Ebook Harrison''s manual of medicine (16th edition): Part 1

HARRISON’S

Manual of
Medicine


EDITORS
Dennis L. Kasper, MD, MA(HON)
William Ellery Channing Professor of Medicine,
Professor of Microbiology and Molecular Genetics,
Harvard Medical School;
Director, Channing Laboratory,
Department of Medicine,
Brigham and Women’s Hospital, Boston

Eugene Braunwald, MD, MA(HON), MD(HON), ScD(HON)
Distinguished Hersey Professor of Medicine,
Harvard Medical School;
Chairman, TIMI Study Group,
Brigham and Women’s Hospital, Boston

Anthony S. Fauci, MD, ScD(HON)
Chief, Laboratory of Immunoregulation; Director,
National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Bethesda

Stephen L. Hauser, MD
Robert A. Fishman Distinguished Professor and Chairman,
Department of Neurology, University of
California– San Francisco,

San Francisco

Dan L. Longo, MD
Scientific Director, National Institute on Aging,
National Institutes of Health,
Bethesda and Baltimore

J. Larry Jameson, MD, PhD
Irving S. Cutter Professor and Chairman,
Department of Medicine,
Northwestern University Feinberg School of Medicine;
Physician-in-Chief, Northwestern
Memorial Hospital, Chicago


HARRISON’S

Manual of
Medicine
EDITORS
Dennis L. Kasper, MD
Eugene Braunwald, MD
Anthony S. Fauci, MD
Stephen L. Hauser, MD
Dan L. Longo, MD
J. Larry Jameson, MD, PhD

McGraw-Hill

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DOI: 10.1036/0071466983

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CONTENTS
Contributors
Preface

xiii
xv
SECTION 1

CARE OF THE HOSPITALIZED PATIENT
1 Initial Evaluation and
Admission Orders for the
General Medicine Patient
2 Assessment of Nutritional
Status
3 Electrolytes/Acid-Base
Balance
4 Enteral and Parenteral
Nutrition
5 Transfusion and Pheresis
Therapy

6 Principles of Critical Care
Medicine
7 Respiratory Failure
8 Pain and Its Management
9 Procedures Commonly

Performed by Internists
10 Diagnostic Imaging in
Internal Medicine
11 Gastrointestinal Diseases

1
2
5
14

19
22
23
28
32
34

17

SECTION 2

MEDICAL EMERGENCIES
12 Acute Respiratory Distress
Syndrome (ARDS)
13 Cardiovascular Collapse
and Sudden Death
14 Shock
15 Sepsis and Septic Shock
16 Acute Pulmonary Edema
17 Confusion, Stupor,

and Coma
18 Stroke
19 Subarachnoid Hemorrhage
20 Increased Intracranial
Pressure and Head Trauma
21 Hypoxic-Ischemic
Encephalopathy

22 Status Epilepticus
23 Poisoning and Drug
Overdose
24 Diabetic Ketoacidosis and
Hyperosmolar Coma
25 Hypoglycemia
26 Infectious Disease
Emergencies
27 Oncologic Emergencies
28 Anaphylaxis
29 Bites, Venoms, Stings, and
Marine Poisonings
30 Hypothermia and Frostbite
31 Bioterrorism

39
41
44
49
53
54
58

66
67

72
74
89
91
94
101
105
106
115
118

69

SECTION 3

COMMON PATIENT PRESENTATIONS
32
33
34
35
36

Chest Pain
Abdominal Pain
Headache
Back and Neck Pain
Fever, Hyperthermia,

Chills, and Rash

133
136
139
147

37
38
39
40

156
v

Pain or Swelling of Joints
Syncope and Faintness
Dizziness and Vertigo
Acute Visual Loss and
Double Vision

161
164
168
171


vi

CONTENTS

41 Paralysis and Movement
Disorders
42 Aphasias and Related
Disorders
43 Sleep Disorders
44 Dyspnea
45 Cough and Hemoptysis
46 Cyanosis
47 Edema
48 Nausea, Vomiting, and
Indigestion
49 Weight Loss
50 Dysphagia

175
179
181
185
187
192
194
197
201
203

51 Acute Abdomen
52 Diarrhea, Constipation, and
Malabsorption
53 Gastrointestinal Bleeding

54 Jaundice and Evaluation of
Liver Function
55 Ascites
56 Azotemia and Urinary
Abnormalities
57 Anemia and Polycythemia
58 Lymphadenopathy and
Splenomegaly

206
208
214
218
224
227
232
235

SECTION 4

DISORDERS OF THE EYE, EAR, NOSE, AND THROAT
59 Common Disorders of
Vision and Hearing

241

60 Infections of the Upper
Respiratory Tract

248

SECTION 5

DERMATOLOGY
61 General Examination of
the Skin

62 Common Skin Conditions

259

255

SECTION 6

HEMATOLOGY AND ONCOLOGY
63 Examination of Blood
Smears and Bone Marrow
64 Red Blood Cell Disorders
65 Leukocytosis and
Leukopenia
66 Bleeding and Thrombotic
Disorders
67 Prevention and Early
Detection of Cancer
68 Cancer Chemotherapy
69 Myeloid Leukemias,
Myelodysplasia, and
Myeloproliferative
Syndrome

70 Lymphoid Malignancies
71 Skin Cancer

265
267

72
73
74
75

272
275
280
284

76
77
78
79
80

290
296
307

81

Head and Neck Cancer
Lung Cancer

Breast Cancer
Tumors of the
Gastrointestinal Tract
Genitourinary Tract Cancer
Gynecologic Cancer
Prostate Hyperplasia and
Carcinoma
Cancer of Unknown
Primary Site
Paraneoplastic Endocrine
Syndromes
Neurologic Paraneoplastic
Syndromes

309
310
316
320
331
334
338
341
344
346


CONTENTS

vii

SECTION 7

INFECTIOUS DISEASES
82 Diagnosis of Infectious
Diseases
83 Antibacterial Therapy
84 Immunization and Advice
to Travelers
85 Infective Endocarditis
86 Intraabdominal Infections
87 Infectious Diarrheas
88 Sexually Transmitted
Diseases and Reproductive
Tract Infections
89 Infections of the Skin, Soft
Tissues, Joints, and Bones
90 Infections in the
Immunocompromised Host
91 HIV Infection and AIDS
92 Hospital-Acquired Infections
93 Pneumococcal Infections
94 Staphylococcal Infections
95 Streptococcal/Enterococcal
Infections, Diphtheria, and
Other Corynebacterial
Infections
96 Meningococcal and Listerial
Infections
97 Infections Caused by
Haemophilus, Bordetella,

Moraxella, and HACEK
Group Organisms
98 Diseases Caused by GramNegative Enteric Bacteria,
Pseudomonas, and
Legionella

351
360
365
372
380
383

393
408
417
424
442
445
448

455
462

99 Infections Caused by Other
Gram-Negative Bacilli
100 Anaerobic Infections
101 Nocardiosis and
Actinomycosis
102 Tuberculosis and Other

Mycobacterial Infections
103 Lyme Disease and Other
Nonsyphilitic Spirochetal
Infections
104 Rickettsial Diseases
105 Mycoplasma Infections
106 Chlamydial Infections
107 Herpesvirus Infections
108 Cytomegalovirus and
Epstein-Barr Virus
Infections
109 Influenza and Other Viral
Respiratory Diseases
110 Rubeola, Rubella, Mumps,
and Parvovirus Infections
111 Enteroviral Infections
112 Insect- and Animal-Borne
Viral Infections
113 Fungal Infections
114 Pneumocystis Infection
115 Protozoal Infections
116 Helminthic Infections

479
485
492
495

506
510

516
517
520

529
533
539
544
547
555
565
569
580

466

471

SECTION 8

CARDIOVASCULAR DISEASES
117 Physical Examination of the
Heart
118 Electrocardiography and
Echocardiography
119 Valvular Heart Disease
120 Cardiomyopathies and
Myocarditis
121 Pericardial Disease

593
596
603
609
612

122 Hypertension
123 ST-Segment Elevation
Myocardial Infarction
(STEMI)
124 Chronic Stable Angina,
Unstable Angina, and NonST-Elevation Myocardial
Infarction

616

621

631


viii

CONTENTS

125 Arrhythmias
126 Congestive Heart Failure
and Cor Pulmonale

638

648

127 Diseases of the Aorta
128 Peripheral Vascular Disease
129 Pulmonary Hypertension

653
655
658

SECTION 9

RESPIRATORY DISEASES
130 Respiratory Function and
Pulmonary Diagnostic
Procedures
131 Asthma and Hypersensitivity
Pneumonitis
132 Environmental Lung
Diseases
133 Chronic Bronchitis,
Emphysema, and Acute
or Chronic Respiratory
Failure

663
668
673

675

134 Pneumonia and Lung
Abscess
135 Pulmonary
Thromboembolism
136 Interstitial Lung Disease
(ILD)
137 Diseases of the Pleura,
Mediastinum, and
Diaphragm
138 Disorders of Ventilation,
Including Sleep Apnea

679
685
687

691
695

SECTION 10

RENAL DISEASES
139 Approach to the Patient with
Renal Disease
140 Acute Renal Failure
141 Chronic Kidney Disease
(CKD) and Uremia
142 Dialysis
143 Renal Transplantation

699
702
707
709
711

144
145
146
147
148
149

Glomerular Diseases
Renal Tubular Disease
Urinary Tract Infections
Renovascular Disease
Nephrolithiasis
Urinary Tract Obstruction

713
720
724
728
731
734

SECTION 11

GASTROINTESTINAL DISEASES
150 Peptic Ulcer and Related
Disorders
151 Inflammatory Bowel
Diseases
152 Colonic and Anorectal
Diseases
153 Cholelithiasis, Cholecystitis,
and Cholangitis

737
742
746
749

154
155
156
157

Pancreatitis
Acute Hepatitis
Chronic Hepatitis
Cirrhosis and Alcoholic
Liver Disease
158 Portal Hypertension

753
757
762

766
769


CONTENTS

ix

SECTION 12

ALLERGY, CLINICAL IMMUNOLOGY, AND RHEUMATOLOGY
159 Diseases of Immediate
Type Hypersensitivity
160 Primary Immunodeficiency
Diseases
161 SLE, RA, and Other
Connective Tissue
Diseases
162 Vasculitis
163 Ankylosing Spondylitis

773
776

779
785
788

164 Psoriatic Arthritis
165 Reactive Arthritis and

Reiter’s Syndrome
166 Osteoarthritis
167 Gout, Pseudogout, and
Related Diseases
168 Other Arthritides
169 Sarcoidosis
170 Amyloidosis

791
792
794
796
799
802
804

SECTION 13

ENDOCRINOLOGY AND METABOLISM
171 Disorders of the Anterior
Pituitary and Hypothalamus
172 Disorders of the Posterior
Pituitary
173 Disorders of the Thyroid
174 Disorders of the Adrenal
Gland
175 Obesity
176 Diabetes Mellitus
177 Disorders of the Male
Reproductive System

807
813
815
823
828
830
835

178 Disorders of the Female
Reproductive System
179 Hypercalcemic and
Hypocalcemic Disorders
180 Osteoporosis and
Osteomalacia
181 Disorders of Lipid
Metabolism
182 Hemochromatosis,
Porphyrias, and Wilson’s
Disease

839
847
852
855

861

SECTION 14

NEUROLOGY
183 The Neurologic
Examination
184 Neuroimaging
185 Seizures and Epilepsy
186 Tumors of the Nervous
System
187 Acute Meningitis and
Encephalitis
188 Chronic Meningitis
189 Multiple Sclerosis (MS)
190 Alzheimer’s Disease and
Other Dementias
191 Parkinson’s Disease
192 Ataxic Disorders

867
873
875
883
886
896
899
904
910
914

193 ALS and Other Motor
Neuron Diseases
194 Trigeminal Neuralgia,

Bell’s Palsy, and Other
Cranial Nerve Disorders
195 Autonomic Nervous
System Disorders
196 Spinal Cord Diseases
197 Peripheral Neuropathies,
Including Guillain-Barre´
Syndrome
198 Myasthenia Gravis (MG)
199 Muscle Diseases
200 Chronic Fatigue Syndrome

917

920
925
932

936
942
944
952


x

CONTENTS

SECTION 15

PSYCHIATRIC DISORDERS AND PSYCHOACTIVE SUBSTANCE USE
201 Psychiatric Disorders
202 Psychiatric Medications
203 Eating Disorders

955
962
969

204 Alcoholism
205 Narcotic Abuse

SECTION 16

ADVERSE DRUG REACTIONS
206 Adverse Drug Reactions

979

SECTION 17

WOMEN’S HEALTH
207 Women’s Health

989

SECTION 18

SCREENING AND DISEASE PREVENTION
208 Health Maintenance and

Disease Prevention

991

SECTION 19

LABORATORY VALUES
209 Appendix: Laboratory
Values of Clinical
Importance

Index

995

1011

972
975


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 editors 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 editors 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 are not responsible for any

errors or omissions or the results obtained from the use of such information. 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 book is accurate and that changes have not been made in
the recommended dose or in the contraindications for administration. This
recommendation is particularly important in connection with new or infrequently used drugs.


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CONTRIBUTORS

Numbers in parentheses refer to contributed chapters in the Manual.

TAMAR F. BARLAM, MD
Associate Professor of Medicine
Boston University School of Medicine
Boston (15, 26, 29, 36, 60, 82– 116, 134, 146)

EUGENE BRAUNWALD, MD, MA(HON), MD(HON), SCD(HON)
Distinguished Hersey Professor of Medicine
Harvard Medical School
Chairman, TIMI Study Group
Brigham and Women’s Hospital
Boston (11, 14, 16, 44– 46, 129, 206)

ANNE CAPPOLA, MD, SCM
Assistant Professor of Medicine and Epidemiology
Division of Endocrinology, Diabetes, and Metabolism
Center for Clinical Epidemiology and Biostatistics

University of Pennsylvania School of Medicine
Philadelphia (4, 24, 25, 30, 49, 171– 182, 203, 207)

PUNIT CHADHA, MD
Fellow in Medicine, Division of Hematology-Oncology
Department of Medicine
Northwestern University Feinberg School of Medicine
Northwestern Memorial Hospital
Chicago (9, 10)

GLENN CHERTOW, MD
Director of Clinical Services
Division of Nephrology
Moffitt-Long Hospitals and UCSF-Mt. Zion Medical Center
Assistant Professor of Medicine in Residence
University of California– San Francisco
San Francisco (3, 47, 56, 139– 145, 147– 149)

DANIEL B. EVANS, MD
Instructor in Medicine
Department of Medicine
Northwestern University Feinberg School of Medicine
Northwestern Memorial Hospital
Chicago (1, 208)

ANTHONY S. FAUCI, MD,
Chief, Laboratory of Immunoregulation
Director, NIAID, NIH
Bethesda (28, 31, 37, 54, 55, 61, 62, 91, 153– 170)

STEPHEN L. HAUSER, MD
Robert A. Fishman Distinguished Professor and Chairman
Department of Neurology
University of California– San Francisco
San Francisco (8, 17– 22, 34, 35, 38– 43, 59, 81, 183– 205)
xiii
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xiv

CONTRIBUTORS

J. LARRY JAMESON, MD, PHD
Irving S. Cutter Professor and Chairman
Department of Medicine
Northwestern University Feinberg School of Medicine
Physician-in-Chief
Northwestern Memorial Hospital
Chicago (4, 23– 25, 30, 49, 172– 182, 203, 207, 209)

DENNIS L. KASPER, MD, MA(HON)
William Ellery Channing Professor of Medicine
Professor of Microbiology and Molecular Genetics
Harvard Medical School
Director, Channing Laboratory
Department of Medicine
Brigham and Women’s Hospital
Boston (15, 26, 29, 36, 60, 82– 116, 134, 146)

CAROL A. LANGFORD, MD
Associate Professor of Medicine,
Department of Rheumatic and Immunologic Diseases,
Cleveland Clinic Foundation
Cleveland (37, 54, 55, 61, 62, 153, 154, 161– 170)

LEONARD S. LILLY, MD
Associate Professor of Medicine
Harvard Medical School
Chief, Brigham and Women’s/Faulkner Cardiology
Boston (13, 32, 117– 128)

DAN L. LONGO, MD
Scientific Director, National Institute on Aging
NIH
Bethesda and Baltimore (5, 27, 33, 48, 50– 53, 57, 58, 63– 80, 150– 152)

MICHAEL C. SNELLER, MD
Chief of Immunologic Diseases Section
Laboratory of Immunoregulation
NIAID, NIH
Bethesda (28, 31, 91, 155– 160)

J. WOODROW WEISS, MD
Associate Professor of Medicine
Harvard Medical School, Chief, Division of Pulmonary, Critical Care and
Sleep Medicine
Beth Israel Deaconess Medical Center
Boston (6, 7, 12, 130– 133, 135– 138)

PREFACE

Harrison’s Principles of Internal Medicine (HPIM) has always been a premier resource for clinicians and students, who require a detailed understanding of the biological and clinical aspects of quality patient care. As demands
increase, especially given the expanding medical knowledge base and the
increased patient-care responsibilities typical of modern health care settings, it is not always possible to read a full account of a disease or presentation before encountering the patient. It is for this reason, among others,
that the Editors have condensed the clinical portions of HPIM into this
pocket-sized Harrison’s Manual of Medicine. Like previous editions, this
new edition presents key features of the diagnosis and treatment of major
diseases that are likely to be encountered on a medical service.
The purpose of the Manual is to provide on-the-spot summaries in preparation for a more in-depth analysis of the clinical problem. The value of
the Manual lies in its abbreviated format, which is useful for initial diagnosis and management in time-restricted clinical situations. The Manual
has been written for easy reference to the full text of HPIM, and the Editors
recommend that the full textbook— or Harrison’s On Line— be consulted
as soon as time permits.
This new edition of the Manual includes a number of timely revisions.
The first section, focusing on care of the hospitalized patient, is completely
new and reflects the growing importance of in-patient-specific approaches.
Within this section are practical and valuable chapters on admitting orders,
common clinical procedures, and approach to the patient in critical care.
A brand new chapter on key concepts in radiographic imaging is also
included. Section 2 addresses the assessment and initial management of
common medical emergencies, including the distillation of three important
new chapters in HPIM on the likely biological, chemical, and radiologic
agents of terrorism. Chapters on cardinal disease manifestations and on the
management of common medical diseases have been completely revised
and updated to reflect important developments.
The increasing time demands on clinicians are being partially offset by
wider use of digital information delivery. The last edition of the Manual
was the first to be made available in PDA format. This new edition of the

Manual is also available digitally for PDA, and the PDA version now includes the full complement of tables and diagrams found in the print version
of the Manual. In addition, Harrison’s On Line includes the full text of
HPIM and a number of other valuable features. Taken as a portfolio, Harrison’s is now available in a variety of formats suitable for all levels of
medical training and for all varieties of health care settings.
We have developed this edition of the Manual with the able assistance of
selected contributors. The Editors also wish to acknowledge contributors to
past editions of this companion handbook, whose work formed the basis for
many of the chapters herein: Joseph B. Martin, MD, PhD; Daryl R. Gress,
MD; John W. Engstrom, MD; Kenneth L. Tyler, MD; Sophia Vinogradov,
MD. We thank Elizabeth Robbins, MD, for her editorial assistance.
xv

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SECTION 1
CARE OF THE HOSPITALIZED PATIENT

1
INITIAL EVALUATION AND ADMISSION ORDERS
FOR THE GENERAL MEDICINE PATIENT
Patients are admitted to the hospital when (1) they present the physician with a
complex diagnostic challenge that cannot be safely or efficiently performed in
the outpatient setting; or (2) they are acutely ill and require inpatient diagnostic
tests, interventions, and treatments. The decision to admit a patient includes
identifying the optimal clinical service (i.e., medicine, urology, neurology), the
level of care (observation, general floor, telemetry, ICU), and necessary consultants. Admission should always be accompanied by clear communication

with the patient, family, and other caregivers, both to procure relevant information and to outline the anticipated events in the hospital.
The scope of illnesses cared for by internists is enormous. During a single
day on a typical general medical service, it is not unusual for physicians, especially residents in training, to admit ten patients with ten different diagnoses
affecting ten different organ systems. Given this diversity of disease, it is important to be systematic and consistent in the approach to any new admission.
Physicians are often concerned about making errors of commission. Examples would include prescribing an improper antibiotic for a patient with pneumonia or miscalculating the dose of heparin for a patient with new deep venous
thrombosis. However, errors of omission are also common and can result in
patients being denied life-saving interventions. Simple examples include: not
checking a lipid panel for a patient with coronary heart disease, not prescribing
an angiotensin-converting enzyme (ACE) inhibitor to a diabetic with documented albuminuria, or forgetting to give a patient with an osteoporotic hip
fracture calcium, vitamin D, and an oral bisphosphonate.
Inpatient medicine typically focuses on the diagnosis and treatment of acute
medical problems. However, most patients have multiple medical problems, and
it is equally important to prevent nosocomial complications. Prevention of common hospital complications, such as deep venous thromboses (DVT), peptic
ulcers, line infections, and pressure ulcers, are important aspects of the care of
all general medicine patients.
A consistent approach to the admission process helps to ensure comprehensive and clear orders that can be written and implemented in a timely manner.
Several mnemonics serve as useful reminders when writing admission orders.
A suggested checklist for admission orders is shown below and it includes
several interventions targeted to prevent common nosocomial complications.
Computerized order entry systems are also useful when designed to prompt
structured sets of admission orders.
Checklist mnemonic: ADMIT VITALS AND PHYSICAL EXAM

• Admit to: service (Medicine, Oncology, ICU); provide status (acute or observation).
• Diagnosis: state the working diagnosis prompting this particular hospitalization.
• MD: name the attending, resident, intern, student, primary care MD, and
consultants.
• Isolation requirements: state respiratory or contact isolation and reason for
order.
1

Copyright © 2005, 2002, 1998, 1995, 1991, 1988 by The McGraw-Hill Companies, Inc. Click here for terms of use.


2

SECTION 1 Care of the Hospitalized Patient

• Telemetry: state indications for telemetry and specify monitor parameters.
• Vital signs (VS): frequency of VS; also specify need for pulse oximetry and

orthostatic VS.
• IV access and IV fluid or TPN orders (see Chap. 3).
• Therapists: respiratory, speech, physical, and/or occupational therapy needs.
• Allergies: also specify type of adverse reaction.
• Labs: blood count, chemistries, coagulation tests, type & screen, UA, special
tests.
• Studies: CT scans (also order contrast), ultrasounds, angiograms, endoscopies, etc.
• Activity: weight bear/ambulating instructions, fall/seizure precautions and
restraints.
• Nursing Orders: call intern if (x/y/z), also order I/Os, daily weights, and blood
glucose.
• Diet: include NPO orders and tube feeding. State whether to resume diet
after tests.
• Peptic ulcer prevention: proton-pump inhibitor or misoprostil for high-risk
patients.
• Heparin or other modality (warfarin, compression boots, support hose) for
DVT prophylaxis.
• Yank all Foley catheters and nonessential central lines to prevent iatrogenic
infections.
• Skin care: prevent pressure sores with heel guards, air mattresses, and RN

wound care.
• Incentive spirometry: prevent atelectasis and hospital-acquired pneumonia.
• Calcium, vitamin D, and bisphosphonates if steroid use, bone fracture, or
osteoporosis.
• ACE inhibitor and aspirin: use for nearly all patients with coronary disease
or diabetes.
• Lipid panel: assess and treat all cardiac and vascular patients for hyperlipidemia.
• ECG: for nearly every patient Ͼ50 years at the time of admission.
• X-rays: chest x-ray, abdominal series; evaluate central lines and endotracheal
tubes.
• Advanced directives: Full code or DNR; specify whether to rescind for any
procedures.
• Medications: be specific with your medication orders.
It may be helpful to remember the medication mnemonic “Stat DRIP” for
different routes of administration (stat, daily, round-the-clock, IV, and prn medications). For the sake of cross-covering colleagues, provide relevant prn orders
for acetaminophen, diphenhydramine, calcium carbonate, and sleeping pills.
Specify any stat medications since routine medication orders entered as “once
daily” may not be dispensed until the following day unless ordered as stat or
“first dose now.”

2
ASSESSMENT OF NUTRITIONAL STATUS
Stability of body weight requires that energy intake and expenditures are balanced over time. The major categories of energy output are resting energy expenditure (REE) and physical activity; minor sources include the energy cost


CHAPTER 2 Assessment of Nutritional Status

3

of metabolizing food (thermic effect of food or specific dynamic action) and

shivering thermogenesis. The average energy intake is about 2800 kcal/d for
men and about 1800 kcal/d for women, though these estimates vary with age,
body size, and activity level. Dietary reference intakes (DRI) and recommended
dietary allowances (RDA) have been defined for many nutrients, including 9
essential amino acids, 4 fat-soluble and 10 water-soluble vitamins, several minerals, fatty acids, choline, and water (Tables 60-1 and 60-2, pp. 400 and 401,
in HPIM-16). The usual water requirements are 1.0– 1.5 mL/kcal energy expenditure in adults, with adjustments for excessive losses. The RDA for protein
is 0.6 g/kg body weight. Fat should comprise Յ30% of calories, and saturated
fat should be Ͻ10% of calories. At least 55% of calories should be derived
from carbohydrates.

Malnutrition
Malnutrition results from inadequate intake or abnormal gastrointestinal assimilation of dietary calories, excessive energy expenditure, or altered metabolism
of energy supplies by an intrinsic disease process.
Both outpatients and inpatients are at risk for malnutrition if they meet one
or more of the following criteria:

• Unintentional loss of Ͼ10% of usual body weight in the preceding 3 months
• Body weight Ͻ90% of ideal for height (Table 2-1)
• Body mass index (BMI: weight/height2 in kg/m2) Ͻ 18.5
Table 2-1
Ideal Weight for Height
Men
a

a

Women

Height

Weight

Height

Weight

Height

Weight

Height

Weight

145
146
147
148
149
150
151
152
153
154
155
156
157
158
159
160

161
162
163
164
165

51.9
52.4
52.9
53.5
54.0
54.5
55.0
55.6
56.1
56.6
57.2
57.9
58.6
59.3
59.9
60.5
61.1
61.7
62.3
62.9
63.5

166
167

168
169
170
171
172
173
174
175
176
177
178
179
180
181
182
183
184
185
186

64.0
64.6
65.2
65.9
66.6
67.3
68.0
68.7
69.4
70.1

70.8
71.6
72.4
73.3
74.2
75.0
75.8
76.5
77.3
78.1
78.9

140
141
142
143
144
145
146
147
148
149
150
151
152
153
154
155
156
157

158
159
160

44.9
45.4
45.9
46.4
47.0
47.5
48.0
48.6
49.2
49.8
50.4
51.0
51.5
52.0
52.5
53.1
53.7
54.3
54.9
55.5
56.2

161
162
163
164

165
166
167
168
169

56.9
57.6
58.3
58.9
59.5
60.1
60.7
61.4
62.1

a

Values are expressed in cm for height and kg for weight. To obtain height in inches, divide by
2.54. To obtain weight in pounds, multiply by 2.2.
Source: Adapted from GL Blackburn et al.: Nutritional and metabolic assessment of the hospitalized patient. J Parenter Enteral Nutr 1:11, 1977; with permission.


4

SECTION 1 Care of the Hospitalized Patient

A body weight Ͻ90% of ideal for height represents risk of malnutrition,
body weight Ͻ85% of ideal constitutes malnutrition, Ͻ70% of ideal represents
severe malnutrition, and Ͻ60% of ideal is usually incompatible with survival.

In underdeveloped countries, two forms of severe malnutrition can be seen:
marasmus, which refers to generalized starvation with loss of body fat and
protein, and kwashiorkor, which refers to selective protein malnutrition with
edema and fatty liver. In more developed societies, features of combined protein-calorie malnutrition (PCM) are more commonly seen in the context of a
variety of acute and chronic illnesses.
ETIOLOGY The major etiologies of malnutrition are starvation, stress
from surgery or severe illness, and mixed mechanisms. Starvation results from
decreased dietary intake (from poverty, chronic alcoholism, anorexia nervosa,
fad diets, severe depression, neurodegenerative disorders, dementia, or strict
vegetarianism; abdominal pain from intestinal ischemia or pancreatitis; or anorexia associated with AIDS, disseminated cancer, or renal failure) or decreased
assimilation of the diet (from pancreatic insufficiency; short bowel syndrome;
celiac disease; or esophageal, gastric, or intestinal obstruction). Contributors to
physical stress include fever, acute trauma, major surgery, burns, acute sepsis,
hyperthyroidism, and inflammation as occurs in pancreatitis, collagen vascular
diseases, and chronic infectious diseases such as tuberculosis or AIDS opportunistic infections. Mixed mechanisms occur in AIDS, disseminated cancer,
COPD, chronic liver disease, Crohn’s disease, ulcerative colitis, and renal
failure.
CLINICAL FEATURES

• General— weight loss, temporal and proximal muscle wasting, decreased

skin-fold thickness
• Skin, hair, nails— easily plucked hair, easy bruising, petechiae, and perifollicular hemorrhages (vit. C), “flaky paint” rash of lower extremities (zinc),
hyperpigmentation of skin in exposed areas (niacin, tryptophan); spooning of
nails (iron)
• Eyes— conjunctival pallor (anemia), night blindness, dryness and Bitot spots
(vit. A), ophthalmoplegia (thiamine)
• Mouth and mucous membranes— glossitis and/or cheilosis (riboflavin, niacin, vit. B12, pyridoxine, folate), diminished taste (zinc); inflamed and bleeding
gums (vit. C)
• Neurologic— disorientation (niacin, phosphorus), confabulation, cerebellar

gait, or past pointing (thiamine), peripheral neuropathy (thiamine, pyridoxine,
vit. E), lost vibratory and position sense (vit. B12)
Laboratory findings include a low serum albumin, elevated PT, and decreased cell-mediated immunity manifest as anergy to skin testing. Specific
vitamin deficiencies may also be present.

For a more detailed discussion, see Dwyer J: Nutritional Requirements and
Dietary Assessment, Chap. 60, p. 399; Halsted CH: Malnutrition and Nutritional Assessment, Chap. 62, p. 411; and Russell RM: Vitamin and Trace
Mineral Deficiency and Excess, Chap. 61, p. 403, in HPIM-16.


CHAPTER 3 Electrolytes/Acid-Base Balance

5

3
ELECTROLYTES/ACID-BASE BALANCE
SODIUM
In most cases, disturbances of sodium concentration [Naϩ] result from abnormalities of water homeostasis. Disorders of Naϩ balance usually lead to hypoor hypervolemia. Attention to the dysregulation of volume (Naϩ balance) and
osmolality (water balance) must be considered separately for each pt (see below).
HYPONATREMIA This is defined as a serum [Naϩ] Ͻ 135 mmol/L and
is among the most common electrolyte abnormalities encountered in hospitalized pts. Symptoms include confusion, lethargy, and disorientation; if severe
(Ͻ120 mmol/L) and abrupt, seizures or coma may develop. Hyponatremia is
often iatrogenic and almost always the result of an abnormality in the action of
antidiuretic hormone (ADH), deemed either “appropriate” or “inappropriate,”
depending on the associated clinical conditions. The serum [Naϩ] by itself does
not yield diagnostic information regarding the total-body Naϩ content. Therefore, a useful way to categorize pts with hyponatremia is to place them into
three groups, depending on the volume status (i.e., hypovolemic, euvolemic,
and hypervolemic hyponatremia).
Hypovolemic Hyponatremia Mild to moderate degrees of hyponatremia
([Naϩ] ϭ 125– 135 mmol/L) complicate GI fluid or blood loss for two reasons.

First, there is activation of the three major “systems” responsive to reduced
organ perfusion: the renin-angiotensin-aldosterone axis, the sympathetic nervous system, and ADH. This sets the stage for enhanced renal absorption of
solutes and water. Second, replacement fluid before hospitalization or other
intervention is usually hypotonic (e.g., water, fruit juices). The optimal treatment of hypovolemic hyponatremia is volume administration, either in the form
of colloid or isotonic crystalloid (e.g., 0.9% NaCl or lactated Ringer’s solution).
Hypervolemic Hyponatremia The edematous disorders (CHF, hepatic cirrhosis, and nephrotic syndrome) are often associated with mild to moderate
degrees of hyponatremia ([Naϩ] ϭ 125– 135 mmol/L); occasionally, pts with
severe CHF or cirrhosis may present with serum [Naϩ] Ͻ120 mmol/L. The
pathophysiology is similar to that in hypovolemic hyponatremia, except that
perfusion is decreased due to (1) reduced cardiac output, (2) arteriovenous
shunting, and (3) severe hypoproteinemia, respectively, rather than true volume
depletion. The scenario is sometimes referred to as reduced “effective circulating arterial volume.” The evolution of hyponatremia is the same: increased
water reabsorption due to ADH, complicated by hypotonic fluid replacement.
This problem may be compounded by increased thirst. Pts with a variety of
causes of chronic kidney disease may also develop hypervolemic hyponatremia,
due principally to salt and water retention due to reduced GFR, and to the
diseased kidneys’ inability to osmoregulate.
Management consists of treatment of the underlying disorder (e.g., afterload
reduction in heart failure, large-volume paracentesis in cirrhosis, glucocorticoid
therapy in some forms of nephrotic syndrome), Naϩ restriction, diuretic therapy,
and, in some pts, H2O restriction. This approach is quite distinct from that
applied to hypovolemic hyponatremia.
Euvolemic Hyponatremia The syndrome of inappropriate ADH secretion
(SIADH) characterizes most cases of euvolemic hyponatremia. Common causes


6

SECTION 1 Care of the Hospitalized Patient

of the syndrome are pulmonary (e.g., pneumonia, tuberculosis, pleural effusion)
and CNS diseases (e.g., tumor, subarachnoid hemorrhage, meningitis); SIADH
also occurs with malignancies (e.g., small cell carcinoma of the lung) and drugs
(e.g., chlorpropamide, carbamazepine, narcotic analgesics, cyclophosphamide).
Optimal treatment of euvolemic hyponatremia is H2O restriction to Ͻ1 L/d,
depending on the severity of the syndrome.

TREATMENT
The rate of correction should be relatively slow (0.5 mmol/L per h of Naϩ).
A useful “rule of thumb” is to limit the change in mmol/L of Naϩ to half of
the total difference within the first 24 h. More rapid correction has been associated with central pontine myelinolysis, especially if the hyponatremia has
been of long standing. More rapid correction (with the potential addition of
hypertonic saline to the above-recommended regimens) should be reserved
for pts with very severe degrees of hyponatremia and ongoing neurologic
compromise (e.g., a pt with Naϩ Ͻ105 mmol/L in status epilepticus).
HYPERNATREMIA This is rarely associated with hypervolemia, and
this association is always iatrogenic, e.g., administration of hypertonic sodium
bicarbonate. Rather, hypernatremia is almost always the result of a combined
water and volume deficit, with losses of H2O in excess of Naϩ. The most common causes are osmotic diuresis secondary to hyperglycemia, azotemia, or drugs
(radiocontrast, mannitol, etc.) or central or nephrogenic diabetes insipidus (DI)
(see “Urinary Abnormalities,” Chap. 56). Elderly individuals with reduced thirst
and/or diminished access to fluids are at highest risk.

TREATMENT
The approach to correction of hypernatremia is outlined in Table 3-1. As with
hyponatremia, it is advisable to correct the water deficit slowly to avoid neurologic compromise. In addition to the water-replacement formula provided,
other forms of therapy may be helpful in selected cases of hypernatremia. Pts
with central DI may respond well to the administration of intranasal desmoTable 3-1
Correction of Hypernatremia
WATER DEFICIT

1. Estimate total-body water (TBW): 50– 60% body weight (kg) depending
on body composition
2. Calculate free-water deficit: [(Naϩ Ϫ 140)/140] ϫ TBW
3. Administer deficit over 48– 72 h
ONGOING WATER LOSSES

4. Calculate free-water clearance from urinary flow rate (V) and urine (U)
Naϩ and Kϩ concentrations V Ϫ V ϫ (UNa ϩ UK)/140
INSENSIBLE LOSSES

5. ϳ10 mL/kg per day: less if ventilated, more if febrile
TOTAL

6. Add components to determine water of D5W administration rate (typically ϳ50– 250 mL/h)


CHAPTER 3 Electrolytes/Acid-Base Balance

7

pressin. Pts with nephrogenic DI due to lithium may reduce their polyuria
with amiloride (2.5– 10 mg/d) or hydrochlorothiazide (12.5– 50 mg/d) or both
in combination. Paradoxically, the use of diuretics may decrease distal nephron filtrate delivery, thereby reducing free-water losses and polyuria. Occasionally, NSAIDs have also been used to treat polyuria associated with nephrogenic DI; however, their nephrotoxic potential makes them a less attractive
therapeutic option.

POTASSIUM
Since potassium (Kϩ) is the major intracellular cation, discussion of disorders
of Kϩ balance must take into consideration changes in the exchange of intraand extracellular Kϩ stores (extracellular Kϩ constitutes Ͻ2% of total-body Kϩ
content). Insulin, ␤2-adrenergic agonists, and alkalosis tend to promote Kϩ uptake by cells; acidosis promotes shifting of Kϩ.

Table 3-2
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. ␤2-Adrenergic agonists (endogenous or exogenous)
3. ␣-Adrenergic antagonists
C. Anabolic state
1. Vitamin B12 or folic acid (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. Hypokalemic periodic paralysis
4. Barium toxicity
III. Increased loss
A. Nonrenal
1. Gastrointestinal loss (diarrhea)
2. Integumentary loss (sweat)
B. Renal
1. Increased distal flow: diuretics, osmotic diuresis, salt-wasting nephropathies
2. Increased secretion of potassium
a. Mineralocorticoid excess: primary hyperaldosteronism, secondary

hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal artery stenosis, hypovolemia), apparent mineralocorticoid excess (licorice, chewing tobacco, carbenoxolone), congenital adrenal hyperplasia, Cushing’s syndrome, Bartter’s syndrome
b. Distal delivery of non-reabsorbed anions: vomiting, nasogastric
suction, proximal (type 2) renal tubular acidosis, diabetic ketoacidosis, glue-sniffing (toluene abuse), penicillin derivatives
c. Other: amphotericin B, Liddle’s syndrome, hypomagnesemia


8

SECTION 1 Care of the Hospitalized Patient

HYPOKALEMIA Major causes of hypokalemia are outlined in Table 32. Atrial and ventricular arrhythmias are the major health consequences of hypokalemia. Pts with concurrent magnesium deficit (e.g., after diuretic therapy)
and/or digoxin therapy are at particularly increased risk. Other clinical manifestations include muscle weakness, which may be profound at serum [Kϩ]
Ͻ 2.5 mmol/L, and, if prolonged, ileus and polyuria. Clinical history and urinary
[Kϩ] are most helpful in distinguishing causes of hypokalemia.

TREATMENT
Hypokalemia is most often managed by correction of the acute underlying
disease process (e.g., diarrhea) or withdrawal of an offending medication (e.g.,
loop or thiazide diuretic), along with oral Kϩ supplementation with KCl, or,
in rare cases, KHCO3 or K-acetate. Hypokalemia may be refractory to correction in the presence of magnesium deficiency; both cations may need to
be supplemented in selected cases (e.g., cisplatin nephrotoxicity). If loop or
thiazide diuretic therapy cannot be discontinued, a distal tubular K-sparing
agent, such as amiloride or spironolactone, can be added to the regimen. ACE
inhibition in pts with CHF attenuates diuretic-induced hypokalemia and protects against cardiac arrhythmia. If hypokalemia is severe (Ͻ2.5 mmol/L) and/
or if oral supplementation is not tolerated, intravenous KCl can be administered through a central vein at rates which must not exceed 20 mmol/h, with
telemetry and skilled monitoring.
HYPERKALEMIA Causes are outlined in Table 3-3. In most cases, hyperkalemia is due to decreased Kϩ excretion. Drugs can be implicated in many
cases. Where the diagnosis is uncertain, calculation of the transtubular K graTable 3-3
Major Causes of Hyperkalemia
I. “Pseudo”-hyperkalemia

A. Thrombocytosis, leukocytosis, in vitro hemolysis
II. Intra- to extracellular shift
A. Acidosis
B. Hyperosmolality; radiocontrast, hypertonic dextrose, mannitol
C. Beta2-adrenergic antagonists (noncardioselective agents)
D. Digoxin or ouabain poisoning
E. Hyperkalemic periodic paralysis
III. Inadequate excretion
A. Distal K-sparing diuretic agents and analogues
1. Amiloride, spironolactone, triamterene, trimethoprim
B. Decreased distal delivery
1. Congestive heart failure, volume depletion, NSAIDs, cyclosporine
C. Renal tubular acidosis, type IV
1. Tubulointerstitial diseases
a. Reflux nephropathy, pyelonephritis, interstitial nephritis, heavy
metal (e.g., Pb) nephropathy
2. Diabetic glomerulosclerosis
D. Advanced renal insufficiency with low GFR
E. Decreased mineralocorticoid effects
1. Addison’s disease, congenital adrenal enzyme deficiency, other
forms of adrenal insufficiency (e.g., adrenalitis), heparin, ACE inhibitors, AII antagonists