypertension)

SPECIAL

biopsy), open lung biopsy

(MDS, lymphoproliferative diseases, radiation)

· CLINICAL FEATURES —about 50% of cases

pre-ceded by viral-like respiratory infection

Symptoms include dyspnea on exertion,

per-sistent non-productive cough, and weight loss

· DIAGNOSIS—characteristic findings on CXR and CT chest include bilateral, diffuse, ill-defined alveolar opacities distributed periph-erally PFT shows mainly restrictive lung disease pattern

· TREATMENTS — prednisone 1 mg/kg PO daily

PATHOPHYSIOLOGY

ABNORMAL PHARYNX ANATOMY —decreased

upper airway muscle tone and reduced reflexes

protecting pharynx from collapse, increased

leads to snoring and hypopnea, full collapse leads

arousals lead to hypersomnolence Severe chronic

hypoxemia leads to pulmonary hypertension

ASSOCIATIONS —obesity, hypothyroidism,

acro-megaly, amyloidosis, neuromuscular disease,

vocal cord paralysis, nasopharyngeal carcinoma,

Down syndrome (macroglossia)

COMPLICATIONS —hypertension, pulmonary

hypertension, CAD, CVA, increased motor vehicle accidents

CLINICAL FEATURES

HISTORY —daytime sleepiness, habitual snoring,

witnessed apneic episodes, poor sleep hygiene, morning headaches, fall asleep while driving, dyspnea, cough, exercise capacity, short-term memory loss, excessive caffeine intake, alcohol intake, past medical history (weight gain, thyroid disease, neurological disease), and medications The Epworth Sleepiness Scale and STOP-Bang Questionnaire may be used as a screening tool

PHYSICAL —vitals (hypertension, hypoxia)

Asterixis and plethora secondary to hypercapnia Check for low-hanging soft palate, large uvula,

nigri-cans Perform respiratory and cardiac examination (hypertension and pulmonary hypertension, restrictive lung disease) Inspect for potential causes such as nasopharyngeal carcinoma, hypo-thyroidism (goiter), acromegaly (course facial structures), and amyloidosis (periorbital infiltrate, shoulder pad sign)

Related Topics

CPAP (p. 105) Hypertension (p. 65) Pulmonary Hypertension (p. 17)

SPECIFIC ENTITIES CONT’D SPECIFIC ENTITIES CONT’D

DIFFERENTIAL DIAGNOSIS OF SLEEP DISORDERS

HYPERSOMNOLENCE

(OSA), periodic limb movement disorder

· INADEQUATE SLEEP TIME —medicine residents,

shift workers

· INCREASED SLEEP DRIVE —narcolepsy, primary

CNS hypersomnolence, head injury, severe

depression, medications

INSOMNIA

illness, medications (steroids), illicit drugs

(stimulants)

· CHRONIC—conditioned, psychiatric

disor-ders, poor sleep hygiene, medical disordisor-ders,

pain, restless leg syndrome, circadian

rhythm disorder

PARASOMNIA —sleep walking, sleep terrors,

nocturnal seizures, rapid eye movement

behav-ior disorder

PATHOPHYSIOLOGY CONT’D