Current Essentials of Medicine (4th Edition) PDF

a LANGE medical book CURRENT ESSENTIALS of MEDICINE Fourth Edition Edited by Lawrence M. Tierney, Jr., MD Professor of Medicine University of California, San Francisco Associate Chief of Medical Services Veterans Affairs Medical Center San Francisco, California Sanjay Saint, MD, MPH Associate Chief of Medicine, Ann Arbor VA Medical Center Director, VA/UM Patient Safety Enhancement Program Professor of Internal Medicine, University of Michigan Medical School Ann Arbor, Michigan Mary A. Whooley, MD Professor of Medicine, Epidemiology and Biostatistics University of California, San Francisco Department of Veterans Affairs Medical Center San Francisco, California New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto Copyright © 2011, 2005, 2002, 1997 by The McGraw-Hill Companies, Inc. All rights re- served. 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Neither McGraw-Hill nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise. To Katherine Tierney: a sister whose absolute commitment to her par- ents at the end of their lives provides a model for anyone fortunate enough to know her. Lawrence M. Tierney, Jr. To my father, Prem Saint, and father-in-law, James McCarthy, whose commitment to education will inspire generations. Sanjay Saint In memory of my mother, Mary Aquinas Whooley (1940–2003). Mary A. Whooley This page intentionally left blank Contents Contributors............................................ vii Preface................................................ xi 1. Cardiovascular Diseases............................... 1 2. Pulmonary Diseases................................. 37 3. Gastrointestinal Diseases............................. 66 4. Hepatobiliary Disorders............................... 92 5. Hematologic Diseases............................... 109 6. Rheumatologic & Autoimmune Disorders................ 147 7. Endocrine Disorders................................ 178 8. Infectious Diseases................................. 202 9. Oncologic Diseases................................. 286 10. Fluid, Acid–Base, and Electrolyte Disorders............. 309 11. Genitourinary and Renal Disorders..................... 325 12. Neurologic Diseases................................ 350 13. Geriatrics......................................... 372 14. Psychiatric Disorders................................ 381 15. Dermatologic Disorders.............................. 399 16. Gynecologic, Obstetric, and Breast Disorders............ 450 17. Common Surgical Disorders.......................... 468 18. Common Pediatric Disorders.......................... 481 19. Selected Genetic Disorders........................... 500 20. Common Disorders of the Eye......................... 509 21. Common Disorders of the Ear, Nose, and Throat.......... 529 22. Poisoning......................................... 540 Index................................................ 565 Tab Index....................................... Back Cover This page intentionally left blank Contributors Timir Baman, MD Cardiolology Fellow, University of Michigan Medical School, Ann Arbor, Michigan Cardiovascular Diseases Alex Benson, MD Fellow, Department of Pulmonary and Critical Care Medicine, University of Colorado Hospital, Aurora, Colorado Pulmonary Diseases Aaron Berg, MD Clinical Lecturer and Hospitalist, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan Fluid, Acid–Base, and Electrolyte Disorders Jeffrey Critchﬁeld, MD Associate Professor of Clinical Medicine, Department of Medicine, San Francisco General Hospital, University of California, San Francisco School of Medicine, San Francisco, California Rheumatologic & Autoimmune Disorders Vanja Douglas, MD Assistant Clinical Professor, Department of Neurology, University of California, San Francisco, California Neurologic Disorders Rebecca A. Jackson, MD Associate Professor & Chief, Obstetrics, Gynecology and Reproductive Sciences, San Francisco General Hospital, University of California, San Francisco, California Gynecologic, Obstetric, and Breast Disorders viii Contributors Kirsten Neudoerffer Kangelaris, MD Research Fellow, Division of Hospital Medicine, University of California, San Francisco, California Selected Genetic Disorders Helen Kao, MD Assistant Professor, Division of Geriatrics, Department of Medicine, University of California, San Francisco, San Francisco, California Geriatrics Kewchang Lee, MD Associate Clinical Professor of Psychiatry, University of California, San Francisco; Director of Psychiatry Consultation, San Francisco Veterans Affairs Medical Center, San Francisco, California Psychiatric Disorders Joan C. Lo, MD Research Scientist, Division of Research, Kaiser Permanente Northern California; Associate Clinical Professor of Medicine, University of California, San Francisco, Oakland, California Endocrine Disorders Michael P. Lukela, MD Director, Medicine-Pediatrics Residency Program, University of Michigan Medical School, Ann Arbor, Michigan Common Pediatric Disorders Read G. Pierce, MD Chief Resident, Internal Medicine, University of California, San Francisco, San Francisco, California References Jack Resneck, Jr., MD Associate Professor of Dermatology and Health Policy, Department of Dermatology and Phillip R. Lee Institute for Health Policy Studies, University of California, San Francisco School of Medicine, San Francisco, California Dermatologic Disorders Michael Rizen, MD, PhD, and Stephanie T. Phan, MD Eye Clinic of Bellevue, Ltd, P.S., Bellevue, Washington Common Disorders of the Eye Contributors ix Amandeep Shergill, MD Assistant Clinical Professor of Medicine, Division of Gastroenterology, Department of Medicine, San Francisco Veterans Affairs Medical Center & University of California, San Francisco, San Francisco, California Gastrointestinal Diseases Hepatobiliary Disorders Sanjay Shewarkramani, MD Clinical Assistant Professor, Department of Emergency Medicine, Georgetown University Hospital, Washington, DC Poisoning Emily Shuman, MD Clinical Lecturer, Department of Internal Medicine, Division of Infectious Diseases, University of Michigan, Ann Arbor, Michigan Infectious Diseases Jennifer F. Waljee, MD, MS Department of Surgery, University of Michigan, Ann Arbor, Michigan Common Surgical Disorders Sunny Wang, MD Assistant Clinical Professor of Medicine, Hematology/Oncology, University of California, San Francisco & San Francisco VA Medical Center, San Francisco, California Hematologic Diseases Oncologic Diseases Suzanne Watnick, MD Medical Director, VA Dialysis Unit, Associate Professor of Medicine, Portland VA Medical Center and Oregon Health & Science University, Portland, Oregon Genitourinary and Renal Disorders Katherine C. Yung, MD Assistant Professor, Department of Otolaryngology-Head and Neck Surgery, Division of Laryngology, University of California, San Francisco, California Common Disorders of the Ear, Nose, and Throat This page intentionally left blank Preface The fourth edition of Current Essentials of Medicine (originally titled Essentials of Diagnosis & Treatment) continues a feature introduced in the second edition: a Clinical Pearl for each diagnosis. Pearls are time- less. Learners at every level, and in many countries, remember them as crucial adjuncts to more detailed information about disorders of every type. Ideally, a Pearl is succinct, witty, and often colloquial; it is stated with a certitude suggesting 100% accuracy. Of course, nothing in med- icine is so, yet a Pearl such as “If you diagnose multiple sclerosis over the age of ﬁfty, diagnose something else” is easily committed to memory. Thus, Pearls should be accepted as offered. Many have been changed since the previous editions, and we urge readers to come up with Pearls of their own, which may prove to be more useful than our own. The fourth edition, like its predecessors, uses a single page to con- sider each disease, providing the reader with a concise yet usable sum- mary about most of the common diseases seen in clinical practice. For readers seeking more detailed information, a current reference has been provided for each disease. We have expanded the number of diseases from the previous edition and updated the clinical manifestations, diag- nostic tests, and treatment considerations with the help of our con- tributing subject-matter experts. We hope that you enjoy this edition as much as, if not more than, the previous ones. Lawrence M. Tierney, Jr., MD San Francisco, California Sanjay Saint, MD, MPH Ann Arbor, Michigan Mary A. Whooley, MD San Francisco, California This page intentionally left blank 1 Cardiovascular Diseases Acute Coronary Syndrome Essentials of Diagnosis Classiﬁed as ST-segment elevation (Q wave) myocardial infarction (MI), non–ST-segment elevation (non-Q wave) MI, or unstable angina Prolonged (> 30 minutes) chest pain, associated with shortness of breath, nausea, left arm or neck pain, and diaphoresis; can be painless in diabetics S4 common; S3, mitral insufﬁciency on occasion Cardiogenic shock, ventricular arrhythmias may complicate Unrelenting chest pain may mean ongoing jeopardized myocardium Differential Diagnosis Stable angina; aortic dissection; pulmonary emboli Tietze’s syndrome (costochondritis) Cervical or thoracic radiculopathy, including pre-eruptive zoster Esophageal spasm or reﬂux; cholecystitis Pericarditis; myocarditis; Takotsubo’s (stress-induced) cardiomy- opathy Pneumococcal pneumonia; pneumothorax Treatment Monitoring, oxygen, aspirin, oral beta-blockers, and heparin if not contraindicated; consider clopidogrel Reperfusion by thrombolysis early or percutaneous coronary inter- vention (PCI) in selected patients with either ST-segment eleva- tion or new left bundle-branch block on ECG Glycoprotein IIb/IIIa inhibitors considered for ST-segment ele- vation MI in patients undergoing PCI Nitroglycerin and morphine for recurrent ischemic pain; also useful for relieving pulmonary congestion, decreasing sympa- thetic tone, and reducing blood pressure Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and aldosterone blockers such as eplerenone improve ventricular remodeling after infarcts Pearl Proceed rapidly to reperfusion in ST-segment elevation MI as time equals muscle. Reference Kumar A, Cannon CP. Acute coronary syndromes: diagnosis and management, part II. Mayo Clin Proc 2009;84:1021. [PMID: 19880693] 1 2 Current Essentials of Medicine 1 Acute Pericarditis Essentials of Diagnosis Inﬂammation of the pericardium due to viral infection, drugs, recent myocardial infarction, autoimmune syndromes, renal fail- ure, cardiac surgery, trauma, or neoplasm Common symptoms include pleuritic chest pain radiating to the shoulder (trapezius ridge) and dyspnea; pain improves with sit- ting up and expiration Examination may reveal fever, tachycardia, and an intermittent friction rub; cardiac tamponade may occur in any patient Electrocardiography usually shows PR depression, diffuse concave ST-segment elevation followed by T-wave inversions; no recip- rocal changes are seen Echocardiography may reveal pericardial effusion Differential Diagnosis Acute myocardial infarction Aortic dissection Pulmonary embolism Pneumothorax Pneumonia Cholecystitis and pancreatitis Treatment Aspirin or nonsteroidal anti-inﬂammatory agents such as ibupro- fen or indomethacin to relieve symptoms; colchicine has been shown to reduce recurrence; rarely, steroids for recurrent cases Hospitalization for patients with symptoms suggestive of signif- icant effusions, cardiac tamponade, elevated biomarkers, or recent trauma or surgery Pearl Patients with pericarditis often present with chest pain that is worse when lying ﬂat. Reference Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idio- pathic acute pericarditis. Heart 2008;94:498. [PMID: 17575329] Chapter 1 Cardiovascular Diseases 3 Acute Rheumatic Fever 1 Essentials of Diagnosis A systemic immune process complicating group A beta-hemolytic streptococcal pharyngitis Usually affects children between the ages of 5 and 15; rare after 25 Occurs 1–5 weeks after throat infection Diagnosis based on Jones’ criteria (two major or one major and two minor) and conﬁrmation of recent streptococcal infection Major criteria: Erythema marginatum, migratory polyarthritis, subcutaneous nodules, carditis, and Sydenham’s chorea; the latter is the most speciﬁc, least sensitive Minor criteria: Fever, arthralgias, elevated erythrocyte sedimen- tation rate, elevated C-reactive protein, PR prolongation on ECG, and history of pharyngitis Differential Diagnosis Juvenile or adult rheumatoid arthritis Endocarditis Osteomyelitis Systemic lupus erythematosus Lyme disease Disseminated gonococcal infection Treatment Bed rest until vital signs and ECG become normal Salicylates and nonsteroidal anti-inﬂammatory drugs reduce fever and joint complaints but do not affect the natural course of the dis- ease; rarely, corticosteroids may be used If streptococcal infection is still present, penicillin is indicated Prevention of recurrent streptococcal pharyngitis until 18 years old (a monthly injection of benzathine penicillin is most commonly used) Pearl Inappropriate tachycardia in a febrile child with a recent sore throat sug- gests this diagnosis. Reference van Bemmel JM, Delgado V, Holman ER, et al. No increased risk of valvular heart disease in adult poststreptococcal reactive arthritis. Arthritis Rheum 2009;60:987. [PMID: 19333942] 4 Current Essentials of Medicine 1 Angina Pectoris Essentials of Diagnosis Generally caused by atherosclerotic coronary artery disease and severe coronary obstruction; cigarette smoking, diabetes mellitus, hypertension, hypercholesterolemia, and family history are estab- lished risk factors Stable angina characterized by pressure-like episodic precordial chest discomfort, precipitated by exertion or stress, relieved by rest or nitrates; unstable angina can occur with less exertion or at rest Stable angina is predictable in initiation and termination; unstable angina is not S4, S3, mitral murmur, paradoxically split S2 may occur transiently with pain Electrocardiography usually normal between episodes (or may show evidence of old infarction); electrocardiography with pain may show evidence of ischemia, classically ST depression Diagnosis from history and stress tests; conﬁrmed by coronary arteriography Differential Diagnosis Other coronary syndromes (myocardial infarction, vasospasm) Tietze’s syndrome (costochondritis) Intercostal neuropathy, especially caused by herpes zoster Cervical or thoracic radiculopathy, including pre-eruptive zoster Esophageal spasm or reﬂux disease; cholecystitis Pneumothorax; pulmonary embolism; pneumonia Treatment Address risk factors; sublingual nitroglycerin for episodes Ongoing treatment includes aspirin, long-acting nitrates, beta- blockers, and calcium channel blockers Angioplasty with stenting considered in patients with anatomically suitable stenoses who remain symptomatic on medical therapy Bypass grafting for patients with refractory angina on medical therapy, three-vessel disease (or two-vessel disease with proximal left anterior descending artery disease) and decreased left ven- tricular function, or left main coronary artery disease Pearl Many patients with angina will not say they are having pain; they will deny it but say they have discomfort, heartburn, or pressure. Reference Poole-Wilson PA, Vokó Z, Kirwan BA, de Brouwer S, Dunselman PH, Lubsen J; ACTION investigators. Clinical course of isolated stable angina due to coronary heart disease. Eur Heart J 2007;28:1928. [PMID: 17562665] Chapter 1 Cardiovascular Diseases 5 Aortic Coarctation 1 Essentials of Diagnosis Elevated blood pressure in the aortic arch and its branches with reduced blood pressure distal to the left subclavian artery Lower extremity claudication or leg weakness with exertion in young adults is characteristic Systolic blood pressure is higher in the arms than in the legs, but diastolic pressure is similar compared with radial Femoral pulses delayed and decreased, with pulsatile collaterals in the intercostal areas; a harsh, late systolic murmur may be heard in the back; an aortic ejection murmur suggests concomi- tant bicuspid aortic valve Electrocardiography with left ventricular hypertrophy; chest x-ray may show rib notching inferiorly due to collaterals Transesophageal echo with Doppler or MRI is diagnostic; angiog- raphy conﬁrms gradient across the coarctation Differential Diagnosis Essential hypertension Renal artery stenosis Renal parenchymal disease Pheochromocytoma Mineralocorticoid excess Oral contraceptive use Cushing’s syndrome Treatment Surgery is the mainstay of therapy; balloon angioplasty in selected patients Twenty-ﬁve percent of patients remain hypertensive after surgery Pearl Intermittent claudication in a young person with no vascular disease should suggest this problem; listen to the back for the characteristic murmur. Reference Tomar M, Radhakrishanan S. Coarctation of aorta: intervention from neonates to adult life. Indian Heart J 2008;60(suppl D):D22. [PMID: 19845083] 6 Current Essentials of Medicine 1 Aortic Dissection Essentials of Diagnosis Most patients between age 50 and 70; risks include hypertension, Marfan’s syndrome, bicuspid aortic valve, coarctation of the aorta, and pregnancy Type A involves the ascending aorta or arch; type B does not Sudden onset of chest pain with interscapular radiation in at-risk patient Unequal blood pressures in upper extremities, new diastolic murmur of aortic insufﬁciency occasionally seen in type A Chest x-ray nearly always abnormal; ECG unimpressive unless coronary artery compromised CT, transesophageal echocardiography, MRI, or aortography usu- ally diagnostic Differential Diagnosis Acute myocardial infarction Angina pectoris Acute pericarditis Pneumothorax Pulmonary embolism Boerhaave’s syndrome Treatment Nitroprusside and beta-blockers to lower systolic blood pressure to approximately 100 mm Hg, pulse to 60/min Emergent surgery for type A dissection; medical therapy for type B is reasonable, with surgery or percutaneous intra-aortic stenting reserved for high-risk patients Pearl The pain of dissection starts abruptly; that of ischemic heart disease increases to maximum over several minutes. Reference Tran TP, Khoynezhad A. Current management of type B aortic dissection. Vasc Health Risk Manag 2009;5:53. [PMID: 19436678] Chapter 1 Cardiovascular Diseases 7 Aortic Regurgitation 1 Essentials of Diagnosis Causes include congenital bicuspid valve, endocarditis, rheumatic heart disease, Marfan’s syndrome, aortic dissection, ankylosing spondylitis, reactive arthritis, and syphilis Acute aortic regurgitation: Abrupt onset of pulmonary edema Chronic aortic regurgitation: Asymptomatic until middle age, when symptoms of left heart failure develop insidiously Soft, high-pitched, decrescendo holodiastolic murmur in chronic aortic regurgitation; occasionally, an accompanying apical low- pitched diastolic rumble (Austin Flint murmur) in nonrheumatic patients; in acute aortic regurgitation, the diastolic murmur can be short (or not even heard) and harsh Acute aortic regurgitation: Reduced S1 and an S3; rales Chronic aortic regurgitation: Reduced S1, wide pulse pressure, water- hammer pulse, subungual capillary pulsations (Quincke’s sign), rapid rise and fall of pulse (Corrigan’s pulse), and a diastolic murmur over a partially compressed femoral artery (Duroziez’s sign) ECG shows left ventricular hypertrophy Echo Doppler conﬁrms diagnosis, estimates severity Differential Diagnosis Pulmonary hypertension with Graham Steell murmur Mitral, or rarely, tricuspid stenosis Left ventricular failure due to other cause Dock’s murmur of left anterior descending artery stenosis Treatment Vasodilators (eg, nifedipine and ACE inhibitors) do not delay the progression to valve replacement in patients with mild to moder- ate aortic regurgitation In chronic aortic regurgitation, surgery reserved for patients with symptoms or ejection function < 50% on echocardiography Acute regurgitation caused by aortic dissection or endocarditis requires surgical replacement of the valve Pearl The Hodgkin-Key murmur of aortic regurgitation is harsh and raspy, caused by leaﬂet eventration typical of luetic aortopathy. Reference Kamath AR, Varadarajan P, Turk R, Sampat U, Patel R, Khandhar S, Pai RG. Survival in patients with severe aortic regurgitation and severe left ventricu- lar dysfunction is improved by aortic valve replacement. Circulation 2009; 120(suppl):S134. [PMID: 19752358] 8 Current Essentials of Medicine 1 Aortic Stenosis Essentials of Diagnosis Causes include congenital bicuspid valve and progressive calci- ﬁcation with aging of a normal three-leaﬂet valve; rheumatic fever rarely, if ever, causes isolated aortic stenosis Dyspnea, angina, and syncope singly or in any combination; sudden death in less than 1% of asymptomatic patients Weak and delayed carotid pulses (pulsus parvus et tardus); a soft, absent, or paradoxically split S2; a harsh diamond-shaped sys- tolic ejection murmur to the right of the sternum, often radiating to the neck, but on occasion heard apically (Gallavardin’s phe- nomenon) Left ventricular hypertrophy by ECG and chest x-ray may show calciﬁcation in the aortic valve Echo conﬁrms diagnosis and estimates valve area and gradient; cardiac catheterization conﬁrms severity if there is discrepancy between physical exam and echo; concomitant coronary athero- sclerotic disease present in 50% Differential Diagnosis Mitral regurgitation Hypertrophic obstructive or dilated cardiomyopathy Atrial or ventricular septal defect Syncope due to other causes Ischemic heart disease without valvular abnormality Treatment Surgery is indicated for all patients with severe aortic stenosis 2 (mean aortic valve gradient > 40 mm Hg or valve area ≤ 1.0 cm ) and the presence of symptoms or ejection fraction < 50% Percutaneous balloon valvuloplasty for temporary (6 months) relief of symptoms in poor surgical candidates Pearl In many cases, the softer the murmur, the worse the stenosis. Reference Dal-Bianco JP, Khandheria BK, Mookadam F, Gentile F, Sengupta PP. Management of asymptomatic severe aortic stenosis. J Am Coll Cardiol 2008;52:1279. [PMID: 18929238] Chapter 1 Cardiovascular Diseases 9 Atrial Fibrillation 1 Essentials of Diagnosis The most common chronic arrhythmia Causes include mitral valve disease, hypertensive and ischemic heart disease, dilated cardiomyopathy, alcohol use, hyperthyroidism, peri- carditis, cardiac surgery; many idiopathic (“lone” atrial ﬁbrillation) Complications include precipitation of cardiac failure, arterial embolization Palpitations, dyspnea, chest pain; commonly asymptomatic Irregularly irregular heartbeat, variable intensity S1, occasional S3; S4 absent in all Electrocardiography shows ventricular rate of 80–170/min in untreated patients; if associated with an accessory pathway (ie, Wolff-Parkinson-White), the ventricular rate can be > 200/min with wide QRS and antegrade conduction through the pathway Differential Diagnosis Multifocal atrial tachycardia; sinus arrhythmia Atrial ﬂutter or tachycardia with variable block Normal sinus rhythm with multiple premature contractions Treatment Control ventricular response with AV-nodal blockers such as digoxin, beta-blocker, calcium channel blocker—choice depend- ing on contractile state of left ventricle and blood pressure Cardioversion in unstable patients with acute atrial ﬁbrillation; elective cardioversion in stable patients once a left atrial throm- bus has been ruled out or effectively treated Antiarrhythmic agents (eg, propafenone, procainamide, amiodarone, sotalol) for highly symptomatic patients despite rate control Chronic warfarin or aspirin in all patients With elective cardioversion, documented therapeutic anticoagu- lation for 4 weeks prior to the procedure unless transesophageal echocardiography excludes a left atrial thrombus; all patients require anticoagulation during and after cardioversion Radiofrequency ablation of pulmonary vein sources of atrial ﬁb- rillation increasingly used in symptomatic patients who fail antiar- rhythmic therapy Pearl In 2010, electrophysiology has allowed pathway or nodal ablation in increasing numbers of patients; remember this option. Reference Hart RG, Pearce LA. Current status of stroke risk stratiﬁcation in patients with atrial ﬁbrillation. Stroke 2009;40:2607. [PMID: 19461020] 10 Current Essentials of Medicine 1 Atrial Flutter Essentials of Diagnosis Common in chronic obstructive pulmonary disease (COPD); also seen in dilated cardiomyopathy, especially in alcoholics Atrial rate between 250 and 350 beats/min with every second, third, or fourth impulse conducted by the ventricle; 2:1 most common Patients may be asymptomatic, complain of palpitations, or have evidence of congestive heart failure Flutter (a) waves visible in the neck in occasional patients Electrocardiography shows “sawtooth” P waves in V1 and the inferior leads; ventricular response usually regular; less com- monly, irregular due to variable atrioventricular block Differential Diagnosis With regular ventricular rate: Automatic atrial tachycardia Atrioventricular nodal reentry tachycardia Atrioventricular reentry tachycardia with accessory pathway Sinus tachycardia With irregular ventricular rate: Atrial ﬁbrillation Multifocal atrial tachycardia Sinus rhythm with frequent premature atrial contractions Treatment Often spontaneously converts to atrial ﬁbrillation Electrical cardioversion is reliable and safe Conversion may also be achieved by drugs (eg, ibutilide) Risk of embolization is lower than for atrial ﬁbrillation, but anti- coagulation still recommended Radiofrequency ablation is highly successful (> 90%) in patients with chronic atrial ﬂutter Pearl A regular heart rate of 140–150 in a patient with COPD is ﬂutter until proven otherwise. Reference Rodgers M, McKenna C, Palmer S, et al. Curative catheter ablation in atrial ﬁb- rillation and typical atrial ﬂutter: systematic review and economic evaluation. Health Technol Assess 2008;12:iii-iv, xi-xiii, 1-198. [PMID: 19036232] Chapter 1 Cardiovascular Diseases 11 Atrial Myxoma 1 Essentials of Diagnosis Most common cardiac tumor, usually originating in the interatrial septum, with 80% growing into the left atrium; 5–10% bilateral Symptoms fall into one of three categories: (1) systemic—fever, malaise, weight loss; (2) obstructive—positional dyspnea and syncope; and (3) embolic—acute vascular or neurologic deﬁcit Diastolic “tumor plop” or mitral stenosis-like murmur; signs of congestive heart failure and systemic embolization in many Episodic pulmonary edema, classically when patient assumes an upright position Leukocytosis, anemia, accelerated erythrocyte sedimentation rate MRI or echocardiogram demonstrates tumor Differential Diagnosis Subacute infective endocarditis Lymphoma Autoimmune disease Mitral stenosis Cor triatriatum Parachute mitral valve Other causes of congestive heart failure Renal carcinoma involving the inferior vena cava Treatment Surgery usually curative (recurrence rate is approximately 5%) Pearl One of the three causes of inﬂow obstruction to the left ventricle, with mitral stenosis and cor triatriatum being the other two. Reference Kuroczyński W, Peivandi AA, Ewald P, Pruefer D, Heinemann M, Vahl CF. Cardiac myxomas: short- and long-term follow-up. Cardiol J 2009;16:447. [PMID: 19753524] 12 Current Essentials of Medicine 1 Atrial Septal Defect Essentials of Diagnosis Patients with small defects are usually asymptomatic and have a normal life span Large shunts symptomatic by age 40, including exertional dysp- nea, fatigue, and palpitations Paradoxical embolism may occur (ie, upper or lower extremity venous thrombus embolizing to brain or extremity rather than lung) with transient shunt reversal Right ventricular lift, widened and ﬁxed splitting of S2, and sys- tolic ﬂow murmur in the pulmonary area ECG may show right ventricular hypertrophy and right axis devi- ation (in ostium secundum defects), left anterior hemiblock (in ostium primum defects); complete or incomplete right bundle- branch block in 95% Atrial ﬁbrillation commonly complicates Echo Doppler with agitated saline contrast injection is diagnos- tic; radionuclide angiogram or cardiac catheterization estimates ratio of pulmonary ﬂow to systemic ﬂow (QP:QS) Differential Diagnosis Left ventricular failure Left-sided valvular disease Primary pulmonary hypertension Chronic pulmonary embolism Sleep apnea Chronic obstructive pulmonary disease Eisenmenger’s syndrome Pulmonary stenosis Treatment Small defects do not require surgical correction Surgery or percutaneous closure devices indicated for patients with symptoms or QP:QS > 1.5 Surgery contraindicated in patients with pulmonary hypertension and right-to-left shunting Pearl Prophylaxis for endocarditis is unnecessary; the low interatrial gradient is the reason. Reference Rosas M, Attie F. Atrial septal defect in adults. Timely Top Med Cardiovasc Dis 2007;11:E34. [PMID: 18301787] Chapter 1 Cardiovascular Diseases 13 Atrioventricular Block 1 Essentials of Diagnosis First-degree block: Delayed conduction at the level of the atrio- ventricular node; PR interval > 0.20 seconds Second-degree block: Mobitz I—progressive prolongation of the PR interval and decreasing R-R interval prior to a blocked sinus impulse as well as “group beating”; Mobitz II—ﬁxed PR inter- vals before a beat is dropped Third-degree block: Complete block at or below the node; P waves and QRS complexes occur independently of one another, both at ﬁxed rates with atrial rate > ventricular rate Clinical manifestations of third-degree block include chest pain, syncope, and shortness of breath; cannon a waves in neck veins; ﬁrst heart sound varies in intensity Differential Diagnosis Causes of ﬁrst-degree and Mobitz I atrioventricular block: Increased vagal tone Drugs that prolong atrioventricular conduction All causes of second- and third-degree block Causes of Mobitz II and third-degree atrioventricular block: Chronic degenerative conduction system disease (Lev’s and Lenègre’s syndromes) Acute myocardial infarction: Inferior myocardial infarction causes complete block at the node, anterior myocardial infarction below it Acute myocarditis (eg, Lyme disease, viral myocarditis, rheu- matic fever) Digitalis toxicity Aortic valve abscess Congenital Treatment In symptomatic patients with Mobitz I, permanent pacing; asymp- tomatic patients with Mobitz I do not need therapy For some with Mobitz II and all with infranodal third-degree atri- oventricular block, permanent pacing unless a reversible cause (eg, drug toxicity, inferior myocardial infarction, Lyme disease) is present Pearl A “circus of atrial sounds” may be created by atrial contractions at dif- ferent rates than ventricular, in any cause of AV dissociation. Reference Dovgalyuk J, Holstege C, Mattu A, Brady WJ. The electrocardiogram in the patient with syncope. Am J Emerg Med 2007;25:688. [PMID: 17606095] 14 Current Essentials of Medicine 1 Cardiac Tamponade Essentials of Diagnosis Life-threatening disorder occurring when pericardial ﬂuid accu- mulates under pressure; effusions rapidly increasing in size may cause an elevated intrapericardial pressure (> 15 mm Hg), lead- ing to impaired cardiac ﬁlling and decreased cardiac output Common causes include metastatic malignancy, uremia, viral or idiopathic pericarditis, and cardiac trauma; however, any cause of pericarditis can cause tamponade Clinical manifestations include dyspnea, cough, tachycardia, hypotension, pulsus paradoxus, jugular venous distention, and distant heart sounds Electrocardiography usually shows low QRS voltage and occa- sionally electrical alternans; chest x-ray shows an enlarged cardiac silhouette with a “water-bottle” conﬁguration if a large (> 250 mL) effu- sion is present—which it need not be if effusion develops rapidly Echocardiography delineates effusion and its hemodynamic sig- niﬁcance, eg, atrial collapse; cardiac catheterization conﬁrms the diagnosis if equalization of diastolic pressures in all four cham- bers occurs with loss of the normal y descent Differential Diagnosis Tension pneumothorax Right ventricular infarction Severe left ventricular failure Constrictive pericarditis Restrictive cardiomyopathy Pneumonia with septic shock Treatment Immediate pericardiocentesis if hemodynamic compromise is noted Volume expansion until pericardiocentesis is performed Deﬁnitive treatment for reaccumulation may require surgical ante- rior and posterior pericardiectomy Pearl Pulsus paradoxus is in fact not paradoxical: it merely exaggerates a normal phenomenon. Reference Jacob S, Sebastian JC, Cherian PK, Abraham A, John SK. Pericardial effusion impending tamponade: a look beyond Beck’s triad. Am J Emerg Med 2009;27:216. [PMID: 19371531] Chapter 1 Cardiovascular Diseases 15 Congestive Heart Failure 1 Essentials of Diagnosis Two pathophysiologic categories: Systolic dysfunction and dias- tolic dysfunction Systolic: The ability to pump blood is compromised; ejection fraction is decreased; causes include coronary artery disease, dilated cardiomyopathy, myocarditis, “burned-out” hypertensive heart disease, and regurgitant valvular heart disease Diastolic: Heart unable to relax and allow adequate diastolic ﬁll- ing; normal ejection fraction; causes include ischemia, hyperten- sion with left ventricular hypertrophy, aortic stenosis, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and small-vessel disease (especially diabetes) Evidence of both common in the typical heart failure patient, but up to 50% of patients will have isolated diastolic dysfunction Symptoms and signs can result from left-sided failure, right-sided failure, or both Left ventricular failure: Exertional dyspnea, orthopnea, paroxys- mal nocturnal dyspnea, pulsus alternans, rales, gallop rhythm; pulmonary venous congestion on chest x-ray Right ventricular failure: Fatigue, malaise, elevated venous pres- sure, hepatomegaly, abdominojugular reﬂux, and dependent edema Diagnosis conﬁrmed by echo, pulmonary capillary wedge meas- urement, or elevated levels of brain natriuretic peptide (BNP) Differential Diagnosis Constrictive pericarditis; nephrosis; cirrhosis Hypothyroidism or hyperthyroidism; beriberi Noncardiogenic causes of pulmonary edema Treatment Systolic dysfunction: Vasodilators (ACE inhibitors, angiotensin II receptor blockers, or combination of hydralazine and isosorbide dini- trate), beta-blockers, spironolactone, and low-sodium diet; for symp- toms, use diuretics and digoxin; anticoagulation perhaps in high-risk patients with apical akinesis even with sinus rhythm; look for ischemia, valvular disease, alcohol use, or hypothyroidism as causes Diastolic dysfunction: A negative inotrope (beta-blocker or calcium channel blocker), low-sodium diet, and diuretics for symptoms Pearl Remember that a normal ejection fraction is the rule in ﬂash pulmonary edema; severe diastolic dysfunction is the problem. Reference Donlan SM, Quattromani E, Pang PS, Gheorghiade M. Therapy for acute heart failure syndromes. Curr Cardiol Rep 2009;11:192. [PMID: 19379639] 16 Current Essentials of Medicine 1 Constrictive Pericarditis Essentials of Diagnosis A thickened ﬁbrotic pericardium impairing cardiac ﬁlling and decreasing cardiac output May follow tuberculosis, cardiac surgery, radiation therapy, or viral, uremic, or neoplastic pericarditis Gradual onset of dyspnea, fatigue, weakness, pedal edema, and abdominal swelling; right-sided heart failure symptoms often pre- dominate, with ascites sometimes disproportionate to pedal edema Physical examination reveals tachycardia, elevated jugular venous dis- tention with rapid y descent, Kussmaul’s sign, hepatosplenomegaly, ascites, “pericardial knock” following S2, and peripheral edema Pericardial calciﬁcation on chest ﬁlm in less than half; electro- cardiography may show low QRS voltage; liver function tests abnormal from passive congestion Echocardiography can demonstrate a thick pericardium and normal left ventricular function; CT or MRI is more sensitive in revealing pericardial pathology; cardiac catheterization demon- strates ventricular discordance with respiration in contrast to restrictive cardiomyopathy Differential Diagnosis Cardiac tamponade Right ventricular infarction Restrictive cardiomyopathy Cirrhosis with ascites (most common misdiagnosis) Treatment Acute treatment usually includes gentle diuresis Deﬁnitive therapy is surgical stripping of the pericardium; effec- tive in up to half of patients Evaluation for tuberculosis Pearl The most overlooked cause of new-onset ascites. Reference Marnejon T, Kassis H, Gemmel D. The constricted heart. Postgrad Med 2008;120:8. [PMID: 18467803] Chapter 1 Cardiovascular Diseases 17 Cor Pulmonale 1 Essentials of Diagnosis Heart failure resulting from pulmonary disease Most commonly due to COPD; other causes include pulmonary ﬁbrosis, pneumoconioses, recurrent pulmonary emboli, primary pulmonary hypertension, sleep apnea, and kyphoscoliosis Clinical manifestations are due to both the underlying pulmonary disease and the right ventricular failure Chest x-ray reveals an enlarged right ventricle and pulmonary artery; electrocardiography may show right axis deviation, right ventricular hypertrophy, and tall, peaked P waves (P pulmonale) in the face of low QRS voltage Pulmonary function tests usually conﬁrm the presence of underlying lung disease, and echocardiography will show right ventricular dilation but normal left ventricular function and elevated right ventricular systolic pressures Differential Diagnosis Other causes of right ventricular failure: Left ventricular failure (due to any cause) Pulmonary stenosis Left-to-right shunt causing Eisenmenger’s syndrome Treatment Treatment is primarily directed at the pulmonary process causing the right heart failure (eg, oxygen if hypoxia is present) In frank right ventricular failure, include salt restriction, diuret- ics, and oxygen For primary pulmonary hypertension, cautious use of vasodilators (calcium channel blockers) or continuous-infusion prostacyclin may beneﬁt some patients Pearl Oxygen is the furosemide of the right ventricle. Reference Weitzenblum E, Chaouat A. Cor pulmonale. Chron Respir Dis 2009;6:177. [PMID: 19643833] 18 Current Essentials of Medicine 1 Deep Venous Thrombosis Essentials of Diagnosis Dull pain or tight feeling in the calf or thigh Up to half of patients are asymptomatic in the early stages Increased risk: Congestive heart failure, recent major surgery, neoplasia, oral contraceptive use by smokers, prolonged inactivity, varicose veins, hypercoagulable states (eg, protein C, protein S, other anticoagulant deﬁciencies, nephrotic syndrome) Physical signs unreliable Doppler ultrasound and impedance plethysmography are initial tests of choice (less sensitive in asymptomatic patients); venog- raphy is deﬁnitive but difﬁcult to perform Pulmonary thromboembolism, especially with proximal, above- the-knee deep vein thrombosis, is a life-threatening complication Differential Diagnosis Calf strain or contusion; ruptured Baker’s cyst Cellulitis; lymphatic obstruction Congestive heart failure, especially right-sided Treatment Anticoagulation with heparin followed by oral warfarin for 3–6 months Subcutaneous low-molecular-weight heparin may be substituted for intravenous heparin NSAIDs for associated pain and swelling For idiopathic and recurrent cases, hypercoagulable conditions should be considered, although factor V Leiden should be sought on a first episode without risk factors in patients of European ethnicity Postphlebitic syndrome (chronic venous insufﬁciency) is common following an episode of deep venous thrombosis and should be treated with graduated compression stockings, local skin care, and in many, chronic warfarin administration Pearl The left leg is 1 cm greater in circumference than the right, as the left common iliac vein courses under the aorta; remember this in evaluat- ing suspected deep venous thrombosis. Reference Blann AD, Khoo CW. The prevention and treatment of venous thromboem- bolism with LMWHs and new anticoagulants. Vasc Health Risk Manag 2009;5:693. [PMID: 19707288] Chapter 1 Cardiovascular Diseases 19 Dilated Cardiomyopathy 1 Essentials of Diagnosis A cause of systolic dysfunction, this represents a group of disor- ders that lead to congestive heart failure Symptoms and signs of congestive heart failure: Exertional dys- pnea, cough, fatigue, paroxysmal nocturnal dyspnea, cardiac enlargement, rales, gallop rhythm, elevated venous pressure, hepatomegaly, and dependent edema Electrocardiography may show nonspeciﬁc repolarization abnor- malities and atrial or ventricular ectopy, but is not diagnostic Echocardiography reveals depressed contractile function and car- diomegaly Cardiac catheterization useful to exclude ischemia as a cause Differential Diagnosis Causes of dilated cardiomyopathy: Alcoholism Infectious (including postviral) myocarditis, human immunode- ﬁciency virus, and Chagas’ disease Sarcoidosis Postpartum Doxorubicin toxicity Endocrinopathies (hyperthyroidism, acromegaly, pheochromocy-toma) Hemochromatosis Idiopathic Treatment Treat the underlying disorder when identiﬁable Abstention from alcohol and NSAIDs Routine management of systolic dysfunction, including with vasodilators (ACE inhibitors, angiotensin II receptor blockers, and/or a combination of hydralazine and isosorbide dinitrate), beta-blockers, spironolactone, and low-sodium diet; digoxin and diuretics for symptoms Many empirically employ chronic warfarin if apical akinesis is noted In a patient with ischemic or nonischemic heart disease and a low left ventricular ejection fraction (< 35%), an implantable cardiac deﬁbrillator (ICD) may be warranted even in the absence of doc- umented ventricular tachycardia Cardiac transplant for end-stage patients Pearl Causes of death: one-third pump failure, one-third arrhythmia, and one-third stroke; arrhythmia and stroke are potentially preventable. Reference Luk A, Ahn E, Soor GS, Butany J. Dilated cardiomyopathy: a review. J Clin Pathol 2009;62:219. [PMID: 19017683] 20 Current Essentials of Medicine 1 Hypertension Essentials of Diagnosis In most patients (95% of cases), no cause can be found Chronic elevation in blood pressure (> 140/90 mm Hg) occurs in 23% of non-Hispanic white adults and 32% of non-Hispanic black adults in the United States; onset is usually between ages 20 and 55 The pathogenesis is multifactorial: Environmental, dietary, genetic, and neurohormonal factors all contribute Most patients are asymptomatic; some, however, complain of headache, epistaxis, or blurred vision if hypertension is severe Most diagnostic study abnormalities are referable to “target organ” damage: heart, kidney, brain, retina, and peripheral arteries Differential Diagnosis Secondary causes of hypertension: Coarctation of the aorta Renal insufﬁciency Renal artery stenosis Pheochromocytoma Cushing’s syndrome Primary hyperaldosteronism Chronic use of oral contraceptive pills or alcohol Treatment Decrease blood pressure with a single agent (if possible) while minimizing side effects; however, those with blood pressure > 160/100 may require combination therapy Many recommend diuretics, beta-blockers, ACE inhibitors, or calcium channel blockers as initial therapy, but considerable lat- itude is allowed for individual patients; these agents can be used alone or in combination; α1-blockers are considered second-line agents If hypertension is unresponsive to medical treatment, evaluate for secondary causes Pearl Increasingly a condition diagnosed by the patient; sphygmomanometers are widely available in pharmacies and supermarkets. Reference Fuchs FD. Diuretics: still essential drugs for the management of hypertension. Expert Rev Cardiovasc Ther 2009;7:591. [PMID: 19505274] Chapter 1 Cardiovascular Diseases 21 Hypertrophic Obstructive Cardiomyopathy (HOCM) 1 Essentials of Diagnosis Asymmetric myocardial hypertrophy causing dynamic obstruction to left ventricular outﬂow below the aortic valve Sporadic or dominantly inherited Obstruction is worsened by increasing left ventricular contractil- ity or decreasing ﬁlling Symptoms are dyspnea, chest pain, and syncope; a subgroup of younger patients is at high risk for sudden cardiac death (1% per year), especially with exercise Sustained, biﬁd (rarely triﬁd) apical impulse, S4 Electrocardiography shows exaggerated septal Q waves sugges- tive of myocardial infarction; supraventricular and ventricular arrhythmias may also be seen Echocardiography with hypertrophy, evidence of dynamic obstruc- tion from abnormal systolic motion of the anterior mitral valve leaﬂet Role for genetic testing including familial screening, but current tests only identify 50–60% of mutations Differential Diagnosis Hypertensive or ischemic heart disease Restrictive cardiomyopathy (eg, amyloidosis) Aortic stenosis; athlete’s heart Treatment Beta-blockers or calcium channel blockers are the initial drugs of choice in symptomatic patients Avoid afterload reducers such as ACE inhibitors Surgical myectomy, percutaneous transcoronary septal reduction with alcohol, or dual-chamber pacing is considered in some Implantable cardiac deﬁbrillator in patients at high risk for sudden death; risk factors include left ventricle thickness > 30 mm, family history of sudden death, nonsustained ventricular tachycardia on Holter, hypotensive blood pressure response on treadmill, previ- ous cardiac arrest, and syncope Natural history is unpredictable; sports requiring high cardiac output should be discouraged All ﬁrst-degree relatives should be evaluated with echocardiography every 5 years if > 18 years of age; every year if < 18 years of age Pearl Hypertrophic obstructive cardiomyopathy is the most common cause of sudden cardiac death in athletes. Reference Elliott P, Spirito P. Prevention of hypertrophic cardiomyopathy-related deaths: theory and practice. Heart 2008;94:1269. [PMID: 18653582] 22 Current Essentials of Medicine 1 Mitral Regurgitation Essentials of Diagnosis Causes include rheumatic heart disease, infectious endocarditis, mitral valve prolapse, ischemic papillary muscle dysfunction, torn chordae tendineae Acute: Immediate onset of symptoms of pulmonary edema Chronic: Asymptomatic for years, then exertional dyspnea and fatigue S1 usually reduced; a blowing, high-pitched apical pansystolic murmur increased by ﬁnger squeeze is characteristic; S3 common in chronic cases; murmur is not pansystolic and less audible in acute Left atrial abnormality and often left ventricular hypertrophy on ECG; atrial ﬁbrillation typical with chronicity Echo Doppler conﬁrms diagnosis, estimates severity Differential Diagnosis Aortic stenosis or sclerosis Tricuspid regurgitation Hypertrophic obstructive cardiomyopathy Atrial septal defect Ventricular septal defect Treatment Acute mitral regurgitation due to endocarditis or torn chordae may require immediate surgical repair Surgical repair or replacement for severe mitral regurgitation in patients with symptoms, left ventricular dysfunction (eg, ejection fraction < 60%), or left ventricular systolic dimension > 40 mm There are no data supporting the use of vasodilators in patients with asymptomatic chronic mitral regurgitation; digoxin, beta-blockers, and calcium channel blockers control ventricular response with atrial ﬁbrillation, and warfarin anticoagulation should be given Pearl The rapid up-and-down carotid pulse may be decisive in separating this murmur from that of aortic stenosis. Reference Mehra MR, Reyes P, Benitez RM, Zimrin D, Gammie JS. Surgery for severe mitral regurgitation and left ventricular failure: what do we really know? J Card Fail 2008;14:145. [PMID: 18325462] Chapter 1 Cardiovascular Diseases 23 Mitral Stenosis 1 Essentials of Diagnosis Always caused by rheumatic heart disease, but 30% of patients have no history of rheumatic fever Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, even hemop- tysis—often precipitated by volume overload (pregnancy, salt load) or tachycardia Right ventricular lift in many; opening snap occasionally palpable Crisp S1, increased P2, opening snap; these sounds often easier to appreciate than the characteristic low-pitched apical diastolic murmur Electrocardiography shows left atrial abnormality, and commonly, atrial ﬁbrillation; echo conﬁrms diagnosis, quantiﬁes severity Differential Diagnosis Left ventricular failure due to any cause Mitral valve prolapse (if systolic murmur present) Pulmonary hypertension due to other cause Left atrial myxoma Cor triatriatum (in patients under 30) Tricuspid stenosis Treatment Heart failure symptoms may be treated with diuretics and sodium restriction With atrial ﬁbrillation, ventricular rate controlled with beta-block- ers, calcium channel blockers such as verapamil or digoxin; long- term anticoagulation instituted with warfarin Balloon valvuloplasty or surgical valve replacement in patients with mitral oriﬁce of < 1.5 cm2 and symptoms or evidence of pul- monary hypertension; valvuloplasty preferred in noncalciﬁed and pliable valves Pearl Think of the crisp ﬁrst heart sound as the “closing snap” of the mitral valve. Reference American College of Cardiology/American Heart Association Task Force on Practice Guidelines; Society of Cardiovascular Anesthesiologists; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons, Bonow RO, Carabello BA, Kanu C, de Leon AC, et al. ACC/AHA 2006 guide- lines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2006;114:e84. [PMID: 16880336] 24 Current Essentials of Medicine 1 Multifocal Atrial Tachycardia Essentials of Diagnosis Classically seen in patients with severe COPD; electrolyte abnor- malities (especially hypomagnesemia or hypokalemia) occasion- ally responsible Symptoms include those of the underlying disorder, but some may complain of palpitations Irregularly irregular heart rate Electrocardiography shows at least three different P-wave mor- phologies with varying PR intervals Ventricular rate usually between 100 and 140 beats/min; if < 100, rhythm is wandering atrial pacemaker Differential Diagnosis Normal sinus rhythm with multiple premature atrial contractions Atrial ﬁbrillation Atrial ﬂutter with variable block Reentry tachycardia with variable block Treatment Treatment of the underlying disorder is most important Verapamil particularly useful for rate control; digitalis ineffective Intravenous magnesium and potassium administered slowly may convert some patients to sinus rhythm even if serum levels are within normal range; be sure renal function is normal Medications causing atrial irritability, such as theophylline, should be avoided Atrioventricular nodal ablation with permanent pacing is used in rare cases that are highly symptomatic and refractory to pharma- cologic therapy Pearl Multifocal atrial tachycardia is the paradigm COPD arrhythmia, electro- cardiographically deﬁned and increasingly treated electrophysiologically. Reference Spodick DH. Multifocal atrial arrhythmia. Am J Geriatr Cardiol 2005;14:162. [PMID: 15886545] Chapter 1 Cardiovascular Diseases 25 Myocarditis 1 Essentials of Diagnosis Focal or diffuse inﬂammation of the myocardium due to various infections, toxins, drugs, or immunologic reactions; viral infection, particularly with coxsackieviruses, is the most common cause Other infectious causes include Rocky Mountain spotted fever, Q fever, Chagas’ disease, Lyme disease, HIV, trichinosis, and toxoplasmosis Symptoms include fever, fatigue, palpitations, chest pain, or symp- toms of congestive heart failure, often following an upper respi- ratory tract infection Electrocardiography may reveal ST-T wave changes, conduction blocks Echocardiography shows diffusely depressed left ventricular func- tion and enlargement Routine myocardial biopsy usually not recommended since inﬂammatory changes are often focal and nonspeciﬁc Differential Diagnosis Acute myocardial ischemia or infarction due to coronary artery disease Pneumonia Congestive heart failure due to other causes Treatment Bed rest Speciﬁc antimicrobial treatment if an infectious agent can be identiﬁed Immunosuppressive therapy is controversial Appropriate treatment of systolic dysfunction: vasodilators (ACE inhibitors, angiotensin II receptor blockers, or combination of hydralazine and isosorbide dinitrate), beta-blockers, spironolac- tone, digoxin, low-sodium diet, and diuretics Inotropes and cardiac transplant for severe cases Pearl In viral myocarditis, remember the following: one-third return to normal, one-third have stable left ventricular dysfunction, and one-third have a severe cardiomyopathy. Reference Schultz JC, Hilliard AA, Cooper LT Jr, Rihal CS. Diagnosis and treatment of viral myocarditis. Mayo Clin Proc 2009;84:1001. [PMID: 19880690] 26 Current Essentials of Medicine 1 Paroxysmal Supraventricular Tachycardia (PSVT) Essentials of Diagnosis A group of arrhythmias including atrioventricular nodal reen- trant, atrioventricular reentrant tachycardias, automatic atrial tachycardia, and junctional tachycardia Attacks usually begin and end abruptly, last seconds to hours Patients often asymptomatic with transient episodes but may com- plain of palpitations, mild dyspnea, or chest pain Electrocardiography between attacks normal unless the patient has Wolff-Parkinson-White syndrome or a very short PR interval Unless aberrant conduction occurs, the QRS complexes are regular and narrow; P wave location helps determine the origin; electro- physiologic study establishes the exact diagnosis Differential Diagnosis No P: Atrioventricular nodal reentry tachycardia Short RP: Typical atrioventricular reentrant tachycardia Orthodromic atrioventricular reentrant tachycardia Atrial tachycardia with 1st degree AV delay Junctional tachycardia Long RP: Atrial tachycardia Sinus tachycardia Atypical atrioventricular nodal reentry tachycardia Permanent junctional reciprocating tachycardia Treatment Many attacks resolve spontaneously; if not, ﬁrst try vagal maneu- vers such as carotid sinus massage or adenosine to transiently block the AV node and break the reentrant circuit Prevention of frequent attacks can be achieved by calcium chan- nel blockers, beta-blockers, or antiarrhythmics if necessary Electrophysiologic study and ablation of the abnormal reentrant circuit or focus, when available, is the treatment of choice Pearl If “Q-wave MI” is the computer readout with a short PR interval, con- sider this: erroneous interpretation may make your patient ineligible for life insurance, when the innocent WPW is the diagnosis. Reference Holdgate A, Foo A. Adenosine versus intravenous calcium channel antagonists for the treatment of supraventricular tachycardia in adults. Cochrane Database Syst Rev 2006;(4):CD005154. [PMID: 17054240] Chapter 1 Cardiovascular Diseases 27 Patent Ductus Arteriosus 1 Essentials of Diagnosis Caused by failure of closure of embryonic ductus arteriosus with con- tinuous blood ﬂow from aorta to pulmonary artery (ie, left-to-right shunt) Symptoms are those of left ventricular failure or pulmonary hyper- tension; many cases are complaint-free Widened pulse pressure, a loud S2, and a continuous, “machinery” murmur loudest over the pulmonary area but heard posteriorly Echo Doppler helpful, but contrast or MR aortography is the study of choice Differential Diagnosis In patients presenting with left heart failure: Mitral regurgitation Aortic stenosis Ventricular septal defect If pulmonary hypertension dominates the picture: Primary pulmonary hypertension Chronic pulmonary embolism Eisenmenger’s syndrome Treatment Pharmacologic closure in premature infants, using indomethacin or aspirin Surgical or percutaneous closure in patients with large shunts, symptoms, or previous endocarditis; controversial in other settings Pearl Patients usually remain asymptomatic as adults if problems have not developed by age 10 years. Reference Schneider DJ, Moore JW. Patent ductus arteriosus. Circulation 2006;114:1873. [PMID: 17060397] 28 Current Essentials of Medicine 1 Prinzmetal’s Angina Essentials of Diagnosis Caused by intermittent focal spasm of an otherwise normal coro- nary artery Associated with migraine, Raynaud’s phenomenon The chest pain resembles typical angina, but often is more severe and occurs at rest Affects women under 50, occurs in the early morning, and typi- cally involves the right coronary artery Electrocardiography shows ST-segment elevation, but enzyme studies are normal Diagnosis can be conﬁrmed by ergonovine challenge during cardiac catheterization Differential Diagnosis Typical angina pectoris; myocardial infarction; unstable angina Tietze’s syndrome (costochondritis) Cervical or thoracic radiculopathy, including pre-eruptive zoster Esophageal spasm or reﬂux disease Cholecystitis Pericarditis Pneumothorax Pulmonary embolism Pneumococcal pneumonia Treatment Statins, smoking cessation, nitrates, and calcium channel block- ers acutely effective and are the mainstay of chronic therapy Prognosis excellent given absence of atherosclerosis Pearl In its classic iteration, vasospasm of the right coronary artery, mostly women, nonexertional, no atherosclerosis, ST elevation at the same time of the day; in 2010, consider cocaine or methamphetamine use. Reference Stern S, Bayes de Luna A. Coronary artery spasm: a 2009 update. Circulation 2009;119:2531. [PMID: 19433770] Chapter 1 Cardiovascular Diseases 29 Pulmonary Stenosis 1 Essentials of Diagnosis Exertional dyspnea and chest pain due to right ventricular ischemia; sudden death occurs in severe cases Jugular venous distention, parasternal lift, systolic click and ejec- tion murmur, delayed and soft pulmonary component of S2 Right ventricular hypertrophy on ECG; poststenotic dilation of the main and left pulmonary arteries on chest x-ray Echo Doppler is diagnostic May be associated with Noonan’s syndrome Differential Diagnosis Left ventricular failure due to any cause Left-sided valvular disease Primary pulmonary hypertension Chronic pulmonary embolism Sleep apnea Chronic obstructive pulmonary disease Eisenmenger’s syndrome Treatment Symptomatic patients with peak gradient > 30 mm Hg: Percutaneous balloon or surgical valvuloplasty Asymptomatic patients with peak gradient > 40 mm Hg: Percutaneous balloon or surgical valvuloplasty Prognosis for those with mild disease is good Pearl If contemplating this as the cause of a murmur, be sure to inquire about ﬂushing; carcinoid syndrome is one of the few causes of right-sided valvular disease. Reference Kogon B, Plattner C, Kirshbom P, et al. Risk factors for early pulmonary valve replacement after valve disruption in congenital pulmonary stenosis and tetral- ogy of Fallot. J Thorac Cardiovasc Surg 2009;138:103. [PMID: 19577064] 30 Current Essentials of Medicine 1 Restrictive Cardiomyopathy Essentials of Diagnosis Characterized by impaired diastolic ﬁlling with preserved left ventricular function Causes include amyloidosis, sarcoidosis, hemochromatosis, scle- roderma, carcinoid syndrome, endomyocardial ﬁbrosis, and postradiation or postsurgical ﬁbrosis Clinical manifestations are those of the underlying disorder; con- gestive heart failure with right-sided symptoms and signs usually predominates Electrocardiography may show low voltage and nonspeciﬁc ST-T wave abnormalities in amyloidosis; supraventricular and ventric- ular arrhythmias may also be seen Echo Doppler shows increased wall thickness with preserved con- tractile function and mitral and tricuspid inﬂow velocity patterns consistent with impaired diastolic ﬁlling Cardiac catheterization shows ventricular concordance with res- piration as compared with constrictive pericarditis Differential Diagnosis Constrictive pericarditis Hypertensive heart disease Hypertrophic obstructive cardiomyopathy Aortic stenosis Ischemic heart disease Treatment Sodium restriction and diuretic therapy for patients with evidence of ﬂuid overload; diuresis must be cautious, as volume depletion may worsen this disorder Digitalis should be used with caution due to increase in intracel- lular calcium Treatment of underlying disease causing the restriction if possible Pearl In a patient with this condition, if the right upper quadrant appears dense on plain chest x-ray, consider hemochromatosis; hepatic iron deposi- tion is responsible. Reference Whalley GA, Gamble GD, Doughty RN. The prognostic signiﬁcance of restric- tive diastolic ﬁlling associated with heart failure: a meta-analysis. Int J Cardiol 2007;116:70. [PMID: 16901562] Chapter 1 Cardiovascular Diseases 31 Sudden Cardiac Death 1 Essentials of Diagnosis Death in a well patient within 1 hour of symptom onset Can be due to cardiac or noncardiac disease Most common cause (> 80% of cases) is ventricular ﬁbrillation or tachycardia in the setting of coronary artery disease Ventricular ﬁbrillation is almost always the terminal rhythm Differential Diagnosis Noncardiac causes of sudden death: Pulmonary embolism Asthma Aortic dissection Ruptured aortic aneurysm Intracranial hemorrhage Tension pneumothorax Anaphylaxis Treatment Aggressive approach obligatory if coronary artery disease is sus- pected; see below Electrolyte abnormalities, digitalis toxicity, or implantable cardiac deﬁbrillator malfunction can be the precipitant and is treated accordingly Without obvious cause, echocardiography and cardiac catheteri- zation are indicated; if normal, electrophysiologic studies thereafter An automatic implantable cardiac deﬁbrillator should be used in all patients surviving an episode of sudden cardiac death second- ary to ventricular ﬁbrillation or tachycardia without a transient or reversible cause Pearl In resuscitated ventricular ﬁbrillation in adults, if myocardial infarction is ruled out, the prognosis is paradoxically worse than if ruled in; it suggests that active ischemia or signiﬁcant structural heart disease is present. Reference Mudawi TO, Albouaini K, Kaye GC. Sudden cardiac death: history, aetiology and management. Br J Hosp Med (Lond) 2009;70:89. [PMID: 19229149] 32 Current Essentials of Medicine 1 Tricuspid Regurgitation Essentials of Diagnosis Causes include infective endocarditis, right ventricular heart fail- ure of any cause, carcinoid syndrome, systemic lupus erythe- matosus, Ebstein’s anomaly, and leaﬂet disruption due to cardiac device leads Most cases secondary to dilation of the right ventricle from left- sided heart disease Edema, abdominal discomfort, anorexia; otherwise, symptoms of associated disease Prominent (v) waves in jugular venous pulse; pulsatile liver, abdominojugular reﬂux Characteristic high-pitched blowing holosystolic murmur along the left sternal border increasing with inspiration Echo Doppler is diagnostic Differential Diagnosis Mitral regurgitation Aortic stenosis Pulmonary stenosis Atrial septal defect Ventricular septal defect Treatment Diuretics and dietary sodium restriction in patients with evidence of ﬂuid overload If tricuspid regurgitation is functional and surgery is performed for multivalvular disease, then tricuspid valve annuloplasty can be considered Pearl Ninety percent of right heart failure is caused by left heart failure. Reference Chang BC, Song SW, Lee S, Yoo KJ, Kang MS, Chung N. Eight-year outcomes of tricuspid annuloplasty using autologous pericardial strip for functional tri- cuspid regurgitation. Ann Thorac Surg 2008;86:1485. [PMID: 19049736] Chapter 1 Cardiovascular Diseases 33 Tricuspid Stenosis 1 Essentials of Diagnosis Usually rheumatic in origin; rarely, seen in carcinoid heart disease Almost always associated with mitral stenosis when rheumatic Evidence of right-sided failure: Hepatomegaly, ascites, peripheral edema, jugular venous distention with prominent (a) wave A diastolic rumbling murmur along the left sternal border, increas- ing with inspiration Echo Doppler is diagnostic Differential Diagnosis Atypical aortic regurgitation Mitral stenosis Pulmonary hypertension due to any cause with right heart failure Constrictive pericarditis Liver cirrhosis Right atrial myxoma Treatment Valve replacement in severe cases Balloon valvuloplasty may prove to be useful in many patients Pearl Almost never encountered in the United States with the wane of rheumatic heart disease; the rare patient with carcinoid syndrome may have it. Reference Guenther T, Noebauer C, Mazzitelli D, Busch R, Tassani-Prell P, Lange R. Tricuspid valve surgery: a thirty-year assessment of early and late outcome. Eur J Cardiothorac Surg 2008;34:402. [PMID: 18579403] 34 Current Essentials of Medicine 1 Unstable Angina Essentials of Diagnosis Spectrum of illness between chronic stable angina and acute myocardial infarction Characterized by accelerating angina, pain at rest, or pain less responsive to medications Usually due to atherosclerotic plaque rupture, spasm, hemor- rhage, or thrombosis Chest pain resembles typical angina but is more severe and lasts longer (up to 30 minutes) ECG may show dynamic ST-segment depression or T-wave changes during pain, but normalizes when symptoms abate; a normal ECG, however, does not exclude the diagnosis Differential Diagnosis Typical angina pectoris; myocardial infarction Coronary vasospasm; aortic dissection Tietze’s syndrome (costochondritis) Cervical or thoracic radiculopathy, including pre-eruptive zoster Esophageal spasm or reﬂux disease Cholecystitis; pneumonia; pericarditis Pneumothorax Pulmonary embolism Treatment Hospitalization with bed rest, telemetry, and treatment similar to acute coronary syndrome Low-dose aspirin (81–325 mg) immediately on admission for all; intravenous heparin of beneﬁt Beta-blockers to keep heart rate and blood pressure in the low- normal range In high-risk patients, glycoprotein IIb/IIIa inhibitors effective, especially if percutaneous intervention likely Nitroglycerin, either in paste or intravenously Cardiac catheterization and consideration of revascularization in appropriate candidates Pearl This condition requires aggressive anticoagulation; give aortic dissec- tion a thought before writing the orders for same. Reference Hitzeman N. Early invasive therapy or conservative management for unstable angina or NSTEMI? Am Fam Physician 2007;75:47. [PMID: 17225702] Chapter 1 Cardiovascular Diseases 35 Ventricular Septal Defect 1 Essentials of Diagnosis Many congenital ventricular septal defects close spontaneously during childhood Symptoms depend on the size of the defect and the magnitude of the left-to-right shunt Small defects in adults are usually asymptomatic except for com- plicating endocarditis, but may be associated with a loud murmur (maladie de Roger) Large defects usually associated with softer murmurs, but com- monly lead to Eisenmenger’s syndrome Echo Doppler diagnostic; radionuclide angiogram or cardiac catheterization quantiﬁes the ratio of pulmonary ﬂow to systemic ﬂow (QP:QS) Differential Diagnosis Mitral regurgitation Aortic stenosis Cardiomyopathy due to various causes Treatment Small shunts in asymptomatic patients may not require surgery Mild dyspnea treatable with diuretics and preload reduction QP:QS shunts over 1.5 are repaired to prevent irreversible pul- monary vascular disease, but decision to close needs to be tailored to individual patient Surgery if patient has developed shunt reversal (Eisenmenger’s syndrome) without ﬁxed pulmonary hypertension Pearl Small defects have a higher risk of endocarditis than large ones; endothelial injury is favored by a small, localized jet. Reference Butera G, Chessa M, Carminati M. Percutaneous closure of ventricular septal defects. State of the art. J Cardiovasc Med (Hagerstown) 2007;8:39. [PMID: 17255815] 36 Current Essentials of Medicine 1 Ventricular Tachycardia Essentials of Diagnosis Three or more consecutive premature ventricular beats; nonsus- tained (lasting < 30 seconds) or sustained Mechanisms are reentry or automatic focus; may occur sponta- neously or with myocardial infarction Other causes include acute or chronic ischemia, cardiomyopa- thy, and drugs (eg, antiarrhythmics) Most patients symptomatic; syncope, palpitations, shortness of breath, and chest pain are common S1 of variable intensity; S3 present Electrocardiography shows a regular, wide-complex tachycardia (usually between 140 and 220 beats/min); between attacks, the ECG often reveals evidence of prior myocardial infarction Differential Diagnosis Any cause of supraventricular tachycardia with aberrant conduc- tion (but a history of myocardial infarction or low ejection frac- tion indicates ventricular tachycardia until proved otherwise) Atrial ﬂutter with aberrant conduction Treatment Depends on whether the patient is stable or unstable If stable: intravenous lidocaine, procainamide, or amiodarone can be used initially If unstable (hypotension, congestive heart failure, or angina): immediate synchronized cardioversion Implantable cardiac deﬁbrillator placement should be strongly considered In a patient with ischemic or nonischemic heart disease and a low left ventricular ejection fraction (< 35%), an implantable cardiac deﬁbrillator is warranted, even in the absence of documented ven- tricular tachycardia Ablation for those with repetitive shocks from deﬁbrillator Pearl All wide-complex tachycardia should be treated as ventricular tachy- cardia until proven otherwise. Reference Aronow WS. Treatment of ventricular arrhythmias in the elderly. Cardiol Rev 2009;17:136. [PMID: 19384088] 2 Pulmonary Diseases Acute Bacterial Pneumonia Essentials of Diagnosis Fever, chills, dyspnea, cough with purulent sputum production; early pleuritic pain suggests pneumococcal etiology Tachycardia, tachypnea; bronchial breath sounds with percussive dullness and egophony over involved lungs Leukocytosis; WBC < 5000 or > 25,000 worrisome Patchy or lobar inﬁltrate by chest x-ray Diagnosis is clinical, but pathogen can be determined from proper sputum Gram stain and/or culture of sputum, blood (positive in ~10%, or pleural ﬂuid; pathogen only determined in 30–60% Principal causes include Streptococcus pneumoniae, Haemophilus inﬂuenzae, Legionella (elderly, smokers), gram-negative rods (alco- holics and aspirators), Staphylococcus (postviral) Differential Diagnosis Atypical or viral pneumonia Pulmonary embolism with infarct Congestive heart failure; acute respiratory distress syndrome (ARDS) Interstitial lung disease Bronchoalveolar cell carcinoma Treatment Empiric antibiotics for common organisms after obtaining cultures; initial dose given in the emergency department Hospitalize selected patients: ≥ 2 of the following CURB-65 cri- teria: confusion, blood urea nitrogen > 20 mg/dL, respiratory rate > 30, systolic blood pressure ≤ 90 mm Hg, age ≥ 65, or patients with signiﬁcant comorbidities or a vital sign, laboratory, or radi- ographic abnormality Pneumococcal vaccine to prevent or lessen severity of pneumo- coccal infections Pearl When diplococci thrive within neutrophils on Gram stain, think staphy- lococci, not pneumococci. Reference Niven DJ, Laupland KB. Severe community-acquired pneumonia in adults: cur- rent antimicrobial chemotherapy. Expert Rev Anti Infect Ther 2009;7:69. [PMID: 19622058] 37 38 Current Essentials of Medicine Acute Pulmonary Venous Thromboembolism 2 Essentials of Diagnosis Seen in immobilized patients, congestive heart failure, malig- nancies, hypercoagulable states, and after pelvic trauma or surgery Abrupt onset of dyspnea and anxiety, with or without pleuritic chest pain, cough with hemoptysis; syncope rare Tachycardia, tachypnea most common; loud P2 with right-sided S3 characteristic but unusual Acute respiratory alkalosis and hypoxemia Elevations in brain natriuretic peptide (eg, BNP > 100 pg/mL) and/or troponins portend a worse prognosis and should prompt an echocardiographic evaluation of right ventricular function Quantitative D-dimer has excellent negative predictive value in patients with low clinical pretest probability CT angiogram is the new gold standard and essentially rules out clinically signiﬁcant pulmonary embolism A ventilation-perfusion scan can be done in patients who cannot tolerate contrast dye; results rely on pretest probability Lower-extremity ultrasound demonstrates deep venous thrombo- sis (DVT) in half of patients Rarely, pulmonary angiography required Differential Diagnosis Pneumonia; myocardial infarction Any cause of acute respiratory distress Systemic inﬂammatory response syndrome (SIRS) Treatment Anticoagulation: Acutely with heparin, start warfarin concurrently and continue for a minimum of 6 months (for reversible cause) to lifelong (unprovoked or irreversible cause) Thrombolytic therapy in selected patients with hemodynamic compromise Intravenous ﬁlter placement for selected patients; consider tem- porary ﬁlter if risk of anticoagulation is time-limited Pearl Ten percent of pulmonary emboli originate from upper-extremity veins; there is more endothelial thromboplastin activity than in the leg veins. Reference Todd JL, Tapson VF. Thrombolytic therapy for acute pulmonary embolism: a crit- ical appraisal. Chest 2009;135:1321. [PMID: 19420199] Chapter 2 Pulmonary Diseases 39 Acute Respiratory Distress Syndrome (ARDS) Essentials of Diagnosis 2 Rapid onset of dyspnea and respiratory distress, commonly in setting of trauma, shock, aspiration, or sepsis Tachypnea, fever; crackles heard by auscultation Arterial hypoxemia refractory to supplemental oxygen, frequently requiring positive pressure ventilation; hypercapnia and respiratory acidosis due to increase in dead space fraction and decrease in tidal volume (lungs become stiff and difﬁcult to expand) Diffuse alveolar and interstitial inﬁltrates by radiography, often sparing costophrenic angles No clinical evidence of left atrial hypertension; pulmonary cap- illary wedge pressure < 18 mm Hg Acute lung injury deﬁned by a Pao2:Fio2 ratio < 300; ARDS is deﬁned by Pao2:Fio2 ratio < 200 Differential Diagnosis Cardiogenic pulmonary edema Primary pneumonia due to any cause Diffuse alveolar hemorrhage Acute interstitial pneumonia (ie, Hamman-Rich syndrome) Cryptogenic organizing pneumonia Treatment Mechanical ventilation with supplemental oxygen; positive end- expiratory pressure often required Low-tidal-volume ventilation, using 6 mL/kg predicted body weight, may reduce mortality A conservative ﬂuid strategy targeting an even total body ﬂuid bal- ance (requires daily diuretics) decreases both time on the venti- lator and time in the ICU Supportive therapy including adequate nutrition, vigilance for other organ dysfunction, and prevention of nosocomial compli- cations (eg, catheter-related infection, UTI, ventilator-associated pneumonia, venous thromboembolism, stress gastritis) Mortality rate is 30–60% Pearl As the Swan-Ganz catheter falls from favor, the cardiac echo becomes increasingly important in ruling out a cardiogenic cause of this problem. Reference Tang BM, Craig JC, Eslick GD, Seppelt I, McLean AS. Use of corticosteroids in acute lung injury and acute respiratory distress syndrome: a systematic review and meta-analysis. Crit Care Med 2009;37:1594. [PMID: 19325471] 40 Current Essentials of Medicine Acute Tracheobronchitis 2 Essentials of Diagnosis Poorly deﬁned but common condition characterized by inﬂam- mation of the trachea and bronchi Due to infectious agents (bacteria or viruses) or irritants (eg, dust and smoke) Consider nasal swab for inﬂuenza if constitutional symptoms present Cough is most common symptom; purulent sputum production and malaise common; hemoptysis occasionally Variable rhonchi and wheezing; fever often absent but may be prominent in cases caused by Haemophilus inﬂuenzae Chest x-ray normal Increased incidence in smokers Differential Diagnosis Asthma Pneumonia Foreign body aspiration Inhalation pneumonitis Viral croup Treatment Symptomatic therapy with inhaled bronchodilators, cough sup- pressants Antibiotics not recommended in most; they shorten the disease course by less than 1 day Treat patients with inﬂuenza according to guideline recommen- dations Patients encouraged to quit smoking Pearl Haemophilus inﬂuenzae and Pseudomonas have a tropism for large airways; study the Gram stain carefully in this syndrome, especially absent underlying lung disease. Reference Wenzel RP, Fowler AA 3rd. Clinical practice. Acute bronchitis. N Engl J Med 2006;355:2125. [PMID: 17108344] Chapter 2 Pulmonary Diseases 41 Allergic Bronchopulmonary Mycosis (Formerly Allergic Bronchopulmonary Aspergillosis) 2 Essentials of Diagnosis Caused by allergy to antigens of Aspergillus species or other fungi colonizing the tracheobronchial tree Recurrent dyspnea, unmasked by corticosteroid withdrawal, with history of asthma; cough productive of brownish plugs of sputum Physical examination as in asthma Peripheral eosinophilia, elevated serum IgE level, precipitating antibody to Aspergillus antigen present; positive skin hypersen- sitivity to Aspergillus antigen Inﬁltrate (often ﬂeeting) and central bronchiectasis by chest radi- ography Differential Diagnosis Asthma Bronchiectasis Invasive aspergillosis Churg-Strauss syndrome Chronic obstructive pulmonary disease Treatment Oral corticosteroids often required for several months Inhaled bronchodilators as for attacks of asthma Treatment with itraconazole (for 16 weeks) improves disease control Complications include hemoptysis, severe bronchiectasis, and pulmonary ﬁbrosis Pearl One of at least three ways this fungus causes illness—all different patho- physiologically. Reference de Oliveira E, Giavina-Bianchi P, Fonseca LA, França AT, Kalil J. Allergic bron- chopulmonary aspergillosis’ diagnosis remains a challenge. Respir Med 2007;101:2352. [PMID: 17689062] 42 Current Essentials of Medicine Asbestosis 2 Essentials of Diagnosis History of exposure to dust containing asbestos particles (eg, from work in mining, insulation, construction, shipbuilding) Progressive dyspnea that appears 20–40 years after exposure, rarely pleuritic chest pain Dry inspiratory crackles and clubbing are common; cyanosis and signs of cor pulmonale occasionally seen Interstitial ﬁbrosis is characteristic (lower lung greater than upper); pleural thickening and diaphragmatic calciﬁcation common but nonspeciﬁc; however, the three together with exposure history establish the diagnosis Exudative pleural effusion develops before parenchymal disease High-resolution CT scan often conﬁrmatory

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