Wound Healing - Alternatives in Management PDF

WOUND HEALING:
Alternatives in
Management
Third Edition
Luther C. Kloth, MS, PT, CWS, FAPTA

Professor
Physical Therapy Department
Marquette University
Milwaukee, WI
Joseph M. McCulloch, PhD, PT, CWS

Executive Associate Dean and Professor, Physical Therapy
School of Allied Health Professions
Louisiana State University Health Sciences Center
Shreveport, LA
F.A. Davis Company
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Philadelphia, PA 19103
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Library of Congress Cataloging-in-Publication Data
Wound healing: alternatives in management/[edited by] Luther C. Kloth, Joseph M.

McCulloch.—3rd ed.
p. cm.—(Contemporary perspectives in rehabilitation ; v. 3)
Includes bibliographical references and index.
ISBN 0-8036-0833-0 (hbk.)
1. Wound healing. I. Kloth, Luther. II. McCulloch, Joseph M. III. Series.
RD94 .W67 2001
617.14—dc21 2001032394
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Dedication
To my wife, Doris; my sons, Eric and Dana; my daughter, Diane; and my friends, colleagues and
students at Marquette University for their support and encouragement. Also, to the chapter au-
thors for their expert contributions to this text. L.C.K.
To my wife, Gail; my sons, Bowen and Brett; other family members; and my friends and profes-
sional colleagues at Louisiana State University Health Science Center who provided support and
encouragement. J.M.M.
Foreword
I have acquired a somewhat bizarre habit, undoubtedly a result of aging. I love to

spend time indexing topics and authors through the PubMed homepage. So, after re-
viewing the third edition of Wound Healing: Alternatives in Management and offering a
few editorial suggestions for Luther Kloth and Joe McCulloch to ponder, I meandered
over to the computer and accessed PubMed to perform a simple search by linking the
terms “wound healing” and “physical therapy.” Much to my dismay, within a few sec-
onds approximately 1100 references appeared before me. Further inspection revealed at
least 32 content areas in which wound healing has been researched in the past 10 years
alone! In addition, the concept of wound healing covered at least six modalities and was
discussed by lead authors with specialty areas as diversified as physical therapy,
surgery, oncology, geriatrics, bioengineering, orthopaedics, rehabilitation medicine,
and nursing. I offer this information as evidence supporting the exponential interest and
growth in the exploration of wound healing and the implementation of novel therapies
to improve everything from skin ulcers to bone healing to macrophage migration to gene
therapy. In short, interest in wound healing appears to be here to stay.
Another expression of interest in this area is found in the remarkable success that
Luther and Joe have experienced with the first two editions of this book. In preparing
for this third and even more comprehensive edition, Luther Kloth wrote to me:
“Because Joe McCulloch and I are constantly around an interdisciplinary group
of professionals at various symposia we attend and committees on which we
serve related to wound care, we have become fully aware of the need to have
chapters in the third edition of our text to reflect the research evidence that sup-
ports and/or refutes the use of various interventions in clinical practice. To this
end, in chapters of our book that cover interventions for wounds, we will indi-
cate whether a particular treatment is based on (1) expert opinion, (2) case stud-
ies, (3) controlled trials, or (4) (randomized clinical trials).”
These words were written over 2-1/2 years ago and reflect the authors’ abilities to
foresee the need to impart information to rehabilitation students and practitioners alike
in terms that are both relevant and essential and to ensure reimbursement for wound
care management in today’s health care environment. The dynamics of their thoughts
are reflected in some of the profound changes in this third edition. Indeed, this book epit-
omizes the philosophy of this series (Contemporary Perspectives in Rehabilitation) by
being not only contemporary in scope but also prognostic in perspective.
There are 5 new chapters among the 14 that make up this text. Chapter 1, The Nor-
mal Process of Healing (Kirsner and Bogensberger) combines information on inflam-
matory responses to wounding, connective tissue responses during the healing process,
and contraction and reepithelialization as part of that process. These concepts occupied
three chapters in the second edition. Jeffrey Davidson provides a new chapter, Growth
Factors, Extracellular Matrix, and Wound Healing (Chapter 5). This excellent presenta-
vii
viii FOREWORD
tion offers insights into cellular and molecular elements contributing to healing of
wounds and the rate-limiting features from which new pharmacological and modality
approaches are spawned. Harriet Loehne also provides a new contribution, Wound De-
bridement and Irrigation (Chapter 7). She offers clinical perspectives based on detailed
decision-making processes and concludes with a case study that follows the Guide to
Physical Therapist Practice.
Given the increasing options for improvement in wound healing, it seemed rea-
sonable that a new chapter be offered to discuss alternative physical interventions for
wound healing. Luther Kloth has performed this task admirably in Chapter 10 by pro-
viding clinical protocols for use with each modality (pulsed diathermy, pulsed ra-
diofrequency stimulation, hyperbaric oxygen, normothermia, negative pressure wound
healing, UV radiation, and ultrasound) and evaluates the utility of each modality ac-
cording to a critical review of available evidence. The last, and totally new, chapter con-
cludes the text and aptly addresses documentation for reimbursement (Chapter 14). Lisa
Barton and Pam Unger provide valuable information on specificity of terminology and
quantification within documentation to facilitate reimbursement for services.
Other chapters have been expanded considerably. For example, Chapter 2, Nutri-
tion and Wound Healing by Brynda Lewis provides considerably more detail than the
same chapter in the previous edition of this text. Bill Ennis and Patricio Meneses have
enhanced the discussion in their chapter, Factors Impeding Wound Healing, by now in-
cluding obesity, temperature, psychological stress, age, gender, and ethnicity as impor-
tant contributing variables and introducing the concept of an “overlap model.” Chapter
4, Bacteriology and Infection Control, by Lynda Britton and Nancy Harkess offers an up-
date on agents that can impede the healing process. Katherine Lampe has expanded the
material in her chapter, Methods of Wound Evaluation (Chapter 6), considerably. Ms.
Lampe has made ample use of the Guide to Physical Therapist Practice related to the in-
tegument system. Involvement of family contributions to the patient history and ways
to evaluate patients more objectively highlight this extremely comprehensive and valu-
able chapter. Anne Myer gives the reader a comprehensive update on indications and
contraindications for dressings used to treat wounds in Chapter 8. The chapter Electri-
cal Stimulation for Wound Healing, by Luther Kloth (Chapter 9) has been completely re-
vised with abundant provision of clinical protocols offered within the context of avail-
able evidence. Jim Birke provides much new material in Chapter 11, Management of the
Insensate Foot. Joseph McCulloch’s Chapter 12, Management of Wounds Secondary to
Vascular Disease, and Chapter 13 from Laurie Rappl and Deb Hagler, Prevention and
Treatment of Pressure Ulcers, have been completely revised and expanded from the sec-
ond edition.
Collectively, this text has grown in scope and direction at the same rate as the ex-
pansion of information. An added advantage of this book is that all chapters have been
written not just to inform and educate readers, but to challenge them as well. One can-
not read any chapter of this book without thinking about the need to provide evidence
and treatment that is compelling and definitive. Not only is this the most comprehen-
sive book to date on how to understand and manage patients with wounds, it will serve
as a prototype for future texts to aid rehabilitation clinicians in their quest to ensure op-
timal care and unequivocal reimbursement.
Steven L. Wolf, PhD, PT, FAPTA

Atlanta, Georgia
Editor-in-Chief, Contemporary Perspectives in Rehabilitation Series
Preface to the Third Edition
The content of this third edition represents several radical changes from the previous
editions.
• The most apparent change is the color insert containing over 50 color pictures of
wounds and related technologies. This section will be especially valuable to students
and novice clinicians in making it easier for them to identify wound types and char-
acteristics and to visualize selected types of equipment.
• Another new feature is the integration of the principles and recommendations es-
poused by the APTA Guide to Physical Therapist Practice into the clinical chapters and
case studies dealing with patients who have wounds of the integument. The new
chapters follow the Guide’s approach to patient examination, evaluation, diagnosis,
prognosis, intervention, and attainment of functional outcomes.
• In addition to these changes, the third edition has 13 new authors, all of whom have
had years of experience in wound care and/or research and education. These authors
have incorporated the latest in wound research findings, technological advances, and
documentation methods into their chapters.
• Another unique feature of the text is found in two new chapters, one dealing with elec-
trical stimulation and the other with six alternative wound interventions. These two
chapters use an evidence-based approach that evaluates the clinical trials related to
each intervention and then rates the wound-healing efficacy of each modality ac-
cording to an A, B, C hierarchy. These chapters provide students, clinicians, and pay-
ors of health-care services with the current research evidence on which reimburse-
ment is increasingly based.
Nineteen authors in the third edition contributed to the writing of 14 chapters.

These chapters are divided into four sections.
The first section, entitled “The Wound-Healing Environment,” contains five chap-
ters, all of which integrate basic scientific information with clinical applications and are
documented by thorough up-to-date literature reviews. When addressing clinical ap-
plications, each chapter provides evidence-based documentation to support the infor-
mation provided. In addition to chapters that address normal wound healing, nutrition,
and factors affecting repair and infection control, there is a new state-of-the-art chapter
on growth factors and skin substitutes.
Section II, Evaluation, consists of one chapter that is devoted entirely to patient and
wound evaluation. This chapter is based on the principles and preferred practice pat-
terns recommended for care of the human integument as outlined in the Guide to Physi-
cal Therapist Practice. The approach described for evaluating the patient with a chronic
wound utilizes six components of patient management: examination, evaluation, diag-
nosis, prognosis, intervention, and management outcomes. These components are sub-
sequently integrated into the case studies in the chapters in Sections III and IV that ad-
dress wound-care interventions and case management and documentation. On reading
the evaluation chapter, the reader will be reminded that thorough wound management
ix
x PREFACE TO THIRD EDITION
goes far beyond local wound care and requires delving into the patient’s history, per-
forming a pertinent systems review, and utilizing appropriate tests and measures. The
evaluation then leads the examiner to the clinical decisions regarding the patient’s sta-
tus upon which the diagnosis, prognosis, and treatment will be based.
Section III, Principles and Techniques, includes four chapters that represent new
coverage of familiar topics related to the principles and techniques of wound care. Chap-
ter 7 addresses in detail all of the available methods of wound débridement, including
OSHA regulations, advantages, disadvantages, indications, contraindications, and dif-
ferentiation of viable and nonviable tissue types. In addition, this chapter discusses
pulsed lavage as both a method of wound irrigation and an adjunct to débridement.
Chapter 8 categorizes and describes the myriad wound dressings, including those that
are well established and the newer ones representing technologies that were nonexistent
in 1995 when the second edition of this book was published. It also describes the uses of
the different dressing categories. Chapter 9 presents the basic terminology, types, and
characteristics of electrical currents and the physical principles of electrical stimulation.
In addition, theories and known responses to electrical stimulation are discussed to aid
understanding of the cytological and physiological mechanisms by which this type of
wound therapy accelerates the rate of healing. A unique feature of this chapter is a
strength-of-evidence rating based on published clinical trials to reflect the efficacy of
electrical stimulation in promoting wound healing. The case study, like those in other
chapters, integrates the principles of patient examination through a systems approach
as described in the Guide to Physical Therapist Practice. Chapter 10 also uses an evidence-
based approach in covering six adjunctive modality interventions that affect wound
healing. Two of these modalities (normothermia and negative pressure wound therapy)
represent newer wound care technologies that have been marketed for less than 5 years,
whereas the others (ultrasound, ultraviolet radiation, hyperbaric oxygen, and pulsed
diathermy) have received variable amounts of use in wound treatment during the past
5 decades. The discussion of each modality begins with a description of the physical en-
ergy source, the characteristics, and the physiological mechanisms and responses that
are elicited to promote wound healing. To establish strength of evidence for determin-
ing the efficacy of each modality, the results of clinical trials are presented and catego-
rized as A, B, or C according to a hierarchy of criteria described in the chapter. The chap-
ter describes components of each modality device or system and presents application
protocols followed by precautions, contraindications, and case studies based on the
Guide to Physical Therapist Practice.
Section IV is entitled Case Management and Documentation. Chapter 11 is devoted
to the evaluation and management of wounds occurring in the diabetic insensate foot
and Chapters 12 and 13 with ulcerations caused by vascular insufficiency and pressure,
respectively. Each of these chapters includes an extensive current review of literature cit-
ing studies that either support or refute specific treatment approaches. As in previous
chapters that address patient care, the case studies are based on the Guide to Physical
Therapist Practice. Chapter 14 provides an introduction to wound care documentation for
reimbursement. To guide patient and wound treatment, the authors recommend that the
therapist use the five-stage management system delineated in the Guide to Physical Ther-
apist Practice, which includes examination, evaluation, diagnosis, prognosis, and inter-
vention. This format has been shown to support reimbursement from third-party pay-
ors. The authors emphasize the need to demonstrate skilled intervention and to include
functional restoration in the patient plan of care. Several patient/wound evaluation and
documentation forms are provided.
When the first edition of this textbook was published in 1990, it was the first con-
PREFACE TO THIRD EDITION xi
temporary book that dealt with clinical wound management. It used a problem-solving
approach that required the clinician to make decisions based on a paucity of scientific
evidence from controlled clinical trials and a plethora of expert opinions. The original
intent of the book was to provide physical therapist clinicians and students with a re-
source on wound healing based on the clinical experiences and research of the authors
and from information gleaned from the literature. However, as the manuscript devel-
oped, we found that we and the other contributors had included information on wound
management that could be useful to clinicians and students in nursing, nutrition, med-
ical laboratory technology, podiatry, and medicine. That information included detailed
discussions of cellular contributions to wound repair during the inflammatory, prolif-
erative, contraction, and remodeling phases of healing. Also presented were the many
factors that compromise healing, including infection, malnutrition, immunosuppres-
sion, topical agents, chemotherapy, and radiation therapy. The section on evaluation in-
corporated clinical measurement methods that could be used by the clinician to objec-
tively document wound-healing progress and to assess the adequacy of peripheral
vascular circulation. Other chapters in the first edition categorized and discussed the
clinical application of wound dressings and pressure-reducing devices, management of
the diabetic patient with a foot wound resulting from loss of protective sensation, and
the use of physical agents such as electrical stimulation, ultrasound, ultraviolet, thermal
energy, and hyperbaric oxygen to promote wound healing.
The second edition, published in 1995, updated, expanded, and broadened the
scope of information and application of the topics in the first edition through extensive
literature reviews, a new chapter on identification and treatment of wound pathogens,
infection control and universal precautions, and the integration of basic and clinical sci-
entific concepts with standard and alternative wound care interventions. Both the first
and second editions included clinical decision-making models and case studies that en-
abled the student and clinician to select the most appropriate methods for treatment of
uncomplicated and complicated wounds.
In 1990, when the first edition was published, the number of new wound care in-
novations was limited. They included the concept of moist wound healing and occlusive
dressings to maintain a moist wound environment and use of the total contact cast,
which had been shown effective in unloading superincumbent body weight and thereby
facilitating closure to plantar ulcers in the diabetic insensate foot. Compression to reduce
lower-extremity edema caused by venous hypertension was becoming recognized as a
significant component of treatment directed toward healing of ankle and leg ulcers re-
sulting from venous insufficiency, and electrical stimulation had been used successfully
for a decade to accelerate closure of chronic wounds.
By comparison, since 1995, when the second edition was published, a plethora of
new wound care products and devices has been brought to market. Along with these
products came a growing body of scientific literature, several new journals, and clinical
research that increasingly supports the efficacy of a variety of new wound care inter-
ventions through evidence-based outcomes.
We regret that Jeffrey A. Feedar, PT, was unable to contribute to this edition of
Wound Healing: Alternatives in Management because he took time off from authoring and
editing to devote his time to raising his son Jon. We wish Jeff and Jon the best.
Luther C. Kloth
Joseph M. McCulloch
Acknowledgments
We wish to thank the following individuals, without whom the publication of this
third edition would not have been possible:
Our contributors, who graciously withstood our critiques and editing of their
manuscripts.
The reviewers and copy editors for their comments and suggestions for improving
the text.
The patients and our colleagues in the Departments of Physical Therapy at Mar-
quette University and Louisiana State University Health Science Center.
The students we have taught at both Marquette University and Louisiana State Uni-
versity Health Science Center for their feedback and constructive comments on the
second edition.
The thousands of physical therapist clinicians and academicians who provided us

with their helpful suggestions for improving this third edition.
The F.A. Davis Company staff, including Jean-François Vilain, Sharon Lee, Jessica
Howie Martin, Jack Brandt, Ona Kosmos, and Maryann Foley.
Steven L. Wolf, PhD, FAPTA of Emory University for his support, guidance, and
encouragement.
xiii
Contributors
Lisa A. Barton, MMSc, PT William J. Ennis, DO
Program Director Department of Surgery, Medical Director
Wound Healing Center Wound Treatment Program
Swedish Medical Center, Providence Christ Hospital and Medical Center
Campus Oak Lawn, Illinois
Seattle, Washington
James A. Birke, PhD, PT, CPed

Director of Rehabilitation Services Deborah Hagler, PT
LSU Health Sciences Center President, Cheyenne Mountain
Diabetes Foot Program Rehabilitation, Inc.
Baton Rouge, Louisiana Colorado Springs, Colorado
Gabriele Bogensberger, MD
Research Fellow
Nancy Harkess, PhD
Department of Dermatology and
Associate Professor (retired)
Cutaneous Surgery
Department of Clinical Laboratory Science
University of Miami School of Medicine
School of Allied Health Professions
Miami, Florida
LSU Health Sciences Center
New Orleans, Louisiana
Lynda A. Britton, PhD
Associate Professor
Department of Clinical Laboratory
Sciences Robert S. Kirsner, MD
School of Allied Health Professions Director, Cedars Medical Center Wound
LSU Health Sciences Center C.U.R.E. Clinic
Shreveport, Louisiana Department of Dermatology and
Cutaneous Surgery
Jeffrey M. Davidson, PhD University of Miami School of Medicine
Professor of Pathology Miami, Florida
Vanderbilt University School of
Medicine
and
Research Career Scientist Luther C. Kloth, MS, PT, CWS, FAPTA
Medical Research Service Professor, Department of Physical
Department of Veterans Affairs Medical Therapy
Center Marquette University
Nashville, Tennessee Milwaukee, Wisconsin
xv
xvi CONTRIBUTORS
Katherine E. Lampe, PT, MPT, CWS Joseph M. McCulloch, PhD, PT, CWS
Assistant Professor Executive Associate Dean
Physical Therapy Department Professor of Physical Therapy
St. Ambrose University School of Allied Health Professions
Davenport, Iowa LSU Health Sciences Center
and Shreveport, Louisiana
Staff Physical Therapist
Physical Medicine and Rehabilitation Patricio Meneses, PhD
Department Adult Medicine Center, Research Coor-
Mercy Medical Center dinator Wound Treatment Program
Dubuque, Iowa Christ Hospital and Medical Center
Oak Lawn, Illinois
Brynda Lewis, BA, MS, RD
Anne Meyer, PT, GCS, CWS
Senior Lecturer and Reader
Wound Specialist
School of Health and Social Science
Coordinated Home Care
University of Wales Institute
Saddleback Memorial Hospital
Cardiff, South Wales, United Kingdom
Laguna Hills, California
and
Research Nutritionist
Laurie Rappl, PT, CWS
Wound Healing Research Unit
Clinical Support Manager
University Department of Surgery
Span-American Medical Systems, Inc.
University of Wales College of Medicine
Greenville, South Carolina
Heath Park, Cardiff, South Wales, United
Kingdom
Pamela Unger, PT, CWS
Partner, Clinical Director
Harriett Baugh Loehne, PT, CWS The Center for Advanced Wound Care
Wound Management Team Leader St. Joseph Medical Center
Acute Care Physical Therapy Reading, Pennsylvania
Wake Forest University Baptist Medical and
Center The Center for Advanced Wound Care
Winston-Salem, North Carolina West Lawn, Pennsylvania
Reviewers
Lucinda L. Baker, PhD, PT Jody Jack Gundrum, PhD, MSPT
Associate Professor Clinical Associate
Department of Biokinesiology and Department of Physical Therapy
Physical Therapy Marymount University
University of Southern California Arlington, Virginia
Los Angeles, California
xvii
Contents
SECTION I: The Wound-Healing Environment . . . . . . . . . . . . . 1
Chapter 1 The Normal Process of Healing . . . . . . . . . . . . . . . . . . . . . . . . 3

Robert S. Kirsner, MD
Gabriele Bogensberger, MD
Wound Characteristics Affecting Wound Healing. . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Wound Depth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Wound Creation Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
Wound Closure Methods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Phases of Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Inflammatory Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6
Proliferative Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
Remodeling Phase . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
Factors Affecting Connective Tissue Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
Measures to Accelerate Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29
Chapter 2 Nutrition and Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . 35

Brynda Lewis, BA, MS, RD
The Nutritional Biochemistry of Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
Protein and Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36
Fats and Fatty Acids and Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
Carbohydrates and Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
Trace Elements and Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38
Vitamins and Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
Nutritional Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42
Body Weight . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42
Anthropometric Indices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
Creatinine Height Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44
Assessment of Visceral Proteins . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44
Assessment of Immune Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
Assessment of Nitrogen Balance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45
Prognostic Indices. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46
Risk Assessment Tools . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
Dietary Assessment Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
Requirement Determinations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
Nutrition, Nutritional Status, and Pressure Scores . . . . . . . . . . . . . . . . . . . . . . . . 50
Malnutrition, Other Types of Wounds, and Wound Healing. . . . . . . . . . . . . . . . . . 55
The Metabolic Response to Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
xix
xx CONTENTS
Nutritional Status and the Postoperative Wound Healing Response. . . . . . . . . 56

Nutrition in Venous Ulceration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
Nutrition in Burn Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
Clinical Decision Making: Case Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 62
Chapter 3 Factors Impeding Wound Healing . . . . . . . . . . . . . . . . . . . . . 68

William J. Ennis, DO
Patricio Meneses, PhD
Theory Associated with Wound Healing Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . 68
Overlap Theory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
Local Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
Bio-burden . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 70
Tissue Perfusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 71
Eschar and Dessication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
Foreign Bodies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
Systemic Factors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
Stress Situations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
Obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
Nutrition. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
Temperature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
Comorbidities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
Clinician-Induced Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
Topical Agents. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
Wound Modalities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
Clinical Decision Making: Case Study 3–1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
Chapter 4 Bacteriology and Infection Control . . . . . . . . . . . . . . . . . . . . . 97

Lynda A. Britton, PhD
Nancy Harkess, PhD
The World of Microbiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
Overview of Bacteriology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98
Wound Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100
Host Defense Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100
Pathogenic Properties of Microbes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
Factors Predisposing to Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101
Sources of Organisms in Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102
Clinical Signs of Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
Organisms Commonly Encountered in Wound Infections . . . . . . . . . . . . . . . . . 103
Infection Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104
Sterilization, Disinfection, and Antisepsis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104
Infectious Waste Disposal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105
CONTENTS xxi
Health-Care Worker Protection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

Patient Protection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107
Wound Care. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
Hand Washing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
Antimicrobial Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
Multiply Resistant Bacteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
The Role of the Microbiology Laboratory . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
Identification of the Agents of Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 114
Interpretation of Culture Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
Antimicrobial Susceptibility Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
Epidemiological Typing for Infection Control . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
Treatment of Wound Infections. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Chapter 5 Growth Factors, Extracellular Matrix, and

Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
Jeffrey M. Davidson, PhD
Wound Repair Terminology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
Components and Mediators in the Skin. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Extracellular Matrix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Adhesive Proteins. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132
Basement Membranes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132
Cell Populations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
Cytokines, Growth Factors, and Their Receptors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
Epidermal Growth Factor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
Platelet-Derived Growth Factor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
Fibroblast Growth Factor. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
Vascular Endothelial Growth Factor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
Connective Tissue Growth Factor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
Transforming Growth Factor- . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
Insulin-Like Growth Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
Growth Factor Production and Regulation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
Cellular Components of the Inflammatory System . . . . . . . . . . . . . . . . . . . . . . . . . . 137
Platelets . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
Neutrophils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
Monocytes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
Lymphocytes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138
Mast Cells. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139
Sequential Events in the Wound Repair Cascade. . . . . . . . . . . . . . . . . . . . . . . . . . . . 139
Granulation Tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140
Re-epithelialization. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 140
Scar Formation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Pathobiology of Wound Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Nonhealing Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
Excessive Healing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142
Wound Healing Research in Animal and Experimental Models . . . . . . . . . . . . . . . 143
Granulation Tissue and Angiogenesis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143
Irritant Injection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
xxii CONTENTS
Implanted Biomaterials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

Excisional Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144
Tissue Biomechanics. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
Scarring. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
Chronic Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
Burns. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
SECTION II: Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
Chapter 6 Methods of Wound Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . 153

Katherine E. Lampe, PT, MPT, CWS
The Guide to Physical Therapist Practice: Integument . . . . . . . . . . . . . . . . . . . . . . . 154
History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 156
Patient Demographic Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157
Occupation or Employment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157
Social Information. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157
Past Medical History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158
Current Health Status . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 158
Risk Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
Patient Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
Wound Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
Periwound Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177
Vascular Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178
Edema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187
Sensation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188
Other Tests, Measures, and Examinations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
Wound Reassessment and Outcome Prediction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197
SECTION III: Principles and Techniques . . . . . . . . . . . . . . . . . . . . 201
Chapter 7 Wound Débridement and Irrigation . . . . . . . . . . . . . . . . . . . . 203

Harriett B. Loehne, PT, CWS
Identification of Tissue Types . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Subcutaneous Layer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Fascia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Skeletal Muscle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Bone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
Cartilage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
Blood Vessels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
Tendon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
Soft Tissue and Drainage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 206
Surgical Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207
CONTENTS xxiii
Sharp Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207

Instruments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208
Preparation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Technique. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Tissue Differentiation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
Precautions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
Mechanical Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Soft Débridement with Gauze or Swab . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Wet-to-Dry Dressing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
Dextranomer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 212
Vacuum-Assisted Closure (V.A.C.)®. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
Hydrotherapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
Enzymatic Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Enzyme Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Recommended Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
Frequency and Duration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
Disadvantages and Advantages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
Autolytic Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224
Chemical Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
Topical Bactericidal Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
Chapter 8 Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232

Anne Myer, PT, GCS, CWS
Dressing Selection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232
Location . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
Wound Stage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
Cavities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
Necrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
Incontinence. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
Drainage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
Wound Edges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Granulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Epithelialization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Gauze (Woven and Nonwoven) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
Indications/Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
Advantages/Disadvantages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
Impregnated Gauze. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
Transparent Films . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
xxiv CONTENTS
Hydrocolloids. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242
Amorphous Hydrogels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244
Hydrogel Sheets. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245
Foams . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
Alginates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 248
Absorptive Fillers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250
Composite Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 252
Collagen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
Biological Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254
Description. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254
Dressings Containing Active Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
Antibacterials (Topical) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 255
Silver Sulfadiazine Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 256
Arglaes and Acticoat Silver Dressings. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257
Iodosorb Gel and Idoflex Pad . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Biofine WDE and Biofine RE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
Appendix 1: Wound Care Product Manufacturers . . . . . . . . . . . . . . . . . . . . . . . . . . 264
CONTENTS xxv
Chapter 9 Electrical Stimulation for Wound Healing . . . . . . . . . . . . . . 271

Terminology of Medical Electricity. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
Polarity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
Charge . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
Charge Density . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
Voltage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
Current . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 272
Therapeutic Electrical Circuit and Electrodes . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
Theoretical Basis of Electrical Stimulation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
Endogenous Electrical Currents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 273
Exogenous Therapeutic Currents for Wound Healing . . . . . . . . . . . . . . . . . . . . . 277
Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
Basic Science Research . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
Clinical Research. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287
Strength of Evidence for ES as a Wound Healing Intervention . . . . . . . . . . . . . . . . 302
Meta-analysis of ES Wound Healing Research Studies . . . . . . . . . . . . . . . . . . . . 303
Guidelines for Wound Treatment with ES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
Precautions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 303
Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 311
Chapter 10 Adjunctive Interventions for Wound Healing . . . . . . . . . . 316

Normothermia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 316
Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 317
Strength of Evidence for Normothermia as a Wound Healing Intervention. . . 319
Components of the Warm Up Wound Therapy System. . . . . . . . . . . . . . . . . . . . 320
Protocol for Normothermic Treatment of Chronic Wounds . . . . . . . . . . . . . . . . 321
Precautions for Warm Up Wound Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322
Contraindications for Warm Up Wound Therapy. . . . . . . . . . . . . . . . . . . . . . . . . 322
Clinical Decision Making: Case Study 10–1. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
Ultraviolet Radiation Therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 326
Physical Properties of Ultraviolet Radiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 327
Strength of Evidence for Ultraviolet Radiation as a Wound Healing
Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
Components of the Derma Wand and Handisol Ultraviolet Systems . . . . . . . . 332
Guidelines for Ultraviolet Treatment of Chronic Wounds. . . . . . . . . . . . . . . . . . 333
UVC Protocol for Treatment of Infected Wounds (Bactericidal Effect) . . . . . . . 333
UVB Protocol for Inducing an Inflammatory Reaction in Chronic Wounds . . . 334
UVB Protocol for Inducing an Inflammatory Reaction in Chronic Wounds . . . 334
UVB Protocol for Stimulating Growth of Granulation Tissue . . . . . . . . . . . . . . . 334
UVB Protocol to Promote Breakdown and Elimination of Necrotic Tissue. . . . 334
Precautions for Ultraviolet Radiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335
Contraindications for Ultraviolet Radiation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 335
xxvi CONTENTS

Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
Negative-Pressure Wound Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
Strength of Evidence for Negative-Pressure Wound Therapy as a
Wound-Healing Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343
Components of the Vacuum-Assisted Closure System. . . . . . . . . . . . . . . . . . . . . 344
Protocols for Vacuum-Assisted Closure of Acute, Subacute, and
Chronic Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344
Protocols for Vacuum-Assisted Closure of Wounds . . . . . . . . . . . . . . . . . . . . . . . 344
Precautions for Vacuum-Assisted Closure of Wounds. . . . . . . . . . . . . . . . . . . . . 345
Contraindications for Vacuum-Assisted Closure of Wounds . . . . . . . . . . . . . . . 346
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349
Hyperbaric Oxygen Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349
Clinical Research. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351
Strength of Evidence for Hyperbaric Oxygen as a Wound
Healing Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353
Components of the Hyperbaric Oxygen Treatment System . . . . . . . . . . . . . . . . 353
Protocol for Hyperbaric Oxygen Treatment of Wounds . . . . . . . . . . . . . . . . . . . 353
Precautions for Treatment of Wounds with Hyperbaric Oxygen Therapy . . . . 354
Contraindications for Treatment of Wounds for Hyperbaric Oxygen
Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 354
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 358
Ultrasound Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 258
Strength of Evidence for Ultrasound as a Wound Healing Intervention . . . . . . 365
Components of a Therapeutic Ultrasound System . . . . . . . . . . . . . . . . . . . . . . . . 365
Protocol for Ultrasound Treatment of Chronic Wounds . . . . . . . . . . . . . . . . . . . 365
Precautions for Ultrasound Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 367
Contraindications for Ultrasound Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369
Thermal and Nonthermal Pulsed Diathermy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 369
Thermal-mode Pulsed Diathermy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 370
Nonthermal-mode Pulsed Diathermy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 371
Strength of Evidence for Thermal-Mode Pulsed Diathermy as a
Wound Healing Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 374
Strength of Evidence for Nonthermal-Mode Pulsed Diathermy as a
Wound Healing Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 375
Components of the Pulsed Diathermy System. . . . . . . . . . . . . . . . . . . . . . . . . . . . 375
Precautions for Thermal and Nonthermal Pulsed Diathermy. . . . . . . . . . . . . . . 375
Contraindications for Thermal and Nonthermal Pulsed Diathermy . . . . . . . . . 375
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376
CONTENTS xxvii
SECTION IV: Case Management and Documentation . . . . . 383
Chapter 11 Management of the Insensate Foot . . . . . . . . . . . . . . . . . . . . . 385

James A Birke, PhD, PT, CPed
Etiology of Foot Ulcerations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 385
Loss of Protective Sensation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 385
Mechanical Stress . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 386
High Foot Pressures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 387
Other Factors Contributing to Tissue Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 387
Examination of the Foot . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388
Foot Screening and Risk Identification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388
History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388
Sensory Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388
Skin Inspection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 390
Muscle Strength Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391
Limitation of Motion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392
Identification of Deformities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 392
Vascular Status Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 393
Evaluation of Footwear . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 393
Prevention and Treatment of Foot Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 393
Wound Care. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394
Devices of Off-Load Stress . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 396
Prevention of Reulceration. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 400
Wound Remodeling and Maturation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 400
Footwear . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 401
Evaluation of Footwear . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 402
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 405
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 405
Chapter 12 Management of Wounds Secondary

to Vascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 409
Joseph M. McCulloch, PhD, PT, CWS
Overview of Vascular System Anatomy and Physiology . . . . . . . . . . . . . . . . . . . . . 409
Venous Insufficiency . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411
Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 411
Theories of Venous Insufficiency Ulceration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412
Clinical Features of Venous Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 414
Treatment of Venous Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 415
Arterial Insufficiency. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418
Pathogenesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 418
Clinical Features of Arterial Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421
Treatment of Arterial Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 421
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 425
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 426
xxviii CONTENTS
Chapter 13 Prevention and Treatment of Pressure Ulcers . . . . . . . . . . 429

Laurie M. Rappl, PT, CWS
Deborah D. Hagler, PT
The Pressure Ulcer Problem. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 430
Incidence and Prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 430
Cause . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 430
Contributory Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 431
Features and Locations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 434
Patients at Highest Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 437
Ideal Positions and Positioning Principles. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 438
Sitting . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 438
Recumbent Postures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 442
Diagnostic Process . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447
History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447
Examination and Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 448
Diagnosis and Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 461
Interventions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 461
Treatment of the Wound Site . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 462
Pressure Reduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 462
Equipment for Positioning and Support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 462
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 490
Additional Readings on Seated Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 490
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 491
Appendix 13–1: Musculoskeletal System: Examples for Seated Position . . . . . . . . 494
Appendix 13–2: Musculoskeletal System: Examples for Recumbent Position. . . . 502
Appendix 13–3: Neuromuscular, Musculoskeletal, Genitourinary,
Psychosocial, Gastrointestinal, and Cardiopulmonary Systems:
Example for Seated Position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510
Appendix 13–4: Neuromuscular, Musculoskeletal, Genitourinary,
Psychosocial, Gastrointestinal, and Cardiopulmonary Systems:
Example for Recumbent Position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 514
Chapter 14 Documentation for Reimbursement . . . . . . . . . . . . . . . . . . . . 517

Lisa A. Barton, MMSc, PT
Pamela Unger, PT, CWS
Interdisciplinary Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517
Risk Assessment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 518
Examination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519
Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 519
Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
Intervention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
Physical Therapy Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521
Correlative Interdisciplinary Documentation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522
Billing Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 525
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 526
CONTENTS xxix
Appendix 1: Braden Scale for Predicting Pressure Sore Risk . . . . . . . . . . . . . . . . . . 527

Appendix 2: Norton Risk Assessment Scale . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 528
Appendix 3: History and Physical Examination. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 529
Appendix 4: Wound Evaluation/Assessment Tool . . . . . . . . . . . . . . . . . . . . . . . . . . 531
Appendix 5: Weekly Measurement Tool . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 532
Appendix 6: Wound Care Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 533
Appendix 7: Weekly Wound Care Progress Not . . . . . . . . . . . . . . . . . . . . . . . . . . . . 537
Appendix 8: Initial Wound Assessment and Treatment Plan. . . . . . . . . . . . . . . . . . 540
Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 541
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 549
CHAPTER 9
Electrical Stimulation for
Wound Healing
Various practitioners have developed and clinically used numerous physical inter-
ventions either as primary wound treatments or as adjuncts to standard wound care. Some
of these modalities, especially electrical stimulation (ES), pulsed electromagnetic field ra-
diation, ultraviolet radiation, and ultrasound have long been associated with physical ther-
apy practice related to wound management. Other physical interventions developed more
recently include devices that promote tissue repair by delivering a controlled level of heat
(normothermia) or vacuum (negative pressure wound therapy) to the wound and/or peri-
wound tissues via occlusive dressings. Another modality that has recently gained popu-
larity among physicians who practice hyperbaric medicine requires the patient to breathe
oxygen at a pressure greater than 1 atmosphere (hyperbaric oxygen therapy).
This and the following chapter will take an evidence-based approach to evaluating
the clinical research that provides strength of evidence for each of these seven modali-
ties regarding their efficacy in accelerating closure of chronic wounds. This chapter ad-
dresses ES only. The next chapter, Chapter 10, will address the other six interventions.
TERMINOLOGY OF MEDICAL ELECTRICITY
Frequently, reviewers of the literature on wound healing with ES have indicated

that they are confused by the wide variety of stimulation parameters reported in the clin-
ical research studies. Much of the confusion may be alleviated with a clear understand-
ing of physical terms associated with medical electricity.
Polarity
Polarity refers to the property of having two oppositely charged conductors (elec-
trodes) in a circuit—one positive, one negative. The negative pole or electrode, the
271
272 WOUND HEALING: ALTERNATIVES IN MANAGEMENT
source of electrons in an electrical circuit, is called the cathode (). The positive pole or
electrode, called the anode (), is the electron depository to which electrons flow.
Charge
Electrical charge (Q) is a fundamental property of matter. Matter can be electrically

neutral or negatively or positively charged. Electrons are negatively charged particles.
An electrically neutral substance that gains an electron becomes negatively charged (),
whereas an electrically neutral substance that loses an electron becomes positively
charged (). Charge is measured in units called coulombs (C), representing a specific
quantity of electrons (e). One coulomb contains 6.28 1018 electrons.1 The amount of
charge delivered into wound tissues through a treatment electrode to enhance healing
is in the microcoulomb (C) range, which will be identified later.
Charge Density
Charge density is a measure of the electrical charge per unit of a cross-sectional area
of an electrode, expressed as Q/cm2. However, because the magnitudes of charge de-
livered to wounds in clinical practice are relatively small, charge densities for ES elec-
trodes are more likely to be expressed as C/cm2. Charge density is inversely related to
electrode size.
Voltage
Voltage (V) refers to the electromotive force or the electrical force capable of mov-
ing electrons (or ions) through a conductor (wound tissues) between two or more elec-
trodes applied to the body. The voltage between the electrodes is created by the separa-
tion of charges between them, such that one electrode has an excess of electrons when
compared to the other. These two electrodes are “polarized” with respect to one another,
one being positive and the other negative.
Current
An electrical current (I) is defined as the rate of flow of charged particles (electrons
or ions) past a specific point in a specific direction. Current flow in a metal wire con-
ductor occurs as a result of the flow of electrons, whereas current flow in tissues is car-
ried by ions (e.g., Na, K, Cl). Current is measured in units of amperes (A) and is de-
fined mathematically as:
I C/t
where I amps; C coulombs; and t time (in seconds [s]). Currents delivered to
wounds that are intended to mimic the bioelectric tissue currents have an order of mag-
nitude that is 1000 times less than 1.0 A, which places them in the milliampere (mA)
range.
CHAPTER 9 ELECTRICAL STIMULATION FOR WOUND HEALING 273
Therapeutic Electrical Circuit and Electrodes
An electrical circuit used for wound healing applications consists of at least two
wires or leads with one lead connected to an electron source (negative jack) and the other
connected to an electron depository (positive jack) of an ES device. The patient end of
each lead is connected to an electrode that is applied to the patient. Electrodes placed in
contact with the tissues of the body are described as being capacitively coupled. When a
unidirectional current flows in the circuit, positively charged ions in the tissues (Na,
K, H) and cells (fibroblast and activated neutrophil) migrate toward the negative elec-
trode (cathode) while negatively charged ions (Cl, HCO3, P) and cells (epidermal,
macrophage, neutrophil) migrate toward the positive electrode (anode) (Table 9–1).
THEORETICAL BASIS OF ELECTRICAL STIMULATION
Endogenous Electrical Currents

Endogenous electrical currents are measurable biological currents. Examples of
these currents include the transmembrane voltages found in cell membranes and the ac-
tion potentials and electrical impulses carried along peripheral nerves to synapses in
skeletal muscle and along the vagus nerve to facilitate cardiac muscle contraction. Mea-
surable currents are also found in the skin and wounds as well as in the cells that facili-
tate wound repair. This section discusses the biologically inherent currents that are as-
sociated with wounding.
SKIN BATTERY POTENTIAL

The human body and the bodies of mammals and amphibians have an endogenous
bioelectric system that contributes to tissue healing.2–6 Since 1945, several investigators
TABLE 9–1 Cellular Galvanotaxis During Wound Healing Phases

Phase of Cells and Current/
Healing Biological Effects Their Polarity Polarity Investigator
Inflammatory Phagocytosis and Macrophage () DC () Orida and Feldman18
autolysis
Neutrophil () DC () Fukushima et al17
Neutrophil () PC () Eberhardt et al24
Neutrophil () DC () Dineur19/Monguio20
Activated
Neutrophil ()
Proliferative Fibroplasia Fibroblast () PC () Bourguignon &
Bourguignon13/
Bourguignon et al67
DC () Canaday and Lee14
DC () Erickson and
Nuccitelli16
DC () Yang et al23
Remodeling Wound contraction Myofibroblast () PC () Stromberg21
Epithelialization Epidermal () DC () Cooper and Schliwa15
PC (/) Mertz et al25
PC () Greenberg et al124
have reported measuring electropositive voltages from the dermis of superficial wounds
and electronegative voltages from the surface of intact skin.3,4,7 These measurable
transepithelial potentials (TEPs) are known to be present as a result of Na channels in
the apical membrane of the skin’s mucosal surface that allow Na to diffuse from the
outside of epidermal cells to the inside (Fig. 9–1).
Foulds and Barker5 measured TEPs of human skin and reported values ranging
from 10 mV to almost 60 mV depending on the region measured. In addition, they
demonstrated the presence of a skin battery in normal human volunteers by placing a
reference electrode in electrical contact with the dermis and a mobile electrode at multi-
ple positions on the skin. They found the average negative potential for all skin sites of
all subjects to be 23.4 mV (Fig. 9–2). Thus, human skin maintains a variable level of
negative electrical charge on its outer surface that results in part from the diffusion of
Na down its chemical gradient from the skin surface to the interior of epidermal cells.
Further experimental evidence supporting the existence of the skin battery has been
demonstrated by applying amiloride (a compound that blocks Na channels in the outer
epidermal membrane) to the skin. This results in inhibition of the skin battery so that
bioelectric current flow cannot be detected.4
NA CURRENT OF INJURY

When a wound occurs in the skin, the TEP provides the electromotive force needed
to drive a steady, measurable current outward through the low wound resistance pro-
vided by the absence of skin (Fig. 9–3). Essentially, an electrical leak occurs that short-
circuits the skin battery at the wound site, allowing current to flow out of the wound.4
In the skin immediately bordering the wound, there is a steep, lateral voltage gradient
that falls from a high of 140 mV/mm at the wound edge to 0 mV/mm just 3 mm lateral
to the wound edge (Fig. 9–4).8 If the wound is allowed to dry, the resistance of the des-
FIGURE 9–1. Diagram of

Na transporting syncytial ep-
ithelium. Sodium ions enter the
outer cells (top) of the epithe-
lium via specific channels in the
outer membranes of these cells,
migrating along a steep electro-
chemical gradient. Once in the
cell, they can diffuse to other
cells of the epithelium via gap
junctions that join the cells of
the epithelium, and they can be
actively transported from all of
these cells via electrogenic
pumps that are in all of the
plasma membranes of the ep-
ithelum except the outer mem-
brane that has the Na chan-
nels. This results in a transport of Na from the water bathing the epithelium to the internal body
fluids of the animal, and the generation of a 50-mV potential across the epithelium. Tight junctions
between cells at the outer edge of the epithelum minimize the escape of the positive charge trans-
ported inward, and therefore minimize the collapse of the potential generated by the epithelium’s elec-
trogenic Na transport. (From Vanable, JW, Jr: Integumentary potentials and wound healing. In Bor-
gans, RB, et al (eds): Electric Fields in Vertebrae Repair. Alan R. Liss, New York, 1989, with
permission.)
FIGURE 9–2. Average hu-

man skin battery potential mea-
sured on a typical person aged
29 years. The exterior of the skin
was found to be electronegative
with respect to the inside of the
body. Measured in millivolts.
(From Foulds, IS, and Barken,
AT: Human skin battery poten-
tials and their possible role in
wound healing. Br J Dermatol
109:515, 1983, with permis-
sion.)
iccated scab blocks the current flowing out of the wound, eliminating the measurable lat-
eral voltage gradient.4 Interestingly, during a 4-day study, Cheng and associates,9 using
a porcine (pig) model, demonstrated that an occlusive wound dressing maintained a
measurable postwounding current of injury at 29.6 8.6 mV, compared to a signifi-
cantly reduced potential of 5.2 12.6 mV recorded from wounds exposed to air over the
FIGURE 9–3. Current path

with wound made through the
stratum corneum in guinea pig
skin. The skin battery drives
positive charges inward that es-
cape through the wound and
return to the region between
the stratum corneum and der-
mis. Only current on the left
side is depicted. (From Jafee,
LF, and Vanalbe, JW, Jr: Elec-
tric fields and wound healing.
Clin Dermatol 2:34, 1984, with
permission.)
FIGURE 9–4. Lateral potential in the vicinity of a wound made in mammalian skin. The
schematic illustration of the circuit diagram of the skin shows the electrodes for measuring
transepithelial potentials in the vicinity of the wound (left), and representative data obtained
from such determination of transepithelial potentials (top). (For actual data and more detailed
information, see Barker and associates.4) When Rw is low, as when the wound is kept moist, cur-
rent driven by the epidermal TEP flows out of the wound and returns to the battery via RII.
When Rw is high, little or no current flows in the circuit, and little or no lateral field exists at the
edge of the wound. Diagrammatic representation of the relevant layers of mammalian skin cor-
responding to the circuit on the left (below right); the lateral field in the vicinity of the wound,
plotted as a function of distance from the wound edge (above) (based on the hypothetical data
plotted on the left). RII resistance of the return path of the current to the epidermal battery,
along which the lateral potential drop occurs near the edge of the wound; Rw resistance of the
wound. (From Vanable, JW, Jr: Integumentary potentials and wound healing. In Borgans, RB,
et al (eds): Electric Fields in Vertebrate Repair. Alan R. Liss, New York, 1989, p 187, with per-
mission.)
same time period. Their study provides evidence that the wound current of injury can
be sustained with occlusive, moisture-retentive dressings, which may contribute to the
accelerated healing that occurs under occlusion.10,11 Occlusive and other types of dress-
ings that trap transudate or serous fluid consisting of 0.9 percent sodium chloride
(NaCl), provide a wound environment that is friendly to cells. With a deficiency of the
wound’s own “physiological saline,” the sterile commercial substitute known as “nor-
mal” saline may be used to mimic transudate fluid, thereby maintaining a moist wound
environment that also provides a conductive medium for maintaining the flow of the bi-
ological injury current.
Wounds closed by new epithelium do not have a measurable current of injury.
McGinnis and Vanable12 have shown that currents escaping through wounds and their
accompanying lateral voltage gradients were reduced and ultimately became nonexis-
tent owing to the resistance created by the epithelium. Whether the Na current of in-
jury actually contributes to wound healing has not been established. However, animal
model in vivo research with amiloride used to block the injury current may help to an-
swer this question.
GALVANOTAXIS
The measurable Na current of injury that flows outward from hydrated wounds has
a positive polarity (wound positive and intact periwound skin negative) with sufficient
field strength to promote cell migration during the healing events of inflammation, fibro-
plasia, contraction and re-epithelialization.6 After wound closure by re-epithelialization,
collagen remodeling occurs despite the fact that the current of injury and the lateral volt-
age gradient no longer exist. Therefore, there is little reason to expect that wound cur-
rents affect the remodeling phase of healing.
Galvanotaxis is the attraction of positively or negatively charged cells toward an
electric field of opposite polarity. Several studies (see Table 9–1) have reported migra-
tion of cells involved in tissue repair toward the anode or cathode created by an electri-
cal field delivered into the tissue culture.13–23 These in vitro studies demonstrate the gal-
vanotaxis theory, which may be used as the basis for selecting the anode or cathode in
the clinical treatment of wounds with ES.
It is important to note that the weak electrical fields used to cause galvanotaxic mi-
gration of cells in tissue culture may well be generated in vivo. A review of the literature
revealed one human study that analyzed the effect of ES on the cell composition in skin
exudate. In 10 wounds treated with ES for 30 minutes, Eberhardt and associates24 found
that 69 percent of 500 cells counted 6 hours after ES were neutrophils compared to 45
percent found for control wounds. The authors suggested that the 24 percent difference
in neutrophil percentage occurred because of the galvanotaxic effect created by the ex-
ogenously applied currents. Mertz and colleagues25 assessed epidermal migration
macroscopically for 7 days after two 30-minute sessions of monophasic pulsed-current
ES of induced wounds in pigs. They observed that wounds treated with negative polar-
ity on day 0 followed by positive polarity on days 1 to 7 demonstrated enhanced ep-
ithelialization by 20 percent compared to those receiving treatment with either positive
(9 percent) or negative (9 percent) alone. In addition, they observed that alternating
/ polarity daily inhibited epithelialization by 45 percent. Thus, evidence indicates
that cells involved in the different phases of wound healing are partly dependent on en-
dogenous bioelectric signals to facilitate their migration and proliferation. Later in the
chapter, the types and characteristics of electrical currents that have been reported to fa-
cilitate healing of chronic wounds will be described.
Exogenous Therapeutic Currents for Wound Healing
Exogenous (externally applied) therapeutic currents are delivered into the wound tis-
sues from ES devices via an electrical circuit consisting of at least two electrodes that are ap-
plied in direct contact (capacitive coupling) with the receiving body part. The exogenous
current is intended to mimic the normal endogenous currents that facilitate wound healing.
TYPES OF ELECTRICAL CURRENTS

Textbooks on physics describe two basic types of electrical currents: direct current
(DC) and alternating current (AC). However, to give more meaningful descriptions to
the “pulsed” waveforms delivered by the majority of electrotherapeutic devices, the

term “pulsed current” (PC) has been adopted as an additional “medical current” by the
section on Clinical Electro-physiology of the American Physical Therapy Association.
This term, described in a monograph titled Electrotherapeutic Terminology in Physical Ther-
apy,1 is not meant to imply that there is an additional type of basic current (there are still
only two, DC and AC). Figure 9–5 provides a flowchart to facilitate easier comprehen-
sion of the complexity of electromedical currents. Only DC and PC have been used in
wound healing studies. Therefore AC will not be discussed.
Direct Current
Direct current is the continuous, unidirectional flow of charged particles for one sec-
ond or longer (Fig. 9–6). In the tissues, the direction of current flow is determined by the
polarity selected, with positively charged ions moving toward the negative electrode
(cathode) and negatively charged ions moving toward the positive electrode (anode).1
Continuous DC has no pulses and subsequently no waveform. However, because DC
flows for 1 second or longer, when it is delivered (through anode and cathode electrodes)
to a solution containing electrolytes, (e.g., NaCl) or to tissues that also contain elec-
trolytes, the current causes the charged ions of Na and Cl to migrate toward the cath-
ode and anode, respectively. At the cathode, Na reacts with H2O to form NaOH and
H2, while at the anode Cl reacts with H2O to form HCl and O2. Thus, when therapeutic
dosages of DC are delivered to the body, the caustic products that form at the electrode-
tissue interface may create alkaline and acid pH changes at the cathode and anode, re-
spectively. If the dosage of DC (for continuous DC dosage is a function of current am-
plitude in milliamperes or microamperes time) is allowed to flow in the skin and
subcutaneous tissues at a sufficiently high amplitude over a long enough time period,
the pH changes at the electrode-tissue interface will cause observable tissue irritation.
The irritation may manifest itself as erythema observed in light skin tones or as blister-
ing from electrochemical burning secondary to a much greater acidic or alkaline pH
change on the skin. These undesirable responses to DC may be diminished somewhat
Monophasic
Pulsed
Symmetric
Current (PC)
Biphasic Balanced
Asymmetric
Unbalanced
Symmetric
Medical Alternating
Balanced
Currents Current (AC)
Asymmetric
Unbalanced
Direct
Current (DC)
FIGURE 9–5. Three types of electromedical currents (AC, DC, PC) with modulation terms
that describe the number of waveform phases, symmetry, charge balance, and geometric shape.
DIRECT CURRENT (D.C.)

AMPLITUDE
0 1 2 3 4 5 6 7 8
TIME (sec)
FIGURE 9–6. Graphic representation of direct current (DC).
by delivering less than 1.0 mA to the electrodes. Current amplitudes under 1.0 mA are
in the microamperage (A) range.
Several clinical studies discussed in more detail later in this chapter have reported
accelerated healing of chronic wounds after treatment with continuous DC delivered to
the wound at 50 to 1000 A.26–29
Pulsed Current
Pulsed current is the brief unidirectional or bidirectional flow of charged particles
(ions) separated by a longer (off ) period of no flow.1 PC is delivered via electrodes to tis-
sues as a series of pulses. Thus, each pulse is an isolated electrical event separated by a
finite off time from the next pulse event. PC is described by its waveform, amplitude,
duration, and frequency.
Waveform refers to the visual configuration of the current or voltage on a plot of am-
plitude and time. Unlike continuous DC, which has no waveform, PC can have two wave-
forms: monophasic (one phase) or biphasic (two opposing phases). A phase describes an
electrical event that begins when the current (or voltage) leaves the isoelectric (zero) base-
line and ends when it returns to the baseline.1 The monophasic pulse represents a very brief
duration of movement of ions in one direction away from the isoelectric zero line, re-
turning to the zero line after a finite period of time (less than 1.0 second) (Fig. 9–7). In a
monophasic pulse, the amplitude and time-dependent (x-y) characteristics of the phase
and pulse are the same. When the duration of a monophasic pulse is less than 1.0 second,
it is not DC and therefore should not be referred to as either pulsed or continuous DC.
With a high enough pulse amplitude in milliamperes or microamperes, when the
monophasic pulse duration progressively exceeds 1.0 second, the caustic acid and alka-
line pH concentrations increase at the anode and cathode, respectively. These chemicals
are the cause of skin irritation and/or burning that may occur with continuous DC or PC
with sufficient amplitude and durations longer than 1.0 second. (The reader may want to
refer to reference 1 for a more detailed discussion of current types and characteristics.)
Monophasic PC waveforms that have been described in the clinical wound healing
literature include the rectangular waveform (Fig. 9–8),30–35 and the twin-peaked wave-
form of high voltage PC (HVPC).36–39 HVPC typically has very-short-duration (2–20 mi-
croseconds), twin triangular pulses that have single-phase charges on the order of 1.6
Q.37 Because HVPC is unidirectional, the assumption is that this type of current may
have the previously described physical properties similar to DC that result in pH changes
that irritate the skin and wound tissues. However, Newton and Karselis40 reported that
FIGURE 9–7. Graphic representations of pulsed current (PC) showing (A) monophasic PC,
(B) asymmetric biphasic PC, and (C) symmetric biphasic PC.
FIGURE 9–8. Graphic representation of monophasic, high-voltage PC (From Nelson, RM,

and Currier, DP: Clinical Electrotherapy, Norwalk, Conn., Appleton and Lange, 1987, p 63,
with permission.)
statistically significant changes in pH did not occur in forearm or lumbar skin in 30

healthy subjects after 30 minutes of HVPC stimulation. No studies were found that in-
vestigated the effects of monophasic PC on pH changes in a moist wound environment.
The biphasic pulse also represents a very brief duration of movement of charged ions.
However, in this case the movement is bidirectional. The waveform of a biphasic pulse
consists of two phases, one of which deviates from the isoelectric zero line, and after a
brief finite time returns to baseline. Then without delay (or in some waveforms, a few
milliseconds’ delay), the second phase leaves the isoelectric zero line in the opposite di-
rection, and after a brief time returns to baseline. The biphasic waveform may be sym-
metrical or asymmetrical about the isoelectric zero line. In the symmetric biphasic wave-
form, all variables (amplitude, duration, rate of rise and decay) are identical with respect
to the isoelectric line for each phase. Therefore, the phase charges of each phase of this
waveform are electrically equal or balanced. In the asymmetric biphasic waveform, one
or more of the waveform variables for each phase are unequal with respect to the iso-
electric line. Asymmetric waveforms may be electrically balanced or unbalanced. Bipha-
sic symmetrical (charge balanced)41–43 and asymmetrical (charge balanced)41,42 wave-
forms have been described in recent wound healing literature (see Fig. 9–7).
LITERATURE REVIEW
Basic Science Research
Two major groups of studies, in vitro studies and animal studies, have been con-
ducted to evaluate the effects of ES. In vitro studies have demonstrated the antibacterial
effects of ES, whereas animal studies have demonstrated the effects of ES on specific as-
pects of wound healing, such as wound scar tensile strength, skin collagen, epithelializa-
tion, capillary density, protein synthesis, and adenosine triphosphate (ATP) generation.
IN VITRO STUDIES (ANTIBACTERIAL EFFECTS OF ES)

Wound healing is slowed or prevented when infection is present. Several in vitro
and in vivo studies have reported that ES either has an inhibitory (bacteriostatic) effect
or a killing (bactericidal) effect on microorganisms that commonly colonize or infect
wounds. The results of these studies suggest that by reducing the number of bacteria in
highly colonized or infected wounds, more nutrients are made available to tissue cells
involved in wound repair, one mechanism by which ES facilitates wound healing. Row-
ley44 reported bactericidal effects in vitro on Escherichia coli B growth rates using catho-
dal microamperage (1.0 mA) and milliamperage ( 1.0 mA) DC. Rowley and col-
leagues45 demonstrated a similar effect using 1000 A of cathodal DC on rabbit skin
wounds infected with Pseudomonas aeruginosa. Barranco and coworkers46 used cathodal
DC to decrease the growth rate of Staphylococcus aureus in infected rat and rabbit femurs
after ES lasting 1 hour. In other in vitro studies that also used microamperage DC, an-
timicrobial effects occurred at the anode when current was delivered to colonized cul-
ture media through a silver electrode.47,48 In these studies, investigators found that 100
A DC delivered to the culture medium via the anode had a bacteriostatic (growth sup-
pression) on five of six Gram-positive bacteria and one fungus, whereas the same cur-
rent and polarity produced a bactericidal effect on six different Gram-negative bacilli.
More recently, investigators compared the in vitro antibacterial effects of mil-
liampere levels of HVPC with milliampere levels of DC applied for two 30-minute ses-
sions.49 They reported that neither anodal nor cathodal HVPC applied at amplitudes
ranging from 50 to 800 mA and a frequency of 100 pulses per second (pps) for 30 min-
utes had inhibitory effects on S. aureus. However, both anodal and cathodal continuous
DC applied at 1, 5, and 10 mA did inhibit S. aureus growth. The findings from this study
suggest that the mechanism by which DC kills bacteria is through the acid and alkaline
pH changes that occur at the anode and cathode of DC, respectively. As mentioned ear-
lier, human skin pH changes at the anode and cathode did not occur in one study with
HVPC applied for 30 minutes.40 However, Kincaid and Lavoie50 did observe pH changes
in vitro when they evaluated the antibacterial effects of HVPC. In their study, the pH of
the culture medium at the cathode increased to between 8.5 and 9.0 with increasing time
or voltage to a maximum after 4 hours of HVPC delivered at 500 V. Despite no change
in pH at the anode, they reported that three microorganisms commonly found in human
wounds were inhibited at both the anode and the cathode when exposed to HVPC for 2
hours at 250 V.
Szuminsky and coworkers51 attempted to identify the mechanisms by which HVPC
is bactericidal in vitro. They observed bactericidal effects at both the anode and cathode
after delivering 500 V into culture mediums containing four different species of bacteria
that commonly colonize wounds. However, they were unable to determine whether the
bactericidal effect was due to the direct action of the current on the organisms, an elec-
trophoretic recruitment of antimicrobial factors, local heat generation, or pH changes.
Although both of the latter studies demonstrated antimicrobial effects in vitro, it is un-
likely that the high voltages used would be tolerated if applied to the wounds of human
subjects.
In summary, in vitro studies have reported that antibacterial effects are more likely
to occur with non-noxious microamperage DC applied to common wound pathogens
through the cathode, whereas the voltages required for antibacterial effects with HVPC
would elicit significant and muscle contractions. No studies were found that examined
the antibacterial effects of other PC waveforms, nor were studies found that compared
the antibacterial effects of ES versus antibiotics. None of the studies cited reported detri-
mental effects of ES on tissues or cells involved in the healing process.
ANIMAL MODEL STUDIES

Numerous animal studies have reported a variety of tissue and cellular effects in re-
sponse to delivering electrical energy into wounds. Direct extrapolation of the findings
reported from these studies to chronic wound healing in humans cannot be made be-
cause of species differences. Additionally, most of the animal studies treated acute
wounds that had been induced by trauma. Also, not all of the animal studies corrobo-
rate with findings that have been reported in human subject studies. Therefore, the
reader will have to draw his or her own conclusions regarding the value of the findings
from the animal studies.
Effect of ES on Wound Scar Tensile Strength

Assimacopoulos52 treated induced wounds in rabbits with 100 A of DC from the
cathode applied continuously until healing was complete. Treated wounds healed 25
percent faster than control wounds. The treated wounds also had larger and stronger
scars composed of dense connective tissue and collagen fibers arranged parallel to the
scar surface. Control wounds took longer to heal, were weaker, and had smaller scars
with less dense connective tissue and collagen fibers arranged perpendicular to the scar
surface. The breaking load required to fail or rupture the scars treated with ES was ap-
proximately twice that required to fail the control scars. In a study by Bigelow and as-
sociates,53 scars of induced wounds in dogs treated with 10 to 20 A of DC from the cath-
ode also had greater tensile strength compared to scars of control wounds, whereas
wounds treated with anodal DC had decreased tensile strength compared to control
wounds.
Increased wound scar tensile strength was also observed in a study by Carey and
Lepley.54 They delivered 200 to 300 A of anodal or cathodal DC continuously through
stainless steel wires placed in parallel incisions in rabbit wounds sutured with silk. In
five animals treated for 3 days, cathodal DC–treated wounds had twice the tensile
strength of anodal DC–treated wounds in four cases. In the fifth animal, tensile strength
of the cathodal DC–treated wound was 50 percent stronger than that of the anodal
DC–treated wound. Without consideration given to polarity, Konikoff55 reported an in-
crease in wound tensile strength of 53 percent after 7 days of DC treatment delivered to
incisions at a mean current density of 8.4 mA/cm2. By straddling treatment and control
wounds with the anode and cathode, Smith and coworkers56 also demonstrated an in-
crease in wound tensile strength in wounds of diabetic mice after delivery of 10 to 20 mA
of DC at 1-minute intervals, 5 days per week for 2 weeks.
Obviously no conclusions can be drawn from the latter two studies regarding the
effects of polarity on wound tensile strength. The findings from the first three of these
five studies contradict the expected findings based on the empirical assumption that
cathodal DC should decrease wound tensile strength, whereas anodal DC should in-
crease it. These assumptions are based on the fact that cathodal DC creates an alkaline
pH, and a base such as dilute bleach (e.g., Dakin’s solution) is known to be sclerolytic
and capable of softening or solubilizing necrotic tissue. Therefore, the cathode would be
expected to decrease the scar tensile strength of the healing wound.
Conversely, anodal DC creates an acid pH with a resultant sclerotic effect that
would be expected to increase rather than decrease the scar tensile strength of the heal-
ing wound, as was observed in three of the studies already mentioned.52–54 Interestingly,
Brown and Gogia57 applied HVPC to induced wounds in rabbits to determine the effects
of cathode polarity on wound closure and tensile strength. They applied the active cath-
ode to wounds of the experimental group and an inactive (sham) cathode to wounds of
the control group for 2 hours twice daily for either 4 or 7 days at 30 to 60 V, 80 pps, and
pulse duration of 100 microseconds. After 4 days, wound scar tensile strength in the ex-
perimental group was 36 percent greater than that in control animals. However, neither
this difference nor the difference in the percentage of wound closure between the two
groups was statistically significant. After 7 days, control wounds demonstrated more
closure than treated wounds. Control wound scars also had significantly greater tensile
strength than treated scars. This tensile strength response at 7 days is the response one
would anticipate with cathodal DC, not cathodal PC. Recall that Newton and Karselis40
demonstrated that HVPC does not create acid and alkaline pH changes on the skin at
the anode and cathode, respectively. Thus, it appears unlikely that HVPC will cause ei-
ther a sclerolytic effect or a sclerotic effect on wound tissues at the cathode and anode,
respectively. Therefore, the mechanism by which cathodal HVPC facilitates an increase
in wound tensile strength may be attributed to galvanotaxis of fibroblasts that secrete
collagen. More basic science research is needed to answer this question definitively.
In a second study using the same research design just described, Brown and col-
leagues58 applied the anode to the wounds of animals in the active treatment group. Af-
ter 4 days, wound closure was significantly less for treated wounds than for control
wounds. Between 4 and 7 days after injury, wound closure values for treated animals in-
creased from 50 to 80 percent. At 7 days after injury, wound closure was similar for the
treatment and control groups. Although no difference in tensile strength between treat-
ment and control wounds was noted after 4 to 7 days of anodal stimulation, histologic
examination revealed that epithelialization had occurred more rapidly in wounds
treated with HVPC. This latter finding suggests that the more rapid rate of epithelial-
ization may have been influenced by the galvanotactic attraction of negatively charged
epidermal cells by the anode, as reported by Cooper and Schliwa.15
In a third study, Brown, and coworkers59 evaluated the effects of HVPC on wound
closure, tensile strength, and mitotic activity in induced wounds in rabbits. Twenty-four
hours after wounding, animals in the treatment group received HVPC for 2 hours, twice
daily for 7 days. Polarity was negative for the first 3 days and then positive for the re-
maining 4 days. Wound closure for HVPC-treated animals was 100 percent, significantly
better than that for control animals (87 percent). No difference in wound scar tensile
strength or mitotic activity between the two groups was noted. In summary, the pre-
ponderance of evidence cited from animal studies suggests that wound tensile strength
may be enhanced with 10 to 300 A of cathodal DC. Unfortunately, the evidence from
studies with HVPC is unclear at this time.
Effects of ES on Other Factors Related to Wound Healing

Many studies have used rat or pig models to investigate the effects of ES on skin
healing. Cheng and colleagues60 analyzed some of the biochemical effects that occur in
rat skin tissue during ES. They reported that 10 to 1000 A of continuous DC (polarity
not mentioned) applied to skin strips 0.5 mm thick for 2 hours in vitro increased the ATP
concentration in the skin fivefold. Optimum increased production of ATP occurred
when the current amplitude was set at 500 A DC. At 1000 A DC, ATP generation
equaled concentrations measured in control skin. In addition, they also reported that 100
to 500 A DC increased amino acid uptake by 30 to 40 percent above control levels and
that a current amplitude of 50 A DC was required to obtain a maximum stimulation ef-
fect on protein synthesis. Alvarez and coworkers10 showed a highly significant increase
in the collagen synthesis and rate of epithelialization in wounds treated with 50 to 300
A of anodal DC.
Winter11 observed that epidermal cells undergoing migration during re-epithelial-
ization in pigskin originate in a strip of intact skin less than 0.5 mm wide on the perime-
ter of the wound. As previously mentioned, Jaffe and Vanable8 measured a steep, lateral
voltage gradient that falls from a high of 140 mV/mm at the wound edge to 0 mV/mm
just 3 mm lateral to the wound edge. Of clinical significance is the finding that when the
perimeter of superficial wounds is allowed to dry, this lateral voltage gradient is sup-
pressed or eliminated, possibly explaining why epithelialization progresses more slowly
in dry wounds than in moist wounds.11 Winter demonstrated that, compared to air-
exposed wounds, cutaneous wounds that are kept moist are covered by epidermis twice
as quickly.
The significant increase in collagen synthesis reported by Alvarez and coworkers10
after anodal ES of induced wounds in pigs has also been reported more recently by sev-
eral other investigators. In one rat study, both DC and AC delivered to skin incisions at
20 A and 100 A, respectively, caused statistically significant increases in collagen con-
centration in and around the wounds compared to control wounds. However, the in-
creases in collagen had no effect on wound tensile strength.61 No explanation was given
for this latter finding, which does not agree with the findings of Nikolaew and cowork-
ers.62 These researchers used the same stimulation parameters and research methodol-
ogy and reported a 200 percent increase in wound tensile strength.
Another study by Castillo and associates63 evaluated the influence of pulsed ES on
healing of burned wounds in rat skin. Using scanning electron microscopy, they evalu-
ated wound tissue that had been treated with biphasic PC (whether it was charge-
balanced or -unbalanced was not identified) at 67 Hz, 0.04 mA, and current density of 0.6
C/cm2 for 20 minutes daily, for 20 days starting immediately after the burn was inflicted
(group A). They also evaluated three other groups of rats including group B, whose burns
were treated twice daily for 20 days with iodine-polyvinylpyrrolidone; group C, which
served as an untreated burned control; and group D, in which the rats were neither
burned nor treated, from which normal skin was obtained. After the first ES treatment
they observed that group A animals could be distinguished by a marked hyperemia, sug-
gesting that the biphasic PC was charge-unbalanced. They found highly significant in-
creases in collagen density for the ES group (A) and the unburned skin group (D) com-
pared to the iodine-treated group (B) and the untreated skin group (C). In addition, the
number of capillaries was statistically greater in the skin of the ES-treated group com-
pared to skin in groups B, C, and D. Furthermore, they observed that wound contraction
was faster for ES-treated wounds than for the other groups. Although wound infections
developed in six rats in group C, no infections occurred in the ES group.
Two other controlled studies investigated the effects of microelectroneuromuscular
stimulation (MENS) on acute wound healing,64,65 histologic changes in rats,64 and histo-
logic changes and subcutaneous partial pressure of oxygen (PsqO2) in Yucatan pigs.65 In
the study on rats, no treatment effect on wound healing was demonstrated, nor were any
effects on epithelial thickness, fibroblast density, or vascular density noted.64 Likewise,
in the Yucatan pig study, there was no evidence of a treatment effect on wound healing
and no changes in PsqO2, collagen deposition, tensile strength, or mast cell degranula-
tion.65 The authors of these two studies attributed the lack of an effect on wound size and
histologic changes to the use of less than optimal stimulation variables (e.g., 100 A at
either 0.1 or 0.3 pps and a 50 percent duty cycle) and small sample sizes that yielded low
statistical power.
Cruz and coworkers66 also studied the effects of ES on burn wounds. They induced
two burns over the paravertebral region in 20 pigs and delivered cathodal HVPC at 175V
and 60 pps for 10 minutes daily for 4 weeks through two active electrodes that straddled
the wounds of 10 pigs. Wounds of 10 control animals received the same protocol with in-
active electrodes. At weekly intervals, the surface area of one wound on each animal was
traced and digitized to evaluate wound contraction, whereas from the second wound on
each animal, tissue was harvested for histologic evaluation of fibroblast count. Results re-
vealed that burn wounds treated with ES had accelerated rates of healing that were sta-
tistically significant (P 0.001) at each weekly interval studied compared to that of the
control wounds. At the end of 4 weeks, 40 percent of the ES-treated wounds were com-
pletely closed, whereas none of the control wounds had closed. Evaluation of the weekly
wound biopsies also revealed a statistically significant increase (P 0.001) in the number
of fibroblasts in ES-treated wounds compared to that of control wounds. Thus, the faster
rate of wound healing in the ES-treated wounds may be explained by the increased pro-
liferation of fibroblasts and their associated collagen production, which has been reported
by other investigators67,68 who stimulated fibroblasts in cell culture with HVPC and ob-
served increased amounts of DNA and collagen synthesis.
In a randomized, controlled trial, Taskan and colleagues69 placed incised wounds
in the backs of 24 rats and treated them with cathodal DC at 300 A continuously for 30
minutes per day for 3 days. Similar incisions were made in 18 rats that received sham
stimulation during the same time period. On days 4 to 6, the active treatment electrode
polarity was changed to the anode, followed by the cathode on day 7 (the last day). His-
tologic analysis of skin samples revealed that collagen was denser and more regular in
arrangement for the active ES group than for the sham ES group on day 7, a finding that
corroborates findings in the literature.13,70,71 The high number of fibroblasts in wounds
of the active ES group on day 7, which is consistent with the literature,57 indicates that
the wound had progressed to the proliferative phase. In summary, the evidence cited
from animal studies regarding the effect of ES on wound collagen production is equiv-
ocal with respect to polarity. However, it is clear from these studies that ES does facili-
tate collagen production in wounds, perhaps by some other biological mechanism.
Effect of ES on Skin Grafts, Donor Sites, and Musculocutaneous Flaps

Chu and associates72 observed that the time required for wound healing, contrac-
tion, and hypertrophic scarring often limits the use of deep, partial-thickness burn
wounds as donor sites for split-thickness grafts. They investigated the effects of weak
anodal DC (20–40 A) delivered through silver nylon dressings for 5 days in a guinea
pig model on (A) healing of partial-thickness scald burns, (B) split-thickness grafts taken
from these wounds when healed, and (C) the resulting donor sites. Scald wounds in 180
animals treated with weak DC re-epithelialized within 12 days after the burn, whereas
only 20 of 40 animals with control wounds that received sham DC had re-epithelialized
within 16 days after the burn. Compared to control grafts, split-thickness grafts taken
from the healed scald wounds showed more rapid revascularization with DC treatment.
Grafts and donor sites treated with DC showed more rapid re-epithelialization, de-
creased contraction, improved hair survival, and decreased dermal fibrosis compared to
controls not treated with DC. Only donor wounds treated with DC could be repeatedly
harvested as donor sites for successful split-thickness autografts. The authors theorized
that DC treatment may not facilitate wound healing, but rather may limit the extent of
tissue destruction as evidenced by DC-treated wounds having less inflammation, gran-
ulation tissue, and fibrosis than control wounds.
Other investigators have studied the effect of cathodal HVPC on macromolecular
leakage from microvessels after induced trauma in hamsters73,74 and rats.75 These stud-
ies have all reported that microvessel leakage was curbed with submotor levels of stim-
ulation. Human subject studies using cathodal HVPC on grafts and donor sites are
needed to determine whether this therapy limits trauma-induced inflammation, edema,
and fibrosis associated with skin grafts and donor sites.
Politis and colleagues76 also used microamperage DC to determine whether ES
could improve the post-traumatic quality of dermis and epidermis in full-thickness skin
grafts in rats. Using an ES device that delivered 4.5 A of DC for 3 days, they studied
the effects of three surgically implanted electrode configurations: anode on top of the
graft, cathode on top of the graft, and an inactive electrode on top of graft. Quantitative
and histologic assessment on postoperative day 7 revealed the presence of necrotic skin
in 80 to 90 percent of graft surface areas in animals treated with cathodal stimulation and
control animals that received no current. In animals treated with anodal DC, only 50 per-
cent of the graft area was necrotic and the significantly thicker dermis had multilayered
patches of intact epidermis.
Two other studies investigated the effect of ES on survival of ischemic skin77 and
musculocutaneous flaps.78 Im and coworkers77 stimulated the ischemic central portion
of bipedicle skin flaps in pigs with a monophasic PC at 35 mA, 128 pps, and a pulse du-
ration of 140 microseconds for 30 minutes twice daily for 9 days after skin-flap elevation.
The skin flaps were stimulated with the cathode on postoperative days 1 to 3, with the
anode on days 4 to 6 and with the cathode on days 7 to 9. Two control pigs received sham
ES treatment, and two others received no treatment. The length of viable flap and the ex-
tent of skin necrosis were measured on postoperative day 21. The mean area of skin flap
necrosis was 28 percent in control animals and 13.2 percent in ES-treated animals (P
0.001). The authors proposed that the initial 3 days of cathodal treatment may have pre-
vented severe ischemia by blocking sympathetic vasoconstriction and also negated
ischemia-reperfusion that may have occurred in the transition zones of the skin flap.
They also theorized that anodal stimulation of the flap in the later stages of tissue repair
might have prevented tissue injury by scavenging superoxide radicals.
The other study that evaluated the effect of ES on flaps used an ES device, transcu-
taneous electrical nerve stimulation (TENS) with an unspecified waveform and para-
meters customarily used to suppress musculoskeletal pain.78 In this study, 10 groups of
rats received different intensities (milliamperes) and pulse-frequency modes for post-
operative treatment of musculocutaneous flaps. A highly significant difference (P
0.001) was noted between the group with the highest percentage of flap survival (94.6
percent)—which received high-intensity (20 mA), high-frequency (80 pps) stimulation
delivered to the base of the flap for three days—compared to the other groups. Also, a
significant difference (P 0.001) in flap survival occurred when high-intensity (20 mA)
treatment was compared to low-intensity (5 mA) treatment. Flap survival was not re-
lated to the ES frequency used. In summary, the evidence cited from animal studies sug-
gests that ES facilitates the survival of failing skin grafts and musculocutaneous flaps.
Clinical studies are needed to substantiate the findings from these animal studies.
Clinical Research
Clinical trials on human subjects, designed to answer research questions pertaining

to the mechanisms responsible for wound healing or questions related to the efficacy of
a particular wound treatment, are highly desirable to clinicians and patients who want
the most effective treatment options, and to third-party payers who base reimbursement
for services on evidence-based clinical studies. This section addresses human subject
studies designed to answer several questions related to the clinical effects of ES.
IMPROVEMENT OF TISSUE OXYGENATION

There is mounting evidence from human subject studies that ES facilitates a tempo-
rary increase in local tissue oxygen tension. It is universally recognized that cells involved
in tissue repair require oxygen to function most efficiently. Cells become inefficient in hy-
poxic tissue environments and die in anoxic environments. Although oxygen is needed
for the survival of cells involved in wound healing, bacterial cells that have detrimental
effects on wound healing processes are adversely affected by elevated levels of tissue oxy-
gen saturation. In fact, PsqO2 decreases resistance to infection by impairing the oxidative
killing of bacteria by neutrophils.79
Gagnier and associates80 tested the effects of ES on the transcutaneous partial pres-
sure of oxygen (TcPO2) in 30 individuals with spinal cord injury (SCI). Ten patients were
assigned to each of three groups that received ES either by a positive or negative
monophasic paired-spiked waveform or by a symmetric biphasic square waveform. All
three groups received submotor stimulation. Thirty minutes before stimulation, during
30 minutes of stimulation, and 30 minutes after stimulation was stopped, the TcPO2 was
monitored and compared with the prestimulation baseline. The TcPO2 increased signif-
icantly compared with prestimulation values in each of the three groups both during
and after stimulation. However, no statistically significant differences in TcPO2 changes
were found among the three different ES waveform groups. The authors suggested that
all three waveforms and the protocol they described could be used with SCI subjects to
increase local TcPO2 to facilitate wound healing.
To further study the effects of ES on cutaneous oxygen levels, Dodgen and col-
leagues81 enrolled 10 diabetic patients and 20 age-matched normal subjects to participate
in three sessions of ES. They delivered current from monophasic, paired spikes through
the cathode placed over the gastroc-soleus muscle group at a stimulus amplitude just be-
low muscle contraction. They also delivered an asymmetric biphasic (balanced) wave-
form via the cathode placed over the gastroc-soleus with the amplitude set to either of
two levels: just below muscle contraction or adequate enough to elicit a 1 level con-
traction. TcPO2 levels were measured by oximetry for 30 minutes before ES, during a 30-
minute stimulation session, and for 30 minutes after the stimulation session. The older
normal subjects demonstrated increased TcPO2 after 30 minutes of stimulation regard-
less of the waveform or level of stimulation used. This increase continued for 30 minutes
after stimulation ended. Diabetic subjects showed no significant increases in TcPO2 after
30 minutes of ES, but they did show significant increases in TcPO2 30 minutes after stim-
ulation ended. Perhaps the delayed response in the diabetic subjects could be attributed
to neuropathic changes compromising sympathetic vasomotor control and/or to sen-
sory nerve dysfunction compromising conduction of sensory afferent impulses.
In a study by Peters and coworkers,82 diabetic patients with impaired vascular func-
tion, who had one foot and lower leg treated with subsensory ES delivered through a sil-
ver mesh sock for 60 minutes on 2 consecutive days, did not have the delayed response
to an increase in TcPO2 that occurred in the study by Dodgen and associates.81 In con-
trast, patients in the former study82 showed a significant increase in perfusion in the
stimulated extremity, reflected by a significant increase in TcPO2 after 5 minutes of ES.
These results suggest that ES increases cutaneous oxygen saturation secondary to in-
creasing local perfusion in diabetic subjects. Therefore, ES may be useful in augmenting
wound healing in diabetic and other patient populations, such as elderly people and per-
sons with SCI, known to have poor healing of chronic wounds (e.g., pressure ulcers, leg
ulcers caused by vascular compromise).
The effect of ES on TcPO2 has also been studied on individuals with SCIs. It is widely
accepted that SCI patients have an altered autonomic nervous system. Some evidence
also suggests that the number of adrenergic receptors in the skin below the level of the
spinal cord lesion could decrease.83 The reduced number of adrenergic receptors could,
in turn, cause abnormal vascular responses in the skin below the level of cord injury.
Other investigators have determined that the TcPO2 in the skin over the sacrum84,85 in
the supine position, and the tibia86 is lower in persons with SCI than in able-bodied in-
dividuals. This evidence indirectly suggests that the abnormal vascular responses in the
skin below the level of the spinal cord lesion may reduce cutaneous blood flow, thereby
lowering tissue oxygenation and predisposing the tissues to pressure ulcer formation.
Mawson and associates87 specifically investigated the effect of ES on TcPO2 in the
sacral skin of SCI patients at high risk for pressure ulcer development in this area. The
objective of their study was to determine whether HVPC stimulation could increase
sacral skin TcPO2 in SCI patients lying prone and supine. The normal TcPO2 range is 60
to 100 mmHg.85 In one group of three subjects (two incomplete quadriplegics and one
complete paraplegic), they applied ES with subjects lying prone, for two 60-minute ses-
sions a few days apart. The cathode was placed at spinal level T6 and the anode at L2.
During the first session for each subject, parameters were set at 50 V and 10 pps. During
the second-session parameters were set at 75 V and 10 pps. After a 5-minute baseline
recording, TcPO2 was recorded at 5-minute intervals during each 60-minute stimulation
period, and during a 20-minute post-stimulation period. For all three subjects in the
prone-lying position, they found that stimulation with HVPC led to a sustained, dose-
related increase in TcPO2 at the sacrum. The increase was more dramatic in two subjects
with baseline TcPO2 values at or below the lower end of the normal range. The authors
noted that stimulation with 100 V had no additional incremental effect on TcPO2 levels
above that achieved with 75 V. In a second group of 29 SCI subjects lying supine, HVPC
was applied with the cathode (polarity assumed) positioned at spinal level T6 and the an-
ode at T12. Before ES was administered, TcPO2 was recorded from sacral skin at the end
of a 15-minute baseline period. The ES parameters used included 75 V, 10 pps delivered
for 30 minutes, followed by a 15-minute poststimulation period of 15 minutes. After 30
minutes of ES, TcPO2 increased 35 percent to 66 mmHg, from a baseline of 49 mmHg (P
0.00001). This level fell slightly to 63 mmHg by the end of the 15-minute poststimula-
tion period. The investigators hypothesized that ES may be able to prevent development
of pressure ulcers by restoring sympathetic tone and vascular resistance below the level
of the cord lesion, resulting in an increase in perfusion to the cutaneous capillary beds.
AUGMENTATION OF CUTANEOUS BLOOD FLOW WITH MOTOR LEVEL

STIMULATION
Numerous studies have investigated the effect of ES on blood flow in the extremi-
ties. In some of these studies investigators have applied ES to the skin of the distal ex-
tremity while measuring changes in arterial perfusion in the same or in other extremi-
ties. Kaada88 successfully treated 10 patients with 19 leg ulcers of various etiologies
using the burst mode from a traditional TENS device. He delivered 15 to 30 mA of pulsed
DC via the cathode for 30 to 45 minutes, three times daily to the web space between the
first and second metacarpals of the ipsilateral hand. The anode was positioned at the ul-
nar border of the ipsilateral wrist. All of the ulcers, which had resisted treatment for sev-
eral months to 4 years, healed completely in response to the remote pulsing stimulation
of muscles underlying the electrodes on the hand and wrist.
Kaada88 proposed that the remote ES of hand muscles improved microcirculation
in tissues of the ipsilateral lower extremity (LE), as evidenced by increased temperature
of the toes and healing of the leg ulcers. He further proposed three mechanisms by which
remote ES of hand muscles may cause vasodilation of small vessels in the ipsilateral LE:
(1) activation of a central serotonergic link that inhibits sympathetic vasoconstriction; (2)
activation and release of vasoactive intestinal polypeptide into the plasma; and (3) acti-
vation of a segmental axon-reflex leading to vasodilation. The finding that serotonin in-
hibitors block the vasodilation response, whereas the opiate antagonist naloxone and an-
tagonists of humoral vasodilators do not affect the responses, provides supportive
evidence for the first-proposed mechanism.88–93
Other investigators have also reported vasodilation responses of hand and digital
vessels to remote transcutaneous stimulation of the skin over the spinal cord94 or ulnar
nerve95 at microamperage DC levels of ES; however, not all studies using such levels
agree with these findings. One study96 reported a reduction in digital temperature, sug-
gesting vasoconstriction of digital vessels after sensory and motor excitation elicited by
noninvasive stimulation of acupuncture points. Ernst and Lee97 applied pulsed mi-
croamperage DC levels of ES to the dorsal web space of the hand with a monophasic
pulse duration of 800 microseconds delivered below the pain threshold at 1 pps. They
reported an increase in sympathetic constrictor tone with subsequent vasodilation after
50 minutes. In a controlled study,98 no change in sympathetic tone was noted after sen-
sory stimulation in patients with chronic pain.
Despite the equivocal research findings related to the use of pulsed microamperage
DC levels of ES and the remote effects produced on circulation in the distal extremities,
this approach to treatment of hand, foot, and digital ulcerations may prove effective in
facilitating increased perfusion and wound repair in patients with primary diagnoses of
Raynaud’s disease, reflex sympathetic dystrophy, and pain associated with diabetic
polyneuropathy. For more information related to the findings of Kaada, the reader is re-
ferred to the literature citations.
AUGMENTATION OF MUSCLE ARTERIAL BLOOD FLOW WITH PULSED

MOTOR LEVEL STIMULATION
Several animal studies have demonstrated that ES applied to innervated skeletal
muscle at low frequencies (2–20 pps) and stimulation intensities greater than 10 percent
of maximum voluntary contraction, causes increased local intramuscular blood
flow.99–103 Likewise, a number of human studies have confirmed that ES applied at an
amplitude high enough to elicit a continuous series of pulsating (nontetanizing) muscle
contractions increases regional blood flow in asymptomatic individuals and patients
with peripheral arterial insufficiency. Currier and associates104 used motor level stimu-
lation to elicit isometric contractions from the calf muscles of healthy subjects equal to
10 and 30 percent of maximum voluntary contraction using 2500 Hz AC with a 50 per-
cent duty cycle. Using a Doppler flowmeter to measure blood flow delivered to the leg
through the popliteal artery, they reported a significant increase in blood flow to the
stimulated leg during the first minute and for a poststimulation period. Tracy and
coworkers105 reported increased blood perfusion through the femoral artery as a result
of pulsed contractions of the quadriceps at frequencies of 10, 20, and 50 pps but not at 1
pps. Skudds and colleagues106 found that pulsating contractions of hand muscles in
asymptomatic individuals increased local blood flow, evidenced by a measurable in-
crease in hand skin temperature.
AUGMENTATION OF MUSCLE ARTERIAL BLOOD FLOW WITH

SUSTAINED TETANIZING CONTRACTION
A number of studies using ES to produce sustained tetanizing contractions in healthy
individuals have reported that muscle blood flow either decreased or was less than blood
flow noted in control subjects.107–109 These studies, in which muscle contractions were sus-
tained with ES, suggest that prolonged, tetanized contractions—whether evoked by ES or
by volition—will likely compress intramuscular arteries long enough to reduce mean ar-
terial blood flow. Thus, eliciting sustained contractions from skeletal muscle would be
counterproductive in the treatment of wounds that are compromised by ischemia.
AUGMENTATION OF FOOT AND CALF MUSCLE PUMPS AND VENOUS

BLOOD FLOW WITH PULSED ES
In the physical therapy management of the patient with venous insufficiency of the
LE, or one at risk for developing deep venous thrombosis (DVT) after surgery, and for
the patient with inefficient or failed foot and calf muscle pumps, ES has an important
role to play in facilitating venous and lymphatic outflow from the limb. Here, the clini-
cal application of pulsed ES is discussed with reference to enhancing venous blood and
lymphatic flow by mimicking the foot and calf muscle pumping systems that normally
propel venous blood and lymph out of the LE during ambulation activities. Chronic
edema of the LE is a common clinical manifestation of venous insufficiency, due in large
part to venous hypertension, incompetent venous valves, and inefficient or failed foot
and calf muscle pumps in some individuals.
Normally, when the individual is in a standing position, the hydrostatic pressure in
the deep veins of the lower leg and foot is about 90 mmHg.110 When distal LE venous
pressure is maintained at this or higher levels as a result of prolonged standing or de-
pendency, pressure in the venules also increases greatly, causing water, electrolytes, and
hydrophilic plasma proteins (especially albumin) to leak out of the capillaries into the
interstices, creating edema. With each step during ambulation, compression of the ve-
nous sinusoids in the foot and contraction of the calf musculature propel venous blood
toward the heart. This momentarily reduces venous pressure in the distal LE to less than
25 mm Hg.110 If LE venous valves are incompetent because of previous damage to them
from DVT or thrombophlebitis, then because of venous reflux, the foot and calf muscle
pumps may become inefficient in promoting venous and lymphatic outflow from the LE.
Total failure of foot and calf pumps and LE edema can occur in the absence of previous
DVT or thrombophlebitis when the calf musculature is severely weakened or paralyzed
from neuromuscular disease, stroke, or SCI. For these conditions, electrically induced,
pulsating muscle contractions may be used clinically to facilitate venous and lymphatic
return, thereby promoting reduction of existing extremity edema by mimicking the vo-
litional calf muscle pumping system.
Studies involving repeated voluntary and electrically elicited muscle contractions
in healthy humans to facilitate venous and lymphatic flow rates is well docu-
mented.111–113 Furthermore, numerous studies have reported that ES of calf musculature
prevents a decrease in the rate of venous blood flow from the LE during surgical proce-
dures, thereby decreasing the occurrence of DVT.114–123 Thus, ES may be used to prevent
DVT in the LE during and after surgery, thereby reducing the likelihood of developing
incompetent venous valves and the complications of venous hypertension and LE
edema. In addition, ES may be used adjunctively to treat existing LE edema secondary
to venous insufficiency. To successfully use ES to augment venous blood flow, prevent
DVT, or reduce existing edema from venous hypertension, ES must elicit moderately
strong, 1-second, pulsating contractions from the foot and calf muscle masses, thereby
emptying the venous sinusoids found in the intrinsic flexor muscles of the foot and calf
muscles. Based on the literature,99,103,111 recommended pulsed stimulation parameters
that produce a pumping effect from foot and/or calf muscles are as follows: pulse fre-
quency, 20 pps; stimulation on-time, 3 seconds; stimulation off-time, 5 seconds; and
stimulus amplitude, set to evoke a contraction of foot and/or calf muscle(s) that is 10 to
20 percent of the patient’s maximum voluntary contraction.
AUGMENTATION OF ANGIOGENESIS IN WOUND TISSUE BY ES

Two recent studies reported increased blood flow secondary to increasing capillary
density in human wounds treated with ES. Junger and coworkers35 reported a mean in-
crease of 43.5 percent in capillary density in the venous leg ulcers of 15 patients whose
wounds had not improved after several months of standard care. They treated the
wounds with monophasic PC for 30 minutes daily for a mean of 38 days. The monopha-
sic PC with a 140-microsecond pulse duration delivered a weak DC component having

an average current of 630 A at 128 pps or 315 A at 64 pps. For the first 7 to 14 days,
they delivered 630 A of current to the wounds via the cathode. They then switched the
treatment electrode polarity to positive for 3 to10 days. After this time, the polarity was
changed back to negative. When the wound had made significant clinical progress to-
ward healing, they reduced the current amplitude to 315 A. Capillary density, as ob-
served by light microscopy, improved from a prestimulation baseline of 8.05 capillar-
ies/mm2 to 11.55 capillaries/mm2 post-stimulation (P 0.039). In addition, the
investigators also measured TcPO2 in the periwound skin before and after the ES treat-
ments. They found that TcPO2 increased from 13.5 to 24.7 mmHg, respectively (normal
is 40 mmHg), and that skin perfusion increased as determined by laser Doppler
fluxmetry.
Angiogenesis was also observed to increase in a recent pilot study by Greenberg
and coworkers.124 They used the same pulsed ES device used in the study by Junger and
colleagues35 to evaluate the effects of positive and negative polarity on epithelialization
and angiogenesis in burn wounds of pigs. They found that re-epithelialization began 2
days earlier in wounds treated with the anode compared to the cathode-treated and con-
trol wounds. Additionally, prominent neovascularity was seen on day 10 in wounds
treated with negative versus positive polarity. The finding of earlier re-epithelialization
agrees with the findings of Mertz and coworkers,25 who observed that pig wounds
treated with the cathode on day 0 and the anode on days 1 to 7, enhanced epithelializa-
tion by 20 percent compared to wounds treated with either positive or negative polarity
alone (see earlier discussion). The enhancement of epithelialization with positive polar-
ity also supports the galvanotaxis theory and the studies that have reported enhanced
epidermal cell migration toward the anode.15,25,124
AMELIORATION OF WOUND-RELATED PAIN WITH ES

Physical therapists have been using ES clinically to treat acute and chronic pain
since the late 1960s. Literally hundreds of studies and numerous textbooks have been
published on electroanalgesia induced by TENS. Only a small sample of the numerous
publications that report positive treatment outcomes from the use of ES to suppress
acute postsurgical pain are cited here as evidence of the significant analgesic effect of ES
on acute wound-related pain.125–127 No studies were found that directly addressed the
use of ES for the treatment of chronic wound-related pain.
Before using electroanalgesia to suppress wound-related pain, the clinician must re-
member that the skin, a protective organ, contains nociceptor receptors that respond to
painful stimuli. Very few, if any, pain receptors reside in subcutaneous soft tissues, in-
cluding granulation and necrotic tissues—both of which can be cut or cauterized with-
out causing the patient any pain. For example, destruction of hypergranulation tissue
with caustic silver nitrate or sharp débridement of necrotic tissue from the wound typi-
cally is painless unless the clinician inadvertently cuts into or cauterizes viable tissue in
the superficial wound margin, where the pain receptors reside. As one proceeds more
deeply into the wound, other tissues that contain varying numbers of pain receptors will
be encountered. Tendon has few, if any, pain receptors; fascia contains some pain re-
ceptors; and periosteum is densely supplied with pain receptors.
When selecting ES parameters to suppress acute wound-related pain, the same
stimulation parameters for treating acute and chronic musculoskeletal pain apply. Thus,
suggested ES parameters for treating acute pain that occurs when the wound is inflamed
or after surgical wide excision of viable tissue or other trauma are as follows:
• Place two small treatment electrodes on the intact periwound skin so that they strad-
dle the wound and a larger nontreatment (dispersive) electrode on intact skin some
distance away from the wound.
• Select a balanced, biphasic or monophasic pulse of short duration (20 to 60 microsec-
onds), set the pulse frequency at 80 to 100 pps, and set the amplitude at a level that
produces a moderately strong but comfortable tingling paresthesia in and around the
wound.
• Increase or decrease the stimulation amplitude as necessary for patient comfort and
pain reduction.
Using these stimulation parameters will provide analgesia as long as the stimulator is
delivering electrical energy to the painful wound and periwound tissues. To produce an
analgesic effect for acute pain associated with larger and deeper wounds (e.g., stage III
and IV pressure ulcers), four electrodes may need to be placed around the wound
perimeter. The patient or a caregiver will need to be instructed in the procedures for ap-
plying electrodes and operation of the TENS device.
For chronic wound-related pain, electrode placement is the same as for acute pain,
just described. Stimulation parameters should be the same as for acute pain initially.
However, if an analgesic effect does not occur within the first hour of treatment, the pa-
rameters should be changed as follows: pulse duration 100 to 200 microseconds, pulse
frequency 2 to 5 pps, and stimulation amplitude set to produce steady, pulsating con-
tractions from the muscles immediately adjacent to the wound.
AMELIORATION OF DIABETIC NEUROPATHIC PAIN WITH ES

Evaluation and treatment of the plantar ulceration that frequently occurs in the di-
abetic insensate foot is covered in Chapter 11. The peripheral neuropathy resulting in
the loss of protective sensation is a common, painful, and often debilitating complica-
tion affecting one-third of individuals with type II diabetes mellitus that increases in
severity with the duration of the disease.128 Because the etiology of diabetic neuropa-
thy is not well understood, only palliative treatments with a variety of pharmaceutical
agents are commonly used to provide symptomatic relief of pain. Some of these agents
have included anticonvulsants, antidepressants, aldose reductase inhibitors, intra-
venous insulin, alpha-adrenergic agonists, topical counterirritants, and intravenous
anesthetics.129–135 The clinical success of these agents in providing symptomatic relief
of neuropathic pain has varied. Also, problems with patient tolerance and adherence
to treatment regimens have occurred as a result of possible side effects from drug
interactions.
Realizing that since the late 1960s ES has been used successfully to treat acute and
chronic musculoskeletal and neuromuscular pain, several investigators have studied the
effects of ES on neuropathic pain in patients with diabetes. Kumar and Marshall136 ran-
domized 31 diabetic patients with neuropathic pain in their lower extremities to active
ES (n 18) or sham-ES (n 13) groups. Before beginning the study and at the end of 4
weeks, each patient’s neuropathic pain level was graded on a scale of 0 to 5, with 0 equal
to no pain and 5 equal to extremely intense, constant, and excruciating pain. The active
ES device (H-wave stimulator, Electronic Waveform Laboratories, Huntington Beach,
CA) generated a biphasic, exponentially decaying pulse with a 4-ms duration, a voltage
range of 25 to 35 V, and a pulse frequency range of 2 to 70 pps. Both groups of patients
treated each of their lower extremities at home for 30 minutes daily for 4 weeks. Indi-
vidual electrodes were applied to the vastus medialis and lateralis muscles, the peroneal
nerve at the neck of the fibula, and the gastrocnemius muscle (Fig. 9–9). Patients in the
active ES group adjusted voltage and pulse frequency to elicit tolerable pulsating mus-
cle contractions. Patients in the control group had their electrodes attached to inactive
ES devices that otherwise looked the same as the stimulators used by patients in the ac-
tive ES group. After 4 weeks, nine patients in the control group crossed over to receive
active ES for 4 weeks. The results revealed that neuropathic symptoms in the sham
group improved in five patients (38 percent) and the mean pain score decreased signif-
icantly (P 0.04), suggesting a placebo-related effect. In the active ES group, sympto-
matic improvement occurred in 15 patients (83 percent) and the mean pain score was
considerably lower (P 0.03), indicating a substantial treatment effect over and above
any placebo influence. Patients in the active ES group reported greater reduction in
symptoms on an analog scale (52 7 percent vs. 27 10 percent in control patients; P
0.05). In addition, ES decreased pain scores from 3.0 to 1.56 (P 0.02) in nine patients
who had received sham ES earlier. The authors pointed out that the results of their study
corresponded closely with pain reduction outcomes reported in studies in which drugs
were used to treat pain.137
In a second placebo-controlled, randomized study using the same ES device and pa-
rameters (see Fig. 9–9), Kumar and coworkers138 compared the effects of the antide-
pressant drug amitryptyline (Elavil) alone to amitryptyline plus active ES and ami-
tryptyline plus sham ES in producing relief of neuropathic pain. Using the same
pain-rating scale from their previous study, they found that amitryptyline alone after 4
weeks produced some degree of pain relief in 15 of 26 patients (60 percent), and pain
scores decreased from 3.8 to 2.9 (P 0.1). In the amitryptyline plus sham ES group (n
9), pain scores decreased from 2.8 to 1.9 (P 0.03). In the amitryptyline plus active ES
group, 12 of 14 patients (85 percent) had symptomatic improvement. Five of these pa-
FIGURE 9–9. H-Wave stimulator with electrodes applied to a lower extremity for treatment
of neuropathic pain. (Courtesy of Electronic Waveform Lab, Inc., Huntington Beach, Calif.)
tients became asymptomatic, and mean pain scores decreased from 3.2 to 1.4 (P 0.01).
The outcomes of this study indicate a substantial effect of active ES over sham ES.
The long-term effects of electroanalgesia on neuropathic pain after treatment with
the same ES device (see Fig. 9–9) used in the Kumar and associates studies136,138 have
been reported by Julka and associates.139 They conducted a follow-up survey of patients
who continued to use the H-wave stimulator after receiving active ES in the 4- and 8-
week Kumar studies. They obtained feedback from 41 of 54 patients (76 percent) who,
using an analog scale, were asked to rate the neuropathic leg pain they experienced be-
fore receiving ES and at the current time. Analysis of the data revealed a 44 percent im-
provement in the neuropathic pain reported by these patients who continued to use the
nonpharmacological treatment modality for an average period of 1.7 years. These data
further suggest that ES, as described in these studies, is effective as an adjunct to anal-
gesic medication in managing neuropathic pain.
One other report described significant success in decreasing neuropathic LE pain.
In this pilot study,140 investigators used a Micro-ZTM stimulator (Prizm Orthopedics,
Duluth, GA) to deliver 50 V (approximately 50 A) of submotor PC at a frequency of 100
pps (pulse duration not reported) for 10 minutes, then 10 pps for 10 minutes to the lower
extremities of diabetic patients. This ES protocol was administered each hour over an 8-
hour period nightly for 1 month through a conductive silver nylon/mesh-stocking elec-
trode (Fig. 9–10) applied to the foot and lower legs of 10 patients experiencing painful,
burning, nocturnal diabetic neuropathy. Subjective pain severity was monitored weekly
FIGURE 9–10. Micro-Z stim-

ulator with Silver-Thera® stock-
ing applied to a lower extremity
for treatment of neuropathic
pain. (Courtesy of Prizm Med-
ical, Inc., Duluth, Ga.)
for 4 weeks during the ES period and for 1 month after ES was terminated using a stan-
dard 10-cm visual analog scale (VAS). Before beginning the ES protocol, the mean VAS
pain score was 7.0. At the end of the 4-week treatment period, the mean pain score was
1.5 (P 0.005). Over the 4-week period, pain scores decreased in a relatively linear fash-
ion. At 1 month after ES treatment, the mean pain score was 2.3, still significantly lower
than the prestudy pain score (P 0.006). The results of this pilot study suggest that
pulsed, submotor ES may be effective in significantly reducing the burning, nocturnal
LE pain associated with diabetic neuropathy.
AUGMENTATION OF AUTOLYSIS WITH ES

No clinical studies dealing with the solubilization or breakdown of necrotic wound
tissue could be identified from the literature. However, information from several animal
studies and an understanding of the electrochemical effects of DC suggest that the alka-
line pH, created by cathodal DC, will solubilize dead tissue just as the mild alkaline pH
from dilute bleach (e.g., Dakin’s solution) causes solubilization of necrotic tissue. Several
studies have shown that cathodal DC solubilizes clotted blood that frequently represents
part of necrotic tissue found in chronic wounds.141–143 In practice there are few, if any, ES
devices on the market that have microamperage DC levels for clinical application.
Some clinicians have claimed that cathodal HVPC also produces the same electro-
chemical pH changes as DC does. This claim is refuted by the research of Newton and
Karselis,40 who demonstrated that HVPC does not produce measurable pH changes at
either the anode or cathode. The only way HVPC could enhance the autolytic break-
down of necrotic wound tissue is by increasing migration of phagocytic cells such as
leukocytes and macrophage into the wound. As discussed earlier in the section on gal-
vanotaxis, these cells have been shown to migrate toward the anode in vitro when the
wound is neither infected nor inflamed.14,15 Human subject studies are sorely needed to
determine how ES changes the wound cellular composition.
ACCELERATION OF WOUND HEALING WITH ES

Numerous controlled as well as randomized, controlled clinical trials support ES as
an efficacious treatment for enhancing the closure of chronic, recalcitrant wounds. On
review of these studies, it was found that few of them were designed to take the wounds
all the way to closure. The main reason for this is that clinical researchers who evaluate
the effect of a particular treatment on wound healing expect that if the intervention is
going to have a measurable effect on healing, the change should occur within some pre-
determined period of time such as 4, 8, or 12 weeks.
Experimental wound treatments studied in clinical trials are often compared with
the so-called standard of care for a particular type of wound (e.g., pressure ulcer, venous
ulcer, diabetic foot ulcer). Standard care for pressure ulcers includes débridement, dress-
ings that maintain a moist wound environment, a pressure-reducing bed and/or wheel-
chair surface, and patient turning/repositioning at 2-hour intervals. Good standard care
can generally close most uncomplicated, small pressure ulcers in 6 to 8 weeks and most
uncomplicated, large pressure ulcers in 8 to 12 weeks. In clinical wound research, if the
experimental wound treatment is closing the wound faster than standard care, or the ex-
perimental treatment plus standard care is closing the wound faster than standard care
alone, then at the end of the preset study period the investigator will be able to make a
statistical statement about the efficacy of the experimental versus the standard treat-
ment. In essence, if the experimental wound treatment consistently closes wounds faster
than standard care, then the experimental treatment will eventually replace or may be
combined with standard care.
Patients involved in wound research assigned to a group that receives standard care
are often categorized as the “control group.” Reviewers of clinical wound healing pub-
lications involving ES often criticize the studies because they do not fully understand
that the experimental group treated with active ES only received one 60-minute ES
wound treatment in a 24-hour period. During the other 23 hours of the research proto-
col, the investigator is ethically bound to provide treatment to the wound, and the treat-
ment that is not always described in published ES studies is almost always standard
care. The point is that in virtually all published, controlled ES wound-healing studies,
the experimental group received ES plus standard care which was then compared
against a control group that received “sham” ES for 60 minutes daily plus standard
wound care during the other 23 hours of the day. So in almost all of the clinical ES
wound-healing studies, ES and standard care are compared against sham ES and stan-
dard care, which in the latter case really amounts to 23 hours of standard care alone plus
1 hour daily of a placebo effect from the sham ES.
The clinical studies that provide evidence-based support for ES as an efficacious
treatment of chronic wounds are reviewed next, according to whether the type of ther-
apeutic current used in the study was DC or PC.
Continuous Microamperage DC Clinical Trials

Between 1969 and 1985, three studies were published in which the investigators
used microamperage levels of DC (recall that microamperage current is defined as 1.0
mA), referring to this current as low-intensity DC (LIDC).27–29 LIDC is continuous DC
with a current amplitude less than 1.0 mA; MENS is PC that also has a current ampli-
tude 1.0 mA. There are no published clinical studies that investigated the effects of
MENS on chronic wound healing. The 1969 and 1976 LIDC studies delivered between
200 and 800 A DC directly into chronic, recalcitrant wounds for 3 hours daily for a
mean of 7.7 weeks in one study27 and 4.7 weeks in the other.28 Patients in these two stud-
ies received 42 hours of ES treatment per week. In the 1985 study, 300 to 700 A DC was
delivered directly into chronic wounds for 4 hours, 5 days per week, for a mean of 5.0
weeks and a total of 20 ES treatment hours.29 In all three studies, wounds were initially
treated with the cathode for 3 days or until infected wounds became aseptic. When sub-
sequent anodal treatment resulted in no measurable progress toward healing, cathodal
polarity was again reapplied until healing stopped, after which anodal stimulation was
reapplied.
Wolcott and colleagues27 reported that of 75 ulcers treated with ES, 45 percent healed
completely in an average of 9.6 weeks, at a rate of 18.4 percent per week. In contrast, 55
percent of the ulcers healed incompletely to an average volume decrease of 64.7 percent
in 7.2 weeks, at a rate of 9.3 percent per week. The average healing rate for all wounds in
their study was 13.4 percent per week. The control group in their study consisted of eight
other patients, six of whom were paraplegic, who had 16 bilateral ischemic ulcers of com-
parable size and location. The eight control ulcers were managed with standard wound
care, as were the eight contralateral ulcers treated with ES. The mean healing rate for the
control ulcers was 5 percent per week compared to 27 percent per week for their ES-
treated counterparts. Interestingly, 71 percent of the patients in this study were para-
plegic, and their rate of tissue repair was approximately 40 percent slower than that for
patients with other primary diagnoses. Despite the overall slower rate of wound healing
for the SCI patients, the ES protocol produced an 81.8 percent wound volume decrease at
a healing rate of 13.4 percent per week for the 75 treated ulcers combined.
Using the same protocol, similar results were reported by Gault and Gatens,28 who
treated 100 ischemic skin ulcers with the same device and protocol used by Wolcott and
associates.27 Six patients with 12 bilateral size-matched ulcers served as the control group.
The six control ulcers that received standard wound care healed at a rate of 14.7 percent
per week compared with 30 percent per week for the six ES-treated ulcers. Three of the
six ES-treated ulcers healed completely, whereas two of the control wounds increased in
size during the 4-week treatment period. The healing rate of 28.4 percent per week for the
100 ulcers in this study, which resulted in complete healing of 48 percent of the ulcers in
4.7 weeks, is comparable to the results reported by Wolcott and associates.27
In both of the studies, a shortage of control wounds is clearly evident. Possibly rec-
ognizing this common deficiency, Carley and Wainapel29 designed a clinical study mod-
ified from the protocol of Wolcott and coworkers.27 In this study, 30 hospital inpatients
with chronic dermal ulcers ranging in duration from 2.3 to 12.3 months were paired ac-
cording to age, diagnosis and wound etiology, location, and size. One member of each
pair was randomly assigned to an experimental group for which wound treatment con-
sisted of microamperage DC stimulation plus standard wound care. The other member
was assigned to a control group treated with standard wound care alone, consisting of
either wet-to-dry dressings or hydrotherapy. The 15 patients in the treatment group re-
ceived 300 to 500 A DC if their wound tissues were normally innervated or 500 to 700
A DC if denervated. The ES was applied directly to the wound via the anode after
cathodal stimulation for the first 3 days. Polarity was reversed for 3 days if measurable
healing stopped. The protocol was modified such that the treatment schedule required
only 20 hours of stimulation per week rather than 42 hours of stimulation per week, as
was required in the studies of Wolcott and colleagues27 and Gault and Gatens.28 Wounds
of patients in the treatment group healed 1.5 to 2.5 times faster than wounds of patients
in the control group. A nonparametric statistical analysis revealed a statistically signifi-
cant and progressively increasing difference between the two groups after 3, 4, and 5
weeks of treatment (P 0.05 at 3 and 4 weeks, P 0.01 at 5 weeks). In all three of these
studies, ES combined with standard wound care promoted faster rates of healing than
standard care alone.
In the three clinical studies just cited, a few days of cathodal wound stimulation pre-
ceded anodal stimulation. A fourth study evaluated the effect of 50 to 100 A DC on
eight venous leg ulcers in existence from 8 months to 5 years.26 All ulcers healed in an
average of 30 days. None recurred during a follow-up period of more than 3 years. Un-
like the other three microamperage DC studies, the current amplitude was considerably
lower and was applied to the wound tissues only through the cathode. From an electro-
chemical perspective, these results are surprising in view of the well-known fact that a
sclerolytic or solubilization effect is produced by the alkaline pH at the cathode. How-
ever, from a galvanotaxic perspective, the cathode facilitates fibroblast migration to the
wound, which would favor connective tissue formation in the proliferative phase.
Pulsed Current Clinical Trials

Two categories of ES devices with voltage outputs are described in terms of either
low or high relative voltage amplitude. The low-voltage category of devices provides PC
in either a monophasic or biphasic waveform, whereas the high-voltage category only
provides monophasic PC. The low-voltage electrotherapeutic devices use relatively long
monophasic or biphasic pulse durations and, therefore, require lower driving voltages
of less than 150 V.1 High-voltage PC devices only deliver monophasic pulses with short
durations less than 10 to 20 microseconds and therefore require a high driving voltage
greater than 150 V.1
Low-Voltage, Monophasic PC Clinical Studies. In the clinical wound healing stud-

ies described in the literature that used monophasic PC, the pulse duration was 140 to 150
microseconds, peak pulse amplitude 30 to 35 mA, and the pulse frequency either 64 or
128 pps.22,32–35 In these studies, the accumulated pulse charge was between 250 and 500
C/s which equates to between 0.89 and 1.78 C/day delivered to the wound. In the first
of these five clinical studies, Weiss and colleagues22 found that 1 month after a 7-day treat-
ment schedule of partial-thickness donor sites with positive-polarity ES, the surgically
induced wounds had softer and flatter scars compared with hypertrophic contralateral
control scars. Histologic findings from bilateral punch biopsies confirmed that electrically
treated scars were reduced in thickness by a mean of 46 percent compared to control scars.
Biopsies also showed that the ES-treated scars had a marked reduction in mast cells that
have been associated with fibrosis. The investigators speculated that the influence of ES
on scar formation could be due partly to a decrease in mast cell migration.
In another study with low-voltage PC, Feedar and associates32 reported the results
of a prospective randomized, controlled, multicenter trial of 4 weeks’ duration, in which
26 chronic dermal ulcers of different etiologies were treated with standard wound care
plus 30 minutes twice daily of active cathodal ES at an initial pulse frequency of 128 pps
and a peak amplitude of 29.2 mA (500 C/s). When the ulcer was débrided or exhibited
serosanguineous drainage, the polarity of the treatment electrode was reversed every 3
days until the wound progressed to a partial-thickness ulcer. Then, with the same peak
amplitude, the pulse frequency was reduced to 64 pps (250 C/s) and the polarity of the
treatment electrode was changed daily until the wound healed. The 24 patients in the
control group were treated with standard wound care and sham ES 30 minutes twice
daily. After 4 weeks, wounds in the treatment and control groups were 44 percent and
67 percent of their initial size, respectively. The weekly healing rates were 14 percent and
8.25 percent, respectively.
Using the same low-voltage PC device, stimulation parameters, and protocol used
in the study just cited, Gentzkow and coworkers33 conducted a double-blind, random-
ized, multicenter trial on 37 patients with 40 pressure ulcers. Nineteen ulcers were
treated with standard wound care plus sham ES, and 21 were treated with standard care
plus active ES. After 4 weeks, the stimulated ulcers had healed more than twice as much
as the sham-treated ulcers (49.8 percent vs. 23.4 percent) at weekly healing rates of 12.5
percent and 5.8 percent, respectively. At the end of the 4-week study period, 15 patients
who had received sham stimulation crossed over to receive active stimulation. In the 15
crossover patients, 4 weeks of active stimulation produced three and one-half times as
much healing as had occurred during the 4 weeks of sham treatment (47.9 percent vs.
13.4 percent). Interestingly, the average healing after 4 weeks of active stimulation for
the 15 crossover ulcers (49.9 percent) was almost identical to the healing after the first 4
weeks of the 21 ulcers in the active treatment group (49.8 percent), which indicates a con-
sistent treatment effect.
In 1993 Gentzkow and associates34 again used the same ES device, stimulation pa-
rameters, and protocol in a prospective, baseline-controlled study on pressure ulcers in
three different health-care facilities over a mean of 8.4 weeks. In this study, a cohort of
61 stage III or IV pressure ulcers served as their own control. The first 4 weeks of the
study consisted of a controlled pretreatment phase (phase 1), during which all wounds
received carefully documented standard wound care, consisting of dressings that main-
tained a moist wound environment, a 2-hour turning/repositioning schedule, a pressure-
reducing bed surface, infection control, and nutritional support. Only wounds that did
not show measurable progress toward closure or deteriorated during the 4-week con-
trol period were enrolled in the second phase of the study. After 4 weeks of optimal stan-
dard wound care, 61 wounds in 51 patients met the inclusion criteria for enrollment in
phase 2, in which patients continued to receive the same standard wound care. In addi-
tion, two 30-minute sessions of active ES were added to their daily wound-care program.
With this research design, subsequent changes in wound dimensions and select charac-
teristics could be attributed to the effects of ES. Progress toward wound healing was de-
fined by the authors as a change of at least one wound stage or two wound characteris-
tics. In the last week of the study (mean, 7.3 weeks) 50 of 61 wounds (82.0 percent) had
improved two or more wound characteristics and 45 of 61 wounds (73.8 percent) had
improved one or more wound stages toward wound closure.
A fourth study, discussed in the previous section related to the effects of ES on an-
giogenesis, also reported using the same low-voltage PC device and stimulation para-
meters used in the studies just described. Junger and colleagues35 reported treating 15
venous leg ulcers with low-voltage PC after standard compression therapy had failed to
show significant evidence of healing over a mean period of 79 months. After a mean of
38 days of wound treatment with ES, the mean ulcer area decreased 63 percent (P
0.01), from 16 to 6 cm.2
An additional study that used low-voltage PC described the current as “pulsed low
intensity direct current” that was delivered to the periwound tissue at 0.5 Hz. Because
the investigators referred to the current as being DC, the assumption is that it was
monophasic but not DC. Recall that the definition of DC is the continuous flow of
charged particles for 1.0 second or longer.1 That means the current used in the study was
delivered at 0.5 Hz, and had a duration of 500 s (0.5 second), which puts it into the
monophasic PC category. The authors, Wood and coworkers,144 described the trial as a
multicenter, double-blind, placebo study in which 71 patients with 74 chronic stage II
and III pressure ulcers were treated with either an active or an inactive “pulsed DC” de-
vice. Active devices were used to treat 43 ulcers and inactive devices were used to treat
31 ulcers, three times per week for 8 weeks. Neither the patient nor the clinician knew
which devices were active or inactive. Both groups also received standard wound care.
The active devices initially delivered 300 A of PC at 0.5 pps through negatively charged
probe electrodes for 1 minute to each of three different periwound sites on opposite sides
of the ulcer, followed by 600 A for 3 minutes at each site. After 8 weeks, 25 of the 43 ul-
cers (58 percent) healed in the active device group, whereas only 1 of 31 ulcers (3 per-
cent) healed in the inactive (placebo) group.
Low-Voltage Biphasic PC Clinical Studies. Three published studies have reported
the effects of low-voltage biphasic PC on wound healing using the technique of placing
treatment electrodes on the periwound skin adjacent to the wound. This technique was
used to purposely stimulate cutaneous nerves rather than deliver current directly into
the wound tissue, as has been done in previous studies. In two of these studies41,42 the
same low-voltage device (Ultrastim [no longer commercially available], Henley Inter-
national, Houston, TX) and stimulation parameters were used. In both of these studies
Baker and colleagues41,42 treated wounds with one of four ES interventions: biphasic
asymmetric waveform (electrically balanced), biphasic symmetric waveform (electri-
cally balanced), MENS, or an ES sham protocol. Because the patients in these studies ei-
ther had SCI41 or diabetes42 with impaired protective sensation in periwound skin, the
authors stated that the purpose of both studies was to evaluate the efficacy of ES in en-
hancing wound healing in patients with neurologically impaired skin, while minimiz-
ing the adverse electrochemical effects of the stimulation on the skin. In the 4-week
study, dermal ulcers in patients with SCI wounds were treated to closure: 35 wounds
treated with the biphasic asymmetric waveform closed, 32 treated with the biphasic
symmetric waveform closed, 18 with MENS closed, and 19 treated with sham ES closed.
A statistically significant difference was found between the group that received the
biphasic asymmetrical waveform and the MENS and sham ES groups. However, no sig-
nificant difference was found between the latter combined two groups (MENS and sham
ES groups) and the group that received the symmetric biphasic waveform. No adverse
electrochemical effects were observed on the skin of patients in this study. Interestingly,
11 control patients treated with standard wound care had a mean weekly healing rate of
9.7 percent after 4 weeks. When these 11 patients were crossed over to be treated with
ES, their mean healing rate was statistically greater during the ES protocol (43.3 percent
per week), and 7 of the 11 wounds closed during the time they received the ES protocol.
The findings of this study agree with those of Stefanovska and associates,145 who also
compared wounds treated with biphasic asymmetric ES versus DC-stimulated and con-
trol wounds. In the second study by Baker and colleagues,42 the increased healing rate
of diabetic foot ulcers treated with the biphasic asymmetrical waveform plus standard
wound care enhanced healing by almost 60 percent over control wounds treated with
standard wound care alone.
High-Voltage PC Clinical Studies. Four published studies investigated the effects
of HVPC on chronic wound healing. In two of the studies, the authors mentioned that
the charge quantities delivered to the wound tissues were 342 C/s37 and 500 C/s.38
These charge values coincide with the range of charge values previously reported in the
five low-voltage PC studies.22–35 In a controlled study, Kloth and Feedar37 randomly as-
signed 16 patients with stage IV dermal ulcers to either an experimental (active ES) or
control (sham ES) group. Wounds of both groups received standard wound care 24
hours per day. In addition, 45 minutes of HVPC was delivered 5 days per week directly
into the nine wounds of the experimental group at 105 pps and the current amplitude
set to just below that which produced a visible muscle contraction. Initially the anode
was placed over the wound, but in four patients whose wounds were treated with ac-
tive ES, the wound electrode polarity was alternated daily each time there was no change
in measurable progress toward wound closure. Seven patients in the control group re-
ceived 45 minutes of placebo ES plus standard wound care to the ulcer 5 days per week.
The wounds of patients in the treatment group healed completely in a mean of 7.3 weeks
at a rate of 45 percent per week. Patients in the control group experienced a mean in-
crease in wound size of 29 percent during a mean period of 7.4 weeks. The wounds of
three patients assigned to a control subgroup treated with standard wound care in-
creased in area by 1.2 percent over 8.7 weeks. However, when these three patients were
reassigned to a treatment crossover group, their wounds healed at an average rate of 38
percent per week, with complete healing occurring in an average of 8.3 weeks.
In a second randomized, controlled study, Griffin and coworkers38 assessed the ef-
ficacy of HVPC for healing stage II, III, or IV pressure ulcers in men with SCI. Of 17 pa-
tients with pressure ulcers in the pelvic region, 8 were randomly assigned to the HVPC
group and 9 to the placebo group. All wounds were treated daily with standard care. In
addition, wounds in the HVPC group received ES for 60 minutes on 20 consecutive days,
with the cathode applied to deliver current directly into the wound. The stimulator was
set to deliver 100 pps and 200 V, which produced 500 C/s at the treatment electrode.
Ulcer surface area was measured before and after ES treatment on days 5, 10, 15, and 20.
Percentage of change from pretreatment ulcer size was calculated for each measurement
interval. On days 5, 15, and 20, ulcers in the HVPC group had significantly greater mean
wound area reductions compared to their pretreatment size than ulcers in the placebo
group.
In two other noncontrolled studies, HVPC was used to treat diabetic foot ulcers and
pressure ulcers. In the diabetic foot wound study, 12 of 15 ulcers (80 percent) healed
completely in a mean period of 2.6 months with anodal stimulation applied for 1 hour 3
days per week.146 In the pressure ulcer study, wounds treated only with HVPC had the
greatest size reduction compared to wounds treated with either whirlpool plus HVPC
or whirlpool alone.147
STRENGTH OF EVIDENCE FOR ES AS A WOUND HEALING

INTERVENTION
The efficacy of ES in promoting wound healing may not be apparent to the reader,
who may be somewhat overwhelmed by the stimulation variables alone that are de-
scribed in the literature. For the healing of chronic wounds by ES, the strength of evidence
based on clinical trials is substantial. The criteria used to rate the strength of evidence
for ES in this chapter and the six adjunctive wound treatments covered in Chapter 10 are
based on clinical and animal trials, case or descriptive studies, or expert opinion. The cri-
teria are modified from the strength-of-evidence rating published in 1994 by the Agency
for Health Care Policy and Research (AHCPR), who rated the efficacy of numerous
wound interventions according to the following scale of A, B, and C.148
A: Results of two or more randomized, controlled, clinical trials on chronic wounds in

humans provide support.
B: Results of two or more controlled clinical trials on chronic wounds in humans pro-
vide support, or when appropriate, results of two or more controlled trials in an an-
imal model provide indirect support.
C: Requires one or more of the following: (1) Results of one controlled trial; (2) results
of at least two case series/descriptive studies on chronic wounds in humans; or (3)
expert opinion.
In 1994, the AHCPR Guideline recommended ES as the only “adjunctive therapy”

with sufficient evidence to warrant recommendation by the panel. The panel recom-
mended “a course of treatment with ES for stage III or IV pressure ulcers that have
proved unresponsive to conventional therapy. ES may also be useful for recalcitrant
stage II ulcers.” In that 1994 document, the strength-of-evidence rating assigned to ES
was “B” based on five “clinical trials” involving 147 patients.29,32,33,37,38 The reader
should note, however, that in the January 1999 issue of the journal Ostomy and Wound
Management, Ovington149 categorized these same five “clinical trials” as randomized,
controlled trials (RCT), updating the 1994 AHCPR literature review through April 1998
for dressings and adjunctive therapies used to treat pressure ulcers. In her review, Ov-
ington indicated that one additional RCT involving the use of ES on pressure ulcers had
been published by Wood and associates144 after the AHCPR Guideline was distributed
at the end of 1994. With this additional RCT, Ovington suggested that the 1999 strength-
of-evidence rating for ES “should perhaps advance from B to A, based on the five orig-
inal randomized, controlled trials plus the 1994 trial.” At the end of the article by Ov-
ington, two highly recognized authorities on chronic wound care gave their
“Interpretations for Practice” based on the literature review by Ovington.
In discussing the overall significance of Ovington’s updated recommendation for
ES and its use in wound care, Krasner and Sibbald149 stated that “it takes the whole
wound care community—researchers, providers, translators, manufacturers, suppliers,
and payors—working together, dialoguing, and yes at times battling, to identify the best
practices for today and to raise the research questions for tomorrow.” Most recently, the
Paralyzed Veterans of America has provided administrative and financial support to de-
velop and publish a Clinical Practice Guideline titled: Pressure Ulcer Prevention and Treat-
ment Following Spinal Cord Injury.150 In this publication, ES was assigned a stand-alone
recommendation (number 17) that no longer classifies it as an adjunctive therapy. The
recommendation, based on a strong strength-of-evidence rating from three RCTs, reads:
“Use electrical stimulation to promote closure of stage III or IV pressure ulcers combined
with standard wound care interventions.”
Meta-analysis of ES Wound Healing Research Studies
Perhaps the most compelling evidence of the efficacy of ES for enhancing the rate
of wound healing is supported by a meta-analysis of 15 ES studies on chronic wound
healing published by Gardner and coworkers.151 The studies they selected for the meta-
analysis included nine RCTs and six nonrandom, controlled trials. Data analyzed from
these studies included 24 ES samples (591 wounds) and 15 control samples (212
wounds). They calculated the average rate of healing per week for the ES and control
samples and found that the rate of healing per week was 22 percent for the ES samples
vs. 9 percent for control samples. This difference represents an increase of 144 percent in
healing rate of ES-treated wounds over control wounds. Based on 95 percent confidence
intervals for ES and control samples, the studies revealed a 90 percent probability that
the net healing effect of ES is 3.7 percent per week or more, which conservatively repre-
sents an increase of 40 percent or more over the control rate. It should be noted that five
of the nine clinical studies29,32,33,37,38 classified as RCTs by Gardner and coworkers151
were previously classified as “controlled trials” in the 1994 AHCPR Guideline,148 and
that classification was used as a basis for the AHCPR to rate ES at a lower level in the hi-
erarchy of wound interventions.
Guidelines for Wound Treatment with ES
The clinical studies cited in the previous section have confirmed that ES combined
with standard wound care accelerates the rate of wound healing faster than standard
care alone, even though the clinical investigators in these studies used a variety of ES de-
vices and stimulation parameters. Despite the positive outcomes reported, critics of ES
literature related to wound healing have frequently argued that there is a lack of con-
sistency in the type of current and stimulation parameters reported. What has been over-
looked by most reviewers of the ES literature is that there is the common denominator
of electrical charge “dosage” delivered into the wound tissues that has been reported in
several of the RCTs.32–35,37,38 The dosage falls within a narrow range of 250 to 500 C/s.
The formulas for calculating electrical charge dosages that are used clinically to enhance
the rate of wound healing with low- and high-voltage PC are shown in Figures 9-11 and
9-12 respectively. To achieve this level of electrical dosage, the guidelines for treating
wounds with ES are proposed in Box 9–1.
Precautions
The only precautions to be considered when ES is selected for wound treatment are
based on anecdotal reports. The level of current required to produce a moderate but
comfortable tingling sensation that is perceived under the electrodes may startle some
patients when the current amplitude is advanced too quickly. This usually can be
FIGURE 9–11
avoided by increasing the voltage or current output more slowly. Occasionally, skin ir-
ritation may occur under the nontreatment electrode(s) that is in contact with the skin.
This may result when the type of ES used has a possible DC component (e.g., continu-
ous DC, monophasic PC with a sufficiently long pulse duration) or is a biphasic, asym-
metrical waveform. Skin irritation is least likely to occur when treatment is provided
with HVPC, as previously recommended.
Contraindications
Only a few clinical situations preclude using ES to promote wound healing:
• Basal or squamous cell carcinoma in the wound or periwound tissues or melanoma

(ES may cause mitogenic activity of the cancer cells).
• Untreated osteomyelitis present in bone in the base of the wound. In this case, ES may
FIGURE 9–12
BOX 9–1 Guidelines for Treating Wounds with Electrical Stimulation (ES)*
Parameter settings
Voltage: 75–150 V (voltage is set at a level within this range to allow the sensate patient to
perceive a moderately strong tingling paresthesia in or around the wound)
Pulse frequency: 100 pps
Polarity of wound treatment electrode: Polarity is changed according to the wound phase
and/or the clinical needs of the wound, as follows:
1. Positive for epithelialization (galvanotaxis of negative epithelial cells)
2. Positive for autolysis and reactivation of inflammatory phase (galvanotaxis of neutrophils
and macrophages)
3. Negative for granulation (galvanotaxis of fibroblasts)
Treatment duration: 60 minutes, 7 days per week until the wound closes
Other considerations
Arrangement and type of electrodes†:
1. Monopolar arrangement: One treatment electrode placed directly over the wound and one
nontreatment (dispersive) electrode placed on intact skin near the wound (15–30 cm from
wound).
2. Bipolar arrangement: Two treatment electrodes placed on intact skin immediately
adjacent to and on opposite sides of the wound cavity. One nontreatment (dispersive)
electrode placed on intact skin 15–30 cm away from wound border.
Type of electrode for monopolar arrangement:
1. Treatment electrode: Remove wound dressing, irrigate wound cavity, and fill it with clean,
saline- or hydrogel-moistened gauze to enhance electrical conductivity. Fold a piece of
heavy-duty aluminum foil that becomes three to four layers thick and is at least 0.5 cm
smaller than the wound perimeter. Apply the foil in contact with the moist gauze in the
wound and connect it to the stimulator lead wire having the polarity that will facilitate
appropriate galvanotaxic cell migration. Secure the foil to the gauze with an appropriate
commercial adhesive product. After the 60-minute ES treatment remove the foil and
dispose of it properly, and then either leave the saline- or hydrogel-moistened dressing in
the wound and secure it with a secondary dressing, or replace it with another standard
dressing that maintains a moist wound environment.
2. Nontreatment (dispersive) electrode: Apply a commercial, self-adhering, well-hydrated
polymer electrode to the intact periwound skin 15–30 cm from the wound (the electrode
should have approximately the same area as the wound surface area). When possible on
subsequent ES treatments, apply this electrode at 12, 3, 6, and 9 o’clock around the
wound perimeter so that the current travels through different tissues of the wound. At the
end of the treatment, remove the electrode and inspect the skin.
Type of electrode for bipolar arrangement:
1. Treatment electrode: If necessary, remove the soiled dressing, irrigate the wound cavity,
and fill it with saline- or hydrogel-moistened gauze to enhance electrical conductivity.
Connect each end of a bifurcated lead wire having appropriate polarity to individual
commercial, self-adhering, well-hydrated polymer electrodes that are each one-half the
area of the wound opening. Apply these electrodes to intact periwound skin at 6–12 or
3–9 o’clock immediately adjacent to the wound perimeter. On subsequent ES treatmens,
alternate the position of these treatment electrodes around the wound perimeter. After
the 60-minute ES treatment, remove these electrodes from the patient, inspect the skin,
and apply the electrodes to their plastic mounting for use during the next treatment. After
treatment, leave the saline- or hydrogel-moistened dressing in the wound, and secure it
with an appropriate secondary dressing or replace it with another standard dressing that
maintains a moist wound environment.
2. Nontreatment (dispersive) electrode: Apply a commercial, self-adhering, well-hydrated
polymer electrode to the intact periwound skin about 30 cm from the wound (the
electrode should have approximately the same are as the wound surface area). Remove
this electrode after the treatment, and inspect the skin.
*Example of ES device: high-voltage pulsed current.
†Both approaches to electrode arrangement have been reported to be effective in accelerating wound
healing.37,38,41,42
305
facilitate premature closure of the wound, which will likely result in abscess forma-
tion. However, if osteomyelitis is responding to antibiotic treatment, ES may be used
to facilitate closure of the soft tissue wound concurrently with resolution of the os-
teomyelitis.
• Application to the neck or thorax by positioning electrodes such that current may flow
through the pericardial area, carotid sinus, phrenic nerve, parasympathetic nerves
and ganglia, or the musculature of the larynx. Similarly, positioning ES electrodes in
a manner that allows current to flow through tissues in which any type of electronic
pacemaker device is implanted is contraindicated. One report on 10 patients who had
had 20 different cardiac pacemakers and had ES applied at four body sites (cervical
spine, distal upper extremity [UE] ipsilateral to cardiac pacemaker, left leg, and lum-
bar area) indicated a lack of interference with the function of the pacemakers.152
CLINICAL DECISION MAKING: CASE STUDY 9–1
EXAMINATION
The patient is a 56-year-old complete L-4 paraplegic and army veteran admitted
to the spinal cord unit of the local Veterans Administration (VA) Medical Center. He
sustained a gunshot injury to his spinal cord at age 24 while taking off in a helicopter
in Vietnam. The gunshot made him lose his grip on the helicopter. Subsequently, he
fell 20 feet onto a bamboo fence and sustained bilateral brachial plexus injuries.
History
During the 32 years since becoming paraplegic, he has had multiple recur-
rences of urinary tract infection and five pressure ulcers, two of which were stage
IV left and right ischial ulcers and three stage III ulcers located on the medial
condyle of his left knee, sacrum, and right heel. For mobility, he uses his right hand
with a joystick to control an electric-powered wheelchair that has a Roho seat cush-
ion (Crown Therapeutics, Inc., Belleville, Illinois). He has chronic obstructive pul-
monary disease from smoking two packs of cigarettes per day, wears a Foley
catheter, and lives in an assisted-living VA facility.
The stage IV pressure ulcer on his right ischial tuberosity dehisced about 1
week after plastic surgery attempted to close the ulcer by rotating a musculocuta-
neous gluteal flap. During the past 3 weeks he has been bedbound, and during this
time the nursing staff has treated the ulcer with standard wound care consisting of
dressings that promote moist wound healing, enzymatic débridement, a pressure-
relieving bed surface, and a 2-hour turning schedule. Little progress has been made
toward closure of the ulcer.
Systems Review
Neuromuscular system: As a result of bilateral brachial plexus and L-4 SCIs, this pa-
tient has severe motor and sensory deficits in both upper and lower extremities.
Musculoskeletal system: The patient is generally debilitated from disuse atrophy of
muscle mass below the umbilicus and from degeneration atrophy of extensor mus-
cles in both upper extremities secondary to the brachial plexus injuries. Both lower
extremities have pronounced bilateral flexion contractures at the hips and knees.
Integumentary system: Trophic changes are observable in the skin of both upper
extremities, accompanied by edema in both hands. Skin of both lower extremi-
ties also exhibits atrophy and trophic changes as a result of autonomic dysfunc-
tion from damage to the sympathetic nervous system. Scar tissue is present at
each of the previous five sites of pressure ulceration (four of five ulcers healed
by secondary intention). Also present is a partial surgical scar in the skin of the
right buttock that ends at the existing pressure ulcer located over the right is-
chial tuberosity.
Tests and Measurements

Manual muscle testing: Manual muscle testing reveals flaccid paralysis of both
lower extremities at the hips, knees, and ankles. Deep tendon reflexes are absent
at the ankle and knee. The patient has grasp present in his right hand but not the
left. He has grade 3 elbow flexors on the right and grade 3.5 on the left.
Range of motion (ROM): Examination reveals the following deficits:
Left LE: Hip 10 extension
Knee 5 extension
Right LE: Hip 12 extension
Knee 20 extension
Right UE: Fingers 3 to 12 extension at metacarpal phalangeal (MP), prox-
imal interphalangeal (PIP), and distal interphalangeal (DIP) joints
Shoulder has full ROM all planes
Elbow 15 extension
Left UE: Fingers 7 to 22 extension at MP, PIP, and DIP joints
Shoulder has full ROM all planes
Elbow 23 extension
Periwound and wound testing: The periwound skin surrounding the right ischial
ulcer is indurated, and scar tissue is present from a previous ulcer that healed
by secondary intention. As verified by an infrared scanning thermometer, the
periwound skin temperature is 1.0 to 1.3 warmer than the skin over the con-
tralateral site, but there is no indication of erythema. The entire wound perime-
ter is free of necrotic tissue, and the epithelial margin has not advanced over the
wound edge. The wound opening measures 3.2 cm from 12 to 6 o’clock and 2.9
cm from 3 to 9 o’clock. Wound depth is 2.4 cm. One centimeter of undermining
is present between 10 and 1 o’clock of the wound perimeter, and 25 percent of
the wound base contains yellow, adherent (collagenous), necrotic tissue.
Wound exudates consist of moderate serosanguineous drainage. Although a
noticeable odor from the wound was perceived after dressing removal, there
was no odor after it was thoroughly irrigated.
EVALUATION OF EXAMINATION DATA

The examination indicates that several problems need to be addressed for this
patient. The nonhealing right ischial pressure ulcer that has failed closure by mus-
culocutaneous flap surgery and by 3 weeks of standard wound care needs to be
managed with an intervention plan that will lead to wound closure in a reasonable
time frame. Wound management should include débridement and other treat-
ments that promote autolysis, granulation tissue growth, and closure of the ulcer.
In addition passive ROM and muscle lengthening is needed to reduce contractures
of UE and LE joints. Appropriate therapeutic positioning is also needed to prevent

the existing ulcer from deteriorating and new pressure ulcers from developing.
DIAGNOSIS
Stage IV right ischial pressure ulcer secondary to loss of protective sensation
and severely restricted mobility. Note: The lack of periwound erythema along with
elevated periwound skin temperature, combined with moderate serosanguineous
drainage and no progress toward closure, suggests that the wound may be in the
chronic inflammatory phase.
PHYSICAL THERAPY INTERVENTIONS

1. Sharp and enzymatic débridement to eliminate necrotic tissue and vulnerabil-
ity to infection.
2. ES combined with standard wound care150 to promote autolytic débridement,
increase blood flow, and wound closure.
3. ROM and muscle lengthening to UEs and LEs to reduce soft tissue contractures
and to increase muscle extensibility and strength.
4. Caregiver education about methods of positioning the recumbent patient (and
the seated patient once the wound has closed).
PROGNOSIS
The prognosis for wound closure and healing is excellent based on clinical re-
search showing that wounds treated with ES combined with standard care heal at
a faster rate than wounds treated with standard care alone.32–34,37,38 The wound will
progress from a reactivated acute inflammatory phase during a period of 10 to 14
days, into the fibroblastic phase during the subsequent 3 to 5 weeks, and finally
into complete closure in 11 weeks.
PHYSICAL THERAPY PLAN OF CARE

Sharp débridement to remove only necrotic tissue will be performed by a
physical therapist preferably credentialed as a Certified Wound Specialist through
the American Academy of Wound Management.153 Enzymatic débridement and
moist wound dressings will be used by the nursing staff between sharp débride-
ment sessions to solubilize necrotic tissue present in the base of the wound. The
goal is to achieve a wound base that is 100 percent beefy red in appearance within
2 weeks. The desired outcome from débridement of all necrotic tissue is a reduction
in patient vulnerability to wound infection.
ES with a HVPC device will be delivered to the wound tissues using the
monopolar electrode placement method, as described in the section titled Guide-
lines for Wound Treatment with ES. The polarity of the treatment electrode must
be selected according to whether the wound needs (1) facilitation of galvanotaxis
for autolysis and/or reactivation of the inflammatory phase (Fig. 9–13), (2) treat-
ment for infection or inflammation (Fig. 9–14), (3) stimulation of fibroplasia (gran-
ulation tissue growth) (Fig. 9–15) in the proliferative phase, or (4) stimulation of
FIGURE 9–13. Electrode

placement and polarity
for promoting autolysis.
(Used with permission
from Advances in Wound
Care 1996 September/
October 9(5):42–45, ©
Springhouse Corporation/
www.springnet.com)

placement and polarity
for promoting antibac-
terial/ antiinflammatory
effect. (Used with permis-
sion from Advances in
Wound Care 1996 Septem-
ber/October 9(5):42–45,
© Springhouse Corpora-
tion/www. springnet.com)

placement and polarity for
promoting granulation tis-
sue growth. (Used with per-
mission from Advances in
ber/October 9(5): 42–45,
© Springhouse Corpora-
tion/www.springnet.com)

placement and polarity for
promoting re-epithelializa-
tion. (Used with permis-
sion from Advances in
ber/October 9(5):42–45, ©
Springhouse Corporation/
www.springnet.com)
epithelial cell migration to resurface the wound (Fig. 9–16). The short-term goal is to
promote autolysis of necrotic tissue that, combined with débridement, results in a
wound base that is 100 percent beefy red within 2 weeks. The long-term goal is to
achieve 50 percent or more measurable progress toward wound closure in 3 to 4
weeks and 100 percent wound closure in 7 to 8 weeks. The desired outcome is to use
computerized pressure mapping to evaluate the patient’s ischial weight loading in
sitting and, when indicated, to begin a progressive sitting program that results in
the patient’s being able to sit in a wheelchair on an appropriate cushion for two 3-
hour periods daily.
Passive ROM exercises to reduce soft tissue contractures, enhance muscle ex-
tensibility, and retard muscle atrophy will be performed on both UEs and LEs
twice daily by a physical therapist assistant. Exercises will also be provided to in-
crease strength on elbow flexors bilaterally. The goal is to achieve 2 to 5 increases
in ROM at all contracted UE and LE joints in 2 weeks. The desired outcome is to en-
able the patient to gain greater function and strength of elbow flexion that will al-
low him to propel his wheelchair for short distances in his home.
The physical therapist will instruct the nursing staff and/or physical therapist
assistant in patient positioning to prevent contractures and new pressure ulcer for-
mation, and to avoid having the patient positioned such that breathing is labored
and weight is borne on the existing right ischial ulcer. The goal is to have caregivers
assist the patient in repositioning every 2 hours, avoid exertion of pressure on the
existing right ischial pressure ulcer, prevent further contractures, and avoid de-
velopment of new pressure ulceration. The desired outcome is to help the patient
achieve increased ability to reposition himself in bed, ultimately with the ability to
sit in a more upright posture in his wheelchair.
DISCHARGE OUTCOME
After 2.5 weeks, the moist wound was 100 percent beefy red granulation tis-
sue without undermining, the entire wound margin had a clean leading edge of
healthy epithelial cells, and the periwound skin temperature was normal. In addi-
tion, measurable increases in ROM had been achieved in both hips and elbows and
the patient had increased strength in both elbow flexor groups. After 4 weeks of ES
wound therapy, the ulcer base had granulated so the wound depth was 1.3 cm, and
the 12- to 6-o’clock and 3- to 9-o’clock measurements were 1.9 and 1.4 cm, respec-
tively. At 8.3 weeks, the ulcer was closed by epithelium, and the patient’s elbow
flexor strength had increased by one full grade bilaterally, enabling him with the
minimal assistance of one person to reposition himself in bed by use of the bed
rails. In week 12 he was evaluated for ischial sitting loads by pressure mapping.
SUMMARY
ES as an intervention for chronic wounds is supported by data from numerous ran-

domized clinical trials. The evidence from several studies is clear. ES combined with
standard wound care accelerates wound closure at a significantly faster rate compared
to standard wound care alone.
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WOUND HEALING:

Luther C. Kloth, MS, PT, CWS, FAPTA

Joseph M. McCulloch, PhD, PT, CWS

Copyright © 2002 by F. A. Davis Company

Printed in the United States of America

Last digit indicates print number: 10 9 8 7 6 5 4 3 2 1

Acquisitions Editor: Margaret Biblis

Library of Congress Cataloging-in-Publication Data

Wound healing: alternatives in management/[edited by] Luther C. Kloth, Joseph M.

I have acquired a somewhat bizarre habit, undoubtedly a result of aging. I love to

Steven L. Wolf, PhD, PT, FAPTA

Nineteen authors in the third edition contributed to the writing of 14 chapters.

The thousands of physical therapist clinicians and academicians who provided us

James A. Birke, PhD, PT, CPed

SECTION I: The Wound-Healing Environment . . . . . . . . . . . . . 1

Chapter 1 The Normal Process of Healing . . . . . . . . . . . . . . . . . . . . . . . . 3

Chapter 2 Nutrition and Wound Healing . . . . . . . . . . . . . . . . . . . . . . . . . 35

Nutritional Status and the Postoperative Wound Healing Response. . . . . . . . . 56

Chapter 3 Factors Impeding Wound Healing . . . . . . . . . . . . . . . . . . . . . 68

Chapter 4 Bacteriology and Infection Control . . . . . . . . . . . . . . . . . . . . . 97

Health-Care Worker Protection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

Chapter 5 Growth Factors, Extracellular Matrix, and

Implanted Biomaterials . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

SECTION II: Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151

Chapter 6 Methods of Wound Evaluation . . . . . . . . . . . . . . . . . . . . . . . . . 153

SECTION III: Principles and Techniques . . . . . . . . . . . . . . . . . . . . 201

Chapter 7 Wound Débridement and Irrigation . . . . . . . . . . . . . . . . . . . . 203

Sharp Débridement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207

Chapter 8 Dressings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232

Chapter 9 Electrical Stimulation for Wound Healing . . . . . . . . . . . . . . 271

Chapter 10 Adjunctive Interventions for Wound Healing . . . . . . . . . . 316

Clinical Decision Making: Case Study 10–2. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 336

SECTION IV: Case Management and Documentation . . . . . 383

Chapter 11 Management of the Insensate Foot . . . . . . . . . . . . . . . . . . . . . 385

Chapter 12 Management of Wounds Secondary

Chapter 13 Prevention and Treatment of Pressure Ulcers . . . . . . . . . . 429

Chapter 14 Documentation for Reimbursement . . . . . . . . . . . . . . . . . . . . 517

Appendix 1: Braden Scale for Predicting Pressure Sore Risk . . . . . . . . . . . . . . . . . . 527

TERMINOLOGY OF MEDICAL ELECTRICITY

Frequently, reviewers of the literature on wound healing with ES have indicated

Electrical charge (Q) is a fundamental property of matter. Matter can be electrically

Therapeutic Electrical Circuit and Electrodes

THEORETICAL BASIS OF ELECTRICAL STIMULATION

Endogenous Electrical Currents

SKIN BATTERY POTENTIAL

TABLE 9–1 Cellular Galvanotaxis During Wound Healing Phases

NA CURRENT OF INJURY

FIGURE 9–1. Diagram of

FIGURE 9–2. Average hu-

FIGURE 9–3. Current path

Exogenous Therapeutic Currents for Wound Healing

TYPES OF ELECTRICAL CURRENTS

the “pulsed” waveforms delivered by the majority of electrotherapeutic devices, the

DIRECT CURRENT (D.C.)

FIGURE 9–8. Graphic representation of monophasic, high-voltage PC (From Nelson, RM,

statistically signiﬁcant changes in pH did not occur in forearm or lumbar skin in 30

Basic Science Research

IN VITRO STUDIES (ANTIBACTERIAL EFFECTS OF ES)

ANIMAL MODEL STUDIES

Effect of ES on Wound Scar Tensile Strength

Effects of ES on Other Factors Related to Wound Healing

Effect of ES on Skin Grafts, Donor Sites, and Musculocutaneous Flaps

Clinical trials on human subjects, designed to answer research questions pertaining