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All the authority of the most trusted brand in medical content in a convenient, portable guide
The Harrison’s Manual, derived from most clinically salient content featured in Harrison's Principles of Internal Medicine, 20th Edition, delivers numerous clinical algorithms in one practical, portable resource. The Manual also includes abundant quick reference tables, plus concise text—providing rapid access to bedside information when decisions need to be made quickly. This full color summary guide covers all diseases and conditions commonly seen in inpatient general medicine, so you can be sure to find invaluable content directly to your workflow and practice.

The 20th edition has been updated to reflect the latest clinical developments in medicine.

The Manual truly makes it easy to find what you need at the point of care. The easy-to-navigate chapters cover symptoms/signs, medical emergencies, specific diseases, and care of the hospitalized patient, with a particular focus on:

• Etiology and Epidemiology
• Clinically Relevant Pathophysiology
• Signs and Symptoms
• Differential Diagnosis
• Physical and Laboratory Findings
• Therapeutics
• Practice Guidelines, and more
Jahr:
2019
Auflage:
20th Edition
Verlag:
McGraw Hill
Sprache:
english
Seiten:
1277
ISBN 13:
9781260455342
Datei:
PDF, 34,63 MB
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PIARRISON'S
1

MANUAL OF
MEDICINE
JAMESON
�.----FAUCI
KASPER
HAUSER
LONGO
LOSCALZO

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EDITORS
J. Larry Jameson, MD, PhD

Robert G. Dunlop Professor of Medicine
Dean, Raymond and Ruth Perelman School of Medicine
Executive Vice President, University of Pennsylvania for the
Health System
Philadelphia, Pennsylvania

Anthony S. Fauci, MD

Chief, Laboratory of Immunoregulation
Director, National Institute of Allergy and Infectious Diseases
National Institutes of Health
Bethesda, Maryland

Dennis L. Kasper, MD

William Ellery Channing Professor of Medicine
Professor of Immunology
Department of Immunology
Harvard Medical School
Boston, Massachusetts

Stephen L. Hauser, MD

Robert A. Fishman Distinguished Professor
Department of Neurology
Director, UCSF Weill Institute for Neurosciences
University of California, San Francisco
San Francisco, California

Dan L. Longo, MD

Professor of Medicine
Harvard Medical School
Senior Physician, Brigham and Women’s Hospital
Deputy Editor, New England Journal of Medicine
Boston, Massachusetts

Joseph Loscalzo, MD, PhD

Hersey Professor of the Theory and Practice of Medicine
Harvard Medical School
Chairman, Department of Medicine
Physician-in-Chief, Brigham and Women’s Hospital
Boston, Massachusetts

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EDITORS
J. Larry Jameson, MD, PhD
Anthony S. Fauci, MD
Dennis L. Kasper, MD
Stephen L. Hauser, MD
Dan L. Longo, MD
Joseph Loscalzo, MD, PhD

New York Chicago San Francisco Athens London Madrid
Mexico City Milan New Delhi Singapore Sydney Toronto

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Copyright © 2020, 2016, 2013, 2009, 2005, 2002, 1998, 1995, 1991, 1988 by McGraw-Hill Education.
All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this
publication may be reproduced or distributed in any form or by any means, or stored in a database or
retrieval system, without the prior written permission of the publisher.
ISBN: 978-1-26-045535-9; 
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contract, tort or otherwise.

Contents

Contributors.............................................................................................................. xiii
Preface..........................................................................................................................xv
Acknowledgments................................................................................................... xvii

SECTION 1   Care of the Hospitalized Patient

1
2
3
4
5
6
7
8
9
10

Electrolytes....................................................................................1
Acid-Base Disorders....................................................................16
Diagnostic Imaging in Internal Medicine.....................................22
Procedures Commonly Performed by Internists............................26
Principles of Critical Care Medicine.............................................32
Pain and Its Management............................................................35
Assessment of Nutritional Status.................................................40
Enteral and Parenteral Nutrition..................................................47
Transfusion and Pheresis Therapy................................................49
Palliative and End-of-Life Care...................................................51

SECTION 2  Medical Emergencies

11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29

Cardiovascular Collapse and Sudden Death.................................59
Shock..........................................................................................62
Narcotic Overdose.......................................................................66
Sepsis and Septic Shock...............................................................68
Acute Pulmonary Edema.............................................................71
Acute Respiratory Distress Syndrome..........................................72
Respiratory Failure......................................................................75
Confusion, Stupor, and Coma......................................................76
Stroke..........................................................................................82
Subarachnoid Hemorrhage..........................................................91
Increased Intracranial Pressure and Head Trauma.........................93
Spinal Cord Compression............................................................98
Hypoxic-Ischemic Encephalopathy............................................100
Status Epilepticus......................................................................101
Diabetic Ketoacidosis and Hyperosmolar Coma.........................103
Hypoglycemia............................................................................106
Oncologic Emergencies.............................................................109
Anaphylaxis...............................................................................114
Bites, Venoms, Stings, and Marine Poisonings............................115

v

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vi

CONTENTS

SECTION 3   Common Patient Presentations

30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58

Fever, Hyperthermia, and Rash..................................................127
Generalized Fatigue...................................................................131
Unintentional Weight Loss........................................................135
Chest Pain.................................................................................137
Palpitations...............................................................................141
Dyspnea....................................................................................141
Cyanosis....................................................................................144
Cough and Hemoptysis..............................................................146
Edema.......................................................................................149
Abdominal Pain.........................................................................153
Nausea, Vomiting, and Indigestion.............................................157
Dysphagia.................................................................................161
Diarrhea, Malabsorption, and Constipation...............................166
Gastrointestinal Bleeding...........................................................174
Jaundice and Evaluation of Liver Function.................................178
Ascites.......................................................................................186
Lymphadenopathy and Splenomegaly........................................189
Anemia and Polycythemia..........................................................194
Azotemia and Urinary Abnormalities.........................................197
Pain and Swelling of Joints.........................................................203
Back and Neck Pain...................................................................207
Headache..................................................................................215
Syncope.....................................................................................223
Dizziness and Vertigo................................................................227
Acute Visual Loss and Double Vision.........................................230
Weakness and Paralysis..............................................................234
Tremor and Movement Disorders..............................................237
Aphasia.....................................................................................240
Sleep Disorders..........................................................................242

SECTION 4  Otolaryngology

59 Sore Throat, Earache, and Upper Respiratory Symptoms............247

SECTION 5  Dermatology

60 General Examination of the Skin...............................................255
61 Common Skin Conditions.........................................................258

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CONTENTS

vii

SECTION 6   Hematology and Oncology

62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79

Examination of Blood Smears and Bone Marrow.......................267
Red Blood Cell Disorders..........................................................269
Leukocytosis and Leukopenia....................................................275
Bleeding and Thrombotic Disorders...........................................278
Myeloid Leukemias, Myelodysplasia, and
Myeloproliferative Syndromes....................................................285
Lymphoid Malignancies............................................................296
Skin Cancer...............................................................................309
Head and Neck Cancer..............................................................312
Lung Cancer..............................................................................314
Breast Cancer............................................................................320
Tumors of the Gastrointestinal Tract..........................................325
Genitourinary Tract Cancer.......................................................337
Gynecologic Cancer...................................................................343
Tumors of the Nervous System...................................................347
Prostate Hyperplasia and Carcinoma..........................................352
Cancer of Unknown Primary Site...............................................355
Paraneoplastic Endocrine Syndromes.........................................359
Neurologic Paraneoplastic Syndromes........................................362

SECTION 7  Infectious Diseases

80
81
82
83
84
85
86
87
88
89
90

Growing Threats in Infectious Disease.......................................367
Infections Acquired in Health Care Facilities..............................371
Infections in the Immunocompromised Host.............................376
Infective Endocarditis................................................................387
Intraabdominal Infections..........................................................398
Infectious Diarrheas and Bacterial Food Poisoning.....................403
Sexually Transmitted and Reproductive Tract Infections.............417
Infections of the Skin, Soft Tissues, Joints, and Bones................433
Pneumococcal Infections...........................................................440
Staphylococcal Infections...........................................................444
Streptococcal/Enterococcal Infections, Diphtheria,
and Infections Caused by Other Corynebacteria and
Related Species..........................................................................453
91 Meningococcal and Listerial Infections......................................463
92 Infections Caused by Haemophilus, Bordetella, Moraxella,
and HACEK Group Organisms.................................................467

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viii

CONTENTS

93 Diseases Caused by Gram-Negative Enteric Bacteria
and Pseudomonads....................................................................473
94 Infections Caused by Miscellaneous Gram-Negative Bacilli........483
95 Anaerobic Infections..................................................................490
96 Nocardiosis, Actinomycosis, and Whipple’s Disease...................498
97 Tuberculosis and Other Mycobacterial Infections.......................503
98 Lyme Disease and Other Nonsyphilitic Spirochetal
Infections..................................................................................515
99 Rickettsial Diseases....................................................................521
100 Mycoplasma pneumoniae, Legionella Species, and
Chlamydia pneumoniae....................................................................531
101 Chlamydia trachomatis and Chlamydia psittaci................................535
102 Infections with Herpes Simplex Virus, Varicella-Zoster
Virus, Cytomegalovirus, Epstein-Barr Virus, and
Human Herpesvirus Types 6, 7, and 8.........................................537
103 Influenza and Other Viral Respiratory Diseases.........................551
104 Rubeola, Rubella, Mumps, and Parvovirus Infections.................555
105 Enterovirus Infections...............................................................561
106 Insect- and Animal-Borne Viral Infections.................................564
107 HIV Infection and AIDS...........................................................572
108 Pneumocystis Pneumonia, Candidiasis, and
Other Fungal Infections.............................................................588
109 Overview of Parasitic Infections.................................................606
110 Malaria, Toxoplasmosis, Babesiosis, and
Other Protozoal Infections........................................................610
111 Helminthic Infections and Ectoparasite Infestations..................625

SECTION 8  Cardiology

112
113
114
115
116
117
118
119
120
121
122

Physical Examination of the Heart.............................................639
Electrocardiography...................................................................644
Noninvasive Examination of the Heart.......................................648
Congenital Heart Disease in the Adult.......................................653
Valvular Heart Disease...............................................................658
Cardiomyopathies and Myocarditis............................................666
Pericardial Disease.....................................................................671
Hypertension.............................................................................676
Metabolic Syndrome..................................................................682
ST-Segment Elevation Myocardial Infarction............................684
Unstable Angina and Non-ST-Elevation
Myocardial Infarction................................................................694

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CONTENTS

123
124
125
126
127
128
129

ix

Chronic Stable Angina...............................................................698
Bradyarrhythmias......................................................................703
Tachyarrhythmias......................................................................706
Heart Failure and Cor Pulmonale...............................................715
Diseases of the Aorta.................................................................721
Peripheral Vascular Disease........................................................724
Pulmonary Hypertension...........................................................727

SECTION 9  Pulmonology

130
131
132
133
134
135
136
137
138
139
140

Diagnostic Procedures in Respiratory Disease............................731
Asthma......................................................................................734
Environmental Lung Diseases....................................................738
Chronic Obstructive Pulmonary Disease....................................741
Pneumonia, Bronchiectasis, and Lung Abscess...........................745
Pulmonary Thromboembolism and Deep-Vein Thrombosis.......754
Interstitial Lung Disease............................................................758
Diseases of the Pleura................................................................763
Diseases of the Mediastinum......................................................766
Disorders of Ventilation.............................................................767
Sleep Apnea...............................................................................768

SECTION 10   Nephrology

141
142
143
144
145
146
147

Acute Renal Failure...................................................................771
Chronic Kidney Disease and Uremia..........................................776
Dialysis......................................................................................778
Renal Transplantation................................................................781
Glomerular Diseases..................................................................784
Renal Tubular Disease...............................................................793
Dysuria, Urinary Tract Infections, Bladder Pain, and
Interstitial Cystitis.....................................................................800
148 Nephrolithiasis..........................................................................805
149 Urinary Tract Obstruction.........................................................807

SECTION 11    Gastroenterology

150
151
152
153
154

Peptic Ulcer and Related Disorders............................................811
Inflammatory Bowel Diseases....................................................817
Colonic and Anorectal Diseases.................................................823
Cholelithiasis, Cholecystitis, and Cholangitis.............................828
Pancreatitis................................................................................835

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x

155
156
157
158

CONTENTS

Acute Hepatitis..........................................................................840
Chronic Hepatitis......................................................................847
Cirrhosis and Alcoholic Liver Disease........................................855
Portal Hypertension...................................................................860

SECTION 12    Allergy, Clinical Immunology,
159
160
161
162
163
164
165
166
167
168
169
170

and Rheumatology

Diseases of Immediate-Type Hypersensitivity.............................863
Primary Immune Deficiency Diseases........................................868
Systemic Lupus Erythematosus..................................................871
Rheumatoid Arthritis................................................................873
The Spondyloarthritides............................................................875
Other Connective Tissue Diseases.............................................882
Vasculitis...................................................................................885
Osteoarthritis............................................................................889
Gout, Pseudogout, and Related Diseases....................................891
Other Musculoskeletal Disorders...............................................896
Sarcoidosis.................................................................................899
Amyloidosis...............................................................................901

SECTION 13     Endocrinology and Metabolism

171 Disorders of the Anterior Pituitary and Hypothalamus...............905
172 Diabetes Insipidus and Syndrome of
Inappropriate Antidiuretic Hormone.........................................912
173 Thyroid Gland Disorders...........................................................915
174 Adrenal Gland Disorders...........................................................924
175 Obesity......................................................................................930
176 Diabetes Mellitus......................................................................932
177 Disorders of the Male Reproductive System...............................941
178 Disorders of the Female Reproductive System............................946
179 Hypercalcemia and Hypocalcemia..............................................955
180 Osteoporosis and Osteomalacia..................................................961
181 Hypercholesterolemia and Hypertriglyceridemia........................966
182 Hemochromatosis, Porphyrias, and Wilson’s Disease..................972

SECTION 14    Neurology

183 The Neurologic Examination.....................................................979
184 Seizures and Epilepsy.................................................................987
185 Alzheimer’s Disease and Other Dementias.................................999

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CONTENTS

186
187
188
189
190
191
192
193
194
195
196
197
198

xi

Parkinson’s Disease.................................................................. 1007
Ataxic Disorders...................................................................... 1014
ALS and Other Motor Neuron Diseases.................................. 1017
Autonomic Nervous System Disorders..................................... 1020
Trigeminal Neuralgia, Bell’s Palsy, and
Other Cranial Nerve Disorders................................................ 1027
Spinal Cord Diseases............................................................... 1034
Multiple Sclerosis.................................................................... 1040
Neuromyelitis Optica............................................................... 1048
Acute Meningitis and Encephalitis........................................... 1051
Chronic and Recurrent Meningitis........................................... 1063
Peripheral Neuropathies, Including Guillain-Barré
Syndrome................................................................................ 1073
Myasthenia Gravis................................................................... 1083
Muscle Diseases....................................................................... 1086

SECTION 15    Psychiatry and Substance Abuse

199
200
201
202
203
204

Psychiatric Disorders............................................................... 1097
Psychiatric Medications........................................................... 1105
Eating Disorders...................................................................... 1114
Alcohol Use Disorder............................................................... 1116
Narcotic Abuse........................................................................ 1120
Cocaine and Other Commonly Used Drugs............................. 1122

SECTION 16    Disease Prevention and Health Maintenance

205
206
207
208
209
210

Routine Disease Screening....................................................... 1127
Vaccines................................................................................... 1131
Cardiovascular Disease Prevention........................................... 1133
Prevention and Early Detection of Cancer................................ 1137
Smoking Cessation.................................................................. 1144
Women’s Health...................................................................... 1147

SECTION 17    Adverse Drug Reactions

211 Adverse Drug Reactions.......................................................... 1151
Index 1153

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NOTICE
Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy
are required. The authors and the publisher of this work have checked
with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted
at the time of publication. However, in view of the possibility of human
error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or
publication of this work warrants that the information contained herein
is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of
the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example
and in particular, readers are advised to check the product information
sheet included in the package of each drug they plan to administer to be
certain that the information contained in this work is accurate and that
changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular
importance in connection with new or infrequently used drugs.

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Contributors

ASSOCIATE EDITORS
S. Andrew Josephson, MD

Professor and Chair, Department of Neurology, University of California,
San Francisco, San Francisco, California

Carol A. Langford, MD, MHS

Harold C. Schott Endowed Chair; Director, Center for Vasculitis Care and Research,
Department of Rheumatic and Immunologic Diseases, Cleveland Clinic, Cleveland,
Ohio

Leonard S. Lilly, MD

Professor of Medicine, Harvard Medical School; Chief, Brigham and Women’s/
Faulkner Cardiology, Brigham and Women’s Hospital, Boston, Massachusetts

David B. Mount, MD

Assistant Professor of Medicine, Harvard Medical School; Renal Division, Brigham
and Women’s Hospital, Renal Division, Boston VA Healthcare System, Boston,
Massachusetts

Edwin K. Silverman, MD, PhD

Professor of Medicine, Harvard Medical School; Chief, Channing Division of
Network Medicine, Department of Medicine, Brigham and Women’s Hospital,
Boston, Massachusetts

Neeraj K. Surana, MD, PhD

Assistant Professor in Pediatrics, Molecular Genetics and Microbiology, and
Immunology, Duke University School of Medicine, Durham, North Carolina

Numbers indicate the chapters written or co-written by the contributor.

Anthony S. Fauci, MD

Chief, Laboratory of Immunoregulation; Director, National Institute of Allergy and
Infectious Diseases, National Institutes of Health, Bethesda, Maryland
28, 44, 45, 49, 60, 61, 107, 153–170

Gregory K. Folkers, MPH

Chief of Staff, Office of the Director, National Institute of Allergy and Infectious
Diseases, National Institutes of Health, Bethesda, Maryland
107, 165

Stephen L. Hauser, MD

Robert A. Fishman Distinguished Professor, Department of Neurology; Director,
UCSF Weill Institute for Neurosciences, University of California, San Francisco,
San Francisco, California
4, 6, 13, 18–24, 50–58, 75, 79, 183–204, 209

J. Larry Jameson, MD, PhD

Robert G. Dunlop Professor of Medicine; Dean, Raymond and Ruth Perelman School
of Medicine; Executive Vice President, University of Pennsylvania for the Health
System, Philadelphia, Pennsylvania
3, 4, 7, 8, 25, 26, 31, 32, 120, 171–182, 205, 210

xiii

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xiv

CONTRIBUTORS

S. Andrew Josephson, MD

Professor and Chair, Department of Neurology, University of California,
San Francisco, San Francisco, California
18-21, 23, 51-54, 57, 183–184, 187, 189, 196–202, 209

Dennis L. Kasper, MD

William Ellery Channing Professor of Medicine;
Professor of Immunology, Department of Immunology, Harvard Medical School,
Boston, Massachusetts
14, 29, 30, 59, 80–106, 108–111, 134, 147, 206

Carol A. Langford, MD

Harold C. Schott Endowed Chair; Director, Center for Vasculitis Care and Research,
Department of Rheumatic and Immunologic Diseases, Cleveland Clinic, Cleveland,
Ohio
28, 44, 45, 49, 60, 61, 107, 153–170

Leonard S. Lilly, MD

Professor of Medicine, Harvard Medical School; Chief, Brigham and Women’s/
Faulkner Cardiology, Brigham and Women’s Hospital, Boston, Massachusetts
11, 12, 15, 33, 34, 36, 112–119, 121–129, 207

Dan L. Longo, MD

Professor of Medicine, Harvard Medical School; Senior Physician, Brigham
and Women’s Hospital; Deputy Editor, New England Journal of Medicine, Boston,
Massachusetts
9, 10, 27, 39–43, 46, 47, 62–74, 76–78, 150–152, 208

Joseph Loscalzo, MD, PhD

Hersey Professor of the Theory and Practice of Medicine, Harvard Medical School;
Chairman, Department of Medicine; Physician-in-Chief, Brigham and Women’s
Hospital, Boston, Massachusetts
1, 2, 5, 11, 12, 15–17, 33–38, 48, 112–119, 121–146, 148, 149, 207, 211

David B. Mount, MD

Assistant Professor of Medicine, Harvard Medical School; Renal Division, Brigham
and Women’s Hospital, Renal Division, Boston VA Healthcare System, Boston,
Massachusetts
1, 2, 38, 48, 141–146, 148, 149

Edwin K. Silverman, MD, PhD

Professor of Medicine, Harvard Medical School; Chief, Channing Division of
Network Medicine, Department of Medicine, Brigham and Women’s Hospital,
Boston, Massachusetts
5, 16, 17, 35, 37, 130–133, 135–140

Neeraj K. Surana, MD, PhD

Assistant Professor in Pediatrics, Molecular Genetics and Microbiology, and
Immunology, Duke University School of Medicine, Durham, North Carolina
14, 29, 30, 59, 80–106, 108–111, 134, 147, 206

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Preface

Harrison’s Principles of Internal Medicine (HPIM), the premier medical textbook for
students and clinicians, provides a comprehensive resource for understanding
of the biological and clinical aspects of quality patient care. Harrison’s Manual of
Medicine aims to fulfill a different need: As a concise, fact-rich resource for pointof-care, the Manual presents clinical information drawn from the 20th edition of
HPIM, covering the key features of the diagnosis, clinical manifestations, and
treatment of the major diseases that are likely to be encountered on a medical
inpatient service and in the clinic.
First published 30 years ago, the Manual is well established as a trusted
resource for rapid access to clinically practical information. With each edition,
it is updated by experts and has become ever more useful with the rapid expansion of medical knowledge and the increasing time constraints associated with
heavy patient-care responsibilities in modern health care settings. The Manual’s
popularity and value reflect its abbreviated format, which has proven extremely
useful for initial diagnosis and management in time-restricted clinical settings.
In particular, the book’s full-color format allows readers to locate and use information quickly. In addition, numerous tables and graphics facilitate decisions at
the point of care.
Although not a substitute for in-depth analysis of clinical problems, the
Manual serves as a ready source of informative summaries that will be useful “on
the spot” and that will prepare the reader for more in-depth analysis through
more extensive reading at a later time. Of note, McGraw-Hill’s Access Medicine
website (www.accessmedicine.com) provides online access to both the Manual
and Harrison’s Principles of Internal Medicine, making it very easy to seek additional information when needed. The Manual is also available in a variety of
eBook and app formats.
Like previous editions, this latest edition of the Manual is intended to keep up
with the continual evolution of internal medicine practices. To this end, every
chapter from the prior edition has been closely reviewed and updated, with
substantial revisions and new chapters provided where appropriate. The Editors
learned much in the process of updating the Manual and we hope that you will
find this edition uniquely valuable as a clinical and educational resource.

xv

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Acknowledgments

The Editors and McGraw-Hill wish to thank their editorial staff, whose assistance
and patience made this edition come out in a timely manner:
From the Editors’ offices: Patricia Duffey; Gregory K. Folkers; Andrew
Josephson, MD; H. Clifford Lane, MD; Carol A. Langford, MD; Julie B. McCoy;
Anita Ortiz; Elizabeth Robbins, MD; Marie E. Scurti; and Stephanie Tribuna.
From McGraw-Hill: James F. Shanahan, Kim J. Davis, and Catherine H.
Saggese.
The Editors also wish to acknowledge contributors to past editions of this
Manual, whose work formed the basis for many of the chapters herein: Tamar F.
Barlam, MD; Gerhard P. Baumann, MD; Eugene Braunwald, MD; Punit Chadha,
MD; Joseph B. Martin, MD, PhD; Michael Sneller, MD; Kenneth Tyler, MD;
Sophia Vinogradov, MD; and Jean Wilson, MD.

xvii

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GLOSSARY
A2

aortic second sound

ABGs
arterial blood gases
ACE	
angiotensin-converting
enzyme
AF
atrial fibrillation
AIDS	
acquired immunodeficiency
syndrome
ALS	
amyotrophic lateral
sclerosis
ANA
antinuclear antibody
ARDS	
acute respiratory distress
syndrome
bid
two times daily
biw
twice a week
bp
blood pressure
BUN
blood urea nitrogen
CAPD	
continuous ambulatory
peritoneal dialysis
CBC
complete blood count
CF
complement fixation
CHF
congestive heart failure
CLL	
chronic lymphocytic
leukemia
CML
chronic myeloid leukemia
CMV
cytomegalovirus
CNS
central nervous system
CPK
creatine phosphokinase
CSF
cerebrospinal fluid
CT
computed tomography
CVP
central venous pressure
CXR
chest x-ray
DIC	
disseminated intravascular
coagulation
DVT
deep-venous thrombosis

HMOM20_IFC.indd 1

EBV
Epstein-Barr virus
ECG
electrocardiogram
EEG
electroencephalogram
ELISA	
enzyme-linked
immunosorbent assay
EMG
electromyogram
ENT
ear, nose, and throat
EOM
extraocular movement
ESR	
erythrocyte sedimentation
rate
FDA	
U.S. Food and Drug
Administration
FEV1
forced expiratory volume in
first second
GFR
glomerular filtration rate
GI
gastrointestinal
	

G6PD	
glucose-6-phosphate
dehydrogenase
Hb
hemoglobin
Hct
hematocrit
HDL
high-density lipoprotein
HIV	
human immunodeficiency
virus
hs
at bedtime
HSV
herpes simplex virus
ICU
intensive care unit
IFN
interferon
Ig
immunoglobulin
IL
interleukin
IM
intramuscular
IP
intraperitoneal
IV
intravenous
IVC
inferior vena cava
IVP
intravenous pyelogram

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GLOSSARY
JVP
jugular venous pulse
LA
left atrium
LAD
left-axis deviation
LBBB
left bundle branch block
LDH
lactate dehydrogenase
LDL
low-density lipoprotein
LFT
liver function test
LLQ
left lower quadrant
LP
lumbar puncture
LUQ
left upper quadrant
LV
left ventricle
MI
myocardial infarction
MIC	minimal inhibitory
concentration
MRI	
magnetic resonance
imaging
NPO
nothing by mouth
NSAIDs	
nonsteroidal
anti-inflammatory drugs
P2
pulmonic second sound
PaO2	
partial pressure of O2 in
arterial blood
PAO2	
partial pressure of O2 in
alveolar blood
PCR
polymerase chain reaction
PFTs
pulmonary function tests

PMNs	
polymorphonuclear cells
or leukocytes
PO
by mouth
PPD	
purified protein
derivative, skin test for
tuberculosis
prn
as needed
pt/pts
patient/patients
PT
prothrombin time
PTT	
partial thromboplastin
time

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PVCs	premature ventricular
contractions
QAM
every morning
qd
every day
qh
every hour
qhs
every bedtime
qid
four times daily
qod
every other day
RA
rheumatoid arthritis
RBBB
right bundle branch block
RBC
red blood (cell) count
RLQ
right lower quadrant
RR
respiratory rate
RUQ
right upper quadrant
RV
right ventricle
S1 . . . S4 heart sounds, 1st to 4th
SARS	
severe acute respiratory
syndrome
SC
subcutaneous
SL
sublingual
SLE	
systemic lupus
erythematosus
SVC
superior vena cava
TIA
transient ischemic attack
tid
three times daily
tiw
thrice a week
TLC
total lung capacity
TNF
tumor necrosis factor
UA
urinalysis
URI	
upper respiratory
infection
UTI
urinary tract infection
UV
ultraviolet
VDRL
test for syphilis
VZV
varicella-zoster virus
WBC
white blood (cell) count

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Care of the Hospitalized Patient

1

SECTION 1

Electrolytes

SODIUM
Disturbances of sodium concentration [Na+] result in most cases from abnormalities
of H2O homeostasis, which change the relative ratio of Na+ to H2O. Disorders
of Na+ balance per se are, in contrast, associated with changes in extracellular
fluid volume, either hypo- or hypervolemia. Maintenance of “arterial circulatory integrity” is achieved in large part by changes in urinary sodium excretion
and vascular tone, whereas H2O balance is achieved by changes in both H2O
intake and urinary H2O excretion (Table 1-1). Confusion can result from the
coexistence of defects in both H2O and Na+ balance. For example, a hypovolemic pt may have an appropriately low urinary Na+ due to increased renal
tubular reabsorption of filtered NaCl; a concomitant increase in circulating
arginine vasopressin (AVP)—part of the defense of effective circulating volume
(Table 1-1)—will cause the renal retention of ingested H2O and the development
of hyponatremia.
■■HYPONATREMIA

This is defined as a serum [Na+] <135 mmol/L and is among the most common
electrolyte abnormalities encountered in hospitalized pts. Symptoms include nausea, vomiting, confusion, lethargy, and disorientation; if severe (<120 mmol/L)
and/or abrupt, seizures, central herniation, coma, or death may result (see Acute
Symptomatic Hyponatremia, below). Hyponatremia is almost always the result
of an increase in circulating AVP and/or increased renal sensitivity to AVP;
a notable exception is in the setting of low solute intake (“beer potomania”),
wherein a markedly reduced urinary solute excretion is inadequate to support
the excretion of sufficient free H2O. The serum [Na+] by itself does not yield diagnostic information regarding total-body Na+ content; hyponatremia is primarily

TABLE 1-1 Osmoregulation versus Volume Regulation
What is sensed
Sensors

OSMOREGULATION
Plasma osmolality
Hypothalamic
osmoreceptors

Effectors

AVP
Thirst

What is affected

Urine osmolality
H2O intake

VOLUME REGULATION
Arterial filling
Carotid sinus
Afferent arteriole
Atria
Sympathetic nervous system
Renin-angiotensin-aldosterone system
ANP/BNP
AVP
Urinary sodium excretion
Vascular tone

Note: See text for details.
Abbreviations: ANP, atrial natriuretic peptide; AVP, arginine vasopressin; BNP, brain
natriuretic peptide.
Source: Adapted from Rose BD, Black RM (eds): Manual of Clinical Problems in
Nephrology. Boston, Little Brown, 1988.

1

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a disorder of H2O homeostasis. Pts with hyponatremia are thus categorized diagnostically into three groups, depending on their clinical volume status: hypovolemic, euvolemic, and hypervolemic hyponatremia (Fig. 1-1). All three forms of
hyponatremia share an exaggerated, “nonosmotic” increase in circulating AVP,
in the setting of reduced serum osmolality. Notably, hyponatremia is often multifactorial; clinically important nonosmotic stimuli that can cause a release of AVP
and increase the risk of hyponatremia include drugs, pain, nausea, and strenuous exercise.
Laboratory investigation of a pt with hyponatremia should include a measurement of serum osmolality to exclude “pseudohyponatremia” due to hyperlipidemia or hyperproteinemia. Serum glucose also should be measured; serum [Na+]
falls by approximately 1.4 mM for every 100-mg/dL increase in glucose, due
to glucose-induced H2O efflux from cells. Hyperkalemia may suggest adrenal
insufficiency or hypoaldosteronism; increased blood urea nitrogen (BUN) and
creatinine may suggest a renal cause. Urine electrolytes and osmolality are also
critical tests in the initial evaluation of hyponatremia. In particular, a urine Na+
<20 meq/L is consistent with hypovolemic hyponatremia in the clinical absence
of a “hypervolemic,” Na+-avid syndrome such as congestive heart failure (CHF)
(Fig. 1-1). Urine osmolality <100 mosmol/kg is suggestive of polydipsia or, in
rare cases, of decreased solute intake; urine osmolality >400 mosmol/kg suggests that AVP excess is playing a more dominant role, whereas intermediate
values are more consistent with multifactorial pathophysiology (e.g., AVP excess
with a component of polydipsia). Finally, in the right clinical setting, thyroid,
adrenal, and pituitary function should also be tested.
Hypovolemic Hyponatremia

Hypovolemia from both renal and extrarenal causes is associated with hyponatremia. Renal causes of hypovolemia include primary adrenal insufficiency
and hypoaldosteronism, salt-losing nephropathies (e.g., reflux nephropathy,
nonoliguric acute tubular necrosis), diuretics, and osmotic diuresis. Random
“spot” urine Na+ is typically >20 meq/L in these cases but may be <20 meq/L in
diuretic-associated hyponatremia if tested long after administration of the drug.
Nonrenal causes of hypovolemic hyponatremia include GI loss (e.g., vomiting,
diarrhea, tube drainage) and integumentary loss (sweating, burns); urine Na+ is
typically <20 meq/L in these cases.
Hypovolemia causes profound neurohumoral activation, inducing systems that preserve arterial circulatory integrity, such as the renin-angiotensinaldosterone (RAA) axis, the sympathetic nervous system, and AVP (Table 1-1).
The increase in circulating AVP serves to increase the retention of ingested-free
H2O, leading to hyponatremia. The optimal treatment of hypovolemic hyponatremia is volume administration, generally as isotonic crystalloid, i.e., 0.9% NaCl
(“normal saline”). If the history suggests that hyponatremia has been “chronic,”
i.e., present for 48 h, care should be taken to avoid overcorrection (see below),
which can easily occur as AVP levels plummet in response to volume-resuscitation; if necessary, the administration of desmopressin (DDAVP) and free water
can reinduce or arrest the correction of hyponatremia (see below). An alternative
strategy is to “clamp” AVP bioactivity by administering DDAVP while correcting the serum [Na+] with hypertonic saline in a more controlled, linear fashion.
Hypervolemic Hyponatremia

The edematous disorders (CHF, hepatic cirrhosis, and nephrotic syndrome)
are often associated with mild to moderate degrees of hyponatremia ([Na+] =
125–135 mmol/L); occasionally, pts with severe CHF or cirrhosis may present
with serum [Na+] <120 mmol/L. The pathophysiology is similar to that in hypovolemic hyponatremia, except that arterial filling and circulatory integrity are

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HMOM20_Sec01_p0001-p0058.indd 3

Assessment of volume status

Euvolemia (no edema)
• Total body water ↑
• Total body sodium ←→

Hypovolemia
• Total body water ↓
• Total body sodium ↓↓

UNa >20

Renal losses
Diuretic excess
Mineral corticoid deficiency
Salt-losing deficiency
Bicarbonaturia with
renal tubal acidosis and
metabolic alkalosis
Ketonuria
Osmotic diuresis
Cerebral salt wasting
syndrome

Extrarenal losses
Vomiting
Diarrhea
Third spacing of fluids
Burns
Pancreatitis
Trauma

Glucocorticoid deficiency
Hypothyroidism
Stress
Drugs
Syndrome of inappropriate
antidiuretic hormone
secretion

UNa >20

Acute or chronic
renal failure

UNa <20

Nephrotic syndrome
Cirrhosis
Cardiac failure

CHAPTER 1

UNa <20

Electrolytes

UNa >20

Hypervolemia
• Total body water ↑↑
• Total body sodium ↑

3

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FIGURE 1-1 The diagnostic approach to hyponatremia. See text for details. (Reprinted from Kumar S, Berl T: Diseases of water metabolism. In: Atlas of Diseases of the
Kidney, Vol I, Schrier RW [ed]. Philadelphia, Current Medicine, Inc, 1999; with permission.)

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decreased due to the specific etiologic factors, i.e., cardiac dysfunction, peripheral vasodilation in cirrhosis, and hypoalbuminemia in nephrotic syndrome.
The degree of hyponatremia is an indirect index of the associated neurohumoral
activation (Table 1-1) and an important prognostic indicator in hypervolemic
hyponatremia.
Management consists of treatment of the underlying disorder (e.g., afterload
reduction in heart failure, intravenous administration of albumin in cirrhosis,
immunomodulatory therapy in some forms of nephrotic syndrome), Na+ restriction, diuretic therapy, and, in some pts, H2O restriction. Vasopressin antagonists
(e.g., tolvaptan and conivaptan) are also effective in normalizing hypervolemic
hyponatremia associated with CHF; hepatic toxicity of tolvaptan limits its clinical utility in cirrhosis.
Euvolemic Hyponatremia

The syndrome of inappropriate ADH secretion (SIADH) characterizes most cases
of euvolemic hyponatremia. Other causes of euvolemic hyponatremia include
hypothyroidism and secondary adrenal insufficiency due to pituitary disease;
notably, repletion of glucocorticoid levels in the latter may cause a rapid drop in
circulating AVP levels and overcorrection of serum [Na+] (see below).
Common causes of SIADH include pulmonary disease (e.g., pneumonia,
tuberculosis, pleural effusion) and central nervous system (CNS) diseases (e.g.,
tumor, subarachnoid hemorrhage, meningitis); SIADH also occurs with malignancies (primarily small cell carcinoma of the lung) and drugs (e.g., selective
serotonin reuptake inhibitors, tricyclic antidepressants, nicotine, vincristine,
carbamazepine, narcotic analgesics, antipsychotic drugs, cyclophosphamide,
ifosfamide). Optimal treatment of euvolemic hyponatremia includes treatment
of the underlying disorder. H2O restriction to <1 L/d is a cornerstone of therapy,
but may be ineffective or poorly tolerated. However, vasopressin antagonists are
predictably effective in normalizing serum [Na+] in SIADH. Alternatives include
the administration of loop diuretics to inhibit the countercurrent mechanism
and reduce urinary concentration, combined with oral salt tablets to abrogate
diuretic-induced salt loss and attendant hypovolemia. More recently, a palatable
form of oral urea has become available; oral urea is equivalent to tolvaptan in
the management of SIADH, increasing urinary solute (urea) and, thus, urinary
H2O excretion.
Acute Symptomatic Hyponatremia

Acute symptomatic hyponatremia is a medical emergency; a sudden drop in
serum [Na+] can overwhelm the capacity of the brain to regulate cell volume,
leading to cerebral edema, seizures, and death. Women, particularly premenopausal women, are particularly prone to such sequelae; neurologic consequences
are comparatively rare in male pts. Many of these pts develop hyponatremia
from iatrogenic causes, including hypotonic fluids in the postoperative period,
prescription of a thiazide diuretic, colonoscopy preparation, or intraoperative
use of glycine irrigants. Polydipsia with an associated cause of increased AVP
may also cause acute hyponatremia, as can increased H2O intake in the setting
of strenuous exercise, e.g., a marathon. The recreational drug Ecstasy (methylenedioxymethamphetamine [MDMA]) can cause acute hyponatremia, rapidly
inducing both AVP release and increased thirst.
Severe symptoms may occur at relatively modest levels of serum [Na+], e.g.,
in the mid-120s. Nausea and vomiting are common premonitory symptoms of
more severe sequelae. An important concomitant is respiratory failure, which
may be hypercapnic due to CNS depression or normocapnic due to neurogenic,
noncardiogenic pulmonary edema; the attendant hypoxemia amplifies the
impact of hyponatremic encephalopathy.

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Electrolytes

CHAPTER 1

5

TREATMENT

Hyponatremia
Three considerations are critical in the therapy of hyponatremia. First, the presence, absence, and/or severity of symptoms determine the urgency of therapy
(see above for acute symptomatic hyponatremia). Second, pts with hyponatremia
that has been present for >48 h (“chronic hyponatremia”) are at risk for osmotic
demyelination syndrome, typically central pontine myelinolysis, if serum Na+ is
corrected by >10–12 mM within the first 24 h and/or by >18 mM within the first
48 h. Third, the response to interventions, such as hypertonic saline or vasopressin antagonists, can be highly unpredictable, such that frequent monitoring of
serum Na+ (initially every 2–4 h) is imperative.
Treatment of acute symptomatic hyponatremia should include hypertonic
saline to acutely increase serum Na+ by 1–2 mM/h to a total increase of 4–6 mM;
this increase is typically sufficient to alleviate acute symptoms from cerebral
edema, after which corrective guidelines for “chronic” hyponatremia are appropriate (see below). A number of equations and algorithms have been developed
to estimate the required rate of hypertonic solution; one popular approach is
to calculate a “Na+ deficit,” where the Na+ deficit = 0.6 × body weight × (target
[Na+] – starting [Na+]). Regardless of the method used to determine the rate of
administered hypertonic saline, the increase in serum [Na+] can be highly unpredictable, due to rapid changes in the underlying physiology; serum [Na+] should
be monitored every 2–4 h during and after treatment with hypertonic saline. The
administration of supplemental O2 and ventilatory support can also be critical
in acute hyponatremia, if pts develop acute pulmonary edema or hypercapnic
respiratory failure. IV loop diuretics will help treat associated acute pulmonary
edema and will also increase free H2O excretion by interfering with the renal
countercurrent multiplier system. It is noteworthy that vasopressin antagonists
do not have a role in the management of acute hyponatremia.
The rate of correction should be comparatively slow in chronic hyponatremia
(<10–12 mM in the first 24 h and <18 mM in the first 48 h), so as to avoid osmotic
demyelination syndrome. Vasopressin antagonists are highly effective in SIADH
and in hypervolemic hyponatremia due to heart failure. Abnormalities in liver
function tests have been reported during the use of tolvaptan, prohibiting use in
cirrhosis; in pts without preexisting liver disease, therapy with this agent should
be restricted to 1–2 months with close monitoring of liver function. Should pts
overcorrect serum [Na+] in response to vasopressin antagonists, hypertonic
saline, or isotonic saline (in chronic hypovolemic hyponatremia), hyponatremia
can be safely reinduced or stabilized by the administration of the vasopressin
agonist DDAVP and the administration of free H2O, typically IV D5W; again,
close monitoring of the response of serum [Na+] is essential to adjust therapy.
Alternatively, the treatment of pts with marked hyponatremia can be initiated with the twice-daily administration of DDAVP to maintain constant AVP
bioactivity, combined with the administration of hypertonic saline to slowly correct the serum [Na+] in a more controlled fashion, thus reducing upfront the risk
of overcorrection.
■ HYPERNATREMIA

This is rarely associated with hypervolemia, where the association is typically iatrogenic, e.g., administration of hypertonic sodium bicarbonate. More commonly,
hypernatremia is the result of a combined H2O and volume deficit, with losses of
H2O in excess of Na+. Elderly individuals with reduced thirst and/or diminished
access to fluids are at the highest risk of hypernatremia due to decreased free

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TABLE 1-2 Correction of Hypernatremia
H2O Deficit
1. Estimate TBW: 50–60% body weight (kg) depending on body composition
2. Calculate free-water deficit: [(Na+ – 140)/140] × TBW
3. Administer deficit over 48–72 h
Ongoing H2O Losses
4. Calculate free-water clearance, CeH2O:

U + UK 
CeH2O = V  1 − Na
SNa 

where V is urinary volume, UNa is urinary [Na+], UK is urinary [K+], and SNa is serum
[Na+].
Insensible Losses
5. ∼10 mL/kg per day: less if ventilated, more if febrile
Total
6. Add components to determine H2O deficit and ongoing H2O loss; correct the
H2O deficit over 48–72 h and replace daily H2O loss.
Abbreviation: TBW, total-body water.

H2O intake. Common causes of renal H2O loss are osmotic diuresis secondary to
hyperglycemia, postobstructive diuresis, or drugs (radiocontrast, mannitol, etc.);
H2O diuresis occurs in central or nephrogenic diabetes insipidus (DI) (Chap. 172).
In pts with hypernatremia due to renal loss of H2O, it is critical to quantify ongoing
daily losses in addition to calculation of the baseline H2O deficit (Table 1-2).
TREATMENT

Hypernatremia
The approach to correction of hypernatremia is outlined in Table 1-2. As with
hyponatremia, it is advisable to correct the H2O deficit slowly to avoid neurologic compromise, decreasing the serum [Na+] over 48–72 h. Depending on the
blood pressure or clinical volume status, it may be appropriate to initially treat
with hypotonic saline solutions (1/4 or 1/2 normal saline); blood glucose should
be monitored in pts treated with large volumes of D5W, should hyperglycemia
ensue. Calculation of urinary electrolyte-free H2O clearance is helpful to estimate
daily, ongoing loss of free H2O in pts with nephrogenic or central DI (Table 1-2).
Other forms of therapy may be helpful in selected cases of hypernatremia, once
water deficits have been repleted. Pts with central DI may respond to the administration of intranasal DDAVP. Stable pts with nephrogenic DI may reduce their
polyuria with hydrochlorothiazide (12.5–50 mg/d). This diuretic is thought to
increase proximal H2O reabsorption and decrease distal solute delivery, thus
reducing polyuria. Pts with lithium-associated nephrogenic DI may respond
to amiloride (2.5–10 mg/d), which decreases the entry of lithium into principal
cells in the distal nephron by inhibiting the amiloride-sensitive epithelial sodium
channel (ENaC). Notably, however, most pts with lithium-induced nephrogenic
DI can adequately accommodate by increasing their H2O intake. Occasionally,
nonsteroidal anti-inflammatory drugs (NSAIDs) or COX-2 inhibitors have also
been used to treat polyuria associated with nephrogenic DI, reducing the negative
effect of local prostaglandins on urinary concentration; however, the nephrotoxic
potential of these drugs typically makes them a less attractive therapeutic option.

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Electrolytes

CHAPTER 1

7

POTASSIUM
Because potassium (K+) is the major intracellular cation, discussion of disorders
of K+ balance must take into consideration changes in the exchange of intra- and
extracellular K+ stores. (Extracellular K+ constitutes <2% of total-body K+ content.)
Insulin, β2-adrenergic agonists, and alkalosis tend to promote K+ uptake by cells;
acidosis, insulinopenia, or acute hyperosmolality (e.g., after treatment with mannitol or D50W) promotes the efflux or reduced uptake of K+. A corollary is that
tissue necrosis and the attendant release of K+ can cause severe hyperkalemia,
particularly in the setting of acute kidney injury. Hyperkalemia due to rhabdomyolysis is thus particularly common, due to the enormous store of K+ in muscle; hyperkalemia may also be prominent in tumor lysis syndrome.
The kidney plays a dominant role in K+ excretion. Although K+ is transported
along the entire nephron, it is the principal cells of the connecting segment and
cortical collecting duct that play a dominant role in K+ excretion. Apical Na+
entry into principal cells via the amiloride-sensitive ENaC generates a lumennegative potential difference, which drives passive K+ exit through apical K+
channels. This relationship is key to the bedside understanding of potassium disorders.
For example, decreased distal delivery of Na+ tends to blunt the ability to excrete
K+, leading to hyperkalemia. Abnormalities in the renin-angiotensin-aldosterone
system (RAAS) can cause both hypo- and hyperkalemia; aldosterone has a major
influence on potassium excretion, increasing the activity of ENaC channels and
the basolateral Na+/K+-ATPase, thus amplifying the driving force for K+ secretion across the luminal membrane of principal cells.
■■HYPOKALEMIA

Major causes of hypokalemia are outlined in Table 1-3. Atrial and ventricular
arrhythmias are the most serious health consequences of hypokalemia. Pts with
concurrent Mg deficit and/or digoxin therapy are at a particularly increased risk
of arrhythmias. Hypokalemia can directly prolong the QT interval and is a significant cofactor in arrhythmias due to other causes of a prolonged QT interval.
Other clinical manifestations include muscle weakness, which may be profound
at serum [K+] <2.5 mmol/L, and, if hypokalemia is sustained, hypertension,
ileus, polyuria, renal cysts, and even renal failure.
The cause of hypokalemia is usually obvious from history, physical examination, and/or basic laboratory tests. However, persistent hypokalemia may
require a more thorough, systematic evaluation (Fig. 1-2). Initial laboratory evaluation should include electrolytes, BUN, creatinine, serum osmolality, Mg2+, and
Ca2+, a complete blood count, and urinary pH, osmolality, creatinine, and electrolytes. Serum and urine osmolality are required for calculation of the transtubular
K+ gradient (TTKG), which should be <3 in the presence of hypokalemia (see also
Hyperkalemia). Alternatively, a urinary K+-to-creatinine ratio of >13-mmol/g
creatinine (>1.5-mmol/mmol creatinine) is compatible with excessive K+ excretion. Further tests such as urinary Mg2+ and Ca2+ and/or plasma renin and aldosterone levels may be necessary in specific cases.
TREATMENT

Hypokalemia
The goals of therapy in hypokalemia are to prevent life-threatening and/or
serious chronic consequences, to replace the associated K+ deficit, and to correct the underlying cause and/or mitigate future hypokalemia. The urgency
of therapy depends on the severity of hypokalemia, associated clinical factors
(cardiac disease, digoxin therapy, etc.), and the rate of decline in serum K+. Pts
with a prolonged QT interval and/or other risk factors for arrhythmia should

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TABLE 1-3 Causes of Hypokalemia
I. Decreased intake
A. Starvation
B. Clay ingestion
II. Redistribution into cells
A. Acid-base
1. Metabolic alkalosis
B. Hormonal
1. Insulin
2. Increased β2-adrenergic sympathetic activity: post–myocardial infarction,
head injury, theophylline
3. β2-Adrenergic agonists: bronchodilators, tocolytics
4. α-Adrenergic antagonists
5. Thyrotoxic periodic paralysis
6. Downstream stimulation of Na+/K+-ATPase: theophylline, caffeine
C. Anabolic state
1. Vitamin B12 or folic acid administration (red blood cell production)
2. Granulocyte-macrophage colony-stimulating factor (white blood cell
production)
3. Total parenteral nutrition
D. Other
1. Pseudohypokalemia
2. Hypothermia
3. Familial hypokalemic periodic paralysis
4. Barium toxicity: systemic inhibition of “leak” K+ channels
III. Increased loss
A. Nonrenal
1. Gastrointestinal loss (diarrhea)
2. Integumentary loss (sweat)
B. Renal
1. Increased distal flow and distal Na+ delivery: diuretics, osmotic diuresis,
salt-wasting nephropathies
2. Increased secretion of potassium
a. Mineralocorticoid excess: primary hyperaldosteronism (APAs),
PAH or UAH, IHA due to bilateral adrenal hyperplasia and adrenal
carcinoma, familial hyperaldosteronism (FH-I, FH-II, congenital
adrenal hyperplasias), secondary hyperaldosteronism (malignant
hypertension, renin-secreting tumors, renal artery stenosis,
hypovolemia), Cushing’s syndrome, Bartter’s syndrome, Gitelman’s
syndrome
b. Apparent mineralocorticoid excess: genetic deficiency of
11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid
excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/
glycyrrhizinic acid and/or carbenoxolone; licorice, food products,
drugs), Liddle’s syndrome (genetic activation of ENaC)
(Continued)

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Electrolytes

CHAPTER 1

9

TABLE 1-3 Causes of Hypokalemia (Continued)
c. Distal delivery of nonreabsorbed anions: vomiting, nasogastric
suction, proximal renal tubular acidosis, diabetic ketoacidosis, glue
sniffing (toluene abuse), penicillin derivatives (penicillin, nafcillin,
dicloxacillin, ticarcillin, oxacillin, and carbenicillin)
3. Magnesium deficiency, amphotericin B, Liddle’s syndrome
Abbreviations: APA, aldosterone-producing adenoma; ENaC, epithelial Na+ channels;
IHA, idiopathic hyperaldosteronism; PAH, primary adrenal hyperplasia; UAH, unilateral
adrenal hyperplasia.

be monitored by continuous cardiac telemetry during repletion. Urgent but
cautious K+ replacement should be considered in pts with severe redistributive
hypokalemia (plasma K+ concentration <2.5 mM) and/or when serious complications ensue; however, this approach has a risk of rebound hyperkalemia following acute resolution of the underlying cause. When excessive activity of the
sympathetic nervous system is thought to play a dominant role in redistributive
hypokalemia, as in thyrotoxic periodic paralysis, theophylline overdose, and
acute head injury, high-dose propranolol (3 mg/kg) should be considered; this
nonspecific β-adrenergic blocker will correct hypokalemia without the risk of
rebound hyperkalemia. It should be noted that hypokalemia is refractory to correction in the presence of Mg++ deficiency, which also should be corrected when
present; renal wasting of both cations may be particularly prominent after renal
tubular injury, e.g., from cisplatin nephrotoxicity.
Oral replacement with K+-Cl− is the mainstay of therapy in hypokalemia.
Potassium phosphate, oral or IV, may be appropriate in pts with combined hypokalemia and hypophosphatemia. Potassium bicarbonate or potassium citrate
should be considered in pts with concomitant metabolic acidosis. The deficit of
K+ and the rate of correction should be estimated as accurately as possible; renal
function, medications, and comorbid conditions such as diabetes should also be
considered so as to gauge the risk of overcorrection. In the absence of abnormal
K+ redistribution, the total deficit correlates with serum K+ such that serum K+
drops by approximately 0.27 mM for every 100-mmol reduction in total-body
stores. Notably, given the delay in redistributing potassium into intracellular
compartments, this deficit must be replaced gradually over 24–48 h, with frequent monitoring of plasma K+ concentration to avoid transient over-repletion
and transient hyperkalemia if otherwise appropriate. If hypokalemia is severe
(<2.5 mmol/L) and/or if oral supplementation is not feasible or tolerated, IV
KCl can be administered through a central vein with cardiac monitoring in an
intensive care setting, at rates that should not exceed 20 mmol/h. KCl should
always be administered in saline solutions, rather than dextrose; the dextroseinduced increase in insulin can acutely exacerbate hypokalemia.
Strategies to minimize K+ losses should also be considered. These measures may
include minimizing the dose of non-K+-sparing diuretics, restricting Na+ intake,
and using clinically appropriate combinations of non-K+-sparing and K+-sparing
medications (e.g., loop diuretics with angiotensin-converting enzyme inhibitors).
■■HYPERKALEMIA

Causes are outlined in Table 1-4; in most cases, hyperkalemia is due to decreased
renal K+ excretion. However, increases in dietary K+ intake can have a major
effect in susceptible pts, e.g., diabetics with hyporeninemic hypoaldosteronism
and chronic kidney disease (CKD). Drugs that impact on the RAA axis are also a
major cause of hyperkalemia.

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10

Yes

Hypokalemia (Serum K+ <3.5 mmol/L)

Emergency?

Pseudohypokalemia?

No
Yes

Clear evidence
of low intake

History, physical examination,
and basic laboratory tests

Clear evidence of
transcellular shift
No

Urine K+

<15 mmol/day OR <15 mmol/g Cr

>15 mmol/g Cr OR >15 mmol/day

Extrarenal loss/remote renal loss

Renal loss

Acid-base status

TTKG
>4

Normal
-Profuse
sweating

Yes

Treat
accordingly

No

No

Metabolic acidosis
-GI K+ loss

No further
workup

Metabolic alkalosis
-Remote diuretic use
-Remote vomiting or
stomach drainage
-Profuse sweating

↑ Distal K+ secretion
BP and/or volume

-Insulin excess
-β2-adrenergic agonists
-FHPP
-Hyperthyroidism
-Barium intoxication
-Theophylline
-Chloroquine

<2
↑ Tubular flow
-Osmotic diuresis

Care of the Hospitalized Patient

Treat accordingly
and reevaluate

Yes

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HMOM20_Sec01_p0001-p0058.indd 11

Non-reabsorbable
anions other than
HCO3–
-Hippurate
-Penicillins

Variable

Low OR normal

High

Acid-base status

Aldosterone

Metabolic acidosis
-Proximal RTA
-Distal RTA
-DKA
-Amphotericin B
-Acetazolamide

Metabolic alkalosis

High

Low

Urine Cl– (mmol/L)

Renin

Cortisol

>20

<10

Urine Ca/Cr
(molar ratio)

-Vomiting
-Chloride
diarrhea
<0.15

-Loop diuretic
-Bartter’s syndrome

-Thiazide diuretic
-Gitelman’s syndrome

Low

High

Normal

-RAS
-RST
-Malignant HTN

-PA
-FH-I

-Cushing’s
syndrome

-Liddle’s syndrome
-Licorice
-SAME

CHAPTER 1

FIGURE 1-2 The diagnostic approach to hypokalemia. See text for details. bp, blood pressure; DKA, diabetic ketoacidosis; FH-I, familial hyperaldosteronism type I;
FHPP, familial hypokalemic periodic paralysis; HTN, hypertension; PA, primary aldosteronism; RAS, renal artery stenosis; RST, renin-secreting tumor; RTA, renal tubular
acidosis; SAME, syndrome of apparent mineralocorticoid excess; TTKG, transtubular potassium gradient. (Reprinted with permission from Mount DB, Zandi-Nejad K:
Disorders of potassium balance. In: Brenner and Rector’s The Kidney, 8th ed, Brenner BM [ed]. Philadelphia, Saunders, 2008.)

Electrolytes

>0.20

High

11

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TABLE 1-4 Causes of Hyperkalemia
I. “Pseudo” hyperkalemia
A. Cellular efflux: thrombocytosis, erythrocytosis, leukocytosis, in vitro hemolysis
B. Hereditary defects in red cell membrane transport
II. Intra- to extracellular shift
A. Acidosis
B. Hyperosmolality; radiocontrast, hypertonic dextrose, mannitol
C. β-Adrenergic antagonists (noncardioselective agents)
D. Digoxin and related glycosides (yellow oleander, foxglove, bufadienolide)
E. Hyperkalemic periodic paralysis
F. Lysine, arginine, and ε-aminocaproic acid (structurally similar, positively
charged)
G. Succinylcholine; thermal trauma, neuromuscular injury, disuse atrophy,
mucositis, or prolonged immobilization
H. Rapid tumor lysis
III. Inadequate excretion
A. Inhibition of the renin-angiotensin-aldosterone axis; ↑ risk of hyperkalemia
when used in combination or at higher than recommended dosages
1. ACE inhibitors
2. Renin inhibitors: aliskiren (in combination with ACE inhibitors or ARBs)
3. ARBs
4. Blockade of the mineralocorticoid receptor: spironolactone, eplerenone,
drospirenone
5. Blockade of ENaC: amiloride, triamterene, trimethoprim, pentamidine,
nafamostat
B. Decreased distal delivery
1. Congestive heart failure
2. Volume depletion
C. Hyporeninemic hypoaldosteronism
1. Tubulointerstitial diseases: SLE, sickle cell anemia, obstructive uropathy
2. Diabetes, diabetic nephropathy
3. Drugs: nonsteroidal anti-inflammatory drugs, COX-2 inhibitors, β blockers,
cyclosporine, tacrolimus
4. Chronic kidney disease, advanced age
5. Pseudohypoaldosteronism type II: defects in WNK1 or WNK4 kinases,
Kelch-like 3 (KLHL3), or Cullin 3 (CUL3)
D. Renal resistance to mineralocorticoid
1. Tubulointerstitial diseases: SLE, amyloidosis, sickle cell anemia,
obstructive uropathy, post–acute tubular necrosis
2. Hereditary: pseudohypoaldosteronism type I: defects in the
mineralocorticoid receptor or ENaCE. Advanced renal insufficiency with
low GFR
E. Advanced renal insufficiency with low GFR
1. Chronic kidney disease
2. End-stage renal disease
3. Acute oliguric kidney injury
F. Primary adrenal insufficiency
1. Autoimmune: Addison’s disease, polyglandular endocrinopathy
2. Infectious: HIV, cytomegalovirus, tuberculosis, disseminated fungal infection
3. Infiltrative: amyloidosis, malignancy, metastatic cancer
4. Drug-associated: heparin, low-molecular-weight heparin
5. Hereditary: adrenal hypoplasia congenita, congenital lipoid adrenal
hyperplasia, aldosterone synthase deficiency
6. Adrenal hemorrhage or infarction, including in antiphospholipid syndrome
Abbreviations: ARB, angiotensin receptor blocker; COX-2, cyclooxygenase 2; ENaC,
epithelial Na+ channels.

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Electrolytes

Emergency
therapy

Yes

K+ ≥6.0
or ECG
changes

Hyperkalemia
(Serum K+

Yes

13

No further
action

No

Evidence of
increased
potassium
load

History, physical
examination,
and basic
laboratory tests

Evidence of
transcellular
shift

No

Treat
accordingly
and
reevaluate

Yes

No
-Hypertonicity
(e.g., mannitol)
-Hyperglycemia
-Succinylcholine
-ε-Aminocaproic acid
-Digoxin
-β-Blockers
-Metabolic acidosis
(non-organic)
-Arginine or lysine
infusion
-Hyperkalemic periodic
paralysis
-↓Insulin
-Exercise

Decreased urinary K+ excretion
(<40 mmol/d)
Decreased
distal
Na+ delivery

Yes

Pseudohyperkalemia?

≥5.5 mmol/L)

No
Treat
accordingly
and
reevaluate

CHAPTER 1

Urine Na+
<25 mmol/L

Urine
electrolytes

TTKG
>8

<5

Reduced tubular
flow

Reduced distal K+ secretion
(GFR >20 mL/min)
9α-Fludrocortisone

Advanced
kidney
failure
(GFR ≤20 mL/min)

Reduced
ECV

TTKG ≥8

TTKG <8
(tubular
resistance)

Low aldosterone
Renin

Drugs
-Amiloride
-Spironolactone
-Triamterene
-Trimethoprim
-Pentamidine
-Eplerenone
-Drospirenone
-Calcineurin
inhibitors

Other causes
-Tubulointerstitial
diseases
-Urinary tract
obstruction
-PHA type I
-PHA type II
-Sickle cell disease
-Renal transplant
-SLE

High
-Primary adrenal
insufficiency
-Isolated aldosterone
deficiency
-Heparin/LMW
heparin
-ACE-I/ARB
-Ketoconazole

Low
-Diabetes mellitus
-Acute GN
-Tubulointerstitial
diseases
-PHA type II
-NSAIDs
-β-Blockers

FIGURE 1-3 The diagnostic approach to hyperkalemia. See text for details. ACEI,
angiotensin-converting enzyme inhibitor; acute GN, acute glomerulonephritis; ARB,
angiotensin II receptor blocker; ECV, effective circulatory volume; LMW heparin,
low-molecular-weight heparin; PHA, pseudohypoaldosteronism; TTKG, transtubular
potassium gradient. (Reprinted with permission from Mount DB, Zandi-Nejad K:
Disorders of potassium balance. In: Brenner and Rector’s The Kidney, 8th ed, Brenner
BM [ed]. Philadelphia, Saunders, 2008.)

The first priority in the management of hyperkalemia is to assess the need
for emergency treatment (ECG changes and/or K+ ≥6.0 mM). This should be followed by a comprehensive workup to determine the cause (Fig. 1-3). History
and physical examination should focus on medications (e.g., ACE inhibitors,
NSAIDs, trimethoprim/sulfamethoxazole), diet and dietary supplements (e.g.,
salt substitute), risk factors for acute kidney failure, reduction in urine output,
blood pressure, and volume status. Initial laboratory tests should include electrolytes, BUN, creatinine, serum osmolality, Mg2+, and Ca2+, a complete blood
count, and urinary pH, osmolality, creatinine, and electrolytes. A urine [Na+]
<20 meq/L suggests that distal Na+ delivery is a limiting factor in K+ excretion;

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volume repletion with 0.9% saline or treatment with furosemide may then be
effective in reducing serum [K+] by increasing distal Na+ delivery. Serum and
urine osmolality are required for calculation of the TTKG. The expected values
of the TTKG are largely based on historic data: <3 in the presence of hypokalemia
and >7–8 in the presence of hyperkalemia.
TTKG =

[K + ]urine × OSM serum
[K + ]serum × OSM urine

TREATMENT

Hyperkalemia
The most important consequence of hyperkalemia is altered cardiac conduction,
with the risk of bradycardic cardiac arrest. Figure 1-4 shows serial ECG patterns
of hyperkalemia; ECG manifestations of hyperkalemia should be considered a
true medical emergency and treated urgently. However, ECG changes of hyperkalemia are notoriously insensitive, particularly in pts with CKD; given these
limitations, pts with significant hyperkalemia (K+ ≥6–6.5 mmol/L) in the absence
of ECG changes should also be aggressively managed.
Urgent management of hyperkalemia constitutes a 12-lead ECG, admission
to the hospital, continuous cardiac monitoring, and immediate treatment. Treatment of hyperkalemia is divided into three categories: (1) antagonism of the cardiac effects of hyperkalemia, (2) rapid reduction in [K+] by redistribution into
cells, and (3) removal of K+ from the body. Treatment of hyperkalemia is summarized in Table 1-5. Kayexalate, a mainstay of hyperkalemia treatment, has

Normal

Mild
hyperkalemia

Moderate
hyperkalemia

Severe
hyperkalemia

FIGURE 1-4 Diagrammatic ECGs at normal and high serum K. Peaked T waves (precordial
leads) are followed by diminished R wave, wide QRS, prolonged P-R, loss of P wave, and
ultimately a sine wave.

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HMOM20_Sec01_p0001-p0058.indd 15

TABLE 1-5 Treatment of Hyperkalemia
MECHANISM
Stabilize
membrane
potential
Cellular K+ uptake

ONSET
1–3 min

DURATION
30–60 min

COMMENTS
Repeat in 5 min if persistent electrocardiographic changes;
avoid in digoxin toxicity.

Insulin

10 U R with 50 mL of D50,
if blood sugar <250
Nebulized albuterol,
10–20 mg in 4-mL saline

30 min

4–6 h

30 min

2–4 h

Kayexalate

30–60 g PO in 20% sorbitol

6h

?

Furosemide
Hemodialysis

20–250 mg IV

15 min
Immediate

4–6 h

Can repeat in 15 min; initiate D10W IV at 50–75 mL/h to
avoid rebound hypoglycemia.
Can be synergistic/additive to insulin; should not be used
as sole therapy; use with caution in cardiac disease; may
cause tachycardia/hyperglycemia.
May cause fatal colonic necrosis; if available, sodium
zirconium cyclosilicate (ZS-9) or patiromer is preferred to
kayexalate.
Depends on adequate renal response/function.
Efficacy depends on pretreatment of hyperkalemia (with
attendant decrease in serum K+), the dialyzer used, blood
flow and dialysate flow rates, duration, and serum to
dialysate K+ gradient.

β2-Agonist
K+ removal

CHAPTER 1

DOSE
10% Ca gluconate,
10 mL over 10 min

Electrolytes

THERAPY
Calcium

15

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Care of the Hospitalized Patient

been linked to fatal colonic necrosis; if available, sodium zirconium cyclosilicate
(ZS-9) or patiromer, newer potassium binders that do not cause colonic necrosis,
should be used in preference to kayexalate.

2

Acid-Base Disorders

Regulation of normal pH (7.35–7.45) depends on both the lungs and kidneys. By
the Henderson-Hasselbalch equation, pH is a function of the ratio of HCO3− (regulated by the kidney) to PCO2 (regulated by the lungs). The HCO3/PCO2 relationship is useful in classifying disorders of acid-base balance. Acidosis is due to
gain of acid or loss of alkali; causes may be metabolic (fall in serum HCO3−) or
respiratory (rise in PCO2). Alkalosis is due to loss of acid or addition of base and
is either metabolic (↑ serum [HCO3−]) or respiratory (↓ PCO2) (Fig. 2-1).
To limit the change in pH, metabolic disorders evoke an immediate compensatory response in ventilation; full renal compensation for respiratory disorders is
a slower process, such that “acute” compensations are of lesser magnitude than
“chronic” compensations. Simple acid-base disorders consist of one primary disturbance and its compensatory response. In mixed disorders, a combination of
primary disturbances is present.
The cause of simple acid-base disorders is usually obvious from history,
physical examination, and/or basic laboratory tests. Initial laboratory evaluation depends on the dominant acid-base disorder, but for metabolic acidosis and
alkalosis this should include electrolytes, BUN, creatinine, albumin, urinary pH,
and urinary electrolytes. An arterial blood gas (ABG) is not always required for
pts with a simple acid-base disorder, e.g., mild metabolic acidosis in the context
of chronic renal failure. However, concomitant ABG and serum electrolytes are
necessary to fully evaluate more complex acid-base disorders. The compensatory
response should be estimated from the ABG; Winter’s formula [PaCO2 = (1.5 ×
[HCO3−]) + 8 ± 2] is particularly useful for assessing the respiratory response
to metabolic acidosis. The anion gap should also be calculated; the anion gap =
[Na+] – ([HCO3−] + [Cl−]) = unmeasured anions – unmeasured cations. The anion
gap should be adjusted for changes in the concentration of albumin, a dominant
unmeasured anion; the “adjusted anion gap” = anion gap + ∼2.5 × (4 – albumin
mg/dL). Other supportive tests will elucidate the specific form of anion-gap acidosis (see below).
■■METABOLIC ACIDOSIS

The low HCO3− in metabolic acidosis results from the addition of acids (organic
or inorganic) or from a loss of HCO3−; causes of metabolic acidosis are classically
categorized by presence or absence of an increase in the anion gap (Table 2-1).
Increased anion-gap acidosis (>12 mmol/L) is due to addition of acid (other than
HCl) and unmeasured anions to the body. Common causes include ketoacidosis
(diabetes mellitus [DKA], starvation, alcohol), lactic acidosis, poisoning (salicylates, ethylene glycol, and methanol), and renal failure.
Rare and newly appreciated causes of anion-gap acidosis include d-lactic
acidosis, propylene glycol toxicity, and 5-oxoprolinuria (also known as pyroglutamic aciduria). d-Lactic acidosis (an increase in the d-enantiomer of lactate)
can occur in pts with removal, disease, or bypass of the short bowel, leading

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CHAPTER 2

Acid-Base Disorders
50

7.7

7.5

pH = 7.4
7.3

45

Ac & chr
met alk

40

Chr
resp acid

7.2

35
30
25

7.1

Ac resp alk

No
ra rma
ng l
e

Bicarbonate, mmol/L

7.6

17

20
15
10

Ac resp acid

7.0

Ac & chr
met acid

Chr
resp alk

6.9
6.8

0

10

20

30

40

50

60

70

80

90

100

PCO 2, mmHg

1

4

8

12

PCO2, kPa

FIGURE 2-1 Nomogram showing bands for uncomplicated respiratory or metabolic acidbase disturbances in intact subjects. Each confidence band represents the mean
±2 SD for the compensatory response of normal subjects or pts to a given primary
disorder. Ac, acute; acid, acidosis; alk, alkalosis; chr, chronic; met, metabolic; resp,
respiratory. (Reprinted with permission from Arbus GS. An in vivo acid-base nomogram
for clinical use. Can Med Assoc J 109:291, 1973.)

to increased delivery of carbohydrates to colon. Intestinal overgrowth of organisms that metabolize carbohydrate to d-lactate results in d-lactic acidosis; a wide
variety of neurologic symptoms can ensue, with resolution following treatment
with appropriate antibiotics to change the intestinal flora. Propylene glycol is a
common solvent for IV preparations of a number of drugs, most prominently
lorazepam. Pts receiving high rates of these drugs may develop a hyperosmolar
anion-gap metabolic acidosis, due mostly to increased lactate, often accompanied
by acute kidney failure. Pyroglutamic aciduria (5-oxoprolinuria) is a high aniongap acidosis caused by dysfunction of the γ-glutamyl cycle that replenishes
intracellular glutathione; 5-oxoproline is an intermediate product of the cycle.
Hereditary defects in the γ-glutamyl cycle are associated with 5-oxoprolinuria;
acquired defects occur in the context of acetaminophen therapy, due to derepression of the cycle by reduced glutathione and overproduction of 5-oxoproline.
Resolution occurs after withdrawal of acetaminophen; treatment with N-acetyl
cysteine to replenish glutathione stores may hasten recovery.

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18

NON-ANION-GAP ACIDOSIS
CLUE
Hx; ↑ K+ drainage
Early chronic kidney disease

Distal—hypokalemic
Distal—hyperkalemic
 Distal—hyporeninemic
hypoaldosteronism
Dilutional
Ureterosigmoidostomy
Hyperalimentation
Acetazolamide, NH4Cl,
lysine HCl, arginine HCl,
sevelamer-HCl

↓ K+, presence of other proximal tubular
defects (Fanconi syndrome)
↓ K+; hypercalciuria; UpH >5.5
↑ K+; nl PRA/aldo; UpH >5.5
↑ K+; ↓ PRA/aldo; UpH <5.5
Massive volume expansion with saline
Obstructed ileal loop
Amino acid infusion
Hx of administration of these agents

CAUSE
DKA
RF
Lactic acidosis
(L-lactate)
Alcoholic ketoacidosis
Starvation
Salicylates
Methanol

Ethylene glycol
d-lactic acidosis
Propylene glycol
Pyroglutamic aciduria,
5-oxoprolinuria

ANION-GAP ACIDOSIS
CLUE
Hyperglycemia, ketones
Late chronic kidney disease
Clinical setting + ↑ serum lactate
Hx; weak + ketones; + osm gap
Hx; mild acidosis; + ketones
Hx; tinnitus; high serum level; + ketones; + lactate
Large AG; concomitant respiratory alkalosis; retinitis; +
toxic screen; + osm gap
RF; CNS symptoms; + toxic screen; crystalluria; + osm gap
Small-bowel disease; prominent neuro symptoms
IV infusions, e.g., lorazepam; + osm gap; RF
Large AG; chronic acetaminophen

Abbreviations: AG, anion gap; DKA, diabetic ketoacidosis; osm gap, osmolar gap; PRA, plasma renin activity; RF, renal failure; RTA, renal tubular acidosis; UpH, urinary pH.

Care of the Hospitalized Patient

CAUSE
Diarrhea enterostomy
RF
RTA
Proximal

SECTION
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1

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TABLE 2-1 Metabolic Acidosis

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Acid-Base Disorders

CHAPTER 2

19

The differentiation of the various anion-gap acidoses depends on the clinical
scenario and routine laboratory tests (Table 2-1) in conjunction with measurement of serum lactate, ketones, toxicology screens (if ethylene glycol or methanol
ingestion are suspected), and serum osmolality. d-Lactic acidosis can be diagnosed by a specific assay for the d-enantiomer; 5-oxoprolinuria can be diagnosed
by the clinical scenario and confirmed by gas chromatographic/mass spectroscopic (GC/MS) analysis of urine, a widely available pediatric screening test for
inborn errors of metabolism (typically “urine for organic acids”).
Pts with ethylene glycol, methanol, or propylene glycol toxicity may have
an “osmolar gap,” defined as a >10-mosmol/kg difference between calculated
and measured serum osmolality. Calculated osmolality = 2 × Na+ + glucose/18 +
BUN/2.8. Of note, pts with alcoholic ketoacidosis and lactic acidosis may also
exhibit a modest elevation in the osmolar gap; pts may alternatively metabolize
ethylene glycol or methanol to completion by presentation, with an increased
anion gap and no increase in the osmolar gap. However, the rapid availability
of a measured serum osmolality may aid in the urgent assessment and management of pts with these medical emergencies.
Normal anion-gap acidosis can result from HCO3− loss from the GI tract. Diarrhea is by far the most common cause, but other GI conditions associated with
external losses of bicarbonate-rich fluids may lead to large alkali losses—e.g.,
in ileus secondary to intestinal obstruction, in which liters of alkaline fluid may
accumulate within the intestinal lumen. Various forms of kidney disease are
associated with non-anion-gap acidosis due to reduced tubular reabsorption of
filtered bicarbonate and/or reduced excretion of ammonium (NH4+). The early
stages of progressive renal disease are frequently associated with a non-aniongap acidosis, with development of an anion-gap component in more advanced
renal failure. Non-anion-gap acidosis is also seen in renal tubular acidosis or
in the context of tubulointerstitial injury, e.g., after acute tubular necrosis, allergic interstitial nephritis, or urinary tract obstruction. Finally, non-anion-gap
acidosis due to exogenous acid loads may occur after rapid volume expansion
with saline-containing solutions, the administration of NH4Cl (a component of
cough syrup), lysine HCl, or treatment with the phosphate binder sevelamer
hydrochloride.
Calculation of the urinary anion gap may be helpful in the evaluation of
hyperchloremic metabolic acidosis, along with a measurement of urine pH. The
urinary anion gap is defined as urinary ([Na+] + [K+]) – [Cl−] = [unmeasured
anions] – [unmeasured cations]); the NH4+ ion is the major unmeasured urinary
cation in metabolic acidosis, wherein the urinary anion gap should be strongly
negative. A negative anion gap thus suggests GI losses of bicarbonate, with
appropriate renal response and increased NH4+ excretion; a positive anion gap
suggests altered urinary acidification, as seen in renal failure or distal renal tubular acidoses. An important caveat is that the rapid renal excretion of unmeasured
anions in anion-gap acidosis, classically seen in DKA, may reduce the serum
anion gap and generate a positive value for the urinary anion gap, despite the
adequate excretion of urinary NH4+; this may lead to misdiagnosis as a renal
tubular acidosis.
TREATMENT

Metabolic Acidosis
Treatment of metabolic acidosis depends on the cause and severity. DKA responds
to insulin therapy and aggressive hydration; close attention to serum [K+] and
administration of KCl is essential, given that the correction of insulinopenia can
cause profound hypokalemia. The administration of alkali in anion-gap acidoses

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Care of the Hospitalized Patient

is controversial and is rarely appropriate in DKA. It is reasonable to treat severe
lactic acidosis with IV HCO3− at a rate sufficient to maintain a pH >7.20; treatment of moderate lactic acidosis with HCO3− is controversial. IV HCO3 is however appropriate to reduce acidosis in d-lactic acidosis, ethylene glycol and
methanol toxicity, and 5-oxoprolinuria.
Chronic metabolic acidosis should be treated when HCO3− is <18–20 mmol/L.
In pts with CKD, there is some evidence that acidosis promotes protein catabolism and may worsen bone disease. There is also evidence that correction of metabolic acidosis in CKD leads to a reduced rate of progression to end-stage renal
disease (ESRD). Sodium citrate may be more palatable than oral NaHCO3. Oral
therapy with NaHCO3 usually begins with 650 mg tid and is titrated upward to
maintain serum [HCO3−].
■■METABOLIC ALKALOSIS

Metabolic alkalosis is due to a primary increase in serum [HCO3−], distinguished
from chronic respiratory acidosis—with a compensatory increase in renal HCO3−
reabsorption—by the associated increase in arterial pH (normal or decreased in
chronic respiratory acidosis). Administered, exogenous alkali (HCO3−, acetate,
citrate, or lactate) may cause alkalosis if the normal capacity to excrete HCO3− is
reduced or if renal HCO3− reabsorption is enhanced. A recently resurgent problem
is “milk alkali syndrome,” a triad of hypercalcemia, metabolic alkalosis, and acute
renal failure due to ingested calcium carbonate, typically taken for the treatment
or prevention of osteoporosis or for symptomatic relief of peptic ulcer disease.
Metabolic alkalosis is primarily caused by renal retention of HCO3− and is
due to a variety of underlying mechanisms. Pts are typically separated into two
major subtypes: Cl−-responsive and Cl−-resistant. Measurement of urine Cl−
affords this separation in the clinical setting (Fig. 2-2). The quintessential causes
of Cl−-responsive alkalosis are GI induced from vomiting or gastric aspiration
through a nasogastric tube, and renal induced from diuretic therapy. Hypovolemia, chloride deficiency, activation of the RAA axis, and hypokalemia play interrelated roles in the maintenance of this hypochloremic or “contraction” alkalosis.
The various syndromes of true or apparent mineralocorticoid excess cause
Cl−-resistant metabolic alkalosis (Fig. 2-2); most of these pts are hypokalemic,
volume expanded, and/or hypertensive.
Common forms of metabolic alkalosis are generally diagnosed from the history, physical examination, and/or basic laboratory tests. ABGs will help determine whether an elevated [HCO3−] is reflective of metabolic alkalosis or chronic
respiratory acidosis; ABGs are required for the diagnosis of mixed acid-base disorders. Measurement of urinary electrolytes will aid in separating Cl−-responsive
and Cl−-resistant forms. Urinary [Na+] may thus be >20 meq/L in Cl−-responsive
alkalosis despite the presence of hypovolemia; however, urinary [Cl−] will typically be very low, except in pts with severe hypokalemia. Notably, urinary [Cl−]
may be variable in pts with diuretic-associated alkalosis, depending on the
temporal relationship to diuretic administration. Other diagnostic tests—e.g.,
plasma renin, aldosterone, cortisol—may be appropriate in Cl−-resistant forms
with high urinary [Cl−] (Fig. 2-2).
TREATMENT

Metabolic Alkalosis
The acid-base disorder in Cl−-responsive alkalosis will typically respond to
saline infusion; however, the associated hypokalemia should also be corrected.
Pts with true or apparent mineralocorticoid excess require specific treatment of

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CHAPTER 2

Acid-Base Disorders

21

Urine [Cl – ]
<20 meq/L

>20 meq/L

Chloride-responsive alkaloses

Chloride-unresponsive alkaloses
Urine K+

Gastric fluid loss

<30 meq/L

Nonreabsorbable anion delivery

Laxative abuse
Severe K+ depletion

High

Diuretics*

Bartter’s or Gitelman’s
Low/normal
syndrome, or
diuretic abuse
Plasma renin

Posthypercapnea
Villous adenoma

High

Congenital chloridorrhea
High unilateral
renal vein renin
Yes
Renovascular HTN
JGA tumor

>30 meq/L
Blood pressure

Normal

Plasma cortisol

No
Malignant or
accelerated HTN

*After diuretic therapy

High

Low
Primary aldosteronism,
bilateral adrenal
hyperplasia, Liddle’s
syndrome, GRA, licorice

Cushing’s
syndrome

FIGURE 2-2 The diagnostic approach to metabolic alkalosis. See text for details. GRA,
glucocorticoid-remediable aldosteronism; HTN, hypertension; JGA, juxtaglomerular
apparatus. (Modified from Dubose TD. Disorders of acid-base balance. In: Brenner and
Rector’s The Kidney, 8th ed, Brenner BM [ed]. Philadelphia, Saunders, 2008 with permission.)

the underlying disorder. For example, hyperactive amiloride-sensitive ENaC
channels cause Liddle’s syndrome, which can respond to therapy with amiloride
and related drugs; pts with hyperaldosteronism may in turn respond to blockade of the mineralocorticoid receptor with spironolactone or eplerenone. Finally,
severe alkalosis in the critical care setting may require treatment with acidifying
agents such as acetazolamide.
■■RESPIRATORY ACIDOSIS

Respiratory acidosis is characterized by CO2 retention due to ventilatory failure.
Causes include sedatives, stroke, chronic pulmonary disease, airway obstruction, severe pulmonary edema, neuromuscular disorders, and cardiopulmonary
arrest. Symptoms include confusion, asterixis, and obtundation.
TREATMENT

Respiratory Acidosis
The goal is to improve ventilation through pulmonary toilet and reversal of bronchospasm. Intubation or noninvasive positive pressure ventilation (NPPV) may be
required in severe acute cases. Acidosis due to hypercapnia is usually mild; however, combined respiratory and metabolic acidosis may cause a profound reduction in pH. Respiratory acidosis may accompany low tidal volume ventilation in
ICU pts and may require metabolic “overcorrection” to maintain a neutral pH.

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SECTION
SECTION12
1

Care of the Hospitalized Patient

■■RESPIRATORY ALKALOSIS

Excessive ventilation causes a primary reduction in CO2 and ↑ pH in pneumonia, pulmonary edema, interstitial lung disease, and asthma. Pain and psychogenic causes are common; other etiologies include fever, hypoxemia, sepsis,
delirium tremens, salicylates, hepatic failure, mechanical overventilation, and
CNS lesions. Pregnancy is associated with a mild respiratory alkalosis. Severe
respiratory alkalosis may acutely cause seizures, tetany, cardiac arrhythmias, or
loss of consciousness.
TREATMENT

Respiratory Alkalosis
Treatment should be directed at the underlying disorders. In psychogenic cases,
sedation or a rebreathing bag may be required.
■■“MIXED” DISORDERS

In many circumstances, more than a single acid-base disturbance exists. Examples include combined metabolic and respiratory acidosis with cardiogenic
shock; metabolic alkalosis and anion-gap acidosis in pts with vomiting and diabetic ketoacidosis; and anion-gap metabolic acidosis with respiratory alkalosis in
pts with salicylate toxicity. The diagnosis may be clinically evident and/or suggested by relationships between the PCO2 and [HCO3−] that diverge from those
found in simple disorders. For example, the PCO2 in a pt with metabolic acidosis
and respiratory alkalosis will be considerably less than that predicted from the
[HCO3−] and Winter’s formula [PaCO2 = (1.5 × [HCO3−]) + 8 + 2].
In “simple” anion-gap acidosis, the anion gap increases in proportion to
the fall in [HCO3−]. A lesser drop in serum [HCO3−] than in the anion gap suggests a coexisting metabolic alkalosis. Conversely, a proportionately larger drop
in [HCO3−] than in the anion gap suggests the presence of a mixed anion-gap
and non-anion-gap metabolic acidosis. Notably, however, these interpretations
assume 1:1 relationships between unmeasured anions and the fall in [HCO3−],
which are not uniformly present in individual pts or as acidoses evolve. For
example, volume resuscitation of pts with DKA will typically increase glomerular filtration and the urinary excretion of ketones, resulting in a decrease in the
anion gap in the absence of a supervening non-anion-gap acidosis.

3

Diagnostic Imaging in
Internal Medicine

Clinicians have a wide array of imaging modalities at their disposal to aid them
in noninvasive diagnosis. Despite the introduction of highly specialized imaging modalities, radiologic procedures such as chest radiographs and ultrasound
continue to serve a vital role in the diagnostic approach to pt care. Increasingly,
ultrasound is used as a point-of-care procedure to assist with intravenous line
placement, and to extend the physical examination of the thyroid thorax, heart,
and abdomen. At most institutions, CT is available on an emergent basis and is
invaluable for initial evaluation of pts with trauma, suspected CNS hemorrhage,
or ischemic stroke. MRI and related techniques (MR angiography, functional

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23

MRI, MR spectroscopy) provide high resolution of many tissues including the
brain, vascular system, joints, and most large organs. Radionuclide scans including positron emission tomography (PET) can provide functional assessment of
organs or specific regions within organs. Combination of PET with MRI or CT
scanning provides highly informative images of the location and configuration
of metabolically active lesions, such as cancers.
This chapter will review the indications and utility of the most commonly
utilized radiologic studies used by internists.

CHEST RADIOGRAPHY (FIG. 3-1)
• Accessible and should be part of the standard evaluation for pts with cardiopulmonary complaints.
• Able to identify life-threatening conditions such as pneumothorax, intraperitoneal air, pulmonary edema, pneumonia, and aortic dissection.
• Often normal in a pt with an acute pulmonary embolus.
• Repeat in 4–6 weeks in a pt with an acute pneumonic process to document
resolution of the radiographic infiltrate.
• Used in conjunction with the physical examination to support the diagnosis
of congestive heart failure. The diagnosis of heart failure is supported by findings of cardiomegaly, cephalization, Kerley B lines, and pleural effusions.
• Repeat frequently in intubated pts to examine endotracheal tube position and
the possibility of barotrauma.
• Features of alveolar or airspace disease include inhomogeneous, patchy opacities and air-bronchograms.
• Helps to document the free-flowing nature of pleural effusions. Decubitus
views should be obtained to exclude loculated pleural fluid prior to attempts
to extract such fluid.

ABDOMINAL RADIOGRAPHY
• Initial imaging modality in a pt with suspected bowel obstruction. Signs of
small-bowel obstruction on plain radiographs include multiple air-fluid levels, absence of colonic distention, and a “stepladder” appearance of smallbowel loops.
• Should not be performed with barium enhancement when perforated bowel,
portal venous gas, or toxic megacolon is suspected.
• Used to evaluate the size of bowel:
1. Normal small bowel is <3 cm in diameter.
2. Normal caliber of the cecum is up to 9 cm, with the rest of the large bowel
up to 6 cm in diameter.

ULTRASOUND
• More sensitive and specific than CT scanning in evaluating for the presence
of gallstone disease.
• Used to assist with central line placement and with peripheral access when
challenging.
• Used to assess the size of the kidneys in a pt with renal insufficiency and to
exclude the presence of hydronephrosis.
• Evaluates for the presence of peritoneal fluid in a pt with blunt abdominal
trauma.
• Evaluates cardiac valves and wall motion.
• Used to localize loculated pleural and peritoneal fluid prior to draining such
fluid.

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Care of the Hospitalized Patient

1
5
6

2

3

7

4

8

9

10
12

11
FIGURE 3-1 Normal chest radiograph-review of anatomy. 1. Trachea. 2. Carina. 3. Right
atrium. 4. Right hemidiaphragm. 5. Aortic knob. 6. Left hilum. 7. Left ventricle. 8. Left
hemidiaphragm (with stomach bubble). 9. Retrosternal clear space. 10. Right ventricle.
11. Left hemidiaphragm (with stomach bubble). 12. Left upper lobe bronchus.

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• Determines the size of thyroid nodules and guide fine-needle aspiration
biopsy.
• Determines the size and location of enlarged lymph nodes, especially in
superficial locations such as in the neck.
• Modality of choice for assessing known or suspected scrotal pathology.
• Effective first imaging modality for evaluating the ovaries.

COMPUTED TOMOGRAPHY
• CT delivers a substantially higher radiation dose than conventional radiography; it should therefore be used judiciously.
• CT of the brain should be the initial radiographic modality in evaluating a pt
with a potential stroke.
• Is highly sensitive for diagnosing an acute subarachnoid hemorrhage and, in
the acute setting, is more sensitive than MRI.
• CT of the brain is an essential test in evaluating a pt with mental status changes
to exclude entities such as intracranial bleeding, mass effect, subdural or epidural hematomas, and hydrocephalus.
• Is better than MRI for evaluating osseous lesions of the skull and spine.
• CT of the chest should be considered in the evaluation of a pt with chest pain
to rule out entities such as pulmonary embolus or aortic dissection.
• CT of the chest is effective for evaluating lung nodules to assess for the presence of thoracic lymphadenopathy.
• CT, with high-resolution cuts through the lungs, is the imaging modality of
choice for evaluating the lung interstitium in a pt with interstitial lung disease.
• Evaluates for the presence of pleural and pericardial fluid and to localize loculated effusions.
• Useful in a pt with unexplained abdominal pain to evaluate for conditions
such as appendicitis, mesenteric ischemia or infarction, diverticulitis, or
pancreatitis.
• CT of the abdomen is also the test of choice for evaluating for nephrolithiasis
in a pt with renal colic.
• Evaluates the presence of an abscess in the chest or abdomen.
• Helps identify the cause of bowel obstruction.
• Identifies abdominal conditions such as intussusception and volvulus in a pt
with abdominal pain.
• Effective for evaluating the retroperitoneum.
• Should be obtained expeditiously in a pt with abdominal trauma to evaluate for the presence of intraabdominal hemorrhage and to assess injury to
abdominal organs.

MAGNETIC RESONANCE IMAGING
• Is more useful than CT in the evaluation of ischemic infarction, dementia,
mass lesions, demyelinating diseases, and most nonosseous spinal disorders.
• Provides excellent imaging of large joints including the kne