Nurse’s Manual
of Laboratory and
Diagnostic Tests
EDITION
Bonita Morrow Cavanaugh, PhD, RN
Clinical Nurse Specialist
Nursing Education
The Children’s Hospital
Denver, Colorado
Clinical Faculty
University of Colorado
Health Sciences Center
School of Nursing
Denver, Colorado
Affiliate Professor
University of Northern Colorado
School of Nursing
Greeley, Colorado
F.A. Davis Company • Philadelphia
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Copyright © 2003 by F. A. Davis Company
Copyright © 1999, 1995, 1989 by F. A. Davis Company. All rights reserved. This book is protected by copyright. No part of it
may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photo-
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Printed in the United States of America
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Developmental Editor: Diane Blodgett
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As new scientific information becomes available through basic and clinical research, recommended treatments and drug
therapies undergo changes. The author and publisher have done everything possible to make this book accurate, up to date,
and in accord with accepted standards at the time of publication. The author, editors, and publisher are not responsible for
errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard
to the contents of the book. Any practice described in this book should be applied by the reader in accordance with professional
standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised always to
check product information (package inserts) for changes and new information regarding dose and contraindications before
administering any drug. Caution is especially urged when using new or infrequently ordered drugs.
Library of Congress Cataloging-in-Publication Data
Cavanaugh, Bonita Morrow, 1952–
Nurse’s manual of laboratory and diagnostic tests. – 4th ed. /
Bonita Morrow Cavanaugh.
p. cm.
Rev. ed. of: Nurse’s manual of laboratory and diagnostic tests /
Juanita Watson. 3rd. ed. c1995.
Includes bibliographical references and index.
ISBN 0-8036-1055-6 (pbk.)
1. Diagnosis, Laboratory —Handbooks, manuals, etc. 2. Nursing-Handbook, manuals, etc. I. Watson, Juanita,
1946– Nurse’s manual of laboratory and diagnostic tests. II. Title.
[DNLM: 1. Laboratory Techniques and Procedures nurses’ instruction
handbooks. QY 39 C377n 1999]
RT48.5.W38 1999
616.07′5—dc21
DNLM/DLC
for Library of Congress 98-50920
CIP
Authorization to photocopy items for internal or personal use, or the internal or personal use of specific clients, is granted by
F. A. Davis Company for users registered with the Copyright Clearance Center (CCC) Transactional Reporting Service, provided
that the fee of $.10 per copy is paid directly to CCC, 222 Rosewood Drive, Danvers, MA 01923. For those organizations that
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Transactional Reporting Service is: 8036-1055/03 0 + $.10.
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To Laurie O’Neil Good, the finest nurse I have ever known.
Love,
Bonnie
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v
This book is designed to provide both students and practitioners of nursing with the informa-
tion they need to care for individuals undergoing laboratory and diagnostic tests and proce-
dures. The content is presented as a guiding reference for planning care, providing specific
interventions, and evaluating outcomes of nursing care.
In this edition, the background information and description of the test or procedure are
followed directly by the clinical applications data, starting with reference values, for each test or
group of tests.
The introductory sections include the anatomic, physiological, and pathophysiological
content necessary for a thorough understanding of the purpose of and indications for specific
tests and procedures. The inclusion of this information makes this book unlike many other
references on this subject matter. This feature enhances the integration of basic science knowl-
edge with an understanding of and application to diagnostic testing. This is extremely helpful
for nursing students in developing critical thinking and clinical judgment.
For each test or study within the respective sections, reference values, including variations
related to age or gender, are provided. Critical values, where appropriate, are highlighted. Both
conventional units and international units are provided. Readers are encouraged to be aware of
some variation in laboratory values from agency to agency.
For all tests, interfering factors are noted where appropriate. Contraindications and Nursing
Alerts are included to provide information crucial to safe and reliable testing and nursing care.
Other features of this manual that contribute to its practical use are presentation of detailed
content in tabular format when appropriate and the use of appendices to provide essential
information applicable to most, if not all, tests and procedures.
Every effort has been made to include tests and procedures currently in use in practice
settings. It is recognized that newer tests and procedures may have become available after this
manuscript was prepared. Readers are encouraged to keep abreast of current literature and
consult with laboratories and agencies in their area for new developments in the field of diag-
nostic tests.
B
ONITA MORROW CAVANAUGH
Preface
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vii
This book would not have been possible without the help, support, and encouragement of a
number of people. Special appreciation is due to the staff of the F. A. Davis Company. I am
particularly indebted to Lisa Deitch, Publisher, for her major contribution in developing the
unique format of this text, for her encouragement, and for always being available for help when
I needed it. I would also like to acknowledge Robert Martone, Nursing Publisher, who encour-
aged me to pursue this project, and Robert H. Craven, Jr., President, for his support and
patience as the book evolved. Special thanks are also due to Ruth De George, Editorial Assistant,
and Michele Reese, Editorial Aide, for their invaluable assistance. Many other individuals at the
F. A. Davis Company contributed to the production of this book, and I wish to extend to all of
them my sincere appreciation for their expertise and dedication to the high standards necessary
to produce a good book. Special recognition in this regard is due to Jessica Howie Martin,
Production Editor, and Bob Butler, Director of Production.
I thank the consultants who served as reviewers of the manuscript for their thoroughness and
generosity in sharing their ideas and suggestions. Your comments proved invaluable! Finally, a
special thanks to those family members, friends, and associates who offered and gave their
support, patience, and encouragement.
B.M.C.
Acknowledgments
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ix
Janice Brownlee, BScN, MAEd
Professor
Canadore College of Applied Arts and
Technology
North Bay, Ontario, Canada
Marie Colucci, BS, MS, EdD
Associate Professor
Riverside Community College
Riverside, California
Mary Jo Goolsby, MSN, ARNP, EdD
Instructor
Florida State University
Tallahassee, Florida
Shelby Hawk, RN, MSN
Instructor
Mid Michigan Community College
Harrison, Michigan
Priscilla Innocent, RN, MSN
Associate Professor
Indiana Wesleyan University
Marion, Indiana
Dr. Fran Keen, RN, DNSc
Associate Professor
University of Miami
Coral Gables, Florida
Dolores Philpot, BSMT, AND, MSN
Instructor
University of Tennessee
Knoxville, Tennessee
Sylvan L. Settle, RN
Vocational Teacher
Tennessee Technology Center
Memphis, Tennessee
Joyce Taylor, RN, MSN, DSN, BA
Associate Professor
Henderson State University
Arkadelphia, Arkansas
Shelley M. Tiffin, ART (CSMLS), BMLSc
Bachelor of Medical Laboratory Science
Program
Department of Pathology and Laboratory
Medicine
University of British Columbia
Vancouver, British Columbia, Canada
Donna Yancey, BSN, MSN, DNS
Assistant Professor
Purdue University
West Lafayette, Indiana
Consultants
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xi
SECTION I • Laboratory Tests, 1
CHAPTER 1
Hematology and Tests of Hematopoietic Function 3
CHAPTER 2
Hemostasis and Tests of Hemostatic Functions 39
CHAPTER 3
Immunology and Immunologic Testing 60
CHAPTER 4
Immunohematology and Blood Banking 96
CHAPTER 5
Blood Chemistry 103
CHAPTER 6
Studies of Urine 221
CHAPTER 7
Sputum Analysis 268
CHAPTER 8
Cerebrospinal Fluid Analysis 274
CHAPTER 9
Analysis of Effusions 283
CHAPTER 10
Amniotic Fluid Analysis 297
CHAPTER 11
Semen Analysis 305
CHAPTER 12
Analysis of Gastric and Duodenal Secretions 311
Contents
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CHAPTER 13
Fecal Analysis 321
CHAPTER 14
Analysis of Cells and Tissues 332
CHAPTER 15
Culture and Sensitivity Tests 352
SECTION II • Diagnostic Tests and Procedures, 361
CHAPTER 16
Endoscopic Studies 363
CHAPTER 17
Radiologic Studies 397
CHAPTER 18
Radiologic Angiography Studies 438
CHAPTER 19
Ultrasound Studies 458
CHAPTER 20
Nuclear Scan and Laboratory Studies 482
CHAPTER 21
Non-Nuclear Scan Studies 528
CHAPTER 22
Manometric Studies 545
CHAPTER 23
Electrophysiologic Studies 558
CHAPTER 24
Studies of Specific Organs or Systems 577
CHAPTER 25
Skin Tests 615
APPENDICES
APPENDIX I
Obtaining Various Types of Blood Specimens 625
APPENDIX II
Obtaining Various Types of Urine Specimens 631
APPENDIX III
Guidelines for Isolation Precautions in Hospitals 634
APPENDIX IV
Units of Measurement (Including SI Units) 636
xii Contents
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APPENDIX V
Profile or Panel Groupings and Laboratory Tests 644
APPENDIX VI
Nursing Care Plan for Individuals Experiencing
Laboratory and Diagnostic Testing 649
INDEX 651
xiiiContents
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1
SECTION
Laboratory
Tests
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3
CHAPTER
Hematology and Tests of
Hematopoietic Function
TESTS COVERED
Bone Marrow Examination, 7
Reticulocyte Count, 9
Iron Studies, 11
Vitamin B
12
and Folic Acid Studies, 13
Complete Blood Count, 14
Erythrocyte (RBC) Count, 20
Hematocrit, 21
Hemoglobin, 21
Red Blood Cell Indices, 22
Stained Red Blood Cell
Examination, 24
Hemoglobin Electrophoresis, 26
Osmotic Fragility, 29
Red Blood Cell Enzymes, 30
Erythrocyte Sedimentation Rate, 31
White Blood Cell Count, 33
Differential White Blood Cell Count, 34
White Blood Cell Enzymes, 37
INTRODUCTION Blood constitutes 6 to 8 percent of total body weight. In terms of
volume, women have 4.5 to 5.5 L of blood and men 5 to 6 L. In infants and children, blood
volume is 50 to 75 mL/kg in girls and 52 to 83 mL/kg in boys. The principal functions of blood
are the transport of oxygen, nutrients, and hormones to all tissues and the removal of meta-
bolic wastes to the organs of excretion. Additional functions of blood are (1) regulation of
temperature by transfer of heat to the skin for dissipation by radiation and convection, (2)
regulation of the pH of body fluids through the buffer systems and facilitation of excretion of
acids and bases, and (3) defense against infection by transportation of antibodies and other
substances as needed.
Blood consists of a fluid portion, called plasma, and a solid portion that includes red blood
cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes). Plasma makes
up 45 to 60 percent of blood volume and is composed of water (90 percent), amino acids,
proteins, carbohydrates, lipids, vitamins, hormones, electrolytes, and cellular wastes.
1
Of the
“solid” or cellular portion of the blood, more than 99 percent consists of red blood cells.
Leukocytes and thrombocytes, although functionally essential, occupy a relatively small portion
of the total blood cell mass.
2
Erythrocytes remain within the blood throughout their normal life span of 120 days, trans-
porting oxygen in the hemoglobin component and carrying away carbon dioxide. Leukocytes,
while they are in the blood, are merely in transit, because they perform their functions in body
tissue. Platelets exert their effects at the walls of blood vessels, performing no known function
in the bloodstream itself.
3
Hematology is traditionally limited to the study of the cellular elements of the blood, the
production of these elements, and the physiological derangements that affect their functions.
Hematologists also are concerned with blood volume, the flow properties of blood, and the
physical relationships of red cells and plasma. The numerous substances dissolved or suspended
in plasma fall within the province of other laboratory disciplines.
4
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HEMATOPOIESIS
Hematopoiesis is the process of blood cell formation.
In normal, healthy adults, blood cells are manufac-
tured in the red marrow of relatively few bones,
notably the sternum, ribs, vertebral bodies, pelvic
bones, and proximal portions of the humerus and
the femur. This production is in contrast to that
taking place in the embryo, in which blood cells are
derived from the yolk sac mesenchyme. As the fetus
develops, the liver, the spleen, and the marrow cavi-
ties of nearly all bones become active hematopoietic
sites (Fig. 1–1). In the newborn, hematopoiesis
occurs primarily in the red marrow, which is found
in most bones at that stage of development.
Beginning at about age 5 years, the red marrow is
gradually replaced by yellowish fat-storage cells
(yellow marrow), which are inactive in the
hematopoietic process. By adulthood, blood cell
production normally occurs in only those bones that
retain red marrow activity.
5
Adult reticuloendothelial cells retain the potential
for hematopoiesis, although in the healthy state
reserve sites are not activated. Under conditions of
hematopoietic stress in later life, the liver, the spleen,
and an expanded bone marrow may resume the
production of blood cells.
All blood cells are believed to be derived from the
pluripotential stem cell,
6
an immature cell with the
capability of becoming an erythrocyte, a leukocyte,
or a thrombocyte. In the adult, stem cells in
hematopoietic sites undergo a series of divisions and
maturational changes to form the mature cells
found in the blood (Fig. 1–2). As they achieve the
“blast” stage, stem cells are committed to becoming
a specific type of blood cell. This theory also explains
the origin of the several types of white blood cells
(neutrophils, monocytes, eosinophils, basophils, and
lymphocytes). As the cells mature, they lose their
ability to reproduce and cannot further divide to
replace themselves. Thus, there is a need for contin-
uous hematopoietic activity to replenish worn-out
or damaged blood cells.
Erythropoiesis, the production of red blood cells
(RBCs), and leukopoiesis, the production of white
blood cells (WBCs), are components of the
hematopoietic process. Erythropoiesis maintains a
population of approximately 25 ϫ 10
12
circulating
RBCs, or an average of 5 million erythrocytes per
cubic millimeter of blood. The production rate is
about 2 million cells per second, or 35 trillion cells
per day. With maximum stimulation, this rate can be
increased sixfold to eightfold, or one volume per day
equivalent to the cells contained in 0.5 pt of whole
blood.
The level of tissue oxygenation regulates the
production of RBCs; that is, erythropoiesis occurs in
response to tissue hypoxia. Hypoxia does not,
4 SECTION I—Laboratory Tests
Figure 1–1. Location of active marrow growth in the fetus and adult. (From Hillman, RS, and Finch, CA: Red Cell
Manual, ed 7. FA Davis, Philadelphia, 1996, p 2, with permission.)
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however, directly stimulate the bone marrow.
Instead, RBC production occurs in response to
erythropoietin, precursors of which are found prima-
rily in the kidney and to a lesser extent in the liver.
When the renal oxygen level falls, an enzyme, renal
erythropoietic factor, is secreted. This enzyme reacts
with a plasma protein to form erythropoietin, which
subsequently stimulates the bone marrow to
produce more RBCs. Specifically, erythropoietin (1)
accelerates production, differentiation, and matura-
tion of erythrocytes; (2) reduces the time required
for cells to enter the circulation, thereby increasing
the number of circulating immature erythrocytes
such as reticulocytes (see Fig. 1–2); and (3) facilitates
the incorporation of iron into RBCs. When the
number of produced erythrocytes meets the body’s
tissue oxygenation needs, erythropoietin release and
RBC production are reduced. Table 1–1 lists causes
of tissue hypoxia that may stimulate the release of
erythropoietin.
5CHAPTER 1—Hematology and Tests of Hematopoietic Function
TABLE 1–1
•
Causes of Tissue Hypoxia That May Stimulate
Erythropoietin Release
Acute blood loss
Impaired oxygen–carbon dioxide exchange in the lungs
Low hemoglobin levels
Impaired binding of oxygen to hemoglobin
Impaired release of oxygen from hemoglobin
Excessive hemolysis of erythrocytes due to hypersplenism or hemolytic disorders of antibody, bacterial, or
chemical origin
Certain anemias in which abnormal red blood cells are produced (e.g., hereditary spherocytosis)
Compromised blood flow to the kidneys
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Threats to normal erythropoiesis occur if suffi-
cient amounts of erythropoietin cannot be
produced or if the bone marrow is unable to
respond to erythropoietic stimulation. People with-
out kidneys or with severe impairment of renal
function are unable to produce adequate amounts of
renal erythropoietic factor. In these individuals, the
liver is the source of erythropoietic factor. The quan-
tity produced, however, is sufficient to maintain only
a fairly stable state of severe anemia that responds
minimally to hypoxemia.
Inadequate erythropoiesis may occur also if the
bone marrow is depressed because of drugs, toxic
chemicals, ionizing radiation, malignancies, or other
disorders such as hypothyroidism. Also, in certain
anemias and hemoglobinopathies, the bone marrow
is unable to produce sufficient normal erythrocytes.
Other substances needed for erythropoiesis are
vitamin B
12
, folic acid, and iron. Vitamin B
12
and
folic acid are required for DNA synthesis and are
needed by all cells for growth and reproduction;
because cellular reproduction occurs at such a high
rate in erythropoietic tissue, formation of RBCs is
particularly affected by a deficiency of either of these
substances. Iron is needed for hemoglobin synthesis
and normal RBC production. In addition to dietary
sources, iron from worn-out or damaged RBCs is
available for reuse in erythropoiesis.
7
Leukopoiesis, the production of WBCs, maintains
a population of 5,000 to 10,000 leukocytes per cubic
millimeter of blood, with the capability for rapid
and dramatic change in response to a variety of
stimuli. No leukopoietic substance comparable to
erythropoietic factor has been identified, but many
factors are known to influence WBC production,
with a resultant excess (leukocytosis) or deficiency
(leukopenia) in leukocytes (Table 1–2).
Note that WBC levels vary in relation to diurnal
6 SECTION I—Laboratory Tests
TABLE 1–2
•
Causes of Altered Leukopoiesis
Physiological Pathological
Leukocytosis
Leukopenia
All types of infection
Anemias
Cushing’s disease
Erythroblastosis fetalis
Leukemias
Polycythemia vera
Transfusion reactions
Inflammatory disorders
Parasitic infestations
Bone marrow depression
Toxic and antineoplastic drugs
Radiation
Severe infection
Viral infections
Myxedema
Lupus erythematosus and other autoimmune disorders
Peptic ulcers
Uremia
Allergies
Malignancies
Metabolic disorders
Malnutrition
Pregnancy
Early infancy
Emotional stress
Strenuous exercise
Menstruation
Exposure to cold
Ultraviolet light
Increased epinephrine secretion
Diurnal rhythms
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rhythms; thus, the time at which the sample is
obtained may influence the results. Overall, leuko-
cytes may increase by as many as 2000 cells per milli-
liter from morning to evening, with a corresponding
overnight decrease. Eosinophils decrease until about
noon and then rise to peak between midnight and 3
AM. This variation may be related to adrenocortical
hormone levels, which peak between 4 and 8
AM,
because an increase in these hormones can cause
circulating lymphocytes and eosinophils to disap-
pear in a few hours.
Evaluation of Hematopoiesis
Abnormal results of studies such as a complete
blood count (CBC)) and WBC count and differen-
tial indicate the need to determine the individual’s
hematopoietic function. Evaluation of hemato-
poiesis begins with the examination of a bone
marrow sample and may subsequently require other
studies and a sample of peripheral blood, either
venous or capillary.
Although the collection of blood specimens is
usually the responsibility of the laboratory techni-
cian or phlebotomist, it is often the responsibility
of the nurse in emergency departments, critical
care units, and community and home care settings.
A detailed description of procedures for obtain-
ing peripheral blood samples is provided in
Appendix I.
BONE MARROW EXAMINATION
Bone marrow examination (aspiration, biopsy)
requires removal of a small sample of bone marrow
by aspiration, needle biopsy, or open surgical biopsy.
Cells normally present in hematopoietic marrow
include erythrocytes and granulocytes (neutrophils,
basophils, and eosinophils) in all stages of matura-
tion; megakaryocytes (from which platelets
develop); small numbers of lymphocytes; and occa-
sional plasma cells (Fig. 1–2). Nucleated WBCs in
the bone marrow normally outnumber nucleated
(immature) RBCs by about 3:1. This is called the
myeloid-to-erythroid (M:E) ratio.
8
Causes of
increased and decreased values on bone marrow
examination are presented in Table 1–3.
Various stains followed by microscopic examina-
tion can be performed on bone marrow aspirate to
diagnose and differentiate among the different
types of leukemia. A Sudan B stain differentiates
between acute granulocytic and lymphocytic
7CHAPTER 1—Hematology and Tests of Hematopoietic Function
TABLE 1–3
•
Causes of Alterations in Bone Marrow Cells
Cell Type Increased Values Decreased Values
Reticulocytes
Neutrophils (total)
Lymphocytes
Plasma cells
Normoblasts
Eosinophils
Compensated RBC loss
Response to vitamin B
12
therapy
Myeloid (chronic) leukemias
Acute myeloblastic leukemia
Lymphatic leukemia
Lymphosarcoma
Lymphomas
Mononucleosis
Aplastic anemia
Myeloma
Polycythemia vera
Bone marrow carcinoma
Lymphadenoma
Myeloid leukemia
Aplastic crisis of sickle cell disease or hereditary
spherocytosis
Aplastic anemia
Leukemias (monocytic and lymphoblastic)
Deficiency of folic acid or vitamin B
12
Aplastic anemia
Hemolytic anemia
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leukemia. A periodic acid–Schiff stain assists in
the diagnosis of acute lymphocytic leukemia and
erythroleukemia. A terminal deoxynucleotidyl
transferase test differentiates between lymphoblastic
leukemia and lymphoma.
9
Because bone marrow examination involves an
invasive procedure with risks of infection, trauma,
and bleeding, a signed consent is required.
INDICATIONS FOR BONE MARROW
EXAMINATION
Evaluation of abnormal results of CBC (e.g.,
anemia), of WBC count with differential (e.g.,
increased numbers of leukocyte precursors), or of
both tests
Monitoring of effects of exposure to bone marrow
depressants
Monitoring of bone marrow response to antineo-
plastic or radiation therapy for malignancies
Evaluation of hepatomegaly (enlarged liver) or
splenomegaly (enlarged spleen)
Identification of bone marrow hyperplasia or
hypoplasia, although the study may not indicate
the cause of the quantitative abnormality
Determination of marrow differential (propor-
tion of the various types of cells present in the
marrow) and M:E ratio
Diagnosis of various disorders associated with
abnormal hematopoiesis:
Multiple myeloma
Most leukemias, both acute and chronic
Disseminated infections (granulomatous,
bacterial, fungal)
Lipid or glycogen storage diseases
8 SECTION I—Laboratory Tests
Reference Values
Cell Type (%) Adults Infants Children
Undifferentiated 0–1.0 — —
Reticulocytes 0.5–2.5 — —
Neutrophils (total) 56.5 32.4 57.1
Myeloblasts 0.3–5.0 0.62 1.2
Promyelocytes 1.4–8.0 0.76 1.4
Myelocytes 4.2–15.0 2.5 18.4
Neutrophilic 5.0–19.0 — —
Eosinophilic 0.5–3.0 — —
Basophilic 0–0.5 — —
Bands (stabs) 13.0–34.0 14.1 0
Lymphocytes 14.0–16.0 49.0 16.0
Monocytes 0.3–6.0 — —
Plasma cells 0.3–3.9 0.02 0.4
Megakaryocytes 0.1–3.0 0.05 0.1
M:E ratio 2.3–3.5:1 4.4:1 2.9:1
Pronormoblasts 0.2–1.3 0.1 0.5
Normoblasts 25.6 8.0 23.1
Basophilic 1.4–4.0 0.34 1.7
Polychromatophilic 6.0–29.0 6.9 18.2
Orthochromic 1.0–4.6 0.54 2.7
Eosinophils 0.5–3.0 2.6 3.6
Basophils 0–0.2 0.07 0.06
Note: There may be differences in normal values among individuals and in values obtained by different laboratory techniques.
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Hypoplastic anemia (which may be caused by
chronic infection, hypothyroidism, chronic
renal failure, advanced liver disease, and a
number of “idiopathic” conditions)
Erythropoietic hyperplasia (which may be
caused by iron deficiency, thalassemias, hemo-
globinopathies, disorders of folate and vitamin
B
12
metabolism, hypersplenism, glucose-6-
phosphate dehydrogenase [G-6-PD] deficiency,
hereditary spherocytosis, and antibody-medi-
ated bacterial or chemical hemolysis)
Lupus erythematosus
Porphyria erythropoietica
Parasitic infestations
Amyloidosis
Polycythemia vera
Aplastic anemia (which may be caused by drug
toxicity, idiopathic marrow failure, or infec-
tion)
CONTRAINDICATIONS
Known coagulation defects, although the test may
be performed if the importance of the informa-
tion to be obtained outweighs the risks involved
in carrying out the test
NURSING CARE BEFORE THE PROCEDURE
Explain to the client:
The purpose of the study
That it will be done at the bedside by a physician
and requires about 20 minutes
The general procedure, including the sensations
to be expected (momentary pain as the skin is
injected with local anesthetic and again as the
needle penetrates the periosteum, the “pulling”
sensation as the specimen is withdrawn)
That discomfort will be minimized with local
anesthetics or systemic analgesics
That the site may remain tender for several weeks
Ensure that a signed consent has been obtained.
Then:
Take and record vital signs.
Provide a hospital gown if necessary to provide
access to the biopsy site or to prevent soiling of
the client’s clothes with the solution used for skin
preparation.
Administer premedication prescribed for pain or
anxiety.
THE PROCEDURE
The client is assisted to the desired position depend-
ing on the site to be used. In young children, the
most frequently chosen site is the proximal tibia; in
older children, vertebral bodies T10 to L4 are
preferred. In adults, the sternum or iliac crests are
the preferred sites.
The prone or side-lying position is used if the
spinous processes are the sites to be used. (These
sites are preferred if more than one specimen is to be
obtained.) The client may also be sitting, supported
by a pillow on an overbed table for a spinous process
site. The side-lying position is used if the iliac crest
or tibia is the site. For sternal punctures, the supine
position is used.
The skin is prepared with an antiseptic solution,
draped, and anesthetized, preferably with procaine,
which is painless when injected. Asepsis must be
meticulous to prevent systemic infection.
For aspiration, a large needle with stylet is
advanced into the marrow cavity. Penetration of the
periosteum is painful. The stylet is removed and a
syringe is attached to the needle. An aliquot of 0.5
mL of marrow is withdrawn. At this time, the
discomfort is a “pulling” sensation rather than pain.
The needle is removed and pressure applied to the
site. The aspirate is immediately smeared on slides
and, when dry, sprayed with a fixative.
For needle biopsy, the local anesthetic is intro-
duced deeply enough to include the periosteum. A
special cutting biopsy needle is introduced through
a small skin incision and bored into the marrow
cavity. A core needle is introduced through the
cutting needle and a plug of marrow is removed. The
needles are withdrawn and the specimen placed in a
preservative solution. Pressure is applied to the site
for 5 to 10 minutes and a dressing applied.
NURSING CARE AFTER THE PROCEDURE
Care and assessment after the procedure include
assisting the client to lie on the biopsied side, if
the iliac crest was entered, or supine, if the verte-
bral bodies were used, to maintain pressure on the
site for 10 to 15 minutes.
For sternal punctures, place the client in the
supine position or other position of comfort.
Provide bed rest for at least 30 minutes after the
procedure.
Assess puncture site every 10 to 15 minutes for
bleeding. Apply an ice bag to the puncture site to
alleviate discomfort and prevent bleeding.
Assess for infection at the site; note any redness,
swelling, or drainage.
Administer analgesics to alleviate discomfort.
RETICULOCYTE COUNT
Reticulocytes are immature RBCs. As RBC precur-
sors mature (Fig. 1–2), the cell nucleus decreases in
size and eventually becomes a dense, structureless
9CHAPTER 1—Hematology and Tests of Hematopoietic Function
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mass.
10
At the same time, the hemoglobin content of
the cell increases. Reticulocytes are cells that have
lost their nuclei but still retain fragments of mito-
chondria and other organelles. They also are slightly
larger than mature RBCs.
11
RBCs normally enter the
circulation as reticulocytes and attain the mature
form (erythrocytes) in 1 to 2 days.
Under the stress of anemia or hypoxia, an
increased output of erythropoietin may lead to an
increased number of circulating reticulocytes (see
Table 1–1). The extent of such an increase depends
on the functional integrity of the bone marrow, the
severity and duration of anemia or hypoxia, the
adequacy of the erythropoietin response, and the
amount of available iron.
12
For example, a normal
reticulocyte count in the presence of a normal
hemoglobin level indicates normal marrow activity,
whereas a normal reticulocyte count in the presence
of a low hemoglobin level indicates an inadequate
response to anemia. This may be a result of defective
erythropoietin production, bone marrow function,
or hemoglobin formation. After blood loss or effec-
tive therapy for certain kinds of anemia, an elevated
reticulocyte count (reticulocytosis) indicates that
the bone marrow is normally responsive and is
attempting to replace cells lost or destroyed.
Individuals with defects of RBC maturation and
hemoglobin production may show a low reticulo-
cyte count (reticulocytopenia) because the cells
never mature sufficiently to enter the peripheral
circulation.
Performing a reticulocyte count involves examin-
ing a stained smear of peripheral blood to determine
the percentage of reticulocytes in relation to the
number of RBCs present.
INDICATIONS FOR RETICULOCYTE COUNT
Evaluation of the adequacy of bone marrow
response to stressors such as anemia or hypoxia:
A normal response is indicated by an increase
in the reticulocyte count.
Failure of the reticulocyte count to increase
may indicate depressed bone marrow function-
ing, defective erythropoietin production, or
defective hemoglobin production.
Evaluation of anemia of unknown etiology to
determine the type of anemia:
Elevated reticulocyte counts are found in
hemolytic anemias and sickle cell disease.
Decreased counts are seen in pernicious
anemia, thalassemia, aplastic anemia, and
severe iron-deficiency anemia.
Monitoring response to therapy for anemia:
In iron-deficiency anemia, therapeutic admin-
istration of iron should produce reticulocytosis
within 3 days and the count should remain
elevated until normal hemoglobin levels are
achieved.
Vitamin B
12
therapy for pernicious anemia
should cause a prompt, continuing reticulocy-
tosis.
Monitoring physiologic response to blood loss:
After a single hemorrhagic episode, reticulocy-
tosis should begin within 24 to 48 hours and
peak in 4 to 7 days.
Persistent reticulocytosis or a second rise in the
count indicates continuing blood loss.
Confirmation of aplastic crisis in clients with
known aplastic anemia as evidenced by a drop in
the usually high level of reticulocytes, indicating
that RBC production has stopped despite contin-
uing RBC destruction
13
NURSING CARE BEFORE THE PROCEDURE
Client preparation is the same as that for any study
involving the collection of a peripheral blood sample
(see Appendix I).
THE PROCEDURE
If the client is an adult, a venipuncture is performed
and the sample is collected in a lavender-topped
tube. A capillary sample may be obtained in infants
and children as well as in adults for whom venipunc-
ture may not be feasible.
NURSING CARE AFTER THE PROCEDURE
Care and assessment after the procedure are the
same as for any study involving the collection of a
peripheral blood sample (see Appendix I).
Abnormal values: Note and report fatigue, weak-
ness, and color changes associated with a decrease
in counts and pain, and changes in mental state
and visual perception associated with an increase
in counts. Increased counts in 4 to 7 days indicate
10 SECTION I—Laboratory Tests
Reference Values
Newborns 3.2% of RBCs,
declining by 2 mo
Infants 2–5%
Children 0.5–4%
Adults 0.5–2% of RBCs; can be
higher in pregnant
women
Reticulocyte index 1.0
Critical values Ͼ20% increase
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that the therapy to treat loss of RBCs is effective,
whereas decreased counts indicate an ineffective
production of RBCs, and further testing and eval-
uation are needed to determine the cause. Assess
for continuing blood loss (pulse, blood pressure,
skin color, weakness, dizziness).
Critical values: Polycythemia with reticulocyte
increases of greater than 20 percent requires
immediate communication to the physician.
Prepare the client for possible phlebotomy to
reduce volume of blood and intravenous fluids
to reduce viscosity of blood. Administer
ordered myelosuppressive drugs.
IRON STUDIES
Iron plays a principal role in erythropoiesis, because
it is necessary for proliferation and maturation of
RBCs and for hemoglobin synthesis. Of the body’s
normal 4 g of iron (somewhat less in women), about
65 percent resides in hemoglobin and about 3
percent in myoglobin. A tiny but vital amount of
iron is found in cellular enzymes, which catalyze the
oxidation and reduction of iron. The remainder is
stored in the liver, bone marrow, and spleen as
ferritin or hemosiderin.
14
Except for blood transfusions, the only way iron
enters the body is orally. Normally, only about 10
percent of ingested iron is absorbed, but up to 20
percent or more can be absorbed in cases of iron-
deficiency anemia. The body is never able to absorb
all ingested iron, no matter how great its need for
iron. In addition to dietary sources, iron from worn-
out or damaged RBCs is available for reuse in
erythropoiesis.
15
SERUM IRON, TRANSFERRIN, AND TOTAL
IRON
-BINDING CAPACITY
Any iron present in the serum is in transit among the
alimentary tract, bone marrow, and available iron-
storage forms. Iron travels in the bloodstream
bound to transferrin, a protein (-globulin) manu-
factured by the liver. Unbound iron is highly toxic to
the body, but generally much more transferrin is
available than that needed for iron transport.
Usually, transferrin is only 30 to 35 percent satu-
rated, with a normal range of 20 to 55 percent. If
excess transferrin is available in relation to body
iron, the percentage saturation is low. Conversely, in
situations of iron excess, both serum iron and
percentage saturation are high.
Measurement of serum iron is accomplished by
using a specific color of reagent to quantitate iron
after it is freed from transferrin. Transferrin may be
measured directly through immunoelectrophoretic
techniques or indirectly by exposure of the serum to
sufficient excess iron such that all the transferrin
present can combine with the added iron. The latter
result is expressed as total iron-binding capacity
(TIBC). The percentage saturation is calculated by
dividing the serum iron value by the TIBC value.
FERRITIN
Iron is stored in the body as ferritin or hemosiderin.
Many individuals who are not anemic and who can
adequately synthesize hemoglobin may still have
decreased iron stores. For example, menstruating
women, especially those who have borne children,
usually have less storage iron. In contrast, persons
with disorders of excess iron storage such as
hemochromatosis or hemosiderosis have extremely
high serum ferritin levels.
16
Serum ferritin levels are used to measure iron-
storage status and are obtained by either radioim-
munoassay or enzyme-linked immunoassay. The
amount of ferritin in the circulation usually is
proportional to the amount of storage iron (ferritin
and hemosiderin) in body tissues. Note that serum
ferritin levels vary according to age and gender (Fig.
1–3).
INDICATIONS FOR IRON STUDIES
Anemia of unknown etiology to determine cause
and type of anemia:
Decreased serum iron with increased transfer-
rin levels is seen in iron-deficiency anemia and
blood loss.
Decreased serum iron and decreased transfer-
rin levels may be seen in disorders involving
diminished protein synthesis or defects in
iron absorption (e.g., chronic diseases,
infections, widespread malignancy, malabsorp-
tion syndromes, malnutrition, nephrotic
syndrome). Percentage saturation of transferrin
11CHAPTER 1—Hematology and Tests of Hematopoietic Function
Figure 1–3. Serum ferritin levels according to sex and
age. (From Hillman, RS, and Finch, CA: Red Cell
Manual, ed 7. FA Davis, Philadelphia, 1996, p 64, with
permission.)
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