Massage Therapy and MedicationsOxford

Massage
Therapy
&
Medications
General Treatment Principles
RANDAL S. PERSAD Dip. Pharm., R.M.T.

FOREWORD BY DR. JOHN YATES Ph.D.
Massage Therapy & Medications
Randal S. Persad Dip. Pharm., R.M.T.
© Copyright 2001
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The author and publisher have made every effort to ensure the accuracy of the
contents of this book. However, appropriate sources should be consulted,
especially for new or unfamiliar information. It is the responsibility of every
practitioner to evaluate the appropriateness of a particular opinion in the context
of actual clinical situations and with due consideration to new developments.
Please respect the time, effort, and commitment that have gone into creating this book by
not copying its contents without permission.
All rights reserved.
Printed and bound in Canada by University of Toronto Press.
Dedication
To my wife Maureen, thank you for your love, support
and the warmth of your soul.
To my father for his inspiration and wisdom,

my mother (in memory of) for her divine guidance,
and my brothers and sisters for their encouragement.
Acknowledgements
The writing of this book has spanned almost a decade; its beginnings are
rooted back in the islands. To Lauren Lumkim, my teacher and mentor, thank
you for believing in and encouraging me during those long hours of
Pharmacy training.
There are many people who have encouraged and supported me in my

writing. Thanks to the staff at Sutherland-Chan School & Teaching Clinic
including Grace Chan, Eric Brown, Murray Pickering, Karen Friedl, Michael
Bard, and Bruce McKinnon.
To the students and staff of the West Coast College of Massage Therapy,
thank you for your questions, suggestions, and unsurpassed support during this
writing adventure. Special thanks to John Ranney, Ron Garvock, Melba 'toast'
Lewis, Natale Rao, Isabell MacDonald, Grace Dedinsky, Dr. Fernando
Villsenior, Will Winram, Clifford Yip, Rich Ingram, Britta Hobkirk, Mike Dixon, and
Steve Anderson. To Dr. Wayne Jakeman and associates, thank you for sharing
and suggesting.
Many thanks to Paul Finch, Peter Becker, Geoff Harrison, and Jean Pascual for
your help with text reading and proofing.
Finally, this project was made possible by the publisher and editor-in-chief
Debra Curties, and the artistic creativity of Bev Ransom. I am especially
grateful for your commitment, and appreciate the time you spent keeping
me focused on deadlines and rewrites.
Foreword
The last two decades have witnessed several remarkable changes in the perceptions
and practice of health care in North America. Dramatic new pharmaceutical agents
have been developed, and they are being made available in a marketing environment
where prescription medications to treat everything from high cholesterol to
hypertension, anxiety, and impotence are being promoted directly to the public via
television and magazine advertisements. Many powerful drugs are now also available
over the counter or via the Internet without a prescription. At the same time, there has
been an enormous groundswell of public interest in and utilization of alternative health
care by all sectors of the population, including the postwar baby-boomers who have
now reached middle age and are experiencing an increase in health problems of every
sort. Many have come to regard non-conventional or alternative therapies as
complementary to medical treatment, and are receiving such treatments while they are
also under the care of a medical doctor for various medical conditions.
Massage is one of the most commonly used of the complementary therapies. It is well
known for its value in relaxation and anxiety reduction, for treatment of many types of
musculoskeletal pain and dysfunction, and for lessening discomforts associated with
chronic disorders like arthritis and fibromyalgia. All of these conditions are also
commonly treated by prescription or over-the-counter medications, and occur in
people who may be using medications for other conditions at the same time. Massage
therapists are more likely than ever before to regularly treat clients who are also using
prescription and non-prescription medications.
Massage Therapy & Medications 1

Unfortunately, although most massage therapists are aware that their clients may be
using medications, many lack formal training in their effects, their potential
interactions with massage therapy modalities, and how to adapt massage treatments in
these situations. Standards for training of massage therapists vary greatly throughout
North America and rarely include a requirement for education about medications. As
a result, few schools have addressed the need for training in basic pharmacology and
the interactions between massage treatment and medications. This book fills a vital
need by providing massage therapists with important basic information on the
properties, mechanisms of action, and side effects of common medications, as well as
how their presence in the client’s body may influence treatment decisions and results.
One section has been devoted to the effects of medications on assessment results.
Massage is performed for a broad spectrum of purposes that range from general
relaxation and stress reduction, to treatment or rehabilitation of a number of injuries
and conditions, to increased psychological comfort and enhanced sense of health and
well-being. Massage therapists rely upon history taking, physical assessment, and
palpation to determine which methods and techniques are most appropriate for the
treatment of each client. The author has provided guidelines for good case history
taking regarding medications, and discusses the various ways that concurrent drug use
can affect assessment findings.
Randal Persad is ideally suited to have written this book. Originally trained as a
pharmacist and employed by Lederle Laboratories, he subsequently became a massage
therapist in 1991. While working in the hotel and spa industry, sports environment, and
in chiropractic and rehabilitative settings, he noticed that many of his clientele were
taking medications, and that the effects of their medications influenced their response
to massage in ways that required him to adapt his treatments. Later, as an instructor at
West Coast College of Massage Therapy in Vancouver, Canada, he was able to use this
integrated knowledge of the actions of pharmaceuticals and the impacts of massage
therapy to create guidelines for undergraduate students that encourage development of
safe and effective treatment plans and minimize adverse reactions. Based on his unique
background and teaching experience, he was asked to develop the medications
component of the curriculum guideline for the College of Massage Therapists of
British Columbia.
Mr. Persad has brought this rich background of knowledge and experience to bear on
the task of providing a practical and useful introduction to pharmacological concepts,
principles, and terminology. His discussion takes a complex subject and makes it easy
to grasp and apply in clinical practice. He also provides the therapist with tools for
better communication with doctors, pharmacists, and other health care professionals.
Both general guidelines for working with clients who are taking medications and
specific guidelines for working around injection sites and implants have been
provided.
2 Massage Therapy & Medications

This book will help therapists develop the skills to interpret and understand the
package information of common drugs and to recognize those drug effects that can
potentially influence a massage treatment. That information can then be interpreted as
it applies to manual therapy, and used to adapt the treatment plan in an appropriate
manner.
Massage Therapy and Medications represents a landmark addition to the literature

available to support high quality education and professional practice by massage
therapists everywhere.
John Yates, Ph.D.
Dr. John Yates received his Ph.D. from the University of Manitoba in 1976. He
developed a strong interest in complementary health care education and research
during a post-doctoral fellowship at the University of Calgary Faculty of Medicine,
following which he joined the Division of Health Promotion and Disease Prevention
in the Department of Health Care and Epidemiology at the University of British
Columbia. Dr. Yates became involved with the West Coast College of Massage
Therapy prior to its opening in 1983, and served as the Academic Education Director
until 1997. Dr. Yates was the founding President of the Physical Medicine Research
Foundation (PMRF) from 1985 to 1990, and was a member of the Medical Advisory
Board of the Western Division of the PMRF from 1990 to 1993. He has also served
as Research Director for the Massage Therapists’ Association of B.C., is a member of
the Editorial Board of the Journal of Soft Tissue Manipulation, was instrumental in
developing the curriculum standard for massage therapy in British Columbia, and is
the author of A Physician’s Guide to Therapeutic Massage, now in its second edition.
Dr. Yates is currently living in Arizona and provides consulting services to
accreditation and certification organizations, professional associations, and colleges
of massage therapy throughout North America.

Outline
MASSAGE THERAPY AND MEDICATIONS
Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1
Outline . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4
Learning Objectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
BASIC CONCEPTS AND GUIDELINES

Chapter 1
Why Massage Therapists Need to Know How Medications Work . . . . . . . . . . . . . . . 11
Chapter 2
Common Pharmaceutical Terms and Concepts . . . . . . . . . . . . . . . . . . . . . . . . . . . . .15
Chapter 3
How Drugs are Administered to the Body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .27
Chapter 4
Drug Processing in the Body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .37
Chapter 5
General Treatment Guidelines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .43
Case History Form . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .48
Letter to Health Care Practitioner . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .53
COMMONLY PRESCRIBED MEDICATIONS AND

TREATMENT PLANNING
Chapter 6
Drugs for Managing Pain and Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .79
Non-Steroidal Anti-Inflammatory Drugs (NSAIDS) . . . . . . . . . . . . . . . . . . . . . . .79
Narcotic Analgesics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .81
Skeletal Muscle Relaxants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .84
Corticosteroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .86
Chapter 7
Drugs for Managing Cardiovascular Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97

Drugs that Improve Heart Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .101
Drugs that Increase Blood Vessel Diameter . . . . . . . . . . . . . . . . . . . . . . . . . . .104
Drugs that Alter Blood Coagulation Mechanisms . . . . . . . . . . . . . . . . . . . . . .109
Drugs that Reduce Blood Volume . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .113
Drugs that Lower Blood Lipid Levels . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .115
Chapter 8
Drugs for Managing Diabetes Mellitus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .125
Insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .127
Oral Hypoglycemic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .131
Chapter 9
Drugs for Managing Respiratory Inflammation and Congestion . . . . . . . . . . . . . . .145
Drugs that Treat/Manage Allergic Reactions . . . . . . . . . . . . . . . . . . . . . . . . .148
Drugs that Increase Airway Diameter . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .150
Drugs that Manage Respiratory Congestion . . . . . . . . . . . . . . . . . . . . . . . . . .153
Drugs that Suppress Coughing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .154
Chapter 10
Drugs for Managing Mood and Emotional Disorders . . . . . . . . . . . . . . . . . . . . . . . . .163
Anti-Anxiety Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .165
Antidepressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .168
Antipsychotic Medications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .173
Chapter 11
Drugs for Managing Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .185
Antineoplastic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .192
Antinausea or Anti-Emetic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .199
Chapter 12
Drugs for Managing HIV/AIDS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .209
Antiviral Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .213
BIBLIOGRAPHY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .226
INDEX . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .231

Learning Objectives
The information presented in this book will give the reader:
• a basic understanding of the concepts and principles of pharmacology

• familiarity with pharmacological terms
• more confidence researching drugs and reading drug profiles
• an introduction to how the body processes and utilizes medications
• an awareness of how drugs are administered and an appreciation of
how different methods of administration affect massage therapy
treatment
• an understanding of the importance of including medication
information in your case history taking
• an appreciation of the categories of drugs that are employed in the
management of a number of common disorders
• basic principles about how the mechanisms of drug action can
interact with the effects of massage therapy
• an awareness of how drugs the client is taking may influence
assessment results
• an understanding of how medication effects can influence selection
and application of massage techniques and hydrotherapy
• an ‘at your fingertips’ reference to common drug side effects
• an awareness of how certain drug effects can contraindicate massage
or make it necessary to postpone treatments
• some pointers about exercise recommendation related to medication
effects
• more confidence in designing safe and effective treatment plans
taking into account the medications the client is using

Basic
Concepts
and
Guidelines
CHAPTER 1
Why Massage Therapists Need to Know

How Medications Work
When the suggestion is made that massage therapists should receive more training in one area
or another, the response is often that the proposed subject is really postgraduate education. It
is argued that practitioners who wish to pursue a particular interest can always elect to do
more training, but the additional education is not necessary for everyday clinical practice.
Whether valid or not in other contexts, this argument is not well founded when applied to
massage therapists and their need for knowledge of basic pharmacology.
While some massage therapists make a definite decision to work in injury rehabilitation,
palliative care, and other such medically intense settings, many say they could not have
predicted at graduation the paths their practices would take. The truth is that most massage
practitioners encounter an unpredictable variety of clinical conditions in their client
populations. Today massage therapists are becoming more and more actively involved in the
integrated health care management of some of our most challenging diseases.
On the surface of things, it is easy to underestimate a massage therapist’s need to know about
medications. Traditionally only members of a mainstream medical profession, like doctors,
nurses, and dentists, have received instruction in pharmacology. The reality is, however, that
massage therapists treat clients on a daily basis who are taking various types of prescribed
drugs. In many cases these medications affect body physiology in ways that make modifying
massage treatment necessary.
Clients who visit massage therapy clinics for relaxation, or seek out massage in settings like
spas or fitness centers, are often taking drugs for heart problems, arthritis, cancer, diabetes,
AIDS, depression, chronic pain, and so on. The fact that the focus of the treatment may be
stress reduction or routine self care does not mean that the interaction between the client’s
medication and the massage therapy given is a non-issue. This is also true about treatment
modalities that might be considered ‘light’ like lymphatic drainage, or more energy-focused
like craniosacral therapy. Since there is a drug in the client’s body, the practitioner has to have
basic information about how it may impact on the client’s responses to the treatment about to
be given.
A standard definition of pharmacology is “the study of the action of chemicals on living

organisms to produce biological effects.” Pharmacology is subdivided into areas including
pharmacodynamics, pharmacokinetics, pharmacy, and toxicology, all of which support the
understanding and utilization of medications in medical treatment.

Massage therapy is generically defined as “the manipulation of the soft tissues of the body for
a therapeutic response.” In addition to direct manual manipulation of tissues, other modalities
are often used during treatment. Examples include hydrotherapy, actinotherapy, and
aromatherapy, as well as specific manual techniques like joint mobilization, manual lymph
drainage, muscle energy techniques, and myofascial release methods. All are geared towards
producing physical changes for the benefit of the client.
Both pharmacy and massage therapy, although very different disciplines, attempt to create
physiologic and psychological changes important to the achievement of better health and
quality of life.
All medications affect the normal responses of the body in some way. While some of these
effects are not relevant to massage practice, in many cases the combined physiological results
enhance or alter the impact of massage therapy modalities. At times the outcome can be
adverse. For example:
• Centrally acting skeletal muscle relaxants (e.g. cyclobenzaprine) depress

various parts of the central nervous system. This can alter the normal
protective stretch reflexes in skeletal muscles so that there is potential for
damage from manual techniques.
• The phenothiazines (e.g. trifluoperazine) are used for their anti-psychotic
properties. They often alter the temperature regulating mechanisms of the
body, creating an important hydrotherapy concern.
• Corticosteroids (e.g. dexamethasone) are a group of drugs widely used in
medicine to control pain, inflammation, and immune responses. These
drugs are also known to weaken connective tissues including skin, fascia,
ligaments, and muscle.
Let’s take a look at two scenarios that illustrate why a massage practitioner needs to know
basic information about drug effects and interactions:
1. The massage technique of petrissage creates hyperemia, while the application

of heat either locally (a hot pack) or systemically (sitting in a whirlpool or
hot herbal bath) creates vasodilation. Both have the direct effect of
increasing blood flow into the affected tissues. If your client is taking
medications for a cardiovascular complaint, the response to such modalities
may be altered due to the effects of the medication on the circulatory system.
A predisposition to adverse reactions is therefore created. For example,
petrissage can cause bruising in someone taking an anticoagulant, and a hot
systemic treatment such as a whirlpool may promote fatigue, dizziness, and
even fainting in combination with a vasodilator medication.
2. A client with a sore shoulder is taking a pain-relieving drug, such as aspirin
or ibuprofen, and also seeks out massage treatment. The client requests

“deep work” to get to the root of the problem, which is a combination of
tendinitis and old scar tissue. The therapist complies and gives a rigorous
deep treatment. The next day the client is very bruised and in much worse
pain. If the therapist had been aware that aspirin and ibuprofen have
anticoagulant properties as well as reducing the ability to give accurate
feedback about how painful a technique is, it would have been clear that the
‘deep work’ approach was not indicated at that time.
The general population is increasingly combining allopathic medicine (using drugs to treat a
condition and/or alleviate symptoms) and non-drug therapies such as massage. This
combining of therapies by the American public was first documented in a study published in
1993.1 The data indicated that 83% of individuals interviewed saw both their medical doctor
and providers of “unconventional” medicine2 in their search for better health, even when they
had serious medical conditions. The study additionally found that 72% did not inform their
physician that they were receiving these other therapies while under medical care. Whatever
the reasons for this are, it speaks to the need for practitioners of complementary health care
methods to have independent awareness of the implications of combining their treatments
with common allopathic modalities.
When a client reports: “My doctor has prescribed muscle relaxants for me,” or “I have been
taking a painkiller since the accident,” or “I got a steroid shot for the bursitis,” the massage
therapist needs to understand the significance of these statements as they relate to massage
treatment planning. The practitioner is responsible for both the effectiveness and the safety
of the therapy provided.
To provide safe and effective treatment, massage therapists should have:
• a basic understanding of the actions and effects of commonly used drugs, and
the ability to research the effects of other medications encountered
• knowledge of how massage affects the body's physiology and the ability to
apply this knowledge to varying client presentations
It is not the intention of this text to provide extensive coverage of all drugs or detailed
discussion of the chemical structures of drugs. Nor does the mention of specific drugs or
brand names imply their superiority over others or constitute a recommendation for their
specific use.
When therapists require specific information about a medication, there are a number of good
resource texts such as The Physicians Desk Reference (PDR), The United States
Pharmacopeial Drug Information (USP DI), and the Compendium of Pharmaceuticals and
Specialties (CPS), which is a Canadian reference for health care professionals. In some cases,
the pharmacist or attending physician is also an important resource.

Massage therapists can feel at a loss when approaching a doctor or researching in such
reference texts because the language used to discuss medications can be quite technical. It is
also important to be aware that the available resources usually do not reflect an understanding
of the effects of massage therapy and the impact of combining massage modalities with the
drug in question.
A useful resource in understanding how massage therapy affects the body is A Physician's
Guide to Therapeutic Massage by Dr. John Yates. This book presents research findings that
discuss the physiologic effects of massage therapy on the various body systems. Research
into how massage therapy influences the body physiologically is still limited and is ongoing;
therapists are reminded to use the available information as a guide and to stay alert for
individual client reactions.
This text is designed to help massage therapists understand the language and concepts of
pharmacology and how the use of medications relates to massage therapy. It also provides
information about the potential impact that drugs can have on a massage treatment and offers
guidelines for preventing practitioner-induced adverse effects through appropriate planning
and treatment adaptation.
1. Eisenberg, D.M., et al., “Unconventional Medicine in the United States, Prevalence, Cost and
Patterns of Use,” New England Journal of Medicine, January 28, 1993.
2. Unconventional medicine was defined as “…medical interventions not taught widely at U.S.
medical schools or generally available at U.S. hospitals. Examples include acupuncture,
chiropractic, and massage therapy.”

CHAPTER 2
Common Pharmaceutical
Terms and Concepts
To have a clearer understanding of how drugs work therapists must be able to read and
understand drug profiles or monographs. Reading a drug profile can be quite challenging
because it is often difficult to understand the language of pharmacology. This chapter explains
commonly used terms that therapists will encounter when reading information about drugs.
1. DRUG NAMES
Drugs are known by either their generic name or their brand name.
Generic Name
The generic name of a drug is a simplified term that reflects the official chemical name and
structure of the drug. As can be seen in the example below, the generic name diazepam is
much simpler and easier to use than the chemical name of the same compound.
Generic name: diazepam
Official chemical name:

7 chloro-1,3dihydro-1-methyl-5-phenyl-2H-1,4-benzodiazepin-2-one (C16H13ClN2O)
Sometimes a drug may have more than one generic name. For example, acetaminophen is also
known as paracetamol. In this text, the most common generic name will be used.
Brand Name
When a drug is developed, researched, tested, and produced for sale in the marketplace by a
drug manufacturing company, the formulation is assigned a brand name. The brand name is
the registered trademark ® for a generic drug by a drug manufacturer.
The generic drug called acetaminophen or paracetamol is more commonly known by its brand
name Tylenol. Another example is the generic drug ibuprofen, which is known by several
brand names including Motrin, Advil, Nuprin, and Brufen.
The use of a brand name in this book does not imply its superiority over a brand name not
included, nor is it intended to be a recommendation for its use.

Brand Name
The registered name of a generic drug by a drug manufacturer.
Motrin
Advil ibuprofen
Brufen
Nuprin
Clinical Relevance
In today's very competitive medication market an increasing number of companies are
manufacturing generic drug preparations that typically sell at a cheaper price than the
corresponding brand name version. Although these preparations meet official requirements,
concerns about their therapeutic effectiveness and tolerability do sometimes arise when
compared to their brand name counterparts. On the other hand, they can be more efficacious
for some people.
You will no doubt encounter clients who have changed their medication from a brand name
drug to the generic version or from a generic to the brand name. If it is a prescribed change,
most likely the physician will be monitoring the client. However, it is also possible to
voluntarily change a medication by obtaining a prescription from another doctor or by
ordering it over the Internet. If the change is not being professionally monitored, and the
client experiences adverse reactions such as dizziness, nausea, or headaches, these symptoms
may not be correctly attributed to the generic/brand name drug switchover.
Another concern about this type of medication change is that the client may not experience
the same degree of therapeutic effectiveness as with the version of the drug originally being
taken. This can be life threatening if the client has a serious condition and is making the switch
without appropriate medical supervision. It may also make reactions to massage therapy
suddenly less amenable.
Massage practitioners are encouraged to be alert to clients changing medications between

generic and brand name versions, and to inquire about any adverse reactions or side effects
experienced since the change.
2. DRUG CLASSIFICATION
Drugs can be classified in several ways. For example, for the purposes of regulatory bodies
they can be broadly classified as:
• non-prescription drugs
• prescription drugs
• restricted and controlled drugs

Drugs can also be classified according to their medicinal and chemical properties. They are
often grouped according to their:
• therapeutic properties
• action or effect on a specific body system
• chemical structures
The recommendation of a specific member of a drug class by a physician depends on various

factors such as cost, patient tolerance, and pharmacokinetic properties.
When a massage therapist is reading a drug profile, particular attention should be paid to the
classification of drugs according to their therapeutic effects, and what body systems are most
affected.
Classification by Therapeutic Effect

When drugs have been placed together in a class based on similar therapeutic properties, this
is because they are generally used in the management of a particular disorder or disease. As
a result, when a specific effect is needed the physician can select from a range of drugs. For
example, if the desired therapeutic effect is to reduce blood pressure, the physician can
prescribe either one or a combination of drugs that are known to have an antihypertensive
effect. This class includes drug categories like the diuretics, beta blockers, calcium channel
blockers, and vasodilators. Regardless of how they act to reduce blood pressure, these
chemicals are classified as ‘antihypertensive drugs.’
Let’s look at another example. If the desired therapeutic effect is to reduce pain, the physician
can prescribe either one or a combination of drugs that are known to have an analgesic effect.
This is a large class of medications involving many categories. Examples include the non-
steroidal anti-inflammatory drugs, the narcotic analgesics, and the centrally acting skeletal
muscle relaxants.
Classification by Effect on a Specific Body System

When drugs are classified according to their body system effects, their placement in a class
does not necessarily reflect what their therapeutic use might be. For example, drugs that affect
the central nervous system (CNS) include the CNS stimulants, such as caffeine, and CNS
depressants like the narcotic analgesics. Drugs that affect the function of the gastrointestinal
tract include the antacids, which are used to neutralize stomach acidity; laxatives, used for the
management of constipation; and antidiarrheal drugs for the management of diarrhea.
Classification by Chemical Structure

When drugs are classified according to their chemical structure they often show related
therapeutic properties. Slight changes in chemical structure can create drugs with weaker or
stronger therapeutic effects and different side effects. This can be observed in the range of

medications included in large groupings like the corticosteroids, narcotics, beta blockers, and
non-steroidal anti-inflammatories.
Clinical Relevance
A client may not remember the name of the medication(s) he or she is taking, but will be able
to tell you the reason it was prescribed, for example to lower blood pressure. Until more
specific information is provided by the client, knowledge of this systemic drug classification
should guide you toward planning an appropriate assessment and treatment that pays attention
to the cardiovascular system problem.
Clients may also not fully comprehend why a specific drug has been prescribed, for example
for back pain. Regardless of the exact cause of pain, which is a subject the massage therapist
will want to explore further, the fact that the client is taking an analgesic always necessitates
having an awareness of analgesic-related concerns, like reduced accuracy of client feedback.
3. USES OR INDICATIONS
The section of a drug profile called “Uses” or “Indications” lists the diseases or disorders for
which the drug is officially recommended. These are the uses approved by the Food and Drug
Administration (FDA) or similar Health and Welfare department of the country of origin.
Sometimes drugs are employed in an unofficial or experimental manner. An illustration of this

is the current recommendation of aspirin in cardiovascular disease. The official use for aspirin
is the management of mild to moderate pain. However, because of its anticoagulant effects
aspirin is now being widely recommended to help prevent heart attacks and strokes. It is also
showing very promising results when used in the treatment and management of certain types
of colon cancer.
Information about non-official uses of medications can usually be obtained through sources
like the local library or pharmacist, the Internet, or a medical health care provider.
As more research and testing is conducted, a once experimental use of a drug may receive
regulatory body approval and become an official use.
Clinical Relevance
A single medication can have several approved and non-approved uses. Therapists should
always inquire about why a client is taking a particular medication. Looking at the range of
uses for aspirin given on the next page, you can see that the reason a client is taking it is
important to discern, as the approach to assessment and treatment for a headache will be quite
different than that for treating an inflamed joint.

headaches
fever
aspirin pain
cardiovascular uses
joint inflammation
4. EFFECTS OF MEDICATIONS
The effects of medications can be grouped into three categories:
• therapeutic effects
• side effects or adverse effects
• unpredictable effects
Drug effects are influenced by factors such as dosage, age and gender of the patient, lifestyle,
pathologies present, and the person's own unique constitution.
Therapeutic Effect
The therapeutic effect is the desired effect of the drug. For example, a therapeutic effect of
aspirin is to reduce the pain and inflammation of arthritis, and the therapeutic effect of the
anti-anxiety drug diazepam is to calm and relax the user. The therapeutic effect of a drug is
intended to help the user get better.
Side Effect
Also referred to as adverse effects, side effects are the undesirable reactions a drug can
produce. They may be related to the therapeutic effect of the drug, being in essence a stronger
than typically experienced response. For example, in some individuals diazepam can promote
a greater degree of calming and relaxation than desired. The result may be drowsiness to an
extent where the ability to drive or operate machinery is impaired.
Side effects can also be the result of additional actions a drug may have. Aspirin, aside from
its desired therapeutic effects, irritates the lining of the stomach. This irritation can lead to the
development of gastric ulcers and even severe gastrointestinal bleeding.
Side effects may also be created by interactions among two or more medications. In other
words, two drugs that individually may not produce problematic responses, when combined,
can result in new or intensified adverse effects.

Therapeutic Effect
Analgesia
aspirin
Side Effect
GI Irritant
Therapeutic Effect
Antianxiety
diazepam
Side Effect
Drowsiness
Side effects may be caused by additional actions of a drug, for example aspirin irritating the stomach
lining, or an intensification of a drug’s actions, as in the case of valium producing drowsiness.

Unpredictable Effect
Unpredictable effects of a drug tend to occur in two types:
• allergic or hypersensitivity reactions

• idiosyncratic reactions
Allergic or Hypersensitivity Reactions

Some people react allergically to some drugs. These types of reactions can range from fairly
mild to quite severe. Mild reactions usually manifest as skin eruptions such as hives. Other
mild allergic reactions to drugs can include joint pain, fever, and swollen lymph nodes.
If the allergic response is more severe, the client can experience an anaphylaxis reaction or
anaphylactic shock. Anaphylaxis is a medical emergency situation characterized by seriously
decreased blood pressure and restricted airflow, the latter being a result of contraction of the
bronchial smooth muscle and swelling of the throat and mouth.
Idiosyncratic Reactions
Idiosyncratic reactions are unexpected or highly unusual effects of a medication, occurring
uniquely in individuals or in very small numbers of people. This type of effect can be difficult
to explain, although genetic predisposition may play a role. When compared to the expected
therapeutic response or typical side effects of the drug, idiosyncratic reactions can be
accelerated, toxic, or opposite effect responses.
Clinical Relevance
Clients can be experiencing effects from their medications other than the desired therapeutic
ones. In some cases a client’s chief complaint may actually be a drug side effect. Therapists
are encouraged to always check with clients concerning what side effects they have
experienced, and/or what they have been told may occur. Common side effects are usually
listed in drug profiles. In a later section of this book, side effect tables are presented for the
drug classes commonly seen in massage therapy practice. It is important to keep in mind that
such lists can never be considered exhaustive given the range of responses to medications that
may occur.
Practitioners should always monitor client symptomatology and be alert for unusual aspects,
unexpected changes, or atypical responses to massage treatment modalities. If adverse or
unpredictable drug effects are suspected, the client should be advised to schedule a follow-up
session with the prescribing medical practitioner.
When clients are taking more than one medication there is an increased likelihood that the
combination of drug effects may result in side effects or idiosyncratic reactions, some of
which may contribute to their musculoskeletal and general health complaints.

5. MECHANISM OF ACTION
This term describes what a drug does inside the body to produce its therapeutic effect(s).
Drugs do not create new functions; instead they alter existing cellular activities. The
processes through which medications influence body physiology are varied and often
biochemically complex. With some drugs these biochemical reactions are well researched and
documented, while for others the exact processes and mechanisms involved are not fully
understood, or not known.
Drug mechanisms of action are created through one or a combination of the following:
• By Combining with Specific Cellular Receptors

In order for a drug to exert its biological effect there must be an interaction between the drug
molecules and the target cells. The “lock and key” theory postulated in 1894 by Emil Fischer,
a German chemist and enzymologist, offers an explanation as follows: All cells have receptor
sites on their membranes that will only fit with molecules of a certain size, shape, or charge
(+ve or -ve). When a drug molecule is a good match with a cell membrane’s receptor sites, it
can produce changes inside the cell such as altering internal ion channels, messenger systems,
or enzyme reactions. These changes adjust how the cell functions in order to create the drug’s
effects. The interaction between the drug molecule and the cell membrane is compared to the
fit between a lock (cell) and key (drug molecule).
Drug C
A Drug B
Drug Drug D
Lock and key configuration between drug and cell receptor: Drugs A and B each fit into a matching
receptor on the cell surface and will therefore be able to alter the cell’s functions. Drugs C and D
do not have matching shapes and will not have any impact on the cell.

To give some clinical examples:
1. A drug may interact with a muscle cell receptor site to cause prolonged opening of an
internal calcium channel. This results in increased calcium utilization in the cell and
produces the drug’s effect, which in this instance is an increase in the force of muscle
contraction. Such an effect can be useful in supporting a weakened heart, for example.
2. If the mechanism of action of a drug is to increase the sensitivity of cell membranes
to insulin, the result being to decrease blood glucose levels, the drug is useful in the
management of Type II diabetes.
• By Chemically Altering Body Fluids

A common example of this mechanism of action is taking an
antacid to neutralize excess stomach acidity and reduce or
prevent digestive discomfort.
• By Chemically Altering Cell Membranes

Drugs can act on a cell’s membrane to alter its electrical stability and therefore influence its
responsiveness to stimuli. Typically, the drug will influence the membrane’s permeability,
causing speeding up or slowing down of the movement of ions into and out of the cell. Some
examples of medications that act this way include lithium and the general anaesthetic gases.
K+
K+
Na+
Drug
This neuron is being influenced by a medication to be less easily depolarized. This effect is desirable
in a number of circumstances, for example to produce local anaesthesia or prevent seizures.

• By Interacting with Extracellular Enzyme Systems
Enzymes are protein molecules that facilitate or catalyse all chemical reactions of living cells,
causing them to respond in various ways. By influencing enzyme behaviors, medications can
have numerous types of impacts on tissue function.
A. Injury Resulting in Pain

Injury
Cell
Arachidonic Acid
Cyclo-oxygenase
PGG2
Pain
B. The NSAID Mechanism of Action
Arachidonic Acid
NSAIDS
Illustration of how aspirin and other non-steroidal anti-inflammatory drugs reduce pain by blocking
the activity of the cyclooxygenase enzyme, resulting in inhibition of prostaglandin synthesis.

Clinical Relevance
Knowledge of the mechanism of action of a drug increases one’s understanding of why the
drug is being used for a particular condition or conditions, and why the drug produces its
effects. More importantly, it is often the basis for the practitioner’s awareness of how massage
therapy might promote intensified or adverse reactions. Alternatively, it may explain why
massage therapy will have limited effectiveness while the drug is being taken. Numerous
examples of how drug mechanisms of action can influence the impact of massage modalities
will be discussed in later sections of this book.
6. HALF-LIFE
Half-life in the pharmaceutical context is the time it takes for the body's normal metabolic and
elimination processes to reduce the blood concentration of the drug to one half, or 50%. For
example, if there is 100 mg of a medication in the bloodstream, the half-life of the drug is the
time it would take to reduce its blood concentration to 50 mg. Each drug has its own
individual half-life.
Assuming a half-life of 20 minutes, the table that follows illustrates how much of the drug
mentioned above would be in the bloodstream after 100 minutes.
TIME IN MINUTES BLOOD CONCENTRATION (mg)

start amount 100
20 50
40 25
60 12.5
80 6.25
100 3.125
Clinical Relevance
There are many biochemical processes involved in the metabolism and elimination of drugs
from the body. The kidneys and liver are key organs in these processes. Clients who have
dysfunction of either of these organs may be especially vulnerable to adverse and toxic
reactions because of ineffective removal of drugs and their metabolites. Therapists are
encouraged to inquire about the health and function of these organs and be alert to the
potential implications of dysfunction.
7. ONSET OF ACTION
This term refers to the time it takes before the user feels the effects of the drug. The key factor
is usually how the drug was administered. For example, the onset of action can be felt almost
immediately following an intravenous injection, but most solid orally administered

preparations take about half an hour. Some drugs require concentration accumulation in target
body parts. An example of this is the accumulation of an anti-inflammatory medication within
the synovial joint, which can involve several days before peak onset of action is experienced.
Clinical Relevance
Knowing the expected onset of action of a drug can help the practitioner determine optimal
scheduling of massage therapy. Wherever possible, appointments should be planned when the
effect of the medication is most conducive to safe and effective treatment. In some cases, this
will be when the drug is exercising maximum effect and in others when it is not. Guidelines
elaborating these relationships will be offered in a later chapter. Therapists are expected to
exercise professional judgement, and to consult with the appropriate health care provider
when necessary.
8. BIOAVAILABILITY
The term bioavailability describes the amount of a drug that actually enters the systemic
circulation and is available to produce its effects. A key factor affecting bioavailability is how
the drug has been administered into the body (the route of administration). For example, if
50 mg of a drug is taken orally but the amount that actually reaches the circulation, due to the
impact of digestive processes, is 25 mg, the drug has a 50% bioavailability. If, however, 50
mg of the drug is administered directly into the bloodstream via intravenous injection, it is
100% bioavailable.
When a medication has a low bioavailability only a small quantity of the drug is available in
the blood. Most of the administered dose is either changed into another form or excreted
before it enters the bloodstream. On the other hand, drugs with high bioavailability have high
available concentrations in the systemic circulation and are usually rapidly absorbed after
administration.
Other factors that influence drug bioavailability include dosage and frequency and the
person’s age and general health. The presence of any pathologies that affect how the drug is
absorbed, for example gastrointestinal disorders if the drug is administered orally, will also
play a role.
Clinical Relevance
Like onset of action, bioavailability can be a factor in massage treatment scheduling and
design. Having information about a medication’s bioavailability adds to the elements the
massage therapist brings together to create a safe and appropriate treatment plan. For
example, if the client is being massaged in hospital and is receiving an analgesic medication
via IV, the impact of the drug will be consistently strong and the massage therapist will need
to take into account the client’s inability to give trustworthy feedback about depth of
technique. On the other hand, when a client is taking an analgesic orally, treatment can be
organized around whether the maximum analgesic effect is helpful (e.g. in palliative care) or
of concern, for example when frictioning a tendinitis.

CHAPTER 3
How Drugs are Administered

to the Body
“Route of administration” is the term used to describe how a drug is administered to the body.
Drugs can be administered to a specific body area for a local effect or they can be applied in
a manner that has a systemic effect.
The routes of administration discussed in this chapter include:
• oral (into the gastrointestinal tract in solid or liquid form)

• mucous membrane application (under the tongue, inhaled, rectal)
• topical (application to the ears, eyes, skin)
• parenteral (by injection)
• implanted catheters and drug pumps
The route of administration influences the rate and completeness of absorption of the drug
into the bloodstream. This in turn affects several pharmacologic properties of the drug,
including its bioavailability, onset, and intensity of action. Knowledge of routes of
administration will have an impact on the timing and design of the massage treatment, as will
be discussed later.
1. ORAL ADMINISTRATION
The oral route of administration is by far the most popular
way of introducing drugs into the body. The medication is
swallowed in the prescribed dose and absorption occurs
into the blood from the gastrointestinal tract. Solid oral
preparations include tablets, caplets, and capsules; liquid
preparations include syrups, elixirs, and suspensions.
Depending on the form of oral administration (liquid or
solid) it usually takes between a few minutes and an hour
before the drug is absorbed and distributed in the
bloodstream and the person begins to experience its
effects. The maximum effect occurs when a peak level is
achieved in the blood.

Solid preparations will typically dissolve in the stomach and be absorbed into the blood from
the intestines a half to one hour after administration. Enteric coated and timed release
preparations are an exception to this. Enteric coated tablets/caplets have a specially designed
layer of material that dissolves in the intestines instead of the stomach, sparing the stomach
from direct exposure to the drug. Drugs that irritate the stomach lining, such as aspirin and
other non-steroidal anti-inflammatory drugs (NSAIDs), usually have an enteric coat. Enteric
coated drugs may take a slightly longer time to be absorbed into the bloodstream, and the
onset of action of these preparations can depend on several factors including whether or not
there is food in the stomach, and how fast the stomach empties.
Timed release preparations are also referred to as “controlled release” or “slow release.”
Following oral administration only a certain amount or part of the preparation will become
available for absorption into the blood. The remaining parts will dissolve at later times as the
preparation passes through the intestines. This property of dissolving at different times
ensures a constant level of medication in the blood. Timed release preparations are usually
administered once or twice a day.
Liquid medications are generally absorbed into the circulation within 15 minutes after oral
administration and usually have a faster onset of action when compared to the solid oral
preparations.
2. APPLICATION TO MUCOUS MEMBRANES

Mucous membranes contain mucus-secreting cells and cover the internal surfaces of body
passages. The digestive, respiratory, reproductive, and urinary tracts are all lined by mucous
membranes.
Mucous membranes are highly vascularized. They have extensive networks of blood vessels
that tend to pose fewer restrictions to drug access than the skin or intestinal cells. Local
applications are used to address infections and inflammations, for example a canker sore in
the mouth, but their vascularization also makes mucous membranes a good route of
administration when a systemic effect with a more rapid onset of action is needed.
A common example of a
systemic use in a situation
that requires quick action is
the management of angina
attacks. At the beginning of
the attack the client places a
nitroglycerine tablet under
his or her tongue (sublingual
administration). The tablet
dissolves and is absorbed
across the mucous membrane

of the oral cavity directly into the bloodstream. Its symptom relieving effect on the heart
occurs within minutes.
Drugs are applied to mucous membranes as:
• suppositories or enemas applied into the rectum

• inhalations in powder, gas, dust, or vapour forms that are usually
administered into the respiratory tract from specialized devices
• sprays and drops applied into the oral and respiratory tracts
• swabs, powders, sublingual and buccal (dissolved in the cheek
pouch) tablets applied into the mouth and throat
• douches, foams, creams, and pessaries (vaginal suppositories)
applied into the vagina
3. TOPICAL APPLICATIONS
Topical applications are preparations applied:
• into the ear (otic)

• into the eye (ophthalmic)
• onto the skin (dermal)
They are generally used to treat local complaints such as ear infections, eye irritations, and
itchy skin.
Otic Administration
Medications are usually administered into the ear as drops. The drops are applied as close to
body temperature as possible to avoid overstimulation of the auditory nerve. Occasionally
clients may experience vertigo type symptoms. Often a piece
of dry cotton will be inserted into the ear after application to
absorb any excess medication.
Ophthalmic Administration
Drops or ointments are the usual way of administering drugs
into the eye. The preparations must be kept as sterile as
possible because the eyes are very susceptible to infection.
Administration of eye medications may be followed by periods
of blurred vision.

Dermal Administration
Dermal applications are becoming a more and more popular way of administering
medications. They are used in several ways, including:
• to treat local skin conditions such as rashes, dry skin, infections, and
abrasions
• for the relief of muscle and joint pain
• for the systemic administration of drugs
The skin, which is the largest organ of the body, has many functions. It is waterproof; it
protects against invasion of microorganisms; and it acts as a barrier to ultraviolet radiation.
Under normal conditions the skin also acts as a barrier to most chemicals. However, because
of differences in thickness (e.g. thin behind the ears and in the inner upper forearm, thick on
the palm of the hand and sole of the foot), and the penetrating nature of certain chemicals, the
ability of substances to penetrate the dermal boundary varies. Chemicals that are able to cross
the skin’s barriers and enter the circulation will have a systemic effect on the body.
Drugs are applied to the skin as ointments, creams, gels, solutions, and more recently as the
skin patch.
Topical Skin Applications for Local Use

Topical applications of creams, ointments, gels, and lotions are used to treat local skin
conditions like cuts and rashes. They tend to contain ingredients such as antibiotics,
antihistamines, corticosteroids, moisturizers, and analgesics. These preparations are designed
to act specifically on the affected area. They are not intended to enter the systemic circulation;
any such absorption that does occur is usually minute and of little concern.
Topical Skin Applications for Relief of Muscle and Joint Pain

Creams, ointments, liniments, and certain types of medicated plasters are regularly used for
the relief of low-grade muscle and joint pain. Sometimes referred to as counter-irritants, they
contain ingredients such as capsaicin, menthol, wintergreen, and various types of essential and
medicinal oils that are quite volatile, meaning that they evaporate quickly. The exact action
of each ingredient will differ, but they all affect the local circulation and superficial nerves in
ways that can relieve pain and stiffness. Primarily, they tend to cause an increase in local
blood flow that improves oxygen and nutrient delivery and removes metabolic wastes from
the affected tissues.
When such a counter-irritant is applied, especially if it contains a medicinal oil in high

concentration, the person may experience an initial coolness followed by a sensation of
warmth. When this happens the oil applied to the skin surface has absorbed body heat causing
it to evaporate from the skin, hence the coolness at first, and the warmth that follows
represents an increase in blood flow into the area of application.

Topical Skin Applications for Systemic Administration of Drugs
Specially formulated ointments, and products like the skin patch, are increasingly becoming
popular routes for the systemic administration of medications. The preparations involved are
'transdermal,' meaning that the drug is formulated in a special gel-like matrix that is able to
pass through the skin barrier and enter the systemic circulation. Nicotine and hormone
replacement therapy patches are common examples of this type of application. They are stuck
onto the skin in much the same way we apply a Band-Aid.
Drugs like nitroglycerine are also available in special ointment formulations

for transdermal absorption. A prescribed amount of the ointment is
squeezed onto a strip that is then applied securely to the patient’s skin at a
chosen site. The medication is absorbed in a slow steady way to ensure a
good concentration in the bloodstream over a period of time.
Therapists should remember that transdermal preparations do cross the skin barrier and must
not be confused with the regular local ointments and creams described earlier. While a
practitioner should always take precautions against removing a dermal preparation, when the
application is being used to maintain a controlled medication level in the blood the
implications of wiping it off or disengaging a patch are more serious. The practitioner can
also be ‘dosed’ by the medication if it comes in contact with his or her skin.
4. PARENTERAL ADMINISTRATION
The term parenteral refers to any route of administration other than the oral or gastrointestinal
routes. In common usage, however, this term is closely associated with injections and that is
how it will be interpreted in this text.
Situations in which the parenteral route of administration is selected include:
• when oral administration would be ineffective; for example, insulin is usually

delivered by injection because if taken orally it is destroyed in the stomach
• during emergency situations where a very rapid physiologic response is
needed, e.g. to prevent an anaphylactic reaction following an insect bite
• for continuous provision of a steady supply
of a drug via intravenous drip, usually in a
medical setting like a hospital or hospice
• when a patient is vomiting and cannot take
medication orally
• for administering vaccines
• when a preparation is being injected directly
into a tissue, for example into an
osteoarthritic joint (intra-articular injection)

The table that follows lists routes of administration for injections, time frames for their onsets
of action, and common sites of administration.
Route of Injection Onset of Action Site of Administration
intradermal – within the within a few minutes often in the forearm (e.g. allergy
dermis of the skin testing), or where needed for local
anaesthesia
subcutaneous – within can be quick, within a few outer surface of the upper arm, the
the subcutaneous minutes if there is good abdomen, the anterior thigh
layer of the skin vascular supply
intramuscular – within very quick to within a few the middle deltoids, the ventrogluteal
the muscle minutes; some are prepared in area, dorsogluteal: in the region of
slow release form gluteus medius or gluteus maximus, in
the vastus lateralis, in the middle third
of the thigh between the greater
trochanter and the knee
intra-articular – directly may take up to several hours joints of the body, most commonly:
into a joint before full effect is felt; shoulder, elbow, wrist, hand, hip,
occasionally the person may intervertebral, pelvis, knee, ankle, foot,
experience a flare up after the sacroiliac joints
injection
sometimes administered in slow

release or long acting form ;
effects from one injection can
last up to 6 weeks
intravenous – directly very quick to within a few median cubital, cephalic, median, and
into a vein minutes basilic veins of the elbow, forearm and
dorsum of the hand
intra-arterial – directly very quick to within a few use is restricted to special cases such
into an artery minutes as diagnostic procedures, or during
chemotherapy
intrathecal – directly very quick to within a few common example is the epidural
into the spinal column minutes (lower body anaesthesia)
intralesional – directly very quick to within a few for example, into trigger points or
into a lesion minutes tumours
perineural (nerve block) usually within a few minutes close to nerves, at nerve roots, in facet
– in the immediate joints
vicinity of a nerve

Commonly used injection sites. All sites indicated with the exception of the buttocks are frequently
used for subcutaneous injections. The muscles most commonly utilized for intramuscular injections
are the deltoids, the gluteals, and the quadriceps.
When a prolonged medication effect is needed, a specially prepared long-acting

formulation called a depot (Fr: storage) is used. Drugs are administered in this manner by
intramuscular, intra-articular, and subcutaneous injection. For example, when a person
with osteoarthritis is given intra-articular injections of corticosteroids, depending on the
type of corticosteroid used, the effect of the drug can last for as long as six weeks.
Some drug depot preparations are also implanted subcutaneously, for example
contraceptives. The drug is slowly released and absorbed into the bloodstream. This type
of contraceptive can last for up to five years.

5. IMPLANTED CATHETERS AND DRUG PUMPS
Drug pumps and implanted catheters are another means of delivering drugs into the body.
These devices are often used with patients with special requirements, for example for:
• frequent blood sample taking

• delivering many injections into the bloodstream
• giving several types of transfusions
• supplying ongoing nutritional support
• providing greater control over the administration of their medication
Implanted Catheters
An implanted catheter device is surgically fitted so that most of it is lying beneath the skin.
There are two incisions made during the implantation, for entrance and exit sites. The exit
site is the location where the catheter exits through the skin surface. A small length of catheter
fitted with an injection cap extends beyond the exit site.
The entrance site is made in the tissue at the location where the drug is to be administered.
Depending on what the medication is, and where it has to be delivered, the placement of the
catheter varies. For example, if what is required is an epidural for analgesia, the catheter’s
entrance site is implanted into the epidural space, and if the catheter is being used to deliver
insulin, the entrance site is in the subcutaneous tissues.
When the drug must be

delivered directly into the
catheter in circulation, the catheter is
the right internal usually placed into a central
entrance site jugular vein
vein. This is known as a
central venous catheter (CVC).
exit site The entrance site portion is
implanted with its tip threaded
into a large vein, providing
easy access to the vascular
system without having to put a
needle into a blood vessel
every time a procedure is
performed. The veins usually
injection cap used are the large cervical
veins.
The part of the catheter between the entrance and exit sites lies within a surgically created
subcutaneous tunnel. An injection cap (the visible piece) is attached to the catheter at the exit
site. This is the mechanism through which a needle is inserted to deliver medications.

For CVCs, the exit site of the catheter is usually on the anterior chest wall, and for epidurals
on the anterior lateral flank area.
Drug Pumps
Drug pumps are sometimes used to deliver
medications into the bloodstream via an
intravenous line or an implanted catheter. They
are ‘pushing’ devices in the form of an external
machine or a subcutaneously implanted
apparatus. With both types of pumps patients
have a certain amount of control over
administering their own medication.
In the external pump set-up the drug to be

administered is stored inside the pump. The
patient pushes a button on the pump mechanism
to release a predetermined dose of the
medication into the bloodstream. The pump
usually regulates the intervals at which the drug
can be taken to avoid overdose.
Internal pumps are subcutaneously

implanted and can stay in place for as
self-sealing material
long as 1 to 2 years. Medications are
injected through the skin surface into
reservoir pump device
a reservoir within the pump. The
skin surface patient controls the release of the
subcutaneous medication by activating the pump
tissue with an external device much like a
TV remote control. Once released the
vein drug travels through a catheter that
begins at the reservoir and terminates
in a central vein.
Clinical Relevance
Knowledge of routes of administration and their implications is very useful in planning
massage treatments to minimize the chances of inducing medication-related adverse
reactions. For example, a client who is on short term use of oral anti-inflammatory tablets
will probably give more accurate feedback about depth of technique during the treatment if it
is performed when the drug's bioavailability is at its lower levels. Giving the treatment before

or just after scheduled doses might be appropriate. On the other hand, when treating an
insulin dependent diabetic, the medical stability of the client is of primary importance.
Scheduling treatments in time periods following insulin injections so that the medication is at
peak bioavailability is less likely to destabilize the diabetic condition.
Implanted catheters and drug pumps must be properly maintained by the patient and carefully
monitored medically. Everyone involved with the client’s care needs to maintain an
awareness that infections and blood clots can develop at the entry and exit sites. A more
serious concern with internally implanted drug pumps is malfunction of the pump or a
blockage or kink in the delivery catheter. Such disruptions can lead to symptoms of over or
under dosage of the drug.
There are a number of massage treatment guidelines that stem from specific aspects of the
various routes of administration. These will be elaborated in Chapter 5.

CHAPTER 4
Drug Processing in the Body
In this chapter we will discuss what happens to a drug after it is administered into the body.
Although there are differences that stem from individual drug characteristics and variations
based on routes of administration, all drugs are subjected to various physiological processes
that can modify their capacity to affect their target cells. These include:
• dissolving and dissociating; making the drug particles available for

absorption from the gastrointestinal tract
• metabolism; processes that can change the chemical nature and activity of
the drug
• distribution; delivery of the drug to its site(s) of action
• elimination; removal of the drug and its metabolites from the body
These processes have the potential to impact significantly on the therapeutic activities of
drugs and properties such as their bioavailability.
1. DISSOLVING AND DISSOCIATING

During the manufacture of solid oral medications (e.g. tablets, caplets,
capsules) several inactive substances called excipients are included in
the preparations. They are present in varying amounts and serve two
main functions: to help the preparation maintain its stability while
stored on the pharmacy shelf, and to ensure that it can readily dissolve
and dissociate in the gastrointestinal tract. In the latter case they
facilitate the ‘breaking up’ of the preparation into much smaller
particles suitable for movement from the GI tract into the bloodstream.
Tablets and capsules that quickly dissolve and dissociate are more
rapidly absorbed. This increases the drug's bioavailability and tends to
make the onset of action faster.
Orally administered liquid preparations generally contain their drug ingredients in a dissolved
form, making them readily available for absorption.

Absorption of a drug into the blood is influenced by many factors. Some of these include:
• its chemical nature; for example aspirin, a weak acid, is more readily
absorbed from the acidic environment of the stomach, while griseofulvin, an
anti-fungal agent, is best absorbed when taken with a fatty meal
• its dosage; higher drug dosages are typically absorbed more rapidly
• its form of administration (see Chapter 3)
• the size of its particles; for example griseofulvin ultramicrosize tablets are
absorbed more readily than griseofulvin microsized tablets
• the presence of any gastrointestinal pathologies (ulcers, gastritis, etc.) that
can affect the amount and quality of absorption
2. METABOLISM
Following oral administration and absorption from the intestines, a drug is transported to the
liver via the portal circulation. The liver is the most important organ of metabolism. Drug
profiles often contain statements such as “This drug undergoes rapid hepatic
biotransformation,” or “This drug is extensively metabolized by the liver.” Metabolism
involves a number of complex biotransformational processes which change potentially
damaging substances into ones that will not be harmful to body tissues.
An aspect of metabolism that can affect drug

bioavailability is called the “first pass effect.”
This term refers to the effects of liver
processes on a drug that has just entered the
blood from the GI tract. Before it can access
the rest of the body via the general
circulation, it is exposed to the actions of the
liver’s metabolizing enzymes. However, not
all drugs are affected by these processes in
the liver. A drug can be unaffected by
metabolism, in which case it is usually
excreted or eliminated in its original form.
When a drug does undergo metabolism, substances called metabolites are formed. Most drug
metabolites are inactive and harmless compounds, but some show various degrees of
pharmacological activity. These metabolites may produce desired therapeutic effects or they
may be responsible for undesired side effects. For example, describing the pharmacology of
the anti-anxiety drug ketazolam, one reference text states: “The main half life of ketazolam
is approximately 2 hours while half-lives of its metabolites are much longer (32-52 hours) …
The main active metabolites are diazepam, …1” In this example both the drug and its
metabolites demonstrate pharmacologic activity and produce anti-anxiety effects.

Although the liver is the key organ of metabolism, other body tissues are also involved. They
include the lungs, skin, kidneys, and gastrointestinal tract. Certain enzymes found in the
blood, and in neurons, are also responsible for metabolizing drugs.
Sometimes other routes of administration are used to make a drug available to its target
tissues before breakdown can occur in the liver, in other words to bypass the first pass
effect. For example, with sublingual administration a drug can be absorbed into the
circulation through the buccal mucous membranes. From there it is transported by the
superior vena cava to the heart and distributed throughout the body. Similarly, with
suppository application a medication can be absorbed through the rectal mucous
membranes into the circulation and enter the heart via the inferior vena cava. In both
examples the heart initially distributes the drug systemically, allowing it to reach its target
cells before it is taken to the liver. Intravenous or intramuscular injections are also routes
of administration that allow a drug to avoid the first pass effect. By entering the systemic
circulation before contacting the liver, a medication’s bioavailability can be maximized
and its effects experienced within a few minutes. In the normal course of blood
circulation it will eventually be taken to the liver and exposed to its enzymes, at which
point its bioavailability will go down.
When a systemic effect is needed very quickly, and a parenteral route is not
appropriate, the sublingual route is most often employed. The example of sublingual
nitroglycerine use at the onset of angina pains has already been mentioned. The
resulting therapeutic effect occurs within minutes. If the nitroglycerine were taken as a
swallowed tablet, the processes it would have to undergo in the gastrointestinal tract
and the liver would greatly reduce its bioavailability, the timeliness of its onset of action,
and its therapeutic effect.
3. DISTRIBUTION
This term refers to how a drug is transported from its site of absorption to its site(s) of action,
metabolism, and excretion. There are many complex pharmacologic and physiologic factors
that support the distribution of drugs throughout the body. The ones discussed below provide
a general overview of circulatory factors that can affect drug distribution.
• The Rate of Blood (and Therefore Drug) Flow to the Various Tissues
Because tissues like the kidneys, liver, and brain (for drugs that cross the blood brain barrier)
consistently receive high volumes of blood, they will initially receive higher drug
concentrations than do tissues like fat and muscles. As the drug is subsequently recirculated
through the body, more even distribution will occur.
• How Much Drug is Bound to Plasma Proteins

Drugs in the bloodstream are often ‘bound’ to plasma proteins (mainly albumin) to form
drug-protein complexes. Each drug has its characteristic degree of plasma protein binding.

For example, if a drug is described as 60% bound to plasma proteins this means that at any
given time only 40% of the drug is ‘free’ in the blood to diffuse to the target tissues and cause
cellular reactions. Regardless of the drug concentration, 60% will always be plasma protein
bound and only 40% free in the blood.
This binding of drugs to albumin is reversible. There is constant movement of drug molecules
from the bloodstream into the intercellular spaces, and reformation of new drug-protein
complexes within the blood. Throughout these processes a drug’s characteristic equilibrium
between protein bound and free drug concentrations is maintained. Drugs that are typically
highly bound to plasma proteins tend to remain in the body longer than drugs that are less so.
• Mechanisms that Control Brain Access

The blood brain barrier (BBB) consists of tightly packed endothelial cells and surrounding
astrocytes which, among other things, help protect brain tissue from potentially harmful
effects of drugs. How they perform their function is not fully understood, but they appear to
identify substances that are potentially damaging and obstruct them from leaving the blood to
enter the brain interstitium.
Drug "B"
Drug "A"
neuron
cell body
blood
capillary
astrocyte
Drug A is being permitted to pass through the capillary wall and the astrocyte to gain access to the
neuron; Drug B is not being allowed past the ‘blood brain barrier.’

The solubility of a drug also appears to be a determining factor in whether it will gain access
to the brain. Lipid soluble drugs such as the barbiturates cross the blood brain barrier much
more easily than drugs with poor lipid solubility like the penicillin antibiotics.
Research also seems to suggest that a specific set of transport mechanisms are in place that
influence which substances will gain access into the brain. For example glucose, which is
necessary for neuron function and is water rather than lipid soluble, is transported into brain
tissue dissolved in plasma.
4. ELIMINATION
Drugs and other toxic substances are prepared
for elimination from the body by various
metabolic processes in the liver. The
metabolites are biochemically altered to make
them harmless to body tissues and more readily
eliminated.
The kidneys are the main organs involved in

elimination; however, other routes include the
sweat glands, bile, bowels, lungs, and even
mother's milk. Drug monographs will include
statements like “60% of the dose was excreted
in the urine with the remaining drug
undergoing fecal excretion.”
Clinical Relevance
In Chapter 2, differences between generic and brand name drugs were discussed and the
suggestion was made that clients who change their medication from one to another may
experience adverse reactions or altered therapeutic effects. This chapter should shed more
light on this issue. During the production of solid oral preparations such as tablets and
capsules, the quality of excipients or inactive substances used by manufacturers varies. Since
these excipients play an important role in facilitating dissolving and dissociating of the drug
in the gastric environment, a tablet that dissolves and dissociates poorly will not be absorbed
as readily as a tablet of higher quality. Less absorption of the drug into the bloodstream leads
to lower bioavailability, slower onset of action, and questionable therapeutic effectiveness.
Clients with gastrointestinal disturbances such as vomiting and diarrhea, or who have GI
disorders like ulcers or Crohn’s Disease, will tend to experience impaired drug absorption
and/or increased elimination of the drug from the GI tract.
The health and function of the liver and kidneys are extremely important for the normal
removal of drugs and other toxic substances from the body. When drugs and their metabolites
are not properly eliminated they tend to accumulate in the various organs and tissues of the

body and produce adverse effects. Clients who present with either past or present disorders
of these organs may be especially sensitive to the effects of drugs.
The health of the client can affect the amount of free drug in the blood. For example, clients
who are fasting (unsupervised) or those with liver or kidney disease will often have a decrease
in plasma albumin levels. Under these conditions, there will be more free drug to interact with
target cells. If the dose of the drug is not modified the client is at risk for drug toxicity.
1. 1993 Compendium of Pharmaceutical Specialties, 28th ed., Canadian Pharmaceutical Press,

Ontario, Canada.

CHAPTER 5
General Treatment Guidelines
In Chapter 1 reference was made to a research study that investigated the combining of
allopathic and complementary therapies by the American public. An important finding was
that a large percentage of individuals did not inform their doctors that they were receiving
complementary therapies while still under medical care.
Regardless of place of work or treatment style, today’s massage therapists encounter many
clients who are taking drugs. The potential for adverse interactions between a client's
medications and the massage therapist’s choice of treatment modalities, which could include
hydrotherapy, stretching, deep tissue work, lymph drainage, and so on, must raise the question
of client safety in the practitioner’s mind. In treatment planning, the therapist must consider
all factors that could compromise client safety; one such factor is medications.
Chapters 1 through 4 introduced the reader to basic concepts in pharmacology, including

interpretation of key pharmacological terms, description of the routes of administration of
medications, and discussion of some of the drug processing mechanisms in the body. When
possible, an appropriate connection to massage therapy was made; for example, concerns
were raised about the reliability of client feedback when an analgesic is being taken, and about
the importance of understanding a drug’s bioavailability and plasma levels in relation to
scheduling treatments. To promote client safety, therapists need to have a basic understanding
of pharmacologic principles, and the ability to interrelate this knowledge with the
physiological effects of massage therapy modalities and approaches.
Let’s look at a drug profile and relate the information to massage treatment planning. The
following excerpt1 contains information about the anticonvulsant (used in the treatment of
epilepsy) drug carbamazepine.
“The absorption of carbamazepine in man is relatively slow. When taken in a single oral dose
the carbamazepine tablets and chewable tablets yield peak plasma concentrations of
unchanged carbamazepine within 4-24 hours. Only 2-3% of the dose, whether given singly
or repeatedly, is excreted in the urine in unchanged form. The primary metabolite is the
pharmacologically active 10, 11-epoxide. After repeated doses the elimination half-life of
unchanged carbamazepine is 16-24 hours depending on the duration of the medication.
“Because the onset of potentially serious blood dyscrasias [abnormal conditions of blood
cells] may be rapid, patients should be made aware of early toxic signs and symptoms of a
potential hematological problem, as well as symptoms of dermatological or hepatic reactions.

If reactions such as fever, sore throat, rash, ulcers in the mouth, easy bruising, petechial or
purpuric hemorrhage [purplish red spots caused by the release into the skin of a very small
quantity of blood from a capillary] appear, the patient should be advised to contact his or her
physician immediately.
“Other adverse reactions include: skin sensitivity reactions and rashes, photosensitivity,
hypertension or hypotension, nausea, vomiting, and aggressive behavior.”
How would a massage therapist use the above information and relate it to massage treatment?
• Since carbamazepine is used in the treatment of epilepsy, the stability of the

client’s condition is of concern. Treatments should be scheduled when peak
levels of the drug are expected – according to the drug profile this occurs at
least 4 hours after taking a dose.
• Good clinical practice would include taking a BP reading at the start of each
treatment. If you observe significant changes, inform the client and suggest a
follow up visit to the medical practitioner.
• The health and function of the liver and kidneys are
extremely important for maintenance of therapeutic
levels of medications in the blood. The long half-life
of this drug, and the fact that the primary metabolite is
pharmacologically active, suggest that the client can
quickly develop adverse effects if normal elimination
processes are compromised by poor organ health.
Complaints such as fever, and reddish or purplish bruises
as mentioned in the drug profile, are early indications of
drug toxicity. The practitioner will want to stay alert to
the symptoms and complaints of the client. When there
are indicators of drug toxicity present, massage
treatments are contraindicated until the client is
evaluated and 'cleared' by the attending physician.
This chapter draws on information presented in earlier chapters and focuses on decision-
making for the massage therapist, integrating clinical implications of clients’ medication use
into general guidelines for massage therapy that promote safe and effective treatment. These
include guidelines for:
• assessment
• treatment planning
• hydrotherapy
• therapeutic exercise prescription and client self care
• treating around injection sites, skin patches, and implant devices

1. GUIDELINES FOR ASSESSMENT
Most clients have a limited ability to distinguish the multitude of factors that can contribute
to their symptoms. This is especially likely if the complaints are related to medication effects.
If the massage therapist is unaware of the mechanisms of action of medications and the
potential impact of side effects, interpretation of the client’s symptom picture and assessment
findings can lead to misleading conclusions. This in turn can result in development and
administration of ineffective or harmful treatment plans and poor client recovery.
At the end of this section you will find a sample letter to a medical practitioner addressing a
situation where the massage therapist believes a medication side effect may be contributing to
a client’s clinical presentation.
A client’s medications have the potential to alter the results of the massage therapist’s
assessment of his or her case. In this section we will explore how drugs can affect:
• the client's complaints

• case history taking
• observation
• palpation
• movement examination/special and neurological testing
You will also be introduced to the Medication Case History Intake Form.
The Client’s Complaints
Listening to the client characterize the problem is an especially important part of conducting
an assessment. With experience, the practitioner can often form an accurate clinical
impression just by listening to the client’s description of his or her complaint. When

medication effects are contributing to a client’s presentation, the therapist may notice that the
symptoms and test results do not ‘add up’ to a typical diagnostic picture, or may be puzzled
that the symptoms exceed or differ from what might be expected. These situations should be
referred to the doctor for evaluation.
It is also true that medication side effects can mimic common complaints seen in massage
therapy practice, for example headaches, fatigue, swollen ankles, and muscle and joint pain.
This awareness can help the practitioner to anticipate the involvement of medications in some
cases, or to follow through appropriately if massage treatment does not have the expected
result in addressing the complaint.
The chart below gives examples of this type of overlap.
Side Effects That Mimic Common Complaints
Anti- Anti- Anti-

Complaint NSAIDs Hypertensives Corticosteroids Depressants Anxiety Meds
Headaches yes yes yes yes yes

Drowsiness yes yes yes yes
Dizziness yes yes yes yes yes
Fatigue yes yes yes yes yes
Swollen ankles yes yes yes
Rash yes yes yes yes yes
Numbness or tingling yes yes
Muscle or joint pain yes yes yes

Case History Taking
In addition to having clients fill
out general case history forms, it
can be very useful to incorporate a
specific form to document each
client’s medications, remedies,
and supplements. Unless asked
specifically, clients will often
forget to inform you about some of
the substances they are using.
Those who are taking several
types of over-the-counter (OTC)
and/or prescribed medications
may need to take the form home
and check their medicine cabinets
in order to complete the
information as requested.
The reasons for having a medication case history form include:
• to have a clear record of which drugs and other substances are being taken
and why
• to identify and initiate follow-up if the client does not know the reason for
taking a drug
• to have a reference for sorting client complaints in light of potential
relationships to medication use
• to identify if the drugs being used are from the same group (the client is
potentially “double-dosing” and may be more predisposed to adverse
reactions)
• to identify the full profile of what is being taken and the potential for multi-
substance side effects (it can sometimes be enlightening to see how many
drugs are being used by one person and to determine whether any one doctor
is aware of the full profile)
• to have a quick reference for treatment planning
• as a service to the client – building a medication/remedy profile may prove
helpful as a reference in the long-term management of his or her health

Medication Case History Intake Form*
On these two pages you will find a sample case history form specifically for medications,
remedies, and supplements.
Medication Case History - Intake Form Date

Your health and well-being are important to us, so please take a few moments to complete the form provided. The information will help us plan a safer
and more effective treatment for you. All information obtained will be confidential.
NAME __________________________________________ AGE _____ OCCUPATION _______________________________

ADDRESS __________________________________________________________________________________________________
PHONE NUMBERS (H) ___________________________ (W) ________________________________
FAMILY DOCTOR ____________________________________________________________ PHONE _____________________
Within the last 4 weeks: YES NO

Has your medical doctor prescribed any new medications or changed your medications? O O
Has your naturopath or medical herbalist prescribed any remedies for you? O O
Has your dentist prescribed any medications for you? O O
Have you purchased any over-the-counter items for health purposes from a pharmacy or health food shop? O O
Are you presently taking any herbal, Chinese medicine, or homeopathic remedies? O O
Are you presently taking any vitamin or mineral supplements? O O
Name & Strength Date Started # Per Day Reason for Use
List any prescribed or

over-the-counter items
you are presently
taking orally:
List any herbal,

Chinese medicine, or
homeopathic remedies
you are presently
taking orally:
List any vitamin or

mineral supplements
you are presently
taking orally:
© 2001 Curties-Overzet Publications To order: 1-888-649-5411 p.t.o.

Medication Case History - Intake Form page 2
YES NO If yes, please answer the following:

Are you presently using O O Name of preparation: (1) ________________________ (2) _________________________
any medicinal creams or Reason for use: _____________________________________________________________
ointments? Date started: ________________________________________________________________
Area (on the body) of use: ____________________________________________________
How often do you apply it: ___________________________________________________
Are you presently using any O O Name of preparation: (1) ________________________ (2) _________________________
medicinal eye, ear or nose Reason for use: _____________________________________________________________
preparations? Date started: ________________________________________________________________
How often do you apply it: ___________________________________________________
skin patch preparation? Reason for use: _____________________________________________________________
Date started: ________________________________________________________________
How often do you apply it: __________________________________________________
medicinal preparation in the Reason for use: _____________________________________________________________
vagina or the rectum? Date started: ________________________________________________________________
How often do you apply it: __________________________________________________
Are you self-injecting any O O Name of preparation: (1) ________________________ (2) _________________________
medication? (insulin, pain Reason for use: _____________________________________________________________
killers, testosterone, etc.) Date started: ________________________________________________________________
Area (on the body) of injection: _______________________________________________
How often do you self-inject: _________________________________________________
Do you have any medication O O Name of preparation: (1) ________________________ (2) _________________________
delivery implant devices? Reason for use: _____________________________________________________________
Date started: ________________________________________________________________
Area and route of implantation: _______________________________________________
Do you drink coffee or tea on O O If yes, how many cups per day: _________ or per week: ______
a regular basis?
Do you drink alcoholic O O If yes, how many drinks per day: _______ or per week: ______
beverages on a regular basis?
Do you smoke? O O If yes, how many packs per day: ________ or per week: ______
Within the last week have you
used any recreational drugs?
O O
Have you experienced any of the following since starting the medication/natural remedy therapy?
anxiety insomnia irritability blurred vision liver infection decreased appetite
headaches joint pain drowsiness muscle aches yeast infection difficulty breathing
fatigue depression swelling frequent flu difficult urination cold hands and feet
dizziness confusion dry skin stomach pain high blood pressure shortness of breath
fever nausea bitter taste athletes foot heart palpitations low blood pressure
chills tremors loss of taste weight gain/loss increased tiredness prolonged menses
bruising numbness skin rash muscle weakness bladder infection stomach irritation
diarrhea vomiting constipation joint swelling kidney infection decreased sex drive
hair loss tingling chest pain other: ________________________________________________________
Are you allergic to any substances? (e.g. oils, drugs, aromas, metals, etc.) Yes O No O If yes, please specify:
___________________________________________________________________________________________________________________
Additional Comments: ______________________________________________________________________________________________
Signature: ______________________________________________ Date: ______________________
* You may want to use this form as a reference in designing your own, or you can contact Curties-Overzet
Publications to purchase these forms in bulk.

To enhance the usefulness of the information gathered on the medication intake form,
therapists need to consider the impact of the following:
When more than one medication is prescribed for the treatment of a single condition, for
example:
• Hypertension is often managed with a combination of diuretics and

betablocker medications.
• Following soft tissue injury, muscle relaxants and anti-inflammatories are
often prescribed together.
• The common flu is often managed with cough and cold medications, and
sometimes antibiotics to treat/prevent secondary infections.
The combination of medications may cause an increased incidence of side effects or perhaps
unpredictable effects experienced by the client.
A single medication can be used in the management of more than one condition, for
example:
• Aspirin is normally recommended for mild to moderate pain; however, it is

also increasingly used in the management of cardiovascular diseases for its
anticoagulant effect.
• Corticosteroids are used in treating several conditions, including asthma,
bronchitis, arthritis, ulcerative colitis, and various types of autoimmune and
allergic disorders.
Therapists are encouraged to make sure it is clear why a particular medication is being used,
and to assess whether there is more than one purpose for the client taking the drug. Knowing
what the client is being treated for makes for better treatment planning.
When one or more of the medications is a long-term prescription:
• Long-term use of medications is an indication that the client's condition may

be serious. Before treating, it is important to be clear about the nature and
progression of the condition.
• Concerns arise about the health of the liver and kidneys, since these organs
are responsible for the metabolism and elimination of drugs and are more
likely to be compromised by long-term medication use. The client's
symptoms/complaints may be related to accumulation of metabolites in the
body. Inquire in detail about side effects that have been experienced, or
might be anticipated.
• Long-term use of some medications can lead to the development of another
pathology. For example, prolonged corticosteroid use can promote
osteoporosis. Postmenopausal women and the elderly are especially
predisposed.

• The health of the other body systems, i.e. the cardiovascular, respiratory,
digestive, and so on, needs to be monitored ongoingly for stresses or side
effects imposed by long-term medication use. As an example, long-term use
of morphine for analgesia can cause constipation and long-term aspirin use
can lead to ulcers.
• Several medications when taken long-term can reduce the integrity of the
body’s tissues, a particular concern for massage therapists. Be alert for
dry/cracked skin, open lesions, edema, tissue dystrophy, and sensory
impairment; assess for reduced resilience of connective tissue structures like
ligaments and tendons. Ask for medical guidance as needed.
When the client is taking a mix of traditional and non-traditional substances:
Since there are many gaps in this area of knowledge, it is often not easy to find out about the
potential interactions among medications and the remedies and supplements that many clients
are taking. If the client is seeing another health care professional, for example a naturopath or
homeopath, this person can be an important source of information. Existing studies can also
be searched out at the library or on the Internet. A helpful website is www.onemedicine.com.
An alert practitioner will always keep in mind the possibility that the client’s clinical picture
and assessment findings may be affected by such substance mixing.
Observation
Observation, or the ‘looking phase,’ begins when the therapist greets the client; it is an
important source of information about the client’s health. This part of an assessment includes
observing for:
• facial expression • physical deformity

• gait and movement patterns • standing and sitting posture
• skin color and health • limb size and shape
• edema
Let’s look at an example of how a client’s medication can affect the interpretation of observed
information.
A client on long-term use of a calcium channel blocker

medication will be predisposed to developing an altered gait
pattern. This is because accumulation of edema in the feet and
ankles is often associated with this group of drugs. The massage
therapist who is unaware of this side effect may interpret the
altered gait as caused by a hip or lower back disorder and plan
a treatment to focus on these areas. The edema may be
perceived as secondary rather than primary in the etiology of the
problem.

To resolve the altered gait, and any secondary complaints of the client such as hip and lower
back pain, the edema in the feet and ankles must be treated. As well, the physician needs to
be informed of the degree to which the medication is affecting the client’s musculoskeletal
system.
Palpation
Changes in tissue health, muscle tone (hypo- or hypertonicity), skin temperature and
moisture, fascial mobility, myofascial trigger points, and tissue fluid levels are all palpable by
massage therapists.
Here are a few examples of how the use of medications can cause palpable changes:
• Muscle relaxants and other CNS depressants will alter the tone of the skeletal
muscles so that they feel ‘loose’ and are too easily overstretched.
• Long-term use of oral corticosteroids will lead to breakdown of connective
tissues including the skin, muscle, and lymphatic tissues. Edema may be
present, the skin will often feel fragile, and muscles tend to be soft and
hypotonic.
• Ibuprofen, an easily available anti-inflammatory, can cause increased
perspiration. On palpation, the skin will feel cool and moist.
• Repeatedly used injection sites can feel edematous, nodular, and fibrotic,
with fascial mobility restrictions; such sites can also be a source of pain.
Movement Examination/Special and Neurological Tests

During the testing portion of the assessment, the client is asked to perform certain movements
and/or the therapist moves the client’s body through special tests that target the structures
being assessed. The test findings help determine which tissue structures are involved, and to
what degree, in the presenting complaint.
Let's look at two examples of how medications can alter responses to movement and special
tests:
• Medications such as anti-inflammatories and narcotic analgesics alter the

client’s pain perception. When asked to do active movements, the client may
be able to perform normal or near normal range of motion without showing
signs of pain and discomfort that would accurately reflect the stresses being
applied to the tissues. Passive movement results are likely to be skewed in a
similar fashion.
• Centrally acting skeletal muscle relaxants depress the CNS. The results of
neurological testing on, for example, deep tendon reflexes, dermatomes, and
myotomes will be altered. Responses of muscles to manual testing will be
weakened and they will show signs of fatigue more easily.

Sample Letter to Medical Practitioner
The letter that follows is an example of the type of correspondence a massage therapist might
send to the doctor of a shared client in a case where, from the therapist’s viewpoint, a
medication side effect may be playing a role in the client’s presentation. It is important to
keep in mind that such letters must be as brief as possible, well organized, and written in a
neutral, professional tone.
Massage Therapy Center,

Suite 123, Femur Drive, Patellaville
Tel/Fax: 000-123-4567
November 12, 2001
Dr. Rectus Femoris

345 Adductor Drive,
Patellaville
RE: Possible Medication Side Effect
Dear Dr. Femoris,
I am writing in connection with a patient in your practice, Mr. Iliac Crest, who has recently begun receiving
massage therapy.
Client's Complaint: Mr. Crest presented at my clinic two weeks ago complaining of right hip pain and sore,
swollen ankles and feet. He described the hip pain as “dull and achy,” occurring especially after activities
involving prolonged standing or walking, and stated that the peripheral edema is most uncomfortable in the
evenings.
Client History: Mr. Crest had his quarterly medical evaluation with you three months ago. As his blood pressure
was up, you prescribed an additional antihypertensive medication, a calcium channel blocker. Six weeks ago Mr.
Crest visited your clinic complaining of an achy right hip and tired feet. You prescribed an anti-inflammatory,
ordered X-rays of the hip and lumbar spine, and suggested that he elevate his feet at the end of the day.
Clinical Assessment: Changes in gait and pelvic mobility patterns were observed. Bilateral leg edema was
evident, with right side prominence. Orthopedic assessment revealed hypertonicity of the hip and lumbar
musculature, but suggested no specific lesion. The anti-inflammatory did not reduce the symptoms. There is no
history of trauma to the hip joint, and I understand the X-ray report indicated no abnormalities. Mr. Crest
informed me that the swelling began about 4 weeks after his quarterly visit to you.
Clinical Impression: Mr. Crest’s altered gait may be causing his hip pain and discomfort. As you know,
peripheral edema can be a side effect of calcium channel blockers. The time frame links his symptom onset with
beginning the new medication, as does the progression, with early symptoms of peripheral edema causing foot
and ankle discomfort followed later by hip pain. The massage therapy sessions have been aimed at reducing the
edema and addressing the increased muscle tone. Although temporary alleviation was effected, there has not
been substantial improvement. I would be happy to provide additional information regarding the massage
therapy sessions if you wish.
I look forward to hearing your decision in this matter.
Yours truly,
Tib Anterior, R.M.T.

2. GUIDELINES FOR TREATMENT PLANNING
Treatment planning involves being familiar with the general health of the client, having a
good understanding of the nature and progression of the presenting condition(s), and
designing a safe and effective approach to achieving the massage treatment goals.
The massage treatment plan should complement other types of care the client might be
receiving. Providing safe and effective treatment compatible with a client’s medications can
be challenging for the practitioner. This section will elaborate several guidelines related to
how drugs can affect:
• the scheduling of treatments

• treatment focus and duration
• techniques used during treatment
• client cooperativeness
Drugs Can Affect Treatment Scheduling

It is beyond the massage therapist’s scope of practice to tell clients when to take their
medications. However, by adjusting when massage therapy is given, the practitioner can
work to best coincide treatment with the bioavailablity cycles of drug use.
Let's look at two important considerations:
• Medical Stability of the Client

A client whose condition necessitates long-term drug use usually requires a certain medication
level in the blood to ensure that the condition remains stable. Here are a few examples:
• an insulin dependent diabetic must have regular doses of insulin to maintain

acceptable levels of glucose in the blood
• a client being treated for a chronic pain syndrome requires pain medication
for physical and emotional stability
• an epileptic client needs to maintain peak blood levels of anticonvulsant
medication to stabilize the central nervous system and reduce the likelihood
of seizures
Treatment planning must take into account that the circulatory and neural effects of massage
therapy may tend toward destabilizing this type of client. In addition to judicious treatment
modification, the practitioner should consider scheduling treatment sessions at a medication-
appropriate time after the client’s scheduled dosage. The purpose is to ensure maximal
bioavailability of the medication, and therefore better stability of the client during and after
the treatment.

• Client Feedback Implications
As previously discussed, drugs such as non-steroidal anti-inflammatories, narcotic analgesics,
and central nervous system depressants can alter a client’s ability to give accurate feedback
about the comfort of techniques and modalities used during massage treatment. These
medications alter normal pain responses that warn of potential tissue injury. Techniques or
modalities that would normally cause some discomfort become more tolerable than they should.
Consider a client taking an anti-inflammatory for a few days because of a minor injury. The
client seeks massage therapy to assist with the healing process; however, the drug’s analgesic
properties will compromise the client’s ability to comment on what the injured tissues are
experiencing during the treatment. The client, who has a reduced perception of pain, provides
misleading information to the therapist, saying things like “you can go deeper if you want.”
If the therapist responds by doing deeper massage in such a situation, there is a likelihood of
causing more tissue damage and promoting more bruising.
For clients taking medications short-term for minor conditions, recommended treatment
scheduling is just before or soon after the medication dose. With lower bloodstream
bioavailability of the drug the client is likely to give more accurate feedback about the
techniques and modalities used. However, the massage therapist should still be cautious since
the drug’s onset of action can mask symptoms of overtreatment. If unsure about how to judge
the ideal timing of a massage treatment for tissue safety, the therapist is encouraged to discuss
this concern with the client and/or the attending physician.
Drugs Can Require Adapting/Shortening the Treatment
• Energy Level of the Client

Fatigue is a common side effect of many medications, including the hypertension
medications, anti-anxiety drugs, and many of the antidepressants. In this case massage
therapy may cause even more fatigue, and a shorter, more specific treatment design is needed.
The client should be asked to monitor during and after treatments for decreased energy or
other adverse effects, so that the massage therapist can evolve a treatment design most suited
to the circumstance.
• Emotional Stability of the Client

Long-term use of some drugs, for example
corticosteroids, is associated with mood
fluctuations; depression and anxiety are side effects
of many medications. It is possible that with the
additional physical/emotional effects of massage
therapy, some clients may feel emotionally volatile
or overwhelmed, and this may warrant ending the
treatment early or planning for shorter sessions.
Discuss this possibility with the client in advance
and together develop a plan of action.

Drugs Can Influence the Selection of Manual Techniques
Many medications will influence how manual techniques are to be applied during a massage
session. In the chapters that follow, as drug group applications are discussed in more detail,
more specific guidelines will be elaborated on. Let’s look here at some examples that give rise
to general guidelines:
• Some Drugs Alter Blood Clotting Mechanisms

Clients will be predisposed to bruising when taking medications that alter the normal blood
clotting process. Examples include anticoagulants, platelet inhibitors, and aspirin and the
other non-steroidal anti-inflammatory drugs.
Massage techniques like muscle stripping,

deep kneading, ischemic compressions (for
trigger point therapy), and cross fiber frictions
must be modified or avoided. These
techniques, when used on normal healthy
connective tissue to promote good fiber
alignment, often produce a mild inflammatory
response that is easily resolved. However,
when the client is taking a medication with
anticoagulant properties they can result in
excessive bruising and inflammation.
• Some Drugs Alter Protective Responses

Several medications, including centrally acting muscle relaxants, narcotic analgesics, and
anti-anxiety drugs, depress nervous system reactions to sensory feedback from the stretch and
tension receptors in muscle and joint tissues. Firing from these sensory organs (muscle
spindle, golgi tendon organ, joint capsule and ligament receptors) may not elicit expected
responses to techniques that place stress or stretch on them. Massage therapists tend to rely
on such responses to determine when the pressure is deep enough or a stretch is being applied
optimally. When the tissue does not tighten as a signal, manual techniques can inadvertently
be applied too aggressively and tissue damage caused. Techniques such as aggressive
contract-relax stretching and deep tissue work must be eliminated from the treatment plan, or
used very cautiously.
While the usual effect is to reduce the potency of protective reflexes, in some cases
overreactions can occur, leading to muscle spasm and reflex muscle guarding.
• Some Drugs Compromise Tissue Integrity

The corticosteroids in particular, especially when used long term, cause atrophy and
weakening of skin, ligaments, joint capsules, bones, and muscles and their tendons. When
injected into joints for arthritic conditions, they can induce breakdown of articular cartilage.

Any massage approaches that involve placing direct pressure or stress on tissue structures will
need to be employed carefully. Techniques such as rib springing, heavy tapotement, passive
forced stretching, muscle stripping, deep kneading, frictions, and joint mobilization should be
significantly modified or avoided. Be particularly careful with clients who are at risk for
developing osteoporosis, for example post-menopausal women and the elderly.
Normal health, function, and sensitivity of the skin are also compromised by prolonged
topical corticosteroid use. Skin rolling, frictions, and wringing techniques can result in
bruising and inflammation of the subcutaneous tissues.
The therapist should note that the conditions caused by such medication use will also impair
repair processes in body tissues, resulting in healing time frames that are often longer than the
‘norm’ and prolonged tissue fragility after injury.
• Some Drugs Mask Pain Responses
Trigger Point
Pain Referral
+
+
+ +
Pectoralis
Major &
Minor
Since assessment results can be compromised in the absence of normal pain sensation, the test
findings of clients using anti-inflammatories or analgesics, either orally or topically, can make
their tissues appear more healthy and resilient than they truly are. The unaware practitioner
may plan to use more aggressive treatment techniques than is appropriate. It is important to
rely less on client feedback and more on observation and palpation, as well as on medical
advice as needed.

Drugs Can Alter a Client’s Cooperativeness
Various drugs, especially those that depress the central nervous system like the narcotic
analgesics and anti-anxiety agents, can make a client less communicative and seemingly
indifferent to supplying information in a complete way, either during case history taking or in
the course of treatment. The therapist will often need to spend more time and take a
determined approach, asking specific questions and making sure that feedback is frequently
solicited.
3. GUIDELINES FOR HYDROTHERAPY

Hydrotherapy is generally defined as “the use of water in any of its three forms, solid, liquid
and gas, used internally or externally for a therapeutic response.” All physiologic systems of
the body are influenced in one way or another by the combination of hydrotherapy modalities
and medications. Since hydrotherapy is a common component of massage therapy treatment
plans, and practitioners often suggest hydrotherapy as home care, an appreciation of how
client medication use impacts on hydrotherapy decisions is important.
This section will look at how the concurrent use of drugs can affect:
• blood vessel reactions to hot and cold stimuli

• sensitivity of the skin to temperature changes
• the body's temperature control mechanisms
Some Drugs Alter How Blood Vessels React to Hot and Cold
Blood vessels generally react to hot applications by dilating (vasodilation), to brief cold
applications by constricting (vasoconstriction), and to prolonged cold by first constricting and
then dilating. Contrast applications (alternating hot and cold) cause the blood vessels to
alternately vasodilate and vasoconstrict, and are aimed at strengthening vasomotor functions.
Factors that influence the nature or degree of any of these reactions will alter responses to
hydrotherapy modalities.
Let’s consider the following scenario:
A client is diagnosed with moderate hypertension, work-related stress being a major

contributing factor. On the recommendation of a friend the client visits a local day spa for
some relaxation therapy. After review of the treatments offered, the decision is made to
proceed with a 20-minute hot tub followed by a full body massage.
The client is taking an antihypertensive medication that lowers blood pressure by causing
dilation of the peripheral blood vessels. During the hot tub the client begins to feel
lightheaded, and on emerging from it complains to the massage therapist of dizziness, fatigue,
nausea, and headache. These symptoms relate to the combined effects of the antihypertensive

medication and the systemic heat application. Massage therapy might heighten these effects
and is no longer indicated.
The hydrotherapy choice in this situation is not appropriate given the medication use, and if
the spa therapists are unaware of such implications, client safety can be compromised. In
addition to antihypertensive medications, several other drugs, including for example the
narcotic analgesics, also cause peripheral vasodilation.
Some drugs act on receptors in blood vessel walls to cause vasoconstriction. They are used:
• to treat migraine headaches – e.g. sumatriptan (Imitrex)
• for congestion (ephedrine and pseudoephedrine are commonly found in
decongestant preparations)
• to treat children with Attention Deficit Hyperactivity Disorder (ADHD)
– methylphenidate (Ritalin)
• to promote weight loss, e.g. a CNS stimulant like dextroamphetamine
(Dexedrine)
• in medical emergencies, for example shock, hypotension, and other types of
circulatory emergencies, to increase blood pressure
• in topical anaesthetic preparations to extend the time period that the
anaesthetizing agent stays in the area

When the vasodilation capacity of blood vessels is compromised by drug use, all extreme
temperature hydrotherapy is contraindicated. With hot applications, the normal dilation
response helps distribute the heat evenly through the tissue and tends to prevent burning at the
site of application. Blood vessels that are held in constriction are less effective in this role
and the client may be burned. On the other hand, if a cold modality is used, the constricted
blood vessels may respond to the application by going into spasm. This leads to tissue
ischemia and can be quite painful.
When drugs are influencing the contractility of blood vessel walls to impair either
vasoconstriction or vasodilation responsiveness, hydrotherapy modalities must be moderated
and cautiously applied.
Some Drugs Change Skin Sensitivity to Temperature

Skin receptors play an important role in the interpretation of hot and cold sensations.
Prolonged topical corticosteroid use, local skin creams and ointments used for muscle and
joint pain, and CNS depressant medications can cause decreased sensitivity of the skin to
temperature stimuli.
Consider another client, who regularly complains of anxiety-related headaches and a stiff
shoulder, and is taking prescribed anti-anxiety medication twice daily, codeine tablets for
headache, and using a topical OTC analgesic rub for the shoulder discomfort.
This client presents for massage treatment complaining of the sore shoulder and of
interscapular pain. On palpation, the shoulder and periscapular muscles feel hypertonic, and
there is decreased mobility of the local vertebral and costovertebral joints. The therapist
applies a hot pack for 15 minutes before beginning manual treatment. The combined effects
of the oral and topical medications have the potential to reduce the client’s ability to ‘feel’ the
hot pack. Tissue sensation will become even more inexact, risking burning, and feedback
about the manual techniques used next will be additionally compromised. Since the therapist
will not receive accurate feedback about the hydrotherapy application or the subsequent
massage work, the client will probably be bruised and in more pain the next day.
Some Drugs Alter the Body's Temperature Control Mechanisms

Medications like the phenothiazines (used in psychiatric medicine) suppress the hypothalamic
centers that regulate central and peripheral temperature control mechanisms. Homeostatic
regulation of body temperatures is affected.
In both hot/humid and hot/dry conditions the ability of the body to sweat and thereby cool
itself can be reduced. Hydrotherapy modalities like steams, saunas, hot baths, and sweating
herbal wraps produce similar conditions. Clients are at risk for developing heat intolerance,
indicated by symptoms such as confusion, inability to sweat, hot dry skin, nausea, and muscle
weakness.

The chilled client can pose a similar concern. For example, therapists working at ski resorts
see clients who have spent the day on the slopes and are complaining of feeling chilled. It
makes sense to warm them up with a steam or hot tub. If any of these clients are taking
medications that alter body temperature controls, the choice of warming hydrotherapy must
be much more moderate, incorporating modified application temperature and a less full body
focus.
In addition to steams and hot tubs, cold plunges are becoming more popular at spas and other
destination resorts. Cold plunge modalities are contraindicated for any client taking
medications that alter body temperature control mechanisms.
Quick Guide to Hydrotherapy Case History Questions
In addition to asking directly about a client’s medication related hydrotherapy effects,

general information elicited in case history taking may point to hydrotherapy concerns
that need more follow up. This can be significant in helping amalgamate all the case
information to create a safe and effective treatment plan.
• the client's preferences related to hot and cold – are there any
medically advised hydrotherapy or temperature restrictions?
• blood pressure and pulse – what is normal for the client? is the BP high or
low? requiring medication control?
• daily bath or shower temperatures (use as a guide for what is being well
tolerated when making hydrotherapy application decisions)
• areas of impaired circulation, including cold hands/feet, varicosities
• areas of sensory deficit
• time of last meal, for two reasons;
• if the last meal was more than 6 hours ago full body modalities such
as herbal baths or steam treatments will increase the cellular
metabolic rate and can cause a drop in blood sugar levels
• full body hydro treatments should be delayed at least 2 hours after a
large meal
• past experience with hydrotherapy – reactions to previous treatments?
• the condition of the skin and underlying connective tissues
• allergies or sensitivities to essential oils, bath additives, etc.
• pregnancy: what trimester, any medical restrictions related to
temperature use, blood pressure problems?
• presence of systemic conditions such as fibromyalgia, lupus, diabetes,
cancer, respiratory conditions (asthma, emphysema, bronchitis),
circulatory or cardiovascular problems including angina, stroke, etc.

Quick Guide to Hydrotherapy Treatment Modifications
This information is offered to assist the therapist in making hydrotherapy choices and
monitoring client reactions to treatment in order to minimize adverse occurrences.
Options for modifying hydrotherapy treatments to reduce their intensity include:
• shorter duration: Each treatment has a
customary duration. For example, herbal 5
baths generally last 10-20 minutes. Clients
recovering from conditions like the flu can
benefit from the effects of an herbal bath,
but may still be on antibiotics or other
medications and will be generally weakened.
Shorter treatment times are recommended.
• local hydrotherapy versus systemic: A client
who is recovering from a sinus infection can
benefit from the effects of steam on the
respiratory system. During the recovery period a local treatment like a facial steam
may be less fatiguing than a systemic treatment like a medicated steam bath.
• modified treatment temperatures: Although each treatment modality has its ‘ideal’
temperature, modifying the temperature/temperature range can make
hydrotherapy applications more enjoyable and safer for the client. For example:
1. With contrast hydrotherapy treatments, the greater
the temperature difference between the hot and cold
applications, the more intense the effects on the blood
vessels. Strong contrast hydrotherapy applications
involve temperature differentials of 10-40 C (50-104 F).
A factor like long-term use of corticosteroid medication
can affect the health and contractile ability of the
blood vessels, and suggests temperature modifications
to somewhere in the 20-30 C range (68-86 F) would be
more appropriate.
2. A systemic treatment like a medicinal/herbal bath
is usually administered at 36-38 C, 97-100 F. At this
temperature there will be an elevation of the body’s
basal metabolic rate, which potentially increases the workload of the heart. For the
hypertensive client or client with a weakened heart, this can be cause for concern. Such
clients will benefit from a tepid or neutral bath (35-36 C, 95-97 F).
Recognizing and Handling an Adverse Reaction to a Hydrotherapy Treatment

If a client reports feeling lightheaded/dizzy, experiencing nausea, or getting a
headache, or if the skin becomes swollen, blotchy, or marbled (red/blue spots), stop the
application immediately. Place the client in a comfortable rest position in a neutral
temperature environment and provide room temperature water to be drunk in sips. Stay
close and monitor for signs of improvement. Milder adverse reactions, especially when
recognized early, usually begin to reverse in a short period of time; more serious reactions,
or unusually prolonged ones, should be evaluated medically.

4. GUIDELINES FOR THERAPEUTIC EXERCISE PRESCRIPTION
AND CLIENT SELF CARE
The overall goal of any exercise or self care program is to return the client to normal pain-free
activities of daily living (ADLs). Exercises suggested by the massage therapist should
complement any other medically supervised program. Self care activities for clients with
systemic conditions such as hypertension, asthma, multiple sclerosis, or those recovering
from a stroke or heart attack, should be developed closely with the medical team,
physiotherapist, or qualified exercise trainer.
Exercise intolerance or adverse reactions to exercise include breathing difficulty, palpitations,

chest pain, dizziness, nausea, vomiting, lightheadedness, or other symptoms that cause alarm.
There are a few simple generic guidelines to consider when suggesting an exercise program:
• give one or two activities at a time and monitor how the client responds
• develop a progressive exercise plan; begin with mild activities and progress
to more challenging types
• develop the exercise plan around the client’s lifestyle
The client’s medication use can impact on exercise prescription by influencing the:
• desired frequency, intensity, and duration of the exercises

• time of day the exercises should be performed
• medical stability of client while performing the exercises
Some Drugs Will Influence Exercise Frequency, Intensity, and Duration (FID)
When introducing an activity such as
walking, your instructions to the
client might be: “Take a moderately
paced [intensity] walk around your
neighborhood block. It should be no
longer than 10-15 minutes [duration]
once a day for a week [frequency].”
Exercise prescription needs to take

into account the physiological effects
that medications can have on the
client’s body. Fatigue, low energy, drowsiness, and muscle weakness are common drug side
effects. As well, clients who are taking medications that depress the CNS or mask pain
symptoms (for example, muscle relaxants and analgesics) will be at risk to injure or re-injure
tissues if an aggressive exercise plan is recommended.

Some Drugs Influence the Time of Day Exercises Should Be Performed
Exercising in bright sunlight or on hot
humid days can be quite risky when using
certain medications. For example, clients
taking medications in the phenothiazine
family often experience sensitivity to
sunlight. The metabolites from these
medications accumulate in the skin and
react with the sunlight to produce a deep
blue-black discoloration. Clients who are
predisposed to photosensitivity reactions
should plan their activities for early
morning or wait until later in the day, should
exercise inside or in shaded areas, and
should wear a hat and be well clothed when
outdoors. Exercising in direct sunlight is not
recommended.
As previously mentioned, drugs like the

phenothiazines also affect the temperature control
mechanisms in the hypothalamus. Vigorous exercise
on hot humid days is not recommended since there is
increased risk of developing heat stroke.
Other drug groups that can cause photosensitivity

reactions include antibiotics, sulfa drugs, muscle
relaxants, and asthma medications. While it is difficult
to predict who will experience these reactions, and how
intensely, the elderly and very young are most at risk
for adverse responses.
Some Drugs Impact the Medical Stability of the Exercising Client

Clients with systemic conditions like asthma, diabetes, and hypertension require special
consideration in exercise program planning. For example, since exercise increases metabolic
demands on the body, it is usually best for the insulin dependent diabetic client to exercise
soon after taking his or her medication to ensure an adequate blood glucose level for cellular
function.
Asthmatic clients need to keep triggering factors at a minimum when exercising. For
example, it would not make sense to advocate swimming for a client who reacts to cold water
or chlorine, or running through the woods at a high pollen time of year. Prescribed exercises
should avoid exposures that tend to trigger asthma attacks as well as being well suited to the
effects of the drugs the client is taking. The practitioner needs to ask about the client’s
medical guidelines for medication use and exercise and suggest compatible activities.

Some asthmatics cannot exercise at all without medication support. In these cases, it is best
to rely on the exercise regime prescribed by the physician and/or physiotherapist.
Antihypertensive medications like the diuretics, vasodilators, and calcium channel blockers
often produce side effects of joint pain, cramps, difficult breathing, fatigue, and reduced
tolerance of heat. Clients who are using medications for heart disease and blood pressure
control must be carefully monitored during any exercise program.
5. GUIDELINES FOR TREATING AROUND INJECTION SITES, SKIN

APPLICATIONS, AND IMPLANT DEVICES
Treating on or around injection sites, skin patches, and implanted devices poses a challenge
for massage therapists because not much is known about how massage and hydrotherapy
modalities affect the release or uptake of medication from these sites. The information that is
available can sometimes add to the sense of confusion. For example:
“Massage of subcutaneous insulin injection sites markedly increased the

absorption rate of insulin.”2
“Contrary to what might have being expected, our study of local massage
suggests that the maneuver caused delay in the absorption of drug
[fluphenazine decanoate] for at least the first hour.”3
A Japanese study4 on massage during epidural block reports: “We conclude

that peripheral sensory stimulation as weak as gentle massage may initiate a
series of indirect mechanisms that lead to accelerated regression of sensory
analgesia.”
Taking the side of caution, it makes sense for massage therapists to assume that any
manipulation on or around such a site, in particular an injection site or skin patch, has the
potential to alter the pharmacokinetics of the drug being administered.
Injection sites can also be locations of tissue damage and degenerative change, posing
concerns about how resilient the tissue is, how best to work with the tissue, and when to avoid
local treatment:
“If you received a cortisone type injection, make sure that you protect that area
from hard exercise for at lease two months after you receive the injection.”5
“Certain drugs, especially the lipid (fat) soluble drugs, seem to cause direct
damage to the muscle cell membrane resulting in muscle fiber necrosis.”6
(Although this study was done on laboratory animals, the implication for
human tissue cannot be ignored.)

This section will explore the issues related to assessing and treating around injection sites,
skin applications, and implant devices, including how to:
• assess the medication site

• recognize adverse reactions at the site
Guidelines will then be suggested for the practitioner to follow when working with clients
who have cutaneous or subcutaneous medication sites.
Assessing the Medication Site

The practitioner must perform a thorough assessment before making decisions about
whether/how to treat at or near a medication site. A good assessment will include:
• case history questions

• observation of the site
• palpation on and around the site
• movement assessment of the area
The therapist’s questions are intended to elicit specific information about the reason for the
injection, skin patch, or implant device, and any related concerns or medical guidelines.
Close observation of the site will detect signs of inflammation, irritation, infection, bruising,
or skin reactions; palpation and movement assessment give the therapist more detailed
information about the health and strength of the connective tissues around the site.
Case History Questions

• reason for injection/patch/implanted device
• location of the site(s) – remember, some devices have entry and exit sites
• if a patch or implanted device, how long has it been there? is it changed or
replaced regularly?
• if a regular injection site, how often is it used?
• are alternate sites used for injections? where?
(e.g. diabetic client)
• when injections are administered, method of
administration: intramuscular, intravenous,
intra-articular, etc.
• is the injection self-administered, or administered
by medical personnel?

• how long does the effect of the injection last?
• inquire about any side effects experienced currently or previously
• any history of infection at the site? if yes, what was the treatment and
management? how long did it take to resolve?
• ask about any related abnormal sensation, muscle weakness, etc.
• any previous injections/patches/devices – reason for use, site of application,
how long ago, etc.
Observation
• compare the body part/body area bilaterally
• is the site inflamed? does it look irritated?
• are there any signs of bruising, skin rashes, etc.
• does the skin look unusually dry or moist?
• is there any swelling proximal or distal to the site?
• is the site discolored?
• does the client show signs of apprehension or protectiveness of the site?
Palpation
Using thoroughly washed hands, or gloves:
• compare the body part/body area

bilaterally
• clearly identify the boundaries of the
patch or device
• palpate around the site, not over the site
– does palpation cause pain?
(note your depth of palpation)
• assess for loss of sensation – can the
client ‘feel’ you palpating?
• assess for edema; if present, gently push into the edema – is it pitted?
• does the skin feel unusually hot, dry, moist?
• does the tissue surrounding the site feel dense or fibrotic?
• what is the tissue mobility like – normal, loose, taut, fragile, adhered?
• palpate the local musculature – any pain or discomfort?

Movement Assessment
A movement assessment of the medication site typically involves the therapist assessing
active (AROM), passive (PROM) and resisted (RROM) ranges of motion. If the test area
seems irritated, instruct the client to move only within pain tolerance.
• AROM: The client performs active movements. For example, if the

injection was given in the middle deltoid, having the client perform shoulder
abduction helps the therapist assess the strength and degree of irritation of
the deltoid muscle and its supporting connective tissue.
• PROM: The therapist moves the part and assesses for articular and
connective tissue compliance, and range and smoothness of movement.
Passive testing is especially indicated for intra-articular injections.
• RROM: The therapist resists the client’s movements. If the site is not
irritated, or is an old site, this will assess muscle integrity and strength and is
especially indicated for intramuscular injections. RROM is not indicated if
the site is inflamed or irritated.
The therapist needs to use common sense and professional judgment when performing
movement testing; if apprehension or pain are elicited, discontinue and reassess at a later time.
If the site has not been examined medically, in most instances the client should be advised to
have it checked.

Adverse Reactions at the Medication Site
The most common adverse reactions at the medication site involve irritation, inflammation,
or infection. Therapists can be alert to the following:
• If an injection is administered IM, the

drug substance may be a source of
irritation to the muscle tissue. This
can lead to inflammation at the site.
At sites located near nerves, for
example, the gluteals and the sciatic
nerve, nerve irritation may be the
source of the symptoms (numbness,
tingling, muscle weakness, radiating
pain, etc.). Injections into rectus
intermedius can lead to fibrosis and
decreased knee flexion. Fibrosed
injection sites may be tender and
sensitive to touch.
• If an injection is administered IV, the drug substance may cause irritation of
the vein wall, leading to thrombophlebitis. The site will be inflamed, with
local and distal edema, and the client will experience discomfort.
• With injections administered intra-articularly, sometimes an almost
immediate inflammatory reaction will occur. A possible reason for this is
excessive immune reaction to the drug.
• Implanted devices can promote a variety of adverse reactions. Given that
they consist of ‘foreign’ materials implanted through the skin into the tissues
below, tissue irritation, infection, and hypersensitivity reactions can occur.
• Adverse reactions to skin patches are usually hypersensitivity responses.
Clinical Guidelines
The following guidelines are suggested for treating on or around injection sites, implanted
devices, or other skin applications:
In General:
1. Carefully observe and palpate around the medication site for signs of inflammation,
and to determine sensitivity. Be conscientious about hygiene. Assess the site at the
start of each treatment.
• If the site looks red and irritated, leave it alone.

• If infection or inflammation has occurred, determine for how long and

what course of treatment has been pursued medically. The client may be
on antibiotic or anti-inflammatory medications.
• Exercise caution if the client develops a fever, which can sometimes be
caused by injections, for example flu shots. The presence of a fever
indicates that the body is already working hard to mount an immune
response and the additional stimulus of massage may be too taxing.
2. If there is sensory impairment at a medication site, your approach to treatment will

always be more cautious. Work on a small tissue area and monitor the response before
planning deeper or more specific treatments.
3. When working with a client in a hospital or private care setting, ensure that the
attending physician or supervising nurse is aware of your visit. Follow the
institutional guidelines for cleanliness, equipment checks, lubricant use, and so on.
Do not remove any external applications from the client like IV lines, catheters, or
electrodes. Also, keep in mind that your client may be immunocompromised, so if you
feel a ‘bug’ coming on it is best to cancel your visit and reschedule when you are no
longer contagious.

For Injection Sites:
1. Thrombophlebitis can occur with IV injections. Working over or local to the site is
contraindicated until the doctor indicates that the risk of embolism has subsided
(thrombus detaches from the site and occludes a distant blood vessel, resulting in
tissue death).
2. When intramuscular injections are administered, the muscle tissue may be sore and
inflamed for several days following the injection. Local massage should be avoided
during this phase. Inquire about what instructions were given for managing the
inflammation.
3. When short acting injections are used, such as for vaccinations or local anaesthetic,
the drug is typically absorbed and removed from the site within a few hours to a few
days. If clear of all contraindications, an injection site can usually be included in the
treatment after 24 to 48 hours. Safe techniques that can be used over the site include
superficial fascial techniques, gentle stroking, vibrations, lymphatic drainage, and
light petrissage.
4. If the injection is long acting (a depot shot), do not perform any massage over the site.
Consult with the physician about the type of drug used and how long it can be
expected to stay within the tissues (can be as long as 6 weeks). Massaging over such
sites while the drug is still being stored there is contraindicated.
5. Infants who have immunization shots (intervals between 2 to 18 months) often

develop a fever. If there is a fever, even a slight one, do not massage until it has
resolved. If the site begins to show signs of irritation, follow the guidelines as
discussed above.
6. More focused work on the tissue at a site should wait a minimum of 10 days from
discontinuation of use, or longer depending on the tissue recovery time frame in the
case. If an older site is painful on palpation, refrain from treating it for a while longer
to see if the pain subsides. If an older site is pain free, ensure that sensation in the tissue
area is adequate and that the tissue at the site is in fact not more fragile than it appears.
7. Older sites often feel adhered and fibrosed, especially if they were used repeatedly
(e.g. diabetic client). As a general guideline, when working on an older fibrotic
injection site begin cautiously with lighter work and then progress gradually to
introduce hydrotherapy applications and more specific deeper techniques appropriate
to achieving the goals of treatment. The client should be advised to monitor the site
following each treatment for any adverse reactions such as inflammation, soreness, or
bruising. Some reaction to focused work at the site would be expected, but if the post-
treatment effects are stronger than you consider appropriate, reduce the intensity of the
treatment approach.
8. Use of hydrotherapy over injection sites: Application of heat over an injection site or
implanted depot preparation will increase blood flow into the local tissues. This can
Hydro-
collator
Unit
potentially speed uptake of the drug from the site, causing too much to be released into
the bloodstream. The client will likely experience adverse effects as a result. For
example, if a hot pack is placed over a recent insulin injection site, insulin will enter
the blood too quickly and the likelihood is that the client will develop signs of
hypoglycemia. Cold, on the other hand, produces local vasoconstriction and can cause
reduced absorption of medication into the bloodstream, decreasing the rate of drug
delivery to target sites. This can also lead to adverse effects. Although little research
is available in this area, therapists must carefully consider the potential impact of
hydrotherapy over injection sites and other topical and implant devices. Exercise
professional judgment, and if unsure about the impact of a proposed hydrotherapy
application, discuss your plan with the attending medical professional.
For Implanted Devices:

1. When working with a client who has an implanted device, the therapist is responsible
for exercising professional judgment at all times. It is important to ask as many
questions as are needed to understand the type of drug being delivered and its effects,
and the nature and operation of the device. Don’t hesitate to check in with the
attending physician if unsure about anything.
2. Have the client clearly outline the implant’s location and all of its attachment points.
Working outside a 4-6 inch radius of the path of the device is suggested. When
treating around these devices check in regularly with the client regarding comfort and
tolerance of the treatment approach.
3. The main concern is the risk of infection developing at the device’s incision points.
Excellent hygienic practices are absolutely necessary.

For Skin Patches:
1. When a skin patch is present, a similar guideline of working outside a 4-6 inch radius
of the patch is suggested. Performing massage techniques directly over the patch is
contraindicated. It is unclear how massage will affect the pharmacokinetics of the
imbedded drug, but the likelihood is that it could speed uptake of what is intended to
be a time-released medication.
4"
4"
4"
4"
2. The client should never be asked to remove the patch to give the practitioner access to
work on the tissue below. Any such request is outside the massage therapy scope of
practice. In addition, some patches are delivering medications (e.g., nitroglycerine for
angina patients) that are necessary to the client’s medical stability. Other types of
applications (e.g., for birth control or quitting smoking) should also not be interrupted.
3. The therapist needs to be aware that directly manipulating the patch can result in his
or her skin surface being exposed to the drug, with the consequent risk of being
‘dosed.’ Since patches are often placed on the back of the arm and similar less visible
areas, it is important to know and remember their locations to avoid inadvertently
‘massaging’ them.

Summary of General Massage Therapy & Medications Guidelines
1. A thorough case history and assessment of the client is always necessary to obtain
specific information about the client’s use of medications, herbs, vitamins, and so on.
This information is important for planning safe and appropriate treatments.
2. Research the client’s medications by reading the drug profiles. Take note of the
mechanisms of action and potential side effects in each instance. Keep in mind that
the more drugs and other substances a client is taking, the greater the likelihood of
complex or idiosyncratic interactions. Consult with the doctor and other prescribing
practitioners as needed to get a clearer picture.
3. The therapist should always be alert to the possibility that a client’s complaint or
symptom presentation may be an effect or side effect of medication use. Reflect on the
information you have gathered about the medications being taken, as well as
medication start dates in relation to symptom onset. Consider whether there are
indicators of drug toxicity.
4. Remember that assessment results can be altered due to medication effects or side
effects. Drugs that mask pain can create misleading test results.
5. Be prepared to contact the attending physician or health care provider if you perceive
a possible connection between medication effects and the client’s complaints.
Sometimes the assessment results will appear ‘skewed,’ or the client will not be
benefiting from your treatment approach as expected. Create an open line of
communication to discuss such concerns. When communicating with other
practitioners, either verbally or in writing, be brief and well organized in presenting
the information and maintain a balanced perspective.
6. Consider whether the client’s medication should influence your treatment scheduling.
There are two key issues here:
• maximizing bioavailability of drugs needed to stabilize the client’s

medical condition during and after the massage
• maximizing the client’s ability to give feedback during the treatment
7. Consider carefully the physiologic effects of the client’s medications from the
perspective of how safely and effectively they would combine with the effects of your
proposed treatment plan components.
8. When using hydrotherapy modalities, monitor the tissue responses closely, along with
the client’s overall comfort level. When uncertain how well the application will be
tolerated, begin cautiously and assess the response during and post treatment. It is
better to use a well-tolerated modality that is gentler than is customary than to
precipitate adverse effects.

9. Ensure that any exercises you suggest are compatible with the client’s medication
effects and medical advice. Plan a progressive exercise plan around the client’s energy
level and lifestyle. Be alert for complaints of adverse effects like dizziness or
photosensitivity reactions.
10. When working with a client who has an injection site(s), skin application, or implanted
medication delivery device:
• be very careful about hygiene when assessing or treating the site

• identify the exact location; determine the boundaries and route of any
implanted device
• assess the affected tissue thoroughly before treating; do not treat if there
are signs of infection or irritation
• exercise appropriate precautions for treatment and hydrotherapy as
discussed above
• work outside a 4-6 inch radius of skin patches and implanted devices
1. Compendium of Pharmaceutical Specialties, 28th ed., Canadian Pharmaceutical Association,

Ottawa, 1993, pp. 1200-1201
2. Linde, B., “Dissociation of Insulin Absorption and Blood Flow During Massage of a Subcutaneous
Injection Site,” Diabetes Care, 9(6): 570-574, November/December 1986
3. Soni, S.D., et al., “Plasma Levels of Fluphenazine Decanoate, Effects of Site Injection, Massage
and Muscle Activity,” British Journal of Psychiatry, 153: 382-384, 1988
4. Ueda, W., et al., “Effect of Gentle Massage on Regression of Sensory Analgesia During Epidural
Block,” Anaesthesia and Analgesia, 76: 783-5, 1993
5. The Mirkin Report, Bethesda MD, www.wdn.com/mirkin
6. Manor, D. & Sadeh, M., “Muscle Fiber Necrosis Induced by Intramuscular Injection of Drugs,”
British Journal of Experimental Pathology, (4): 457-462, August 1989

Commonly
Prescribed
Medications
and
Treatment Planning
CHAPTER 6
Drugs for Managing

Pain and Inflammation
The most commonly consumed over-the-counter (OTC) preparations in the United States are
the non-steroidal anti-inflammatory drugs (NSAIDs). This drug group includes aspirin and
acetaminophen. In Canada, 1996 sales of OTC analgesics are estimated to have been $197.8
million; in 1997 this figure jumped to $215.9 million.1 Extrapolating to the U.S. market, sales
figures of approximately ten times this amount are likely.
The estimated annual cost associated with toxicity of NSAIDs (excluding non-upper
gastrointestinal hemorrhage and hepatotoxicity) is about $1.35 billion!2 These drugs are also
very frequently taken alongside of other medications. For example, a 1998 study estimated
that almost 20 million patients and 12% of the U.S. population aged 60 or more are taking
NSAIDs and antihypertensive medications concurrently.3 Given the widespread use and ease
of availability of the NSAIDs, massage therapists will be treating an increasing number of
clients who are using these medications for pain and inflammation.
Beyond the volume of over-the-counter sales, prescribed analgesics constitute a very large
percentage of North American medication consumption. This chapter will address the
following drug classes:
• The Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

• The Narcotic Analgesics
• Skeletal Muscle Relaxants
• The Corticosteroids
1. THE NON-STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDS)

Drugs belonging to this group are referred to as the non-steroidal anti-inflammatories to
differentiate them from the corticosteroids, another group of drugs with anti-inflammatory
properties. The primary difference lies in their chemical structures.
Aspirin is the prototype of this group and is used to compare the properties of newer NSAIDs
as they are developed. In addition to acetaminophen (Tylenol), examples of common
NSAIDs include ibuprofen (Advil), naproxen (Anaprox), and diclofenac (Voltaren).

The NSAIDs are widely used in the management of mild to moderate pain and inflammation.
Most members of this group demonstrate all of the following properties:
• anti-inflammatory
• analgesic
• antipyretic (fever lowering)
• anticoagulant
Acetaminophen (Tylenol) is something of an exception in that it produces less anti-

inflammatory action than the other NSAIDS. Instead, it is widely used for its antipyretic and
analgesic properties.
This drug group is very large. Physicians, in choosing which NSAID to prescribe or
recommend, consider factors like age and constitution of the patient, drug cost, and the
pharmacologic activities most required in the situation.
Uses
The NSAIDs are mainly used in the following conditions:
• inflammatory conditions such as rheumatoid arthritis, tendinitis, bursitis

(exception: acetaminophen)
• osteoarthritis
• minor orthopedic/dental surgery, toothache, headaches, sport injuries, etc.
• dysmenorrhea
• more recently, for cardiovascular diseases because of their anticoagulant
effect (aspirin is mainly used for this purpose)
• for cough and cold symptoms such as mild fever and body aches
(primarily acetaminophen)
Mechanism of Action
Cyclooxygenase
Enzyme
PAIN
Arachidonic Acid Prostaglandins INFLAMMATION
CELL AND
from and
TRAUMA Cell Membrane Thromboxanes BLOOD
CLOTTING
The actions of prostaglandins and thromboxanes contribute to the symptoms of tissue trauma.

Irritated or traumatized cells release arachidonic acid into their tissue interstitia. In the
presence of the enzyme cyclooxygenase, arachidonic acid is converted into prostaglandins
and thromboxanes. The NSAIDs inhibit the synthesis and actions of prostaglandins and
thromboxanes, primarily through impairing cyclooxygenase activity.
There are several types of prostaglandins – the ones involved in the inflammatory response
are found in most body tissues. These prostaglandins are produced in high concentrations
following any type of cell irritation or trauma. In addition to inflammation, the increased
prostaglandin volume is associated with pain creation and with increased smooth muscle
contraction in the gastrointestinal, circulatory, and respiratory systems. Through inhibiting the
formation of prostaglandins, the NSAIDs reduce the pain and inflammation associated with
trauma.
NSAIDs
Cyclooxygenase
Enzyme
+
DECREASED
Arachidonic Acid Prostaglandins PAIN AND
CELL INFLAMMATION;
from and
TRAUMA Cell Membrane Thromboxanes BLOOD
THINNING
The NSAIDs reduce the formation of prostaglandins and thromboxanes.
Prostaglandins also play an important role in kidney function and protection of the gastric
mucosa. This is why NSAID drugs, which inhibit prostaglandin formation and function in
varying degrees (aspirin being particularly effective in this respect), are associated with side
effects such as gastric irritation and various forms of kidney dysfunction.
Thromboxanes stimulate platelets to stick together. Persons with high thromboxane

(especially thromboxane A2) levels are more predisposed to thrombosis (blood clot
formation) and other types of cardiovascular problems.
The NSAIDs, especially aspirin, reduce blood clot formation. While a certain amount of
clotting control is good, for example following a stroke (cerebrovascular accident), when the
blood does not clot as it should the person may experience more bleeding and bruising than
usual. Clients using NSAIDs will be at risk for increased bruising following deep tissue work.
2. THE NARCOTIC ANALGESICS

The narcotic analgesics are also referred to as the opiates. The prototype of this group of
drugs is morphine; other members are drugs such as hydrocodone, pethidine, and codeine.

The narcotic analgesics are used to manage moderate to severe pain, both short-term and
chronic.
Because these drugs have the potential to produce physical dependence, they are classified as
controlled substances and require a doctor’s prescription. Codeine is an exception.
Preparations containing high codeine doses are classified as controlled substances; however,
many OTC pain medications combine acetaminophen or aspirin with small doses of codeine.
Uses
The narcotic analgesics are typically used for the management of pain from:
• debilitating injuries
• severe fractures
• major surgery
• terminal diseases
• chronic conditions characterized by severe pain
Mechanism of Action
Although the exact mechanism of action of these drugs is still being examined, they mimic
the activities of the endorphins, enkephalins, and dynorphins, which are the body’s own
naturally produced opiates.
Opioid receptors are found on cells in the brain, spinal cord, and peripheral nerves. Several
different types of opioid receptors have being discovered, each having specific effects. The
narcotic analgesics are believed to act at these sites to alter cellular functions associated with
pain perception and transmission.
Research suggests several possible mechanisms, including:
• altering the flow of calcium and potassium in and out of the cell
Calcium and potassium are important elements needed for proper neuronal function, that is,
transmission and conduction of impulses across synapses and along neurons within CNS
tracts and peripheral nerves. When the normal activities of these substances are interrupted
the transmission of pain signals can also be interrupted.
• affecting cellular second messenger systems

Second messenger systems are intracellular mechanisms of communication that can either
stimulate or inhibit certain cell functions. The opioid drugs are believed to inhibit the
formation of intracellular second messengers such as cyclic adenosine monophosphate, a
possible mechanism of altering pain transmission.

When acting within the central nervous system, the narcotic analgesics:
• reduce the patient’s perception of pain

• alter the reaction and emotional response to pain
• produce sleep
• depress the respiratory, vasomotor, and cough reflex centers
(codeine is often used as a cough suppressant because of this property)
When acting on the peripheral nervous system, the narcotic analgesics affect sensory neurons
at the site of injury/inflammation to produce an analgesic effect. They also directly influence
the smooth muscle cells of the gastrointestinal tract to decrease peristaltic motility and
increase the tone of the intestinal sphincters. (These effects can be useful for managing
diarrhea, but often result in constipation.)
Narcotic Central Action

Analgesics
Analgesia
Peripheral Action

3. SKELETAL MUSCLE RELAXANTS
The skeletal muscle relaxants are used to reduce muscle tone, primarily to manage muscle
spasm and spasticity. These two terms are often used quite loosely and therefore require more
detailed explanation.
Muscle Spasm
As a response to trauma, muscles will often ‘go into spasm’ to protect themselves and
traumatized local tissues against further insult. This is sometimes referred to as muscle
splinting. A spasm is characterized by an abnormally high increase in muscle tone. The result
is usually pain, decreased range of motion, and even inflammation of affected joints.
Spasms can also occur when muscle stretch receptors (the muscle spindles) react strongly to
an unexpected stretch, for example inadvertently stepping off a curb or missing a step. The
muscle spindle reflexes generate alpha motor neuron signals to the overstretched muscle to
produce sudden forceful contraction.
Spasms can also result from intrinsic factors such as electrolyte imbalance.
Spasticity
Spasticity, which is caused by injury or insult to the central nervous system, reflects a loss of
inhibitory input on normal muscle tone from either supraspinal or spinal centers. Normal
muscle tone requires balancing of ascending excitatory signals from the peripheral nerves and
descending inhibitory signals from the central nervous system. These inputs are balanced in
the ventral horn of the spinal cord where the alpha motor neuron cell bodies are located.
Spasticity is usually caused when brain or spinal cord areas responsible for voluntary
movement are harmed. CNS damage from conditions such as multiple sclerosis, cerebral
palsy, spinal cord injuries, and stroke can affect the normal control of muscle tone through
impairing descending inhibitory signals from the brain and spinal cord to the peripheral
reflexes.
Signs and symptoms associated with spasticity include hypertonicity (increased muscle tone
including spasm), clonus (a series of rapid muscle contractions), exaggerated deep tendon
reflexes, reflex spillover effects where motor responses ‘spread’ to other body parts,
scissoring (involuntary crossing of the legs), and fixed joints. Gait, movement, and speech
are usually compromised. Spasticity can vary in degree from mild muscle stiffness to severe,
painful, and uncontrollable spasms.
Uses
The skeletal muscle relaxants are subdivided into two general groups, distinguishing those
that act within the central nervous system from those whose responses are produced primarily
in the periphery.

Centrally acting skeletal muscle relaxants (acting on the CNS) are mainly used to inhibit
painful muscle hypertonicity related to soft tissue injury or inflammation.
The peripherally acting skeletal muscle relaxants have two primary uses:
• in the management of spasticity, where CNS controls are impaired and

therefore cannot be utilized effectively to reduce tone
• as an adjunct to general anaesthesia, to prevent muscle spasms and reflex
reactions during surgery
Mechanism of Action
The centrally acting muscle relaxants, such as cyclobenzaprine, are believed to depress both
sensory and motor impulses at different sites in the brain and at various levels of the spinal
cord. This results in decreased muscle tone, and therefore a reduction in painful occurrences
like spasm. Other drugs whose mechanisms of action include CNS suppression, for example
anti-anxiety medications, can produce similar effects.
The peripherally acting muscle relaxants create their effects through functioning within the
muscle tissue or at the neuromuscular junction to reduce tone. This group includes two main
categories:
• drugs that directly influence the skeletal muscle cell, like Dantrolene
• drugs that act at the neuromuscular junction, such as succinyl-choline
Muscle Relaxants
Central Peripheral
Brain Neuromuscular Junction or
and Spinal Cord within the Muscle Fiber
Dantrolene is believed to act on the sarcoplasmic reticulum of the muscle cell to block
calcium channels. Calcium ion binding with actin and myosin fibers is necessary for muscle
contraction to occur. When a drug like Dantrolene can impair this calcium ion binding, the
contractile ability of the muscle is reduced. This type of effect does not rely on neural input.
Dantrolene is primarily used to manage spasticity. It is not recommended for ‘ordinary’

muscle spasm situations. In therapeutic doses its activities are limited to skeletal muscle, with
no action observed in the heart or smooth muscle structures.

Drugs such as succinyl-choline act at the neuromuscular junction (where the alpha motor
neuron signal makes contact with the muscle cell membrane) to inhibit the normal activities
of the neurotransmitter acetylcholine. Acetylcholine is released from the motor neuron to
stimulate the muscle cell. Drugs that suppress acetylcholine can create temporary flaccid
paralysis in the body’s muscles.
4. THE CORTICOSTEROIDS
The adrenal glands are primarily responsible for producing the two types of
adrenocorticosteroids, namely the mineralocorticoids and the glucocorticoids. The
mineralocorticoids, for example aldosterone, play an important role in fluid and electrolyte
balance. The glucocorticoids, such as cortisol, have several functions including exercising
controls on glucose metabolism, inflammation, and the immune response.
This section will focus on the uses and actions of the synthetically produced glucocorticoids.
These drugs are referred to as the corticosteroids. They are among the most widely used in
medicine, and are available in forms including tablets, liquids, topical creams and ointments,
aerosol sprays, eye/ear drops, and injections.
Uses
The corticosteroids do not actually cure any disease or disorder. Instead, they reduce
associated immune or inflammatory responses, providing a more comfortable, less painful
lifestyle for the patient.
Corticosteroids are utilized in either physiologic or pharmacologic (supraphysiologic) doses.

Physiologic doses are relatively small and are taken to replace the body's daily production of
cortisol. This can be necessary for some adrenal gland disorders, for example Addison’s
Disease.
When administered in pharmacologic doses, which are much higher, the corticosteroids
mimic the actions of naturally produced cortisol to produce anti-inflammatory and
immunosuppressant effects. Medically supervised short-term use (1 to 3 weeks) of
corticosteroids in pharmacologic doses is usually well tolerated with minimal side effects.
However, more long-term use can lead to disruption of adrenal gland functions and an
increased likelihood of undesired effects.
The corticosteroids are used in the medical management of:
• autoimmune disorders, for example rheumatoid arthritis and systemic lupus

erythematosus
• arthritic and degenerative joint disorders such as ankylosing spondylitis
• non-arthritic conditions like tendinitis and bursitis

• allergic disorders like rhinitis, atopic or contact dermatitis, anaphylactic
reactions, and serum sickness (a hypersensitivity reaction that may occur
after antiserum administration or in reaction to certain drug therapies)
• dermatological disorders such as psoriasis, seborrheic dermatitis, and
alopecia
• gastrointestinal diseases, for example ulcerative colitis, chronic hepatitis, and
inflammatory bowel disease
• respiratory disorders like asthma, emphysema, and pulmonary tuberculosis
• transplanted tissue rejection reactions
Therapists should have an appreciation of the widespread use of this group of drugs and make
sure to ascertain why any given client is using a corticosteroid medication.
Mechanism of Action
nucleus
corticosteroid
corticosteroid
receptor
corticosteroid
receptor complex
The corticosteroids are believed to act directly on the nuclei of cells. On entering a cell, the
drug binds to a glucocorticoid receptor in its cytoplasm. The resulting steroid-receptor
complex then travels into the cell’s nucleus and combines with specific sites to stimulate the

transcription of DNA into messenger RNA. Messenger RNA is responsible for protein
synthesis. Several types of proteins are produced, for example enzymes, structural proteins,
and messengers, all of which affect cellular functions in various ways. The corticosteroids
will generate four main categories of effects:
• anti-inflammatory
• immunosuppressant
• catabolic effects on connective tissues
• effects on other cellular functions
Anti-Inflammatory Effects
The corticosteroids reduce the signs and symptoms of inflammation regardless of its cause.
They depress production of several inflammatory substances, including prostaglandins,
leukotrienes, histamine, and kinins. Corticosteroids also appear to stabilize capillaries (reduce
their natural leakiness), and to strengthen the membranes of intracellular organelles to lessen
release of their destructive proteolytic enzymes.
Immunosuppressant Effects
The corticosteroids are thought to inhibit migration of leukocytes and macrophages to sites of
inflammation, and also to reduce their responsiveness to key chemical mediators like the
interferons and interleukins. The quantities of other important immune system cells, including
circulating T-lymphocytes, monocytes, and eosinophils, are also reduced. The overall
combined effect is a suppressed immune system.
A less reactive immune system can be useful when managing autoimmune conditions or
following organ transplant procedures. However, immunosuppression will make a client
more susceptible to contracting infectious diseases.
Catabolic Effects on Connective Tissues

Cortisol has the important metabolic function of maintaining blood glucose and liver
glycogen levels. To achieve this, it directs the breakdown of body tissue proteins and fats into
amino acids and free fatty acids, which in turn undergo gluconeogenesis in the liver. The new
glucose is either released into the blood or stored as glycogen.
In pharmacologic doses the corticosteroids have a similar catabolic effect on the connective
tissues of the body. Muscles and their tendons, bones, ligaments, joint capsules and articular
surfaces, fascial membranes, and blood and lymph vessels can all be broken down. As well,
corticosteroids inhibit fibroblast activity, which will result in reduced connective tissue
rebuilding and thinning of skin.

Let’s look at some examples of how long-term corticosteroid use causes changes to body
tissue structures:
• Injections into joints to manage arthritic conditions can damage articular

cartilage, leading to further compromise of the joint surfaces.
• Prolonged skin applications can result in sensitivity loss and reduced skin
strength and tone.
• Injections into tendons and musculotendinous units to manage inflammation
can reduce the sensitivity of golgi tendon organs and muscle spindles to
stretch and tension changes, resulting in a tearing or rupture risk.
• Injections into the plantar fascia can promote rupture, as well as secondary
pathologies such as tendinitis of the foot muscles.
• Osteoporosis can develop in susceptible individuals.
Effects on Other Cellular Functions

The results of some of the additional ways the corticosteroids can alter cellular functions
include:
• increased resorption of sodium and water in the kidneys (promoting edema

and increased blood pressure)
• changes in behavior and mood
• inhibited calcium absorption from the gastrointestinal tract, having numerous
potential effects on muscle and neuron function, as well as bone health
• impaired osteoblast activity (increases predisposition to osteoporosis)
Therapists should note that all of the effects of the corticosteroids given above, occurring as
they do in combination, will often result in slower healing times, and may lead to a poorer
quality of tissue resolution or repair. It is important not to make assumptions about ‘standard’
healing time frames and to recognize that the effects of a corticosteroid medication in
reducing pain and inflammation can lead a site to appear less acute than it really is.

SIDE EFFECTS – Drugs for Managing Pain and Inflammation
This table lists the common side effects of the groups of medications discussed in this chapter.
Therapists must keep in mind that other side effects may occur, and that reactions will vary in
degree and intensity. Always ask clients about incidence and intensity of any side effects
experienced. When more than one medication is being taken, whether in the same drug group or
not, therapists should appreciate the increased potential for adverse and idiosyncratic effects.
Side Effects NSAID NA MR CSD Side Effects NSAID NA MR CSD

Abdominal Cramps XX X X Libido Changes X
Acne X Lightheadedness X X X
Allergic Reactions XX Loss of Vision X
Anorexia X X Menstrual Irregularities X
Anxiety X X Mood Changes X X
Blurred Vision XX Muscle Weakness X
Blood Dyscrasias XX Nausea XX X X X
Bradycardia X Osteoporosis X
Bruising XXX XX Palpitations XX
Confusion X X Peptic Ulcers XXX X
Constipation XX X Peripheral Edema X X
Depression X X Photosensitivity XX X
Drowsiness XX X X Poor Wound Healing XX XX
Dry Mouth X X Poor Immune Response X
Diarrhea X Postural Hypotension X X
Dizziness XX X X Prolonged Bleeding Time XXX XX
Euphoria X Pruritus X X X
Facial Flushing X Rashes XX X X
Fatigue X X X Respiratory Depression X
Fever X Restlessness X
Fractures X Sedation X
Gastrointestinal Bleeding XXX X Shortness of Breath XX
Headaches XX X X Sweating X
Hepatitis XXX Tachycardia X X
Hiccups X Tendon Injury X XX
Hip or Shoulder Pain X Thrombophlebitis X
Hypertension X X Tinnitus XX
Hypotension X Tremors X
Increased Appetite X Urinary Retention/Frequency X X
Indigestion X Vomiting XX X X X
Insomnia X X Weakness X X
NSAID: Non-Steroidal Anti-inflammatories, NA: Narcotic Analgesics, MR: Muscle Relaxants, CSD: Corticosteroids
The main side effect associated with Dantrolene is liver toxicity.
X – tolerable – notify medical practitioner if bothersome

XX – serious – monitor closely and notify medical practitioner
XXX – very serious – seek medical attention

Quick Guide to Case History Taking
Conditions requiring management of pain and inflammatory reactions range from
musculoskeletal trauma to chronic systemic disorders. It is important to clarify the reasons
for the use of medications addressing pain and inflammation in each client’s case.
Questions
1. What is the cause of the client’s pain? Was a medical diagnosis made?
Musculoskeletal injury, overuse syndrome? Systemic disorder?
2. Is there inflammation? Local or generalized? Current stage of the inflammatory
process? Is this a condition involving flare-ups? If yes, how often? Is there a pattern
to what causes them?
3. When did the pain and inflammation start? Pain location - have client identify
area(s) of discomfort.
4. What is the nature and description of the pain - sharp, shooting, deep, dull, achy?
Have the client rate the pain on a pain scale. Does it affect sleep or daily
activities?
5. With respect to the pain and/or inflammation, what alleviates it? Makes it worse
(specific movement, rest, activity)? How does it respond to touch?
6. Has the condition got better, worse, reached a plateau?
7. What medications are being used to treat the pain and/or inflammation symptoms?
Get details of medication type(s) and reason(s) for use. Any problems with
medication effects? If yes, have they been medically evaluated?
8. Any use of medication delivery devices? Self-administering injections? Patches?
Clarify location(s).
9. What is the general health status of other body systems? Any systemic conditions,
e.g. hypertension, diabetes, asthma? If yes, how are they being managed?
10. Any areas of sensory impairment? Where? Known cause?
11. What other therapies (past or present) have being used to address this problem?
What was the response?
Observations
1. Gait: is it normal, antalgic? Is there compensatory or protective holding? Does the
facial expression indicate pain during walking?
2. Position of comfort during standing and sitting.
3. Ease with which the client removes coat, shoes, etc. Is help required? Is there an
obvious decrease in function or range of motion?
4. Signs of injury and/or inflammation: edema, skin color, bruising, abrasions.
5. Compare bilaterally for size and shape, tissue color, edema, heat/coolness, tissue
atrophy.
6. Ability of client to focus and communicate effectively during the interview.

Quick Guide to Working with Clients Who Have Pain/Inflammation
1. Client Position and Comfort:

Because of the nature of the
condition and/or medication
effects, the client may not be
able to reflect accurately on the
comfort and safety of delicate
body tissues. The practitioner
must pay particular attention to
position choices and transfers.
Swollen tissues need to be well
supported and elevated to
encourage drainage. Use
pillows and other supports to
ensure that any vulnerable body
parts are not compromised.
2. Tissue Health: Pay particular attention to the health and integrity of the skin and
underlying connective tissues. With longstanding or chronic conditions tissues are
generally more fragile, tend to have reduced or otherwise altered sensitivity, and can
be more easily injured from normal use of manual techniques.
3. Systemic Health: Pain and inflammation can be a part of the symptom picture of a
systemic disorder. Familiarize yourself with the condition and the specific clinical issues
it presents. In the chapters that follow several types of painful and/or inflammatory
conditions are addressed, for example respiratory disorders in Chapter 9, cancer in
Chapter 11, and HIV/AIDS in Chapter 12. Evaluate the health of systems like the
cardiovascular system, which is usually affected by generalized conditions. Pain and
inflammation rarely present as unique or independent symptoms – the practitioner
must consider the underlying causes and design the treatment approach accordingly.
4. Effects of Touch: In most cases professional touch in an appropriately designed
treatment approach will help reduce pain. However, it is important to realize that this
is not always true. For individuals in severe pain sometimes being touched causes
overload and results in more distress and discomfort. This can change from day to
day – the practitioner has to be understanding and flexible.
Choice of Techniques
1. In general, client feedback about pain and depth of pressure can be misleading.
'Going deeper,' even if you have the client’s encouragement, may result in bruising,
worsening the injury, or exacerbating an inflammatory reaction.
2. PROM, effleurage, gentle direct or indirect myofascial therapies, lymphatic drainage,
and light reflex techniques like vibrations and stroking and are all effective in treating
the edema and muscle tension that often accompany injuries and flare-ups.

Topical Administration of Pain Medications
In an earlier chapter, topical skin applications for relief of muscle and joint pain were
discussed. Topical analgesics or counter-irritants like Zostrix and Tiger Balm are often
effective in managing pain of the more superficial joints like the knee, hands, and lower
back. These preparations act in a variety of ways on the local circulation and superficial
nerves to relieve pain and stiffness.
Massage Guidelines – Clients Taking Medications for Pain and Inflammation
General Guidelines
1. It is important to always keep in mind that the purpose of these medications is to
relieve pain. Client feedback, although important to solicit and consider, may be
unreliable. The massage therapist must assume more responsibility than is ordinarily
the case for determining what treatment approaches are safe and appropriate.
2. Make sure you are aware of all the medications the client is taking, whether
prescription or OTC. Keep in mind that drugs for managing pain and inflammation
are addressing symptoms. Especially when the cause is a systemic condition, various
other medications may also be employed and will need to be taken into account in
treatment planning. Be alert to the fact that multiple medication use can predispose to
a higher incidence of adverse effects.
3. Schedule treatments around medication taking to maximize the accuracy of the client’s
feedback and to optimize medical stability. These issues are addressed in more detail
in Chapter 5.
4. Nausea and vomiting are potential side effects of all the medication types discussed in
this chapter. Such episodes can leave the client feeling weak and fatigued. Postponing
the session or giving a shorter, more specific treatment may be required.
5. Dizziness, drowsiness, and postural hypotension are also common side effects. These
can be heightened by massage. Ask your client about post treatment reactions – future
treatments may need to be shortened or less intense. Always instruct the client to sit
up slowly and stay seated on the massage table for a minute or so before standing up.
6. Clients taking narcotic analgesics and corticosteroids often experience mood changes
and may be less communicative or responsive. The therapist may notice that the client
is less cooperative, or seems disinterested in responding in a meaningful or thorough
fashion to requests for information or feedback. It can be necessary to exercise a bit
more professional assertiveness.
7. Some clients will experience skin irritations. Ensure proper positioning, and keep in
mind that local massage is contraindicated until the reaction has subsided.

8. Topically administered pain and anti-inflammatory medications act in a variety of
ways on the local circulation and superficial nerves to relieve pain and stiffness. They
tend to compromise local sensation. If on-site work is otherwise appropriate, exercise
caution and modify depth of pressure when working on tissues being influenced by
such topical applications.
Specific Guidelines
1. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
These drugs have both analgesic and anticoagulant properties. Clients may be unable
to give accurate feedback about technique pressures and will be more susceptible to
bruising if treated too aggressively.
Be alert to complaints of gastrointestinal pain and discomfort. The NSAIDs can cause
ulcers and GI tract bleeding, both of which can become life threatening if not
addressed medically. If the client has been diagnosed and is being treated for GI side
effects, abdominal massage and hydrotherapy are contraindicated until the condition
has resolved.
2. Muscle Relaxants and Narcotic Analgesics
The muscle relaxants and narcotic analgesics depress neural responses. Stretching
techniques should be avoided or applied cautiously because sensory feedback from
muscular stretch and tension receptors may be compromised. On palpation, the muscles
whose role it is to protect themselves and their local tissues will feel hypotonic.
Constipation is a common side effect of the narcotic analgesics. The decreased
intestinal motility is not greatly influenced by massage techniques. Prolonged
constipation or bowel restriction must be carefully monitored by the physician.
3. Corticosteroids
The catabolic activity of the corticosteroids, especially with long-term use, can impair
tissue strength, resilience, and sensitivity. Skin integrity may be reduced. The body
tissues are more easily damaged by pressure and stretch. Massage techniques that
place stress on the muscles, bones, and joints of the body must be avoided or modified.
Examples include rib springing, heavy tapotement, and passive overpressure.
Remember that healing times may be longer than expected, and tissue repair may not
be of the best quality. Be particularly careful with clients who are at risk for
developing osteoporosis, like postmenopausal women and the elderly.
The corticosteroids have immunosuppressant effects and can make a client more
susceptible to infection or communicable ‘bugs.’ Hygienic routines become
especially important. As well, the practitioner should be alert to the need to reschedule
such clients’ appointments when personally unwell.

Hydrotherapy Guidelines
Before making treatment decisions, always inquire carefully about areas of sensory
impairment, everyday hydrotherapy tolerance, and any restrictions the doctor has placed on
hydrotherapy use. Small ‘trial’ applications can be useful. In general, local treatments to
specific body areas using modified temperatures are suggested. Always check with the client
to see if there were any post-treatment adverse effects.
Keep in mind that analgesics can modify a client’s perception of when an application
temperature is too hot or too cold for tissue safety.
With use of drugs that depress the CNS, like the skeletal muscle relaxants and narcotic
analgesics, systemic hydrotherapy treatments such as saunas, whirlpool baths, herbal baths,
and medicated steams are not recommended. The effects of the medications in combination
with generalized vasodilation from the treatment can lead to adverse effects like dizziness,
fainting, disorientation, confusion, and edema of the extremities.
Be observant with clients who are taking corticosteroids long-term. Get a sense of their
general constitutional strength and the acuity of their reactions to hot and cold.
Prolonged topical use of corticosteroids not only causes changes in skin sensitivity but can
also affect the reaction of the local blood vessels to hot and cold. Cutaneous blood vessels
may spasm when exposed to even mild temperature differences.
Exercise Recommendation
Medications for pain and inflammation can ‘take the pain away,’ and clients can easily
overwork vulnerable tissues, either inadvertently or hoping that doing more will help them get
better sooner. A progressive exercise plan should be implemented starting with low
resistance, fewer repetitions, and careful monitoring of reactions and progress.
Some people experience photosensitivity reactions from NSAID and muscle relaxant use.
When outdoors such clients should be well clothed and perform exercise activities in shaded
areas or during cooler times of the day.
Clients taking NSAIDs and narcotic analgesics may experience shortness of breath during
exercise. If this occurs the client should be medically evaluated. Exercise frequency,
intensity, and duration will probably need to be modified.
1. Nielsen A.C., Market Track, supplied by the Nonprescription Drug Manufacturers Ass’n of Canada
2. McGoldrick, M.D. & Bailie, G.R., “Nonnarcotic Analgesics: Prevalence and Estimated Economic
Impact of Toxicities,” Annals of Pharmacotherapy, 31(2): 221-7, February 1997
3. Ruoff, G.E., “The Impact of Nonsteroidal Drugs on Hypertension: Alternative Analgesics for
Patients at Risk,” Clinical Therapeutics, 20(3): 376-87, May/June 1998

CHAPTER 7
Drugs for Managing

Cardiovascular Disease
Superior Aorta
Vena Cava
Left
Right Pulmonary
Pulmonary Arteries
Arteries
Left
Right Coronary
Coronary Artery
Artery
Right Left
Ventricle Ventricle
Inferior
Vena Cava
Descending Aorta
The American Heart Association in their Heart and Stroke Statistical Update (Economic Cost
of Cardiovascular Diseases in 2001) projects the cost of cardiovascular diseases and stroke in
the United States in 2001 will be $298.2 billion. This figure includes health expenditures
(direct costs for physicians and other professionals, hospital and nursing home services,
medications, home care, and so on) and lost productivity resulting from morbidity and
mortality.
Cardiovascular disease is so prevalent that it is estimated about 20% of adult North Americans
will develop a cardiovascular condition, most commonly hypertension, atherosclerosis,
angina pectoris, heart attack, cardiac dysrhythmia, or stroke. Someone has a stroke every 53
seconds in the United States; a fatal stroke occurs every 3.3 minutes. Cardiovascular disease
is usually managed with exercise, diet, stress management and other healthy lifestyle changes,
and with a variety of pharmacological and surgical approaches. Massage therapists are
frequently in the position of working with clients who are taking one or more medications for
a cardiovascular disorder.

COMMON CARDIOVASCULAR CONDITIONS
Atherosclerosis
A condition involving build-up of fatty plaques, called atheromas, inside artery walls. The
atheromas project into the blood vessel lumen, reducing flow to supplied tissues and causing
blood turbulence that predisposes to thrombus development.
Thrombus
A clot-like plug formed when platelets are activated inside a blood vessel or heart chamber.
A thrombus consists of aggregated platelets, fibrin strands, and entrapped red blood cells. The
process of thrombus formation is called thrombosis.
Embolus
An embolus is material circulating in the bloodstream that should not be there, for example,
a bone chip or nitrogen bubble. The most common emboli are thrombus pieces
(thromboemboli) that have detached from their sites of origin. An embolism occurs when an
embolus blocks a smaller blood vessel, killing the tissue the vessel supplies.
Angina Pectoris
Episodes of heart pain (intermittent ischemic attacks) brought on by stress and exertion. The
cause is reduced blood flow to the heart muscle due to narrowing of its supplying artery(ies),
usually because of atherosclerosis but sometimes as a result of vasospasm or constrictive
scarring. When the metabolic demand of the myocardial cells exceeds what their
compromised circulation can deliver, lactic acid accumulates and pain results.
Myocardial Infarction (MI)
Death of a section of the heart wall because the supplying coronary artery has become
blocked or has ruptured; in lay language referred to as a heart attack. Occlusion is most
commonly caused by a thrombus developing at an atheroma site.
Hypertension
Chronically elevated blood pressure. Can be idiopathic or as a result of a known cause.
Cardiac Dysrhythmia
Irregular heart beat. There are many possible causes, including conduction system
malfunctions, electrolyte imbalances, scar tissue in the heart wall, and drug reactions.
Cerebrovascular Accident (CVA)
Death of brain tissue as a result of blockage or rupture of a supplying artery; commonly called
a stroke. Hypertension and atherosclerosis complicated by thrombosis are the usual causes.
Transient Ischemic Attack (TIA)
Intermittent ischemic attacks affecting the brain tissue. As with angina pectoris in the heart,
they occur when the lumen of a supplying artery is narrowed due to atherosclerosis, scarring,
or vasospasm. In the brain these attacks can produce any number of symptoms, for example
blurred vision, slurred speech, muscle weakness, loss of sensation, etc., depending on which
tissue area is affected. TIAs are often stroke precursors.
Congestive Heart Failure (CHF)
Weakness of the heart as a pump. The heart struggles to overcome peripheral resistance and
supply enough blood to the tissues. Blood pressure and heart rate are elevated. Acute CHF is
an emergency situation; chronic CHF is a slow progressive diminishment of the heart's strength
and effectiveness.

Blood Pressure, Heart Rate, and Cardiovascular Disease
The role of the cardiovascular system is to provide the body's cells with nutrients and to
remove their metabolic wastes efficiently. It is very sensitive to tissue requirements and, when
healthy, adapts accurately to minute shifts in metabolic need.
The response of the cardiovascular system to heightened tissue demand is to:
• increase the blood pressure

• increase the heart rate
• redirect blood flow to prioritize tissues under stress
These are normal responses designed to enhance delivery of cellular requirements. They are
effective in handling higher demand situations. However, they are intended to be short-term
immediate reactions that subside with the end of the stressor. Let's take a closer look at blood
pressure and heart rate, since these are the mechanisms most influenced by cardiovascular
drug therapies.
• blood pressure
Blood pressure is a measure of the relationship between cardiac output and the total peripheral
resistance. Cardiac output (CO), defined as the volume of blood the heart pumps per minute,
reflects the pumping strength of the heart, its rate and rhythm, and the volume of blood returned
to the heart (venous return). The total peripheral resistance (TPR) is a summation of all the
elements that create resistance to the flow of blood, therefore determining how hard the heart
has to pump to overcome them. The most important factor is blood vessel diameters in the
systemic and pulmonary circulations. The volume and viscosity of the blood also affect TPR.
CO TPR
BP Heart’s Pumping Strength
Heart Rate & Rhythm
Venous Return
Blood Vessel Diameters
Blood Viscosity
Total Blood Volume
When blood pressure is consistently elevated above normal levels concerns arise because of
the stress this places on the heart and vasculature. Monitoring blood pressure is one of the
diagnostic tools routinely used to assess the health of the cardiovascular system.

Chronic blood pressure elevation, called hypertension, is generally defined in an adult as a
systolic pressure of 140 or higher and/or a diastolic pressure of 90 or higher on more than one
visit within two weeks. (Infants and children can also develop hypertension, but different
diagnostic criteria are used.)
Hypertension is classified into two categories:
• primary or idiopathic hypertension, which accounts for 90-95% of cases

• secondary hypertension (caused by another diagnosed condition), which
accounts for 5-10% of cases
The diagnosis of hypertension is almost always an indication of increasing cardiovascular

stress. When high blood pressure is lowered, the stress and work of the heart are reduced and
circulatory efficiency is improved.
• heart rate
The average normal resting heart rate is 70-72 beats per minute. There is considerable range
in what is considered normal, however; children have faster resting heart rates, and elite
athletes generally have much slower ones.
As the heart is asked to do more work, it starts to beat faster. Within physiologic limits, the
faster the heart beats, the more blood it can pump. Signaled by the sympathetic nervous
system, the healthy heart reacts to added demands by increasing both the rate and force of its
pumping action. Again, this is intended to be a short-term response.

The heart muscle is nourished between contractions, so a rapid heart rate reduces the time
frame in which the heart wall itself can be perfused with fresh blood. If the heart rate is
chronically elevated, eventually the tissue is weakened. The weaker heart will tend to beat
faster to compensate, creating an unfortunate cycle characteristic of progressive heart failure.
An elevated heart rate does not necessarily indicate stronger myocardial contractions; in fact,
the opposite is often true.
Medications and Cardiovascular Disease

When drugs are used in the treatment of cardiovascular disorders they are often directed at
managing blood pressure or strengthening heart function, or both. As well, medications are
often employed to prevent or control factors that may lead to blood vessel narrowing or
blockage.
The medications commonly prescribed for cardiovascular conditions are grouped into
categories of drugs that:
• improve heart function

• increase blood vessel diameter
• alter blood coagulation mechanisms
• reduce blood volume
• lower blood lipid levels (reduce blood vessel blockage)
It is important to keep in mind that the drugs we will be discussing in this chapter are often
used in combination with each other – individuals with cardiovascular problems are
frequently taking several medications.
1. DRUGS THAT IMPROVE HEART FUNCTION

This grouping includes two main drug classes:
• the beta blockers (beta-adrenergic blocking drugs)

• the cardiac glycosides
Beta blockers
The betablocker medications are among the most widely used in the management of
cardiovascular diseases. They act on microscopic areas called beta-adrenergic receptors (beta
receptors) located on the surface of the heart. These receptors are normally activated when
sympathetic neurotransmitters like adrenaline and norepinephrine are released during stress.
When the beta receptors are stimulated in this manner, the heart's rate and force of contraction
are increased as part of the 'fright, flight, and fight' survival response. Added work from the

heart is a necessary part of being able to act quickly to avert an accident or escape from a risky
situation.
Concern arises when there is unnecessary or chronic sympathetic stimulation of the beta
receptors. The natural rate and rhythm of the heart can be adversely affected and it can begin
to weaken from overstress and reduced perfusion.
Uses
The beta blockers are primarily used in the management of:
• hypertension, angina pectoris, and dysrhythmia

• vascular headaches (migraines)
• anxiety and tremors
Commonly prescribed betablocker medications include: propranolol (Inderal), nadolol

(Corgard), metoprolol (Lopressor), and timolol (Blocadren).
Mechanism of Action
Sympathetic Sympathetic
Nervous System Nervous System
Stimulation Stimulation
Sympathetic Betablocker
neurotransmitters drugs ‘cover’
stimulate beta receptors the beta receptor
on the heart’s surface. sites, preventing
The result is increased sympathetic
rate and force of stimulation of the
contraction. heart muscle.
The betablocker drugs compete with sympathetic neurotransmitters for the beta receptor sites
on the heart, 'occupying' and blocking them. By preventing sympathetic stimulation of these
sites, the beta blockers relieve cardiac stress by slowing myocardial contractions and
improving their rhythmicity. The beta blockers also seem to have a systemic effect of
reducing blood vessel constriction, thereby assisting in lowering the blood pressure and
easing stress on the heart.

Beta receptors are located in many organs, including the heart, lungs, liver, and skeletal
muscle tissues. Activation of the beta receptors stimulates the formation of the second
messenger cyclic AMP, which then either activates or inactivates certain cellular enzymes.
There are two major types of beta receptors, called beta-1 and beta-2. Stimulation of
beta-1 receptors usually produces an excitatory effect in the target tissue cells, as is the
case with the heart. Beta-2 receptor activation generally results in inhibitory effects; for
example, in the lungs stimulation of such sites reduces constriction of bronchial passages.
The discovery of these specific beta receptors led to the development of beta-selective
drugs. Early beta blockers were non-selective in nature – they occupied both beta-1 and
beta-2 sites. When an individual took one of these beta blockers for a cardiovascular
condition, there was a risk of serious respiratory side effects such as precipitating or
worsening an asthma attack. This risk is reduced with the newer drugs.
Cardiac Glycosides
Cardiac glycosides are commonly found in plants such as milkweed, lily of the valley, the
oleander plant, and foxglove. Medicinal use of these plants for heart conditions dates back at
least 3,000 years – the Egyptians, Romans, and early Europeans all used them. Today, the
cardiac glycosides are mainly derived from various species of the foxglove plant and include
drugs such as digitalis, digitoxin, and digoxin. Collectively these drugs are often referred to
as digitalis, and that is how we will refer to them in this section.
Uses
The cardiac glycosides are primarily used for:
• treatment of congestive heart failure
• prophylaxis and treatment of cardiac dysrhythmias
Congestive heart failure (CHF) results when the heart is not pumping effectively to meet the
demands of the body tissues. CHF can be an acute situation, such as right ventricular failure
due to a pulmonary embolism. This is a life-threatening condition that requires immediate
medical intervention and will not be seen by the massage therapist in everyday practice.
However, massage practitioners are more likely to be working with clients with chronic
progressive heart failure, the incidence of which is quite high in North America. This type of
congestive heart failure is a slower loss of strength and efficiency of the heart that results in
structural and physiological changes and eventual death of the myocardial tissues.
Mechanism of Action
The overall effect of the cardiac glycosides is to reduce the workload of the heart by:
• slowing down the heart rate
• increasing the efficiency of the contraction and refilling phases of the cardiac cycle

Although the exact mechanism is still not completely clear, research suggests two main
actions of the cardiac glycosides:
• Digitalis produces a positive inotropic effect on the heart (increases the force
of myocardial contraction) by altering the normal functioning of the
sodium/potassium pump. An electrolyte imbalance is created that causes an
influx and release of calcium ions within the myocardial cells.
Calcium ions are important for normal and efficient cardiovascular function.
They play a key role in contraction of the heart wall, in contraction of the
muscles of the blood vessels, and in the heart's electrical conduction system.
When the normal progress of calcium ions in and out of their cells is altered,
the contractile and electrical properties of these structures are affected.
Pathways (gates) for the movement of intracellular calcium are regulated by
a number of hormonal, electrical, and chemical processes.
The cardiac glycosides influence this gating activity, elevating intracellular
calcium concentrations to trigger biochemical events that result in more
forceful contraction. Following myocardial contractions the ventricles are
more completely emptied, while on refilling they are more completely filled.
These effects aid in improving blood circulation to the body tissues and
reducing peripheral edema.
• Digitalis also seems to have an effect on the heart’s electrical conductivity
mechanisms. The conduction rate of impulses at the atrioventricular (AV)
node is reduced and there appears to be more vagus nerve stimulation; these
effects decrease the heart's electrical excitability and slow the heart rate.
2. DRUGS THAT INCREASE BLOOD VESSEL DIAMETER

The drugs discussed in this next section all increase vascular diameters. Although their
mechanisms of action differ, their common effect is vasodilation. The purpose is to decrease
peripheral resistance and lower blood pressure.
We will look at four categories of commonly prescribed drugs with vasodilation effects:
• the vasodilators
• the calcium channel blockers
• the angiotensin-converting enzyme (ACE) inhibitors
• the alpha receptor drugs
Vasodilators
The ‘official’ vasodilator medications (those that are actually called the vasodilators) belong
to a group of drugs that are chemically related to the nitrates, for example nitroglycerin. The

nitrates and their derivatives are available in several forms including sublingual tablets,
aerosol sprays, ointments, and skin patches.
Uses
The nitrate family of drugs is used in the management of:
• angina pectoris, acute and chronic

• hypertension
• congestive heart failure
Mechanism of Action
These drugs act directly on the coronary and peripheral blood vessel walls to reduce their
tone. They are metabolized to nitrous oxide in the vascular smooth muscle cells. Nitrous oxide
is a chemical that exists naturally in the body to help regulate blood vessel contractility. It
does so via increasing the concentration of a second messenger called cyclic GMP1 which
produces vasodilation.
It was once believed that the nitrates only dilated the affected vessels of the heart during an
angina pectoris attack. Although some coronary vasodilation is observed, the relief produced
is mainly due to dilation of the systemic vasculature. This lessens the peripheral resistance and
reduces the filling of the ventricles, cutting back quickly on the stress placed on the heart.
When used as directed under the tongue for angina attacks, these effects take place within
2-3 minutes.
Calcium Channel Blockers

These drugs, used very commonly in treating high blood pressure, also produce their effects
by influencing smooth muscle tone in blood vessel walls.

Uses
The calcium channel blockers are widely used in medical practice for:
• hypertension
• tachycardia (rapid heart beat)
• prevention of migraines
• prevention of vascular spasm after brain hemorrhages
Commonly prescribed calcium channel blockers include: Cardizem (Diltiazem), nifedipine
(Procardia), and verapamil (Isoptin).
Mechanism of Action
The calcium channel blockers act on the intracellular calcium gates in cardiac and vascular
smooth muscle cells to block influx and movement of calcium ions. Their key effects, which
work together to reduce stress on the heart, include:
• vasodilation
Vasodilation of the coronary blood supply increases blood flow and oxygen to the heart,
assisting it to function more effectively. The vasodilation of the peripheral vasculature eases
stress on the heart by reducing peripheral resistance and venous return.
• reduction of the rate and force of cardiac contraction

Heart muscle tone is reduced. Some members of this drug group also slow down the electrical
conductivity of the heart. Overall, myocardial excitability is decreased and the heart functions
in a more 'relaxed' manner.
ACE Inhibitors
The ACE inhibitors produce vasodilation by interrupting the activities of one of the enzymes
in the renin-angiotensin system.
The Renin-Angiotensin System

The kidneys play a crucial role in long-term blood pressure control. One of the mechanisms
involved is the renin-angiotensin system, which acts to increase blood pressure back to normal
if it begins to drop.
1. Renin is an enzyme produced mainly in the kidneys and released into the circulation in
response to a decrease in blood pressure. Renin acts on the substance angiotensinogen,
which is made in the liver and is continuously circulating in the blood, converting it to
angiotensin I.
2. Angiotensin I is converted to angiotensin II by an enzyme called angiotensin converting
enzyme (ACE).
3. Angiotensin II has very powerful vasoconstrictor properties. When it circulates in the
bloodstream generalized vasoconstriction occurs and blood pressure goes up.

The renin-angiotensin system is an intrinsic control mechanism that is very useful in
circumstances where the blood pressure is dropping. It functions as a homeostatic response in
minor circumstances and as a life-preserving mechanism in more severe situations like shock
or illness. However, some people develop elevated levels of circulating renin without any
apparent reason. In this scenario, the renin-angiotensin system becomes a factor causing
hypertension.
Uses
The ACE inhibitors are commonly used in the management of:
• hypertension
Commonly prescribed medications in this group include: Captopril (Copoten), enalapril

(Vasotec), and lisinopril (Zestril).
Mechanism of Action
The ACE inhibitors suppress the function of angiotensin converting enzyme, which converts
angiotensin I to angiotensin II. When angiotensin II formation is reduced, its ability to cause
vasoconstriction is decreased. A reduction in peripheral resistance results and systemic blood
pressure is lowered.
The ACE inhibitors also seem to reduce the release of the adrenal hormone aldosterone, which
promotes retention of sodium and water by the kidneys. Aldosterone has the potential to
produce hypertensive effects because it can cause an increase in total blood volume. The ACE
inhibitor drugs, by decreasing the influence of aldosterone on the kidneys and promoting more
excretion of water and sodium, lower the blood volume and help decrease blood pressure.
Alpha Receptor Drugs

Alpha receptors are found in the central nervous system and the smooth muscle of blood
vessel walls. They belong to two groups:
• alpha-1 receptors located on vascular smooth muscle cells

• alpha-2 receptors found in synapses in the autonomic nervous system
The alpha receptors respond to the sympathetic neurotransmitters epinephrine and

norepinephrine to alter blood vessel tone. Alpha-1 receptor activation has a direct effect on
the blood vessels to produce vasoconstriction. When alpha-2 receptors are stimulated there is
a decrease in the number of sympathetic impulses leaving the vasomotor center, which results
in peripheral vasodilation.
Uses
Drugs that act on the alpha receptors are used in the management of:

• hypertension
• Raynaud's vasospasm
Mechanism of Action
Specialized drugs have been designed that can affect sympathetic activity at the alpha receptor
sites to decrease vascular tone:
• by blocking stimulation of alpha-1 receptors in the blood vessels

Drugs that occupy and block the alpha-1 receptor sites against sympathetic stimulation are
called the alpha-adrenergic antagonists. Examples include prazosin (Minipress), doxazosin
(Cardura), and the ergot alkaloid derivatives.
• by stimulating alpha-2 receptors in the CNS

Medications designed to stimulate alpha-2 receptor sites in the brain are known as adrenergic
agonists and include drugs such as clonidine (Catapres) and methyldopa (Aldomet).
In either case, the overall effect is to decrease the sympathetic mediated tone of the vasculature,
causing vasodilation and lowering blood pressure by reducing total peripheral resistance.
Vasodilators
Metabolize to
nitrous oxide inside Calcium Channel
blood vessel walls, Blockers
promoting smooth Act on specialized ACE Inhibitors
muscle relaxation calcium passages Inhibit the
in blood vessel formation of Alpha Receptor
muscle cells to angiotensin II, a Drugs
block the influx of very powerful Reduce the effects
calcium ions vasoconstrictor of sympathetic
stimulation on the
blood vessels
Vasodilation
The total peripheral resistance

of the blood vessels, and
therefore the blood pressure,
is reduced.
Drugs that increase blood vessel diameter

3. DRUGS THAT ALTER BLOOD COAGULATION MECHANISMS
Blood coagulation is a vital biological function necessary to stop bleeding. Under healthy
conditions there is a delicate balance between clot formation and clot breakdown. If clot
formation continues unchecked it leads to thrombosis which can obstruct the blood vessel. On
the other hand, if clot development is inadequate there is excessive bleeding.
Any factor that causes either too much or too little blood coagulation contributes to
cardiovascular stress and disease. Pathological conditions, genetic influences, and the
physiological changes of aging can all impair blood-clotting mechanisms. Hemophilia is an
example of a genetic condition characterized by a defective blood coagulation process – the blood
fails to clot and abnormal bleeding occurs. A different example, thrombocytosis, is a condition of
various causes characterized by a higher number of circulating platelets. This results in increased
blood viscosity, intravascular platelet clumping, and thrombus formation.
This section will focus on drugs that reduce blood clot and thrombus formation, and drugs that
are used to 'break up' clots and thrombi.
Drugs used in the treatment of cardiovascular disease to influence blood coagulation

processes can be subdivided into three categories:
• anticoagulants (affect blood clotting)
• antithrombotics (inhibit thrombosis by altering how platelets adhere together)
• thrombolytics (break down clots and thrombi that have already formed)
Uses
The anticoagulants, antithrombotics, and thrombolytic drugs are used either alone or in
combination with other agents to address:
• deep vein thrombosis
• various thromboembolic and circulatory disorders, including those associated
with heart attacks, cardiac and other types of surgery, pulmonary emboli,
strokes, and transient ischemic attacks
Mechanism of Action
• anticoagulants
The two most commonly used anticoagulant drugs are the orally administered coumarin
derivatives, such as warfarin, and the parenterally administered drug heparin.
Warfarin, which has a similar chemical structure to vitamin K, competes with vitamin K at its
active sites in the liver. Vitamin K functions and dependent processes are suppressed,
resulting in reduced formation of several of the blood clotting factors. It can take a number
of days for the coumarin derivatives to produce their anticoagulant effects.

Vitamin K is necessary for normal blood clotting. It acts as a catalyst during the synthesis
of four of the twelve factors in the clotting cascade: II (prothrombin), VII, IX, and X. It also
plays a role in the conversion of prothrombin to thrombin; thrombin is needed for the
conversion of fibrinogen to fibrin. Fibrin strands form the meshwork of clots and thrombi.
Heparin is only administered by intravenous or subcutaneous injection because it is not

absorbed when taken orally. The body has its own natural source of heparin – it is abundant
in granules of the mast cells that line the vasculature.
Heparin increases the activity of a substance called antithrombin III, which forms complexes
with thrombin. The antithrombin III-thrombin complex inhibits several key enzymes in the
blood clotting process. Unlike warfarin, heparin's onset of action is very quick. These two
drugs are often used in combination for immediate and longer-term effects in the treatment of
venous thrombosis and embolism.
Blood vessel injury

or abnormal blood coagulation process
Clotting cascade
Prothrombinase Prothrombin
Heparin and Ca++

the other
anticoagulants Thrombin
act here
Fibrinogen Fibrin
Clot
The anticoagulants produce their effects by interfering with the production of fibrin.
• antithrombotics
Drugs that prevent or impair platelet aggregation reduce the risk of dangerous thrombus
formation. The antithrombotics are anti-platelet drugs. They are used mainly in the prevention
of arterial thrombosis, especially in the coronary and cerebral arteries.

Unlike blood clots, which form through a “cascade” of clotting factor processes, thrombi
develop as a result of platelet activation. In the presence of the chemical mediator
thromboxane A2, platelets clump together (aggregate). Aggregated platelets, entrapped red
blood cells, and fibrin are the usual components of thrombi.
Platelets play an important role in controlling bleeding, especially following tissue trauma.
However, thrombi can create risky situations if blood vessels are obstructed. Platelets can also
be activated by blood vessel inflammation or elements like atheromas that cause blood
turbulence.
A drug that is increasingly being used as an antithrombotic agent is aspirin. As discussed

previously, aspirin inhibits the formation of thromboxanes. A single dose of aspirin can inhibit
platelet aggregation for up to a week. Since platelet life span is 6-10 days, aspirin (or other
NSAIDs with similar properties) can inactivate platelets for most or all of their short lifespan.
Another example of an antithrombotic medication is dipyridamole (Persantin), which also

inhibits platelet aggregation. It is often used following prosthetic heart valve replacement to
prevent thromboembolic complications.
Blood vessel injury, inflammation, or other wall irregularity

Irritant in the blood, blood turbulence
Arachidonic acid
Aspirin and the other
NSAIDs act here Cyclo-oxygenase
Prostaglandins G2, H2
Thromboxane A2
Platelet aggregation
Thrombus
The antithrombotics produce their effects by impeding platelet aggregation.

• thrombolytics
The thrombolytic drugs promote disintegration of clots and thrombi that have already formed.
This process depends on the presence of plasmin, which is the enzyme responsible for
breaking down fibrin mesh. Any drug or agent that increases plasmin formation and/or
activity has the potential to be used to promote clot and thrombus dissolution.
Streptokinase is an example of a drug in this class. It is an enzyme that combines with

plasminogen (the inactive precursor of plasmin) to form a plasminogen-streptokinase
complex. This complex facilitates plasmin formation.
Another substance that is successfully used pharmacologically as a thrombolytic agent is a

commercial form of the naturally occurring compound tissue plasminogen activator (tPA).
During normal clot breakdown plasminogen is activated by the body's own tPA. DNA
technology has recently made tPA available as a thrombolytic drug.
The thrombolytics are used in the treatment of arterial and venous thrombi, after strokes and
heart attacks, and to clear IV catheters and other such devices.
Blood vessel injury

or abnormal blood coagulation process
Clotting cascade
Prothrombinase Prothrombin
Ca++
Thrombin
Fibrinogen Fibrin
Plasminogen
Thrombolytic/fibrolytic
drugs stimulate
plasmin
Plasmin Clot
The thrombolytic drugs produce their effects by stimulating increased plasmin formation.

4. DRUGS THAT REDUCE BLOOD VOLUME (THE DIURETICS)
The diuretics are usually the first drugs of choice in the pharmacological management of
hypertension and heart disease. They are generally well tolerated and are safely used in
combination with other cardiovascular drugs. The main action of the diuretics is to increase
the formation of urine. They do this through direct action on various parts of the kidney
tubule system. An increase in urine volume leads to a reduction in total blood volume, which
is another avenue for decreasing blood pressure.
The diuretics discussed in this section are classified into three groups:
• the thiazide diuretics
• the loop diuretics
• the potassium sparing diuretics
Uses
The diuretics are used in the management of:
• primary hypertension
• edema due to congestive heart failure, liver disease
• pulmonary edema
• diabetes insipidus
Mechanism of Action
The diuretics act at different sites in the kidney nephrons to increase urine volume.

• thiazide diuretics (e.g. Diuril)
These drugs act at the distal and convoluted tubules to block sodium and chloride ion
resorption. When more of these ions are allowed to pass into the urine, via osmosis more
water goes with them. There is an associated increased loss of potassium ions, which can
cause muscle and nerve dysfunction side effects like cramping and cardiac dysrhythmias.
• loop diuretics (e.g. Lasix)

The loop diuretics act primarily on the ascending loop of Henle to selectively inhibit the
resorption of chloride ions. With increased loss of chloride ions into the renal tubules there
is an accompanying removal of sodium ions and water. Associated potassium loss can be
quite high when taking these drugs.
• potassium sparing diuretics (e.g. Aldactone)

These drugs act on the distal renal tubules. They inhibit the cellular pump that facilitates
elimination of potassium and resorption of sodium. The hormone aldosterone controls this
pump. The result is increased sodium and water excretion with conservation of potassium ions.
Thazide diuretics
Act at the distal and
convoluted tubules
Potassium sparing
diuretics
Act at the distal
renal tubules
Loop diuretics
Act at the ascending
loop of Henle
Urine formation is increased.

Blood volume is decreased.
Blood pressure is reduced.
Drugs that reduce blood volume

5. DRUGS THAT LOWER BLOOD LIPID LEVELS
The lipid lowering drugs (LLDs) are used to manage hyperlipidemia, which is defined as an
abnormally elevated plasma lipoprotein level and is considered a key risk factor for
developing atherosclerosis.
Hyperlipidemia is classified as either:

• primary (due to genetic/familial tendencies)
• secondary (caused by high dietary fat, especially saturated fats, and poor lifestyle)
The relationship between elevated plasma lipoproteins, in particular cholesterol, and coronary
heart disease is well established. An estimated fifty-two million Americans need to comply
with dietary changes to establish adequate plasma lipoprotein levels, and almost thirteen
million require drug therapy.2
The main lipids (fat-like substances) transported in the blood are triglycerides and cholesterol.
Under normal healthy conditions they both have important biological functions. Triglycerides
are the primary form of fat in the body. They play a key role in supplying calories or body
energy. Cholesterol is involved in many cellular functions including formation of cell
membranes and hormone production.
Types of Lipoproteins
Lipoproteins are classified according to their density (weight).
1. Chylomicrons: Containing about 90% triglycerides by weight, chylomicrons are very
large. The fats in the food we eat are digested by the intestines to form chylomicrons
which are transported via the lymphatic system into the blood.
2. Very Low Density Lipoproteins (VLDLs): VLDLs are comprised of about 60% triglycerides
by weight. Unlike the triglycerides of the chylomicrons that come from ingested food,
these are made in the liver from endogenous carbohydrate stores. Triglycerides are
unable to directly penetrate cells like muscle fibers and fat cells. When they require an
energy source, these cells produce an enzyme (lipoprotein lipase) that breaks VLDLs
down into fatty acids and glycerol which are able to enter the cell.
3. Low Density Lipoproteins (LDLs): These lipoproteins contain about 50% cholesterol and
5% triglycerides. LDLs are the remnants of VLDLs. The liver produces about 70% of the
body's cholesterol and most cells can synthesize their own; however if they require
additional amounts they produce receptors on their cell membranes for LDL. When an
LDL combines with a cell receptor it is taken into the cell and degraded. When the cell
has enough cholesterol it stops creating receptors.
4. High Density Lipoproteins (HDLs): HDLs consist of 5% triglycerides and 20% cholesterols.
They are considered the 'good guys' for several reasons. They take cholesterol from
tissue cells to the liver. The liver either breaks down the cholesterol into bile salts or
excretes it into the bile. HDLs also seem to inhibit cellular uptake of LDLs, and may
discourage aggregation of platelets. The higher the HDL levels the less cholesterol in
the bloodstream.

These lipids do not circulate freely in the blood – they bind with protein molecules to form
lipoprotein complexes. Excess volumes of these complexes in the bloodstream promote
atherosclerosis development.
When pharmaceuticals are employed to manage hyperlipidemia, their overall purpose is to

reduce cholesterol and triglyceride concentrations in the plasma. The drugs used for this
purpose fall into four main groups:
• the bile acid sequestrants

• nicotinic acid (niacin)
• the fibric acid derivatives
• HMG Co A reductase inhibitors
Drug Group Mechanism of Action Comments
Bile Acid Sequestrants These drugs are not absorbed The first choice for treating
Drugs belonging to this group from the GI tract. They bind elevated LDL and cholesterol
include Questran, LoCholest, with bile acid to form an levels.3 Maximum effects
and Colestid. Used for insoluble complex excreted in occur after about one month.
managing elevated LDL the feces. This increases the
levels. liver’s utilization of cholesterol
to make bile acids.
Nicotinic Acid (Niacin) Niacin is believed to decrease The oldest lipid lowering drug.
Brand names include Niacor, activity of the enzyme Produces a marked decrease
Niaspan, and Nicolar. Used to triglyceride lipase. This inhibits in triglyceride and LDL levels
lower plasma levels of both formation of VLDLs, and in turn and an increase in HDLs.
LDLs and VLDLs. LDLs.
Fibric Acid Derivatives These drugs activate the Can reduce triglycerides by
Drugs belonging to this group enzyme lipoprotein lipase, and up to 45% while increasing
include Atromid-S, Lopid, and may also interfere with the HDLs.
Tricor. Used primarily to treat production and release of
high triglyceride levels. VLDLs by the liver.
HMG Co A Reductase Inhibitors These drugs inhibit the enzyme LDL plasma levels decrease
Also known as the statins, 3-hydroxyl-3-methyl-glutaryl within two weeks of starting
these drugs are the most coenzyme A, which is therapy. These drugs have an
commonly prescribed in the important for the synthesis of excellent safety and side
U.S. Brand names include cholesterol in the liver. They effect profile.
Lipitor, Baycol, Lescol, also increase the number of
Mevacor, Pravachol, and hepatic LDL receptors. The
Zocor. Used for treating overall effect is a reduction in
elevated LDL levels. LDL plasma levels.

HMG Co A reductase
inhibitors
Inhibit the production of
cholesterol by the liver Fibric acid derivatives
and increase the liver's Stimulate the actions of
sensivity to LDLs the enzyme lipoprotein
Nicotinic acid lipase and decrease VLDL
Inhibits the production
formation of VLDL
by the liver
Bile acid
Liver sequestrants
Increase the excretion
of bile acid in the feces
Gall bladder
Intestines
Cholesterol and triglyceride levels in the blood are decreased.
Drugs that lower blood lipid levels

SIDE EFFECTS – Drugs for Managing Cardiovascular Disease
experienced. When more than one medication is being taken, whether in the same drug group
or not, therapists should appreciate the increased potential for adverse and idiosyncratic effects.
Side Effects BB AC CCB ACE DIU VD CG LLD ARD

Abdominal Cramps X X X XX XX X
Acne X
Allergic Reactions XXX XXX XX X X
Anorexia X XX X
Anemia XX
Angina XXX
Anxiety XX XX X X
Appetite Changes X XX XX
Arthritis X
Back Pain XXX XXX XXX
Blurred Vision X XXX X XX XXX XX X X
Blood Dyscrasias XX XX XXX XXX X
Bradycardia XX XXX
Breathing Difficulty XXX XXX XXX XX
Bruising X XX XX
Bursitis X
Chest Pains XXX XXX XXX X XX
Cold Extremities XXX
Confusion XXX X X X X
Constipation X X XX X
Cough XX XX
Cramps X XX XX X
Cyanosis XXX
Deafness XX
Depression XXX X X X X
Dreams X X X
Drowsiness X XX X X
Dry Eyes X X X
Dry Mouth X X XXX XX XXX X X
Diarrhea XX X XX XX X
Dizziness XX X XX XX X X XX XX
Facial Flushing XX XXX
Fatigue X XX X X X
Fever X XX X X XXX XX
G.I. Bleeding or Pain XXX X XX XX
Gout X
Hallucinations XX X
Headaches X XX X X X XX X XX
Hearing Loss XX
Hematuria XXX
Hepatitis XXX
Hyperglycemia XXX XX X
Hypertension XX XX
Hypotension XX XXX XXX XX XX XX

Side Effects BB AC CCB ACE DIU VD CG LLD ARD
Increased Appetite X
Insomnia XX X XX XX X
Irregular Heartbeat XX XX
Joint Pain XXX XXX XXX XXX XX X
Kidney Dysfunction XXX XXX XX
Libido Changes XX X X X X X
Lightheadedness X X X X
Liver Dysfunction XXX XX
Loss of Hearing XXX XX
Loss of Taste X X X
Loss of Vision XX
Mood Changes XXX XX X
Muscle Weakness X XX XX XXX X
Nausea X X X XX XX X XX X X
Nasal Stuffiness X X
Nosebleeds XX XX
Palpitations X X X XX
Paresthesia XX X XX XX
Peripheral Edema XXX XX XXX XX X XX
Photosensitivity X X X XX
Postural Hypotension X XX XXX XX
Prolonged Bleeding Time XXX
Pruritus X
Rashes XXX X X XXX XXX X
Restlessness X X
Shortness of Breath X XXX XX
Sore Throat XX XX X
Sweating X X X X
Tachycardia X XXX XXX X
Tendon Injury XX
Thirst XX XX
Tinnitus X XX XXX X X
Tiredness X XX X X XX
Tremors X
Urinary Frequency X
Vertigo X X X
Vomiting XX XX XX XX X X
Weakness XX XX X XX XXX X X
Weak Pulse XXX XX
Weight Gain X
BB: Beta blockers, AC: Anticoagulants, CCB: Calcium Channel Blockers, ACE: Angiotensin Converting
Enzyme Inhibitor, DIU: Diuretics, VD:Vasodilators, CG: Cardiac Glycosides, LLD: Lipid Lowering Drugs,
ARD: Alpha Receptor Drugs

NOTE: Clients using an anticoagulant medication must pay particular attention to any incidence of unexplained
bleeding. Signs and symptoms that require immediate attention include: nosebleeds, unusual bruising, blood in
the stools or urine, unusually heavy or unexpected menstrual flow, bleeding from the gums, coughing up blood,
joint pain/stiffness/swelling, and abdominal pain or swelling.

Quick Guide to CV System Case History Taking
The cardiovascular system is responsible for ensuring that each cell of the body has an
adequate supply of oxygen and nutrients, and that metabolites are properly removed. It
is important to keep in mind that when the health of the cardiovascular system is
compromised all tissues and systems of the body can be affected in one way or another.
Similarly, pathologies of other body systems often cause cardiovascular stress.
Questions
1. Identify the cardiovascular disorder(s) for which the client is being treated. Time
frame since diagnosis? Progression of the condition?
2. How is the condition managed? Is it stabilized? Medications, diet, exercise
regimen, herbal remedies, etc? Get medication specifics. If nitroglycerine is being
used, in what form? If tablets, where does the client keep them in case they are
needed? If a patch, location?
3. Has there been any medical emergency? If so, what (heart attack, stroke) and
when? How was it managed? Any heart surgery? Ongoing complications from
any of these?
4. When was the last visit to the medical practitioner? Any recent developments related
to the condition? Was the blood pressure taken? What was it? How does it compare
to the previous reading? Have stress tests been done? What were the results?
5. Any other systemic conditions: asthma, diabetes, autoimmune, etc.? How
managed?
6. Have any restrictions been placed on exercise or hydrotherapy?
7. Circulatory problems, esp. cold hand or feet? Cyanosis? Slower healing times for
cuts or injuries? Any numbness?
8. Any shortness of breath? When does it happen? How much stress or exertion is
involved? Experiencing shortness of breath in any particular positions, e.g. lying flat?
9. In the event of a medical problem (for example an angina attack) while receiving a
treatment, what is the procedure?
Observations
1. Bruising: Note the extent and color. Inquire about how it happened.
2. Varicosities: Bilateral? How torturous or distended are the veins? How resilient is the
skin above them?
3. Peripheral edema: Bilateral? Is it pitted? Color and texture of the local tissues?
4. Breathing difficulties: Is the client out of breath? How much exertion was involved?
It is good clinical practice to take blood pressure and pulse readings for clients with
cardiovascular system challenges. Monitor especially for unexpected changes that may
need medical evaluation, and responses to massage or hydrotherapy treatment.

Quick Guide to Working with Clients Who Have Compromised CV Systems
Client Positioning
• Clients are often asked to begin a massage
treatment in the prone position as a matter
of routine. For the client with a compromised
cardiovascular system this may not be the best
position; in fact with moderate/severe high
blood pressure or recent heart surgery it may
never be appropriate to place the client
prone. Ask about how the client sleeps and
what positions will work best for the treatment.
Use lots of pillows to enhance comfort. Be
prepared to treat in modified supine, sidelying,
or seated positions.
• For clients who have edema, especially of the extremities, ensure that affected areas
are well supported and elevate in a manner that promotes natural lymphatic and
circulatory flow. However, too much elevation can be stressful on a weakened heart
because it increases venous return. For clients with a diagnosis of moderate/severe
CHF, do not elevate the feet above the level of the heart.
• Pay particular attention to client position if there is: a recent cardiac surgery, very high
blood pressure, an implanted device (e.g. pacemaker or catheter), a medicated patch.
• In general, have a strong focus on relaxing and soothing techniques. The goal is to
reduce sympathetic activation, TPR, and the workload of the heart.
• Avoid or modify treatment elements that could activate a sympathetic nervous system
response, for example heavy tapotement, deep tissue work, trigger point release, or
other potentially painful techniques. Make sure the client is warm enough, and is not
caught off guard by anything you are doing.
• Designing the treatment with limb work first helps reduce peripheral resistance.
• Effleurage and petrissage can have potent effects on the circulatory system, especially
long strokes that maximize venous return. Smaller segmental techniques like wringing
and muscle squeezing increase local circulation without causing as much blood flow
back to the heart.
• Avoid excessive elevation or large scale range of motion work when the client has a
significantly weakened heart – both can substantially increase venous return.
• When a client has edema, promoting lymphatic drainage can be helpful, but the scale
of drainage work needs to be modified with the cardiovascularly challenged client. The
lymphatic system empties into the circulatory system and increases blood volume.
• When a client has atherosclerosis or any other condition that predisposes toward
thrombosis, depth of technique should automatically be modified. Any known
thrombus sites are contraindicated for massage.
• If unsure about the efficacy of your planned approach to treatment, consult with the
attending physician.

Massage Guidelines - Clients Taking Medications for Cardiovascular Disorders
General Guidelines
1. Make sure you know all the medications being used and why, including OTCs like
aspirin. Since clients with cardiovascular disorders are often taking multiple
medications affecting various body systems, ask about adverse effects. Research the
drugs being taken to see if any of the client’s complaints may be related to drug
effects.
2. Consider the possibility that massage may destabilize a client with a more severe
cardiovascular condition. Timing of massage therapy in relation to medication use, for
example if the client has angina pectoris or cardiac dysrhythmias, may be important.
3. Postural hypotension, dizziness, and lightheadedness can occur when using the drugs
discussed in this chapter. The client is likely to feel dizzy with fast movements,
especially getting up right after a massage. Instruct the client to sit up slowly and wait
for a few seconds before getting off the table.
4. Check for injection sites, medicated patches, topical preparation use, and implanted
devices. There are cardiovascular medications that are delivered by all these routes.
Review the guidelines laid out in Chapter 5.
Specific Guidelines
1. Drugs that Affect Heart Function
The use of beta blockers can precipitate breathing difficulties, chest pains, and
abnormal heart rate and rhythm. These symptoms vary in intensity from person to
person. They should be carefully monitored medically. Take the client’s blood pressure
every treatment and pay special attention to any significant symptom changes.
Cold extremities, peripheral edema, paresthesias, and joint pain are common
betablocker side effects. Be alert for tissue fragility and decreased sensitivity – when
present adjust your depth of technique. Client feedback may not be reliable.
It is estimated that about 25% of people taking digitalis experience some form of
toxicity. Therapists should be alert to complaints of gastrointestinal irritation, visual
disturbances, confusion, and cardiac abnormalities such as abnormal heart rate or
rhythm. If not managed quickly these reactions can become life threatening.
2. Drugs that Increase Blood Vessel Diameter
Kidney disorders, peripheral edema, changes in heart function, and hypotension

episodes can occur to varying degrees with this group of drugs. These effects increase
the workload of the heart and predispose the client to more serious CV complaints.
Check the blood pressure on an ongoing basis and adapt your client positioning and
treatment approach as appropriate.

• ACE Inhibitors cause some individuals to develop a dry continuous cough within
the first several weeks of therapy. Lying in the supine position can make the
situation worse by aggravating coughing episodes.4 Keep some water handy, and
consider treating the client in a semi-seated position.
• Calcium Channel Blockers and Other Vasodilators can cause swollen, tired
feet and ankles. These clients may be at risk for developing deep venous thrombi.
Be alert to complaints of persistent pain and cramps. Be prepared to refer these
clients to the physician.
• Nitroglycerine Patches and Ointment may produce an itchy feeling at the site of
application. Do not remove the patch or advise the client to wipe off the ointment.
If a rash appears around the patch avoid massaging the affected skin and advise
the client to report it to the physician.
3. Drugs that Alter Blood Coagulation
Clients taking any of the drugs in this group will be predisposed to bruising if treated
aggressively. Deep massage techniques such as muscle stripping, cross fiber frictions,
and deep kneading techniques are not recommended.
Complaints of low back pain may be related to a concurrent kidney dysfunction.

Assess for signs and symptoms of musculoskeletal involvement. If negative, propose
follow up medical evaluation.
4. Drugs that Reduce Blood Volume
Clients taking diuretics may complain of pain, muscle weakness, and

cramping/spasms. These can be signs of electrolyte imbalance. Stretching and
strengthening procedures must be automatically modified. Heart palpitations may also
be related to loss of electrolytes like potassium. These symptoms suggest a need for
electrolyte replacement or re-balancing; if the client’s M.D. is not aware of them,
referral for evaluation is important.
Diuretic use can precipitate occurrences of hyperglycemia. Hyperglycemia signs and

symptoms are outlined in Chapter 8. This is a situation that needs to be medically
assessed and stabilized.
5. Lipid Lowering Drugs
Musculoskeletal, cardiac, blood, nervous, gastrointestinal, and metabolic disorders

can all occur with use of members of this drug group. Familiarize yourself with the
side effect profile of the drug used. Pay attention to chest pain, joint pain, muscle
weakness, easy bruising, hearing loss or changes, and changes in blood pressure. Such
symptoms should be addressed medically.

Always confirm that there are no medically prescribed temperature restrictions, which are
common with cardiovascular conditions and cardiovascular drugs like the beta blockers and
the vasodilator group. Inquire about daily bath or shower temperatures that are well tolerated.
The drugs discussed in this section will all tend to affect responses of the heart and blood
vessels, in one way or another, to temperature changes. The client with a cardiovascular
condition is always more at risk for experiencing adverse reactions to hydrotherapy. Begin
with the mildest applications and progressively increase the hydrotherapy stimulus,
monitoring the client’s responses carefully. Local applications are more likely to be
appropriate than systemic ones like saunas, medicated steams, and whirlpools. Be watchful
for signs of adverse reactions to hydrotherapy. Blood pressure and pulse readings should be
taken at the start and end of treatments.
Keep in mind that if the client is experiencing paresthesias, reactions to temperatures will
likely be altered.
The sympathetic response of the heart and blood vessels to exercise requirements will be
compromised if the client is taking drugs like the beta blockers or alpha receptor drugs. An
aggressive exercise regime puts the client at risk for developing adverse reactions such as
abnormal heart rhythm and palpitations.
Ways in which the client’s medications may interact with the heating effect from exercise
should also be taken into account.
It is important to keep in mind that drugs that affect electrolyte concentrations like the diuretics
will predispose the exercising individual to developing cramps and spasms more easily.
Exercise prescription for the most compromised types of cardiovascular patients is a
specialized field beyond the scope of most massage therapists. With disorders such as
congestive heart failure, a recent stroke or myocardial infarction, and angina pectoris, and
considering the myriad of drugs used to treat them, it is best to work with a health care team
that provides the services of a qualified exercise therapist.
1. Saari, J.T., Dahlen, G.M., “Nitric Oxide and Cyclic GMP are Elevated in the Hearts of Copper-
Deficient Rats,” Medical Science Research, 26: 495-497, 1998
2. Shafeer, R.S., Lacivita, C.L., “Choosing Drug Therapy for Patients with Hyperlipidemia,”
American Academy of Family Physicians, 61: 3371-82, 2000
3. “Management of Hyperlipidlemia,” Website:

www.humana.com/providers/guidelines/hyperlip.asp
4. U.S. Pharmacopeial Convention, Inc., Drug Information for the Health Care Professional (USP DI),
12th ed., pg. 257, Maryland, 1992

CHAPTER 8
Medications for
Managing Diabetes Mellitus
Diabetes is the world’s most common metabolic disease. In 1997 the direct and indirect costs
involved in managing diabetes in the United States totaled an estimated $98 billion.
Approximately 6 percent of the U.S. population has diabetes, and it is the fourth leading cause
of death. Being diabetic can reduce life expectancy by as much as 30 percent.
Diabetes mellitus is primarily a disorder of carbohydrate metabolism. Since carbohydrates

are a basic energy source for cellular activities, such a fundamental problem can give rise to
dysfunctions in virtually every body system. Some of the many complications of diabetes
include nerve damage (diabetic neuropathy), blood vessel damage (diabetic
microangiopathy), skin ulceration, cardiovascular disorders, kidney disease, blindness,
seizures, and amputations of limbs and digits.
The central issue in diabetes mellitus is a problem with the body’s production and/or
utilization of the hormone insulin. One of insulin’s key responsibilities is to move glucose
from the blood into body cells. It is also an anabolic hormone, playing an important role in
tissue growth and repair.
Diabetes is characterized by elevated levels of glucose in the blood (hyperglycemia) and in

the urine (glycosuria). The causes of diabetes mellitus are still under investigation. Several
types have being identified and are presented in the table on the following page.
The pancreas, the organ involved in diabetes, consists of specialized clusters of cells called
the islets of Langerhans. These cells produce and secrete several hormones. There are
three specialized cell types found among the islet cells, each of which is responsible for a
specific hormone:
• A or alpha cells (glucagon)
• B or beta cells – the most abundant (insulin)
• D or delta cells (somatostatin)
Insulin and glucagon are both involved in regulating blood glucose levels. Insulin facilitates
the movement of glucose out of the bloodstream into the peripheral tissues, including
muscles. It therefore decreases blood glucose. Glucagon, an antagonist to insulin,
increases blood glucose concentration. Somatostatin plays a role in gastrointestinal
absorption and may also assist in coordinating insulin and glucagon functions.

Types of Diabetes Mellitus Characteristics and Risk Factors
Type 1 Diabetes Accounts for 5-10% of diagnosed cases of diabetes; usually onsets during
childhood. The pancreas ceases to produce insulin, so proper
Previously called management involves the administration of exogenous insulin.
insulin-dependent diabetes
mellitus (IDDM) or Risk factors for its development, either separately or in
combination, include genetic inheritance, autoimmune
juvenile-onset diabetes
dysfunction, viral infections, and environmental factors.
Type 2 Diabetes Accounts for 90-95% of diagnosed cases. The pancreas still
produces insulin, but its output may be decreased or the insulin
Also referred to as quality may be deficient. Alternatively, the insulin may be normal
non-insulin dependent but peripheral cellular membrane resistance may have
diabetes mellitus (NIDDM) or developed, meaning that body cell insulin receptors malfunction
adult-onset diabetes (for example, in obesity). Another possibility is that the insulin is
being broken down before it completes its physiologic function.
Usually occurs in adults; is typically managed with diet and
lifestyle changes and pharmaceuticals, sometimes with insulin
supplementation.
Risk factors include older age, overweight, family history of
diabetes, prior history of gestational diabetes, impaired glucose
tolerance, physical inactivity, and race/ethnicity (e.g. blacks
and natives have higher risk inheritance factors).
Gestational Diabetes Develops in 2-5% of all pregnancies. Women who are obese or
have a family history of diabetes are at higher risk. Women who
Develops during pregnancy have gestational diabetes are more likely to develop Type 2
but recedes when the diabetes in later life. Managed with insulin and/or oral medications.
pregnancy is over
Diabetes 1-2% of diabetes diagnoses. Linked to specific genetic

From Other Causes syndromes, surgery, drug effects, malnutrition, infections, and
other illnesses. Managed with insulin and/or oral medications.
Management of Diabetes Mellitus

The management of diabetes typically involves:
• use of insulin and/or oral medications

• compliance with a specialized diet that controls sugars and fats
• stress and anxiety management (they increase levels of circulating glucose)
• developing a medically approved exercise plan
• regular medical monitoring
• ideally, becoming a member of a diabetes care support group
In this chapter, we will focus primarily on the pharmaceuticals used in diabetes treatment.

Medication Use in Diabetes
The pharmaceuticals used in managing diabetes include:
• parenteral insulin
• oral hypoglycemic medications
• a combination of insulin and hypoglycemic drugs
1. INSULIN
Insulin is normally released from the pancreas B cells in response to an increased volume of
glucose in the circulating blood, most notably after meals. The insulin stimulates delivery of
the glucose into cells, where it is important for numerous metabolic processes. A normal blood
glucose level is 80-90 mg per 100 ml of blood. The aim of administering exogenous insulin
is to normalize levels of blood glucose in the diabetic.
Liver
• increases glycogen formation

• decreases glucose formation
from amino acids and glycogen
Skeletal Muscle
• increases glucose influx and

utilization in the cell
• increases amino acid and
Effects protein synthesis in the cell
• decreases breakdown of
of glycogen into glucose
Insulin
Fat Cells
• increases storage and synthesis

of fats
• decreases breakdown of stored
fats into free fatty acids
Blood Composition
• decreases circulating glucose

and free fatty acid levels in
the blood

Insulin is utilized in the management of the following:
• type 1 diabetes
• type 2 diabetes when exercise, diet, and oral hypoglycemic drugs are not
effective in controlling blood glucose levels
• gestational diabetes
• pregnancy in type 2 diabetic women
• individuals who become diabetic with severe infections, or following surgery
or injury, or as a result of medication use (e.g. the corticosteroids can have
this effect)
Types of Insulin
There are a number of sources of insulin. Beef and pork insulin are derived by extraction
from the pancreas of the animal. These have been widely used but cause allergic reactions in
some people. Synthetic forms have also been available for some years. A form of insulin has
recently been bioengineered that is identical to human insulin.
Pharmaceutical insulin types vary in their onset, peak, and duration of action, and as such are
used for specific effects.
Type of Insulin Properties and Uses
Brand names include Humulin R and Novolin Toronto.

Rapid Acting Following injection, absorption occurs after 30-60 minutes; peak
or Short Acting action occurs after 2-3 hours. Duration of action varies between
6 to 8 hours. Best taken 30-45 minutes before meals.
Brand names include Lente and NPH.

Following injection, absorption occurs after 3-4 hours; peak effects
Intermediate Acting occur after 7-9 hours. Duration of action varies between 12 to 16
hours. Best use is at bedtime to control glucose levels the next
morning. When taken in the morning peak effects occur in the
afternoon.
Brand names include Humalog (insulin Lispro).

Following injection, absorption is very rapid; peak action occurs
Very Rapid Acting about 30 minutes later. Best used before meals to control
postprandial glucose rise. Can be used as a substitute for short
acting insulin.
Brand names include UltraLenta.

Following injection, absorption is slow; peak effects occur 10-12
Long Acting hours later. Variable duration of action lasting between 16 and 18
hours. Mainly used as a substitute for intermediate acting insulin to
decrease hypoglycemia incidence during the night.

Insulin duration and activity times vary greatly among different insulin types, from individual
to individual, from circumstance to circumstance, and even for the same person using
different injection sites. Therapists are encouraged to learn more about the particular insulin
type(s) a client is using, the dosing method, and how they react to their insulin.
Insulin Administration
Insulin is protein based – if taken orally it is broken down in the gastrointestinal tract. It is
therefore administered by injection, usually subcutaneously.
Insulin can be administered in two different ways:

• multiple daily injections (MDI)
• via an insulin pump
Injection
Managing blood glucose levels may require up to four
insulin injections per day. Clients are generally well
trained in self-injecting insulin in various body locations.
Commonly used areas include:
• the abdominal wall
• the lateral arm
• around the waist and hips
• the thigh
Insulin injected in the vicinity of the stomach appears to have the fastest onset of action. The
second fastest is usually the arm, while slowest onset occurs with injection into
the thigh. The diabetic individual will consistently vary injection sites.
External Insulin Pumps

Insulin pumps are a more recent innovation. They are devices that can be programmed to
automatically release insulin. Worn externally and connected to the diabetic’s bloodstream via
a catheter, design improvements are making insulin pumps increasingly smaller and more user
friendly. If the ultimate goal is to create a device that monitors the diabetic’s blood glucose
and releases insulin exactly as needed (as occurs in the non-diabetic body) insulin pumps have
not yet reached this level. However, many diabetic experts now favor insulin pump use over
injections. The pump offers the user many benefits:
• more ease in carrying and administering insulin
• better blood sugar control
• flexibility of eating patterns
• easier involvement in sports and other activities

The insulin pump consists of several parts:
• a reservoir for insulin
• a small battery-operated pump
• a computer chip that controls insulin delivery
Current versions of the pump are about the size of a deck of cards, weigh about three ounces,
and can be worn on a belt or in a pocket. Connected to the pump is a flexible plastic tube
ending with a needle that is inserted just under the skin in the abdominal area. The site of the
needle is changed every few days. The user programs the pump to deliver a steady amount
(basal dose) of insulin throughout the day. Following meals or at other times when blood
glucose may be high, the user can direct the pump to release a ‘bolus’ dose of insulin.
Other devices that are being tested or are in early use for administering insulin include:
• insulin pens
Insulin pens are a convenient and discreet way to carry insulin. A fine, short needle sits at the
tip of the pen. The user turns a dial to select the desired dose of insulin and presses a plunger
to deliver it. The pens are either disposable or have replacement insulin cartridges.
• insulin jet injectors

These injectors use a high-pressure air mechanism instead of a needle to send a fine spray of
insulin through the skin.
• implantable insulin pumps

These pumps are surgically implanted and can be programmed to deliver insulin in a basal dose
or continuously as needed. Researchers hope that in the future this type of pump will become
a device that can react in the same ways the body would to increased blood glucose.

• insulin inhalers
These are under development and close to clinical trials. The insulin used is specially
manufactured so it can be sprayed and inhaled into the mouth. The insulin coats the mouth,
throat, and tongue and is rapidly absorbed into the bloodstream. These inhalers will most
likely be used in combination with other methods of insulin administration.
Mechanism of Action
Insulin influences the production, transport, and utilization of glucose. Specific insulin
receptors are located on cell membrane surfaces. When insulin binds to an insulin receptor a
series of intracellular biochemical reactions takes place to produce a number of biological
compounds. It is believed that these compounds act as second messengers within the cell to
facilitate its uptake of glucose and/or to increase its glucose storage. Several intracellular
substances including calcium are necessary to these processes.
insulin
cell receptor intracellular molecules
for insulin reactions
Ca++
cellular uptake
and storage
of glucose
glucose
glucose in
entering cell
bloodstream
Most cells have insulin receptors on their cell membranes and are referred to as insulin
dependent cells. However, brain and kidney cells, red blood cells, and those lining the GI
tract do not have insulin receptors. They are able to absorb and use glucose in the
absence of insulin stimulation. These cells are referred to as insulin independent cells.
2. ORAL HYPOGLYCEMIC DRUGS

The oral hypoglycemic drugs are used to lower blood glucose levels. They are subdivided
into four main categories:
• the sulfonylureas
• the biguanides
• competitive inhibitors of intestinal brush-border alpha-glucosidases
• the thiazolidinediones

Sulfonylureas
The sulphonylureas support insulin release and are only helpful when the person’s pancreas
is capable of producing insulin. They are commonly prescribed in combination with diet and
exercise therapy in the long-term management of type 2 diabetes. They are not effective for
type 1 diabetes.
Uses
• type 2 diabetes
• used in conjunction with insulin injections if large amounts of insulin are needed
Commonly prescribed medications in this group include chloropropramide (Diabinese) and

glipizide (Glucotrol).
Mechanism of Action
The sulphonylureas promote insulin release from the pancreas. Insulin production is not
actually increased, but its secretion from beta cells is. In addition, these drugs appear to
enhance the sensitivity of the peripheral tissues to insulin, facilitating glucose uptake into
cells. The overall effect is a reduction in blood glucose. Since these drugs increase blood
insulin levels, they can potentially precipitate hypoglycemic episodes. This issue will be
discussed later in the chapter.
Biguanides
Metformin (Glucophage), a member of this group, has been in use worldwide for the past four
decades. It not only lowers blood glucose but also reduces the risk of atherosclerosis
development by lowering blood cholesterol and triglyceride levels.
Uses
• managing type 2 diabetes when other drugs are ineffective
• combines well with the sulfonylurea drugs to enhance effects
• for patients who show signs of insulin resistance and are obese
Mechanism of Action
The biguanide drugs use a different method than the sulphonylureas to lower blood glucose.
Rather than acting on the pancreas, they target the peripheral tissue cells. Their exact
mechanisms of action are still unclear, but they appear to:
• decrease hepatic glucose production

• decrease intestinal absorption of glucose from food sources
• increase peripheral glucose uptake and utilization by improving insulin
sensitivity in skeletal muscle and fat cells

Two advantages of this group of drugs are that they do not typically cause hypoglycemia, and
they do not promote weight gain. In fact, they are also used to manage some of the
complications associated with insulin resistance that are commonly seen with obesity.
Gastrointestinal distress (stomach upset, cramps, nausea, and vomiting) are common side
effects of the biguanide drugs. These types of GI tract activity can lead to increased
elimination of vitamin B12. Signs of B12 deficiency include fatigue, depression, easy bruising,
skin sensitivity, peripheral neuropathy (numbness and tingling), and loss of appetite.
Alpha-Glucosidase Inhibitors (Starch Blockers)

This class of drugs was first released in the United States in 1995. Their potential for use in
combination with the sulfonylureas and biguanides makes them an important addition to the
medications available for managing type 2 diabetes.
Uses
• type 2 diabetes
A commonly prescribed example of this group is acarbose (Precose).
Mechanism of Action
These drugs act in the intestines by reversibly inhibiting the alpha-glucosidase enzyme. The
role of this enzyme is to break down complex carbohydrates into glucose. Carbohydrate
absorption is forced to take place further along the gastrointestinal tract, producing a more
gradual and delayed rise in postprandial blood glucose concentration.
Thiazolidinediones (TZDs)
This new class of hypoglycemic drugs first became available in the United States in 1997. An
early member of the group, troglitazone, was withdrawn from the market in March 2000
because it was seen to cause severe idiosyncratic liver injuries. Rosiglitazone (Avandia) and
pioglitazone (Actos) have been available since 1999 and have safer profiles.
Uses
• type 2 diabetes
Mechanism of Action
Studies suggest that these drugs increase cell membrane sensitivity to insulin and normalize
a wide range of metabolic problems associated with insulin resistance.
TZDs act on a specific receptor called the peroxisome proliferator activated receptor gamma
(PPAR gamma). PPAR gammas are predominantly found in adipose tissue, macrophages,

vascular smooth muscle cells, endothelial cells, and several cancer cell types. These are all
target tissues for insulin and when stimulated show increased insulin sensitivity.
Beneficial effects of the TZDs include:
• improved glucose uptake in skeletal muscle, adipose tissue, and hepatocytes

• reduced fasting hyperglycemia and insulinemia
• decreased plasma triglyceride, free fatty acid, and LDL-cholesterol levels
• increased plasma HDL-cholesterol concentrations
Biguanides
Sulfonylureas • Decrease liver Alpha-Glucosidase
• Promote release of glucose production
Inhibitors
insulin from the and intestinal
pancreas absorption of • Act in the intestines
glucose to inhibit the enzyme
• Increase the
sensitivity of • Increase peripheral alpha-glucosidase
peripheral tissue glucose uptake and • Delay digestion
cells to insulin utilization and absorption of Thiazolidinediones
complex
• Increase glucose
carbohydrates
uptake in muscle
and fat cells and in
the liver
• Decrease blood
triglyceride, fatty
acid, and cholesterol
levels
Blood glucose levels

are reduced.
Actions of the oral hypoglycemic drugs

SIDE EFFECTS – Drugs for Managing Diabetes
Insulin Sulfonylureas Biguanides Alpha-glucosidase TZD

Side Effects Inhibitors
Abdominal Cramps XX XX XX
Allergic Reactions XX
Anemia X
Blurred Vision X
Bloating XX
Blood Dyscrasias XX
Bruising XX
Confusion X
Constipation X
Drowsiness X
Diarrhea X XX XX
Dizziness X XX
Edema X
Fatigue X XX
Flatulence X
GI Distress XX XX
Headaches X
*Lipodystrophy/Lipohypertrophy X
Liver Dysfunction XX XXX**
Hypoglycemia XXX XXX
Metallic Taste X
Muscle Weakness XX
Nausea X
Paresthesia XX
Photosensitivity X
Rashes X XX
Tinnitus X
Tremors X
Vertigo X
Vit B12 Deficiency XX
Vomiting XX
Weakness XX
Weight Gain XX
Weight Loss X
* refers to changes in the subcutaneous fat at injection sites

** blood tests to monitor liver function are done frequently


Diabetic Instability Reactions
Diabetics are constantly challenged to find the right balance between insulin and blood
glucose. Blood glucose levels that are either too high or too low can cause a number of
symptoms, at their worst progressing to life-threatening destabilization. Even though
medications are central to diabetes management, their use can also be a factor in diabetic
instability episodes.
Hyperglycemia, which is the ‘natural’ diabetic condition, can jeopardize tissues like the brain
whose cells uptake glucose without assistance from insulin and can reach toxic levels if blood
glucose becomes too high. Severe hyperglycemia produces a state called diabetic coma.
Pharmacologically, hyperglycemia can occur from underjudging medication requirements,
from using an insulin product that is not a good match for the patient’s needs, from missing a
dose, or as a medication side effect.
On the other hand, if the diabetic misjudges and uses too much insulin, or does not eat enough
to match insulin intake, or takes too much or too powerful an oral hypoglycemic drug,
available glucose is mobilized into cells and the blood glucose level can become seriously
low. This is called insulin shock. It can be difficult to judge doses on a day-to-day basis
because, as we will discuss shortly, a number of circumstances can alter the diabetic’s
pharmaceutical requirements. Insulin shock can also occur as a medication adverse effect.
In severe or untreated diabetic instability crises, loss of conscious, convulsions, and eventual
death can occur.
Episodes of diabetic instability can onset rapidly or more slowly. In general, hypoglycemia
onsets more quickly and hyperglycemia onsets over a few days. The table below is a quick
reference for signs and symptoms of hypo- and hyperglycemia.
HYPOGLYCEMIA HYPERGLYCEMIA
(leads to insulin shock) (leads to diabetic coma)
stomach pains abdominal pain

hunger anorexia
nervousness thirst
shallow breathing air hunger
pallor and fatigue shortness of breath
sweating facial flushing
weakness polyuria
continuing headaches headaches
tachycardia weight loss
unsteady gait nausea and vomiting
confusion acetone breath
moist and pale skin dry and flushed skin
convulsions constipation
normal eyeballs soft eyeballs

First Aid for Diabetic Instability Episodes
Since diabetic instability can become life-threatening, it is important to have a good
grasp of first aid guidelines. The more the person giving assistance is familiar with the
diabetic person, the more tailored the reaction can be. Unless expert, the first aid
provider should not assume that he or she can distinguish between insulin shock and
diabetic coma. The general rule is:
Always give sugar; never give insulin.
The majority of diabetic destabilizations are insulin shock, so giving sugar is usually
effective. The sugar source must be in a form that is rapidly absorbed (e.g., fruit juice,
candy/chocolate, banana). If the person is not fully conscious, be cautious about
choking risk – place the sweet substance in the cheek pouch or under the tongue.
If it turns out that the person is having a hyperglycemic episode, added sugar will not make
a significant difference in the short term. On the other hand, giving insulin if the person is in
insulin shock could prove fatal.
Having given sugar, keep the person warm and comfortable and watch for improvement.
If you do not see good signs of recovery within 5-10 minutes medical intervention should
be sought.

It is important to remember that there is a great deal of individual variation in what leads to
hyperglycemic and hypoglycemic episodes. Thresholds can change in the same person based
on a number of physical and life circumstances. In general, the better the person’s overall
health and medication stability the more resilient he or she is, but it is good to be prepared and
not depend too much on predictable patterns.
Common examples of factors that can predispose to developing hypoglycemia include:
• incompatible medication type, diabetic medication change

• insulin overdosage
• beginning a new medication of any type (e.g. antibiotic, analgesic)
• drug interactions
• alcohol consumption
• skipping meals/fasting/anorexia
• excessive exercise workouts
• insufficient sleep/sleep disorder/insomnia
• increased stress and anxiety
• significant recent injury
Factors that can predispose to developing hyperglycemia include:
• insufficiently powerful insulin, oral medication dosage is too small

• skipping a dose, irregular medication habits
• drug interactions
• increased psychological or emotional stress
• infection or disease
• alcohol consumption
• high sugar, fast food diet
• thiazide diuretic use
• long-term use of corticosteroid medications
• undiagnosed/untreated diabetes

Quick Guide to Case History Taking for Diabetics
Diabetics can range from having very good health to being quite ill and frail. Case history taking
is key to being able to establish a safe and appropriate treatment plan. Very unstable diabetics
are not good candidates for massage – it is important to evaluate stability of the diabetic
condition and the medication use.
Questions
1. General health, presence of any other conditions.
2. Type of diabetes and date of diagnosis.
3. Progression of the condition. Is it stabilized? Regular medical monitoring?
4. Pharmaceuticals used: insulin, oral medications? Get specifics about types. Taking
medications for any other reason? Get specifics.
Stability of Medication Regimen: Any medication problems? Any recent changes?
If taking insulin, by injection, pump, or other device? Where are the usual sites?
Most recent site?
5. Any recent diabetic crisis? Date, nature of the episode, outcome. Frequency of
destabilizations? Best sugar source to use if client destabilizes – does he or she keep a
supply on hand? Where? Discuss how to proceed if a destabilization occurs.
6. Kidney and cardiovascular health. These systems are generally compromised in
diabetics, especially those who have had the disease for more than 10 years.
CV System: Hypertension, atherosclerosis, history of heart attack or stroke, heart failure
status? Typical BP reading? When last taken and value?
Kidneys: Frequent kidney infections or stones? Kidney failure status?
7. Peripheral tissue status. Any neurovascular changes: tingling, numbness, reduced
sensation anywhere? Leg cramps, muscle weakness? Open sores or lesions – how
managed? Any problems with delayed healing? Any history of gangrene? If yes, get
details. Any amputations?
8. Any problems with vision? Any other diabetic complications?
9. Any current ‘bugs’ or infections?
10. Usual home hydro and exercise practices – any MD restrictions on these? Medically
supervised exercise plan? Glucose stability usually good during exercise?
11. When was the last dose of medication or insulin taken? Last meal? Last glucose level
check? Determine peak stability period.
12. Had massage therapy before? If yes, well tolerated?
Observations
1. Observe for:
• texture and moisture of the skin
• areas of discoloration, open sores or lesions
• fungal infections
• bruising; inquire about how long it takes to resolve
• distal edema
2. Check for locations of altered sensation.

3. With advanced cases of diabetes and significant vascular compromise, a ‘line of
demarcation’ may be observed. This is a defined area on the skin, especially on the lower
extremity, suggestive of poor tissue distal to the line.

Quick Guide to General Treatment Issues with Diabetic Clients
Treating the client with diabetes for stress reduction or musculoskeletal complaints occurs
quite commonly in massage therapy practice. Some general guidelines are offered here.
It is important to also take note of the medications related guidelines coming next in this
chapter.
1. Therapists must consider the pathophysiologic changes in the vasculature and

connective tissues that occur with diabetes mellitus. It is important to have a clear
picture of how resilient the tissues are, especially in the extremities, and whether there
is sensory loss. Healing times can be prolonged and healing quality may be poor. In
the advanced stages of diabetes the connective tissues can be very fragile and
easily injured.
2. With a new client shorter specific sessions are recommended at the beginning. This
approach gives both therapist and client the opportunity to monitor responses to
treatment and make adjustments progressively. Approach hydrotherapy modality
use in a similar way.
3. Diabetics are more susceptible to infection and have more difficulty resolving
infections. Hygienic practices are a priority, especially around areas of skin fragility or
open lesions. Avoid treating vulnerable diabetic clients if you are sick yourself.
4. Keep in mind that there is an increased likelihood of cardiovascular and kidney

systems compromise with longerstanding cases of diabetes. Treatment planning
needs to take into account the whole picture of the client’s health status.
5. Assess the client’s stability before each session. Clients will try to be on time for their
appointments and sometimes rush to do so. This can precipitate a period of mild
hypoglycemia in a diabetic. If a client arrives in a rush, allow him or her to rest for a few
minutes and have a light snack or juice as needed to restabilize. Consider whether the
treatment plan must be modified for this session or whether it is better to re-schedule
the appointment. Diabetic clients should always feel confident that they can
reschedule with you rather than receive massage when they are not feeling stable.
Massage Guidelines – Clients Using Medications for Diabetes Mellitus
General Guidelines
1. Diabetic stability and medication stability are inextricably linked in most diabetics.
For treatment planning, hydrotherapy, and exercise recommendation, the key issues
revolve around stability, and whether the proposed treatment might promote instability
in some way. Consider carefully the general health status of the client, the
medications routine, whether there have been any recent medication problems or
changes of any type, whether any destabilizing factors are present in the situation (see
the information provided earlier in this chapter), and the daily life practices and
tolerances of the client.

2. Diabetic clients know when they are experiencing signs of destabilization and are
usually able to inform you. Discuss this possible scenario with the client in advance
and determine a plan of action. The client should not take medication when
destabilizing unless having been specifically instructed to do so by the physician. Any
acute destabilization is an absolute contraindication to massage.
3. As a general rule, massage therapy should be avoided during periods of medication

change. This applies to changes in medication type, scheduling, or dosage. It is best
to monitor the reaction to the new drug therapy for a week or two before resuming
massage treatments. Wait until the situation has stabilized, especially with type 1
diabetics.
4. Scheduling of massage treatments must relate well to the type(s) of medication used.
Massage, hydrotherapy, and exercise are all stimuli that increase metabolic activity
and consequently have the potential to precipitate a hypoglycemic effect. Unless the
client has prior experience with massage therapy, it is at first something of a ‘guess’
how strong the effect might be. Best practice is to determine the peak bioavailability
time of the client’s diabetic medication and schedule massage appointments then. It is
also important for the client to have eaten sufficiently before each session. Discuss
these logistics together, and if necessary with the physician, to determine how best to
schedule appointments.
5. Diabetics develop cardiovascular and other system complications over time. These
often involve medication controls, for example for high blood pressure or heart failure.
Keeping in mind that multiple medication mixes will tend to promote a higher
incidence of adverse or toxic reactions, be alert for signs and symptoms.
Guidelines Related to Insulin Sites
1. For clients using insulin injections or external pump devices, review the section entitled
Working Around Injection Sites, Skin Patches and Implant Devices in Chapter 5.
2. Do not apply local hydrotherapy modalities or use any direct manual techniques over
recent sites. The various types of insulin have specific onsets of action; massaging or
applying hydrotherapy at the site can alter the insulin pharmacokinetics.
3. Insulin dependent diabetics, especially those who have had the condition for some
time, often have old injection sites that they have stopped using because of
degenerative tissue changes at the site. These tissues tend to be very fibrous on
palpation, often have a ‘hollowed out’ appearance, and lack normal tissue color and
temperature. They also generally have poor local sensation. These sites can cause the
same types of problems as matted scars do, for example, reducing range of motion,
causing painful ‘tugging’ on nearby structures, and creating pockets of distal edema.
The massage therapist may consider using aggressive modalities like deep heat and
friction therapy to address such formations. While hydrotherapy, stretching, and direct

manual techniques can play a role in making these tissues more compliant, this type
of treatment approach must always be considered carefully in light of the problems
with tissue and circulatory integrity that diabetics can have, especially in the
extremities. Each case requires cautious thought and consultation as needed.
Guidelines Related to Oral Hypoglycemic Use
1. Sulfonylureas
These drugs can promote more rapid hypoglycemic destabilization. Be on the alert for
signs of hypoglycemia, such as tingling in the fingers, headaches, blurred vision, and
increased perspiration.
Drug Interaction Alert

Therapists should be aware of the potentially life-threatening drug interaction between
the sulfonylurea drugs and members of the NSAID group including aspirin. A type 2
diabetic client with a musculoskeletal complaint may inadvertently use an OTC pain
preparation without knowledge of this fact. The NSAIDs and the sulfonylurea drugs
compete for the same sites on the plasma protein albumin.1 With greater binding of the
NSAIDs to albumin, more of the sulphonylurea drug remains 'free' or unbonded in the
blood. Since the free drug will interact with pancreatic cells to promote insulin release,
the client is at risk of developing hypoglycemia (insulin shock).
NOTE: Garlic also seems to increase the levels of insulin in the blood.
Rashes and other skin sensitivity reactions can occur with the sulfonylurea drugs. Do
not massage on-site; adapt client positioning to avoid traumatizing the affected skin or
increasing discomfort.
Paresthesias can be a side effect of these drugs, resulting in altered sensation and
reduced accuracy of client feedback.
2. Biguanides
Generalized fatigue and weakness can be side effects of this group of drugs. You may
need to shorten your treatment time or consider more specific regional approaches.
Complaints of muscle cramps, muscle weakness, and numbness and tingling may be
related to electrolyte loss or vitamin B12 deficiency. Muscles and their tendons may
be hyper-or hypo-responsive to the application of standard manual techniques.
The biguanides are often associated with easy bruising. Technique depths should be
modified as a matter of course. Use of more aggressive techniques like muscle
stripping, skin rolling, and cross fiber frictions is not advised.

3. Starch Inhibitors
Encourage clients to “use the bathroom” before the massage session. Gas and bloating
are among the common side effects of these drugs. Therapists must show sensitivity
to unexpected episodes of flatulence since this is a side effect of the medication that
can be heightened by massage work.
4. Thiazolidinediones
Be alert to complaints of fatigue. This group of drugs can cause low blood hemoglobin
levels and anemia. When this type of blood disorder is present it is also important to
keep in mind that the client will be predisposed to bruising easily.
Headaches and edema are also fairly common side effects of these drugs. If such
complaints are not being improved after a reasonable number of massage treatments,
recommend medical evaluation.
Stability is again the key issue. Consider the client’s diabetic stability each time before using
a hydrotherapy modality. Begin with mild approaches and proceed carefully.
With advanced diabetic conditions full body systemic hydrotherapy treatments such as
whirlpools, saunas, and full baths are not recommended. The heat associated with these
treatments increases the workload of the heart and the metabolic demands of the body.
Hypoglycemic reactions are likely to occur despite medication controls. Such modalities are
also likely to be unsafe based on the cardiovascular status/medications of the client (see
Chapter 7).
Remember to identify injection sites and areas of sensory impairment and adjust the
hydrotherapy approach accordingly.
Regular mild to moderate exercise activity promotes glucose utilization by the musculature
(decreases blood glucose levels), improves the health of the circulatory system, and builds
muscle and bone mass. However, because of the additional glucose uptake by exercising
tissues, exercise has the potential to be destabilizing. Types of medication, dosage, and
medication routine are important considerations in determining the nature and scheduling of
exercise programs. Ask about current activity levels and build the exercise plan around the
client’s lifestyle. With advanced cases of diabetes it is best to consult with a health care team
that provides the services of a qualified exercise therapist.
The sulfonylurea drugs increase skin sensitivity to sunlight, so suggesting protective clothing
and exercising in shaded areas will be beneficial.

Gastrointestinal irritations like diarrhea and vomiting can predispose the client to dehydration
and electrolyte deficiencies. Encourage proper hydration and nutrient replacement. If muscle
cramps or spasms occur the client should stop the activity instead of trying to ‘work through it.’
The client may feel generally fatigued and weak. When exercise intensifies these effects,
reassess the frequency, intensity, and duration of the exercise program.
1. Freeman Clarke, J.B., et al., Pharmacological Basis of Nursing Practice, 4th ed., pg, 810, Mosby
Year Book Inc., Missouri, 1993

CHAPTER 9
Drugs for Managing Respiratory

Inflammation and Congestion
Trachea
Bronchi
Bronchiole
Alveoli
Right Lung Left Lung
The respiratory system is responsible for the exchange of oxygen and carbon dioxide between
the body’s tissues and the air. Oxygen is inhaled and added to the circulating blood, while
carbon dioxide is removed from the blood and exhaled as a waste product. Any respiratory
system factors that disrupt this normal exchange mechanism, such as infection, disease, or
chronic irritation, can eventually lead to a form of chronic obstructive pulmonary disease.
Chronic obstructive pulmonary disease (COPD) is a degenerative state involving significant

loss of lung competence to perform the function of ventilation. Respiratory conditions that
commonly contribute to COPD include asthma, bronchitis, and emphysema. The American
Lung Association provides the following statistics, current to 1998, from national surveys and
reports about these three conditions:1,2,3
• the annual economic cost of asthma is about $12.7 billion dollars

• 14.6 million people report having asthma
• asthma is the most common chronic disease in children and causes about 300
childhood deaths each year
• 8.9 million Americans currently have a physician’s diagnosis of chronic
bronchitis
• 3 million Americans are diagnosed with emphysema

CONDITIONS THAT COMMONLY CAUSE COPD
Asthma
Asthma is characterized by smooth muscle spasm, inflammation, and increased mucus
production in the bronchioles. These are the results of mast cell breakdown to liberate
proinflammatory substances including prostaglandins, leukotrienes, bradykinins, and
histamine. The overall effect is congestion, compromise of air passage diameters, and
impaired respiration. Asthma has both acute (asthma attack) and chronic presentations,
and at its most serious can be life-threatening. Shortness of breath, wheezing, and
coughing are experienced in varying degrees of severity.
Asthma is usually activated by allergic or hypersensitivity responses to inhaled substances
like pollen, pollutants, and dust, but can also be a reaction to ingested foods and some
drugs (e.g., aspirin and other NSAIDs, beta blockers), and a sequela of respiratory tract
infections. The causes of asthma are not fully understood.
Emphysema
Emphysema is a degenerative condition characterized by the development of large
empty spaces (bullae) in place of alveolar clusters, destruction of alveolar capillary beds,
and decreased elastic recoil of the lungs. These changes occur over time in response to
irritation and damage, mostly from smoking, but sometimes from occupational or other
exposures to polluted environments.
Emphysema is a dyspneic condition, meaning that it is characterized by shortness of
breath. If the person has a cough it is usually because of concurrent chronic bronchitis
in a long-term smoker or presence of an infection. Individuals with emphysema have
trouble getting enough oxygen through the lungs and into their body tissues; as the
condition progresses they often need supplementary oxygen. The dyspnea is especially
noticed when exhaling – the person has to recruit the accessory muscles of expiration.
Chronic Bronchitis
Chronic bronchitis is characterized by increased mucus activity and congestion,
productive cough (material is coughed up), and a tendency to recurrent respiratory
tract infections. It is a set of degenerative changes in the immune and clearance
functions of the bronchial passageways rather than a distinct disease state. Chronic
bronchitis is generally diagnosed when, in the absence of other pathologies, a cough is
present for at least three months of the year over two consecutive years.
The cause of chronic bronchitis is usually long-term smoking; it can also result from
prolonged respiratory irritation/allergies or repeated bouts of acute bronchitis.
Normal respiratory function involves a combination of good gaseous exchange capacity and
efficient musculoskeletal action to move the thorax. Respiratory disorders often result in
unbalanced use of muscles and stress on joints of the ribcage and thoracic spine, causing
muscle and joint discomforts that can bring a client to massage therapy. For example,
long-term tightness and overuse of the muscles of inspiration often produces ‘barrel chest,’
where the thorax is held in an upward, distended position.

Muscles of Inspiration Muscles of Expiration
Primary Primary
diaphragm none (passive process)
internal intercostals Secondary
Secondary abdominals
scalenes external intercostals
sternocleidomastoid low back muscles
pectoralis muscles
upper trapezius
levator scapula
quadratus lumborum
Upper Respiratory Tract

consists of nasal cavities,
sinuses, pharynx, tonsils,
Respiratory and larynx
System
Lower Respiratory Tract
consists of trachea, bronchi,
bronchioles, and alveoli
Signs and symptoms of respiratory irritation and disease can include:

rhinorrhea (runny nose), face pain and pressure from sinusitis, the sore throat
of laryngitis, productive and non-productive cough, chest pain, dyspnea
(shortness of breath), increased phlegm and mucus production,
musculoskeletal disorders of the neck and thorax, altered breathing patterns,
wheezing, reduced tissue integrity and cyanosis in the extremities, and
clubbing of the fingertips and nailbeds.
When pharmaceuticals are used to manage respiratory congestion and inflammation the
overall effect is to improve clearance of the air passages and optimize conditions for gaseous
exchange in the lungs.
The medications discussed in this chapter include those that:
• treat/manage allergic reactions

• increase airway diameter
• manage respiratory congestion
• suppress coughing

1. DRUGS THAT TREAT/MANAGE ALLERGIC REACTIONS
Antihistamines
The antihistamines are used to control the actions of histamine, which is one of the primary
mediators of the inflammatory response. Rather than reversing current symptoms, they act to
reduce histamine’s ability to produce further effects. Many types of antihistamines can be
purchased without a prescription, and are sold either alone or in combination with other drugs.
Common examples include diphenhydramine (Benadryl) and chlorpheniramine (Chlo-Tripolon).
Histamine
Histamine is an endogenous compound produced and stored in cells, especially mast
cells and blood-borne basophils. It is found in most tissues of the body but is especially
prevalent in the gastrointestinal tract, in the respiratory and cardiovascular systems, and
in certain areas of the central nervous system. Mast cells reside in the connective tissue
membranes that surround blood vessels, nerves, lymphatic tissues, and all organs. Other
cells that make histamine are found in and around parts of the CNS, in tissues undergoing
healing, in the gastric mucosa (mucous membrane), and in epidermal cells.
In order to produce its effects, histamine must be released from the cells that are storing it.
Most typically, this happens in response to tissue injury or infection and in allergic (antigen-
antibody) reactions. Histamine release usually occurs in the presence of bacteria, viruses,
and perceived antigens such as dust, pollen, and some foods, but any number of
substances may act as antigens, including pharmaceuticals. Other factors that can cause
histamine release include cold, physical exercise, and deep pressure into tissues.
Common reactions to histamine release include runny nose, watery eyes, and itchy skin. The
table below lists other more serious effects of histamine.
Body Tissues Effects of Histamine
Heart Increases the rate and force of contraction, decreases the

atrioventricular conduction rate.
Constricts venules, dilates arterioles. This causes plasma leakage

Blood Vessels and edema formation. Generalized release can lead to
hypotension.
Bronchioles Very powerful bronchoconstrictor. Can cause breathing difficulty.
Exocrine Glands Increases salivary, bronchial, and lacrimal gland secretion. Also
increases nasal mucosa production and secretion.
Increases smooth muscle contraction and gastric secretion; can

Gastrointestinal
cause epigastric distress.
Skin Eczema, purpura, urticaria.
Seems to act as a neurotransmitter to generate wakefulness, but

Central Nervous System its exact role is unclear.

Uses
The antihistamines are used in the management of:
• allergic/hypersensitivity reactions
• motion sickness, nausea, vertigo
• insomnia
• cough
• Parkinsonism and related symptoms
Mechanism of Action
Histamine binds with two cellular receptor sites: H1 and H2 receptors. H1 receptors are
primarily located in the gastrointestinal tract, the CNS, and vascular and respiratory smooth
muscle, while H2 receptors are largely found in the GI tract and are mainly involved in gastric
acid secretion.
Antihistamine drugs compete with histamine

for these receptor sites on cell membranes.
The antihistamines discussed in this chapter
target H1 receptor sites.
Because histamines cross the blood-brain

barrier and occupy receptor sites that seem
to be important in wakefulness, drowsiness
is a well-known side effect of antihistamine
medications. They are sometimes used
intentionally to produce sedation. Newer
antihistamines such as Hismanal, Claritin,
and Seldane have been designed to have less
of a sedative effect.
Certain antihistamines (e.g., diphenhydramine) directly suppress the cough reflex center in
the medulla. They also seem to affect other CNS receptors, such as those that respond to
serotonin and acetylcholine, hence their potential for use in managing some CNS disorders.
histamine
antihistamine
occupying cell
receptor site
Cell histamine Cell
receptor sites
on cell membrane

Cromolyn Sodium
Cromolyn sodium stabilizes the membranes of the mast cells in the respiratory tract to prevent
release of proinflammatory substances including histamine. It is primarily used to prevent
bronchospasm when exposure to allergens or to other known predisposing factors is
anticipated. It is utilized alone or in combination with other medications, usually as part of
the management of asthma. Cromolyn is administered via a metered aerosol inhaler or by
using a spinhaler, which is a small hand-held propulsion device designed to facilitate deep
inhalation of medication in powder form.
Commonly prescribed forms of cromolyn sodium include Intal, Intal Inhaler, Nasalcrom,
Crolom, and Opticom.
2. DRUGS THAT INCREASE AIRWAY DIAMETER

The diameters of airway passages can be compromised by:
• inflammation: Respiratory inflammation is usually caused by
allergic/hypersensitivity reactions that result in release of inflammatory
mediators such as histamine, thromboxane, and the leukotrienes.
• hyper-responsiveness of the air passages: The exact reason for this is
unclear, but breakdown of endothelial cells due to irritants like smoking and
infections seems to be a contributing factor. Normally these cells produce
substances that act as bronchodilators to maintain the size of airway
passages. Loss of these cells appears to render the bronchiolar smooth
muscle more likely to hyperreact and go into spasm.
• reflex bronchoconstriction: Bronchoconstriction typically occurs in the
presence of irritating airborne substances, possibly via a protective neural
response. In some instances this response appears to become hyper-reactive
and the air passages go into excessive constriction.
Drugs used to enlarge airway passages include the:

• bronchodilators
• anticholinergic drugs
Uses
Both drug types can be used to:
• manage asthma, emphysema, bronchitis, bronchiectasis, and other chronic
obstructive pulmonary disorders
• manage/prevent exercise-induced asthma
• control allergic/anaphylactic type reactions
• relieve nasal/sinus congestion

Mechanism of Action
• bronchodilators
The commonly prescribed bronchodilators fall into two categories:
• the beta-adrenergic agonists or sympathomimetic agents; examples include
albuterol (Ventolin), fenoterol hydrobromide (Berotec), and epinephrine HCl
(Primatene Mist Solution)
• the xanthine derivatives of which theophylline is the prototype; examples
include Theo-24, Slo-bid, Slo-Phylline, and oxtriphylline (Choldeyl)
Beta-Adrenergic Agonists
In Chapter 7 the role of alpha and beta receptors in the cardiovascular system was discussed,
and mention was made of similar receptors in the lungs. The lungs have beta-2 receptors on
the smooth muscle cells of the respiratory passages. Sympathetic nervous system stimulation
of these receptors initiates a complex series of intracellular responses that results in
bronchodilation.
Beta-adrenergic agonists mimic the actions of the sympathetic neurotransmitter

norepinephrine by stimulating beta-2 receptors to produce dilation of bronchial passages.
These drugs also seem to stimulate the respiratory centers in the brain, and to stabilize the
membranes of cells like mast cells.
The most effective form of administration of the beta-adrenergic agonists is by inhalation. They
are useful during any stage of asthma, and as a pretreatment before exercise or allergen exposure.

Xanthine Derivatives
The xanthine derivatives, which resemble caffeine in chemical structure, stimulate
bronchodilation and improve mucociliary transport function. In addition, they seem to inhibit
intracellular activity that leads to smooth muscle cell contraction. Theophylline, the prototype
of the group, is also believed to suppress intracellular calcium release and inhibit
prostaglandin formation. In combination, these actions improve the size of airway passages
and the overall function of the respiratory system.
Mucociliary Transport System (Mucociliary Elevator)

The membranes that line the respiratory passages contain specialized cells whose purpose is
to clear foreign particles upward toward the throat. There are two types of cells involved in
this function:
• goblet cells: produce mucus that entraps the particles
• ciliated cells: have hair-like structures called cilia that mobilize the mucus out of
the respiratory system
Both types of cells can be damaged or eliminated by chronic irritation. When this happens the
person has to rely more heavily on coughing to eject foreign particles.
• anticholinergic drugs
In addition to beta-2 receptors, cholinergic receptors are also present in the smooth muscle of
the bronchial tree. They react to the neurotransmitter acetylcholine (ACh). When produced
by the parasympathetic nervous system, ACh acts on these cholinergic receptors to cause
bronchoconstriction. Drugs such as ipratropium bromide (Atrovent) block these sites and
reduce bronchoconstriction episodes.
Only a small percentage of respiratory patients (those who do not respond to or who show
sensitivity to the beta-adrenergic agonists and xanthine derivatives) use the anticholinergic drugs.
Beta-adrenergic
bronchial Agonist Drugs
air passage
Sympathetic
Nervous System The beta-adrenergic
stimulation of SymNS agonists mimic
beta-2
these receptors stimulation SymNS stimulation
receptors
produces of these receptors
bronchodilation. to cause bronchodilation.
Parasympathetic The anticholinergic drugs

PSNS
Nervous System block these receptors
cholinergic stimulation
stimulation of from receiving
these receptors receptors
PSNS stimulation,
produces preventing
bronchoconstriction. bronchoconstriction.
Anticholinergic
Drugs

3. DRUGS THAT MANAGE RESPIRATORY CONGESTION
Congestion of the respiratory passageways due to inflammation, irritation, or infection present

(singly or in combination) is typical of many respiratory disorders. Congestion and
inflammation of air passages not only reduces their diameter but can also progress to cause
poor gaseous exchange in the alveoli.
Signs and symptoms of respiratory congestion include runny nose, increased mucus and
abnormal sputum production, and productive cough. The drugs used to manage respiratory
congestion and inflammation include:
• decongestants
• expectorants
• corticosteroids
Decongestants
Decongestants act on the blood vessels that supply the mucosa lining the respiratory tract.
They stimulate alpha-1 adrenergic receptors located in the blood vessel walls to cause
vasoconstriction. Hyperemia, edema, and mucus production are all reduced. These effects
increase the size of bronchial and nasal airways and reduce the congestion associated with
respiratory disorders.
Decongestants are available in nose drops or nasal sprays, and in oral forms as tablets,
capsules, and syrups. Examples of commonly used drugs in this group include oxymetazoline
(Afrin, Coricidin), and pseudoephedrine (Sudafed).
Expectorants
Thickened mucus and static mucus plugs can seriously congest the respiratory tract and
impair gaseous exchange. Most expectorants (guaifenesin is the most widely used) activate a
series of reflexes that stimulate goblet cells in the mucosa to increase fluid production. Other
types, such as potassium iodide, act directly on the mucosal cells to produce the same effect.
The result is increased mucous flow that loosens accumulated secretions and reduces their
viscosity. At the same time the respiratory tract is lubricated. These effects allow the client to
produce a more productive and less frequent cough.
Corticosteroids
The corticosteroids control inflammation and have a number of uses in respiratory disease.
The availability of these drugs in several forms (aerosol sprays, tablets, injections, etc.) offers
versatility in the long-term management of respiratory disorders. The corticosteroids have
already been discussed in Chapter 6, and since they pose some concerns for massage
treatment planning the reader is advised to review this earlier information.

Bronchitis and bronchial asthma are often managed with corticosteroid nasal sprays. The
doses needed in nasal corticosteroids are much smaller than the oral or parenteral ones. It is
presently still unclear whether long-term use of these nasal preparations will have the same
side effects as oral doses, or lead to hyper- or hyposensitivity of the airways.
4. DRUGS THAT SUPPRESS COUGHING
Coughing is a response to irritation of the

respiratory tract. It can be either physiologic or
voluntary. It aids in removing mucus and
irritants to keep the lungs and bronchial tree
free of obstructions. A cough should be deep,
explosive, and effective in clearing the airways.
When problematic coughing episodes disturb
sleep or cause pain, cough suppressants, called
antitussive medications, are prescribed.
Antitussives
Antitussives prevent or relieve coughing
through a variety of means. Some, such as
dextromethorpham hydrobromide (DM in
cough and cold preparations) and the narcotic
analgesics, depress the cough center in the
CNS. Others, for example the antihistamine
diphenhydramine, inhibit the irritant effect of
histamine on the respiratory mucosa, while
benzonatate (Tessalon) has a local anaesthetic
affect on the respiratory tract.
Decongestants, expectorants, antihistamines, and analgesics are the usual primary

ingredients in most OTC cough and cold preparations. In combination they relieve
symptoms such as runny eyes and nose, sinus pressure, coughing episodes, and minor
musculoskeletal aches and pains.

SIDE EFFECTS – Drugs for Respiratory Disorders
Side Effects AH BD CS AT DC EX Side Effects AH BD CS AT DC EX

Abdominal Cramps XX Headaches XX XX XXX X X
Allergic Reactions X Hypertension XX X
Altered Taste XX X Hypotension XX
Anemia XX Insomnia XX X
Angioedema XX XXX Irregular Heartbeat XX X
Anorexia XX X X Joint Pain XXX
Anxiety X XX X Lightheadedness X XX X
Appetite Changes X X Liver Dysfunction X
Blurred Vision X Mood Changes XX
Blood Dyscrasias XX X Muscle Cramps XX
Bradycardia XX XXX Muscle Weakness X XXX
Breathing Difficulty X XXX XXX XXX Nausea XX XX XXX X
Bronchospasm XXX XXX Nasal Stinging XX
Bruising XX Nasal Stuffiness XX X X
Chest Pains XXX X Neuritis XX X
Chills XX Numbness XX
Cold Extremities XX Palpitations XX
Confusion X Paresthesia XX
Constipation XX Photosensitivity XX
Cough X X Rashes XX XXX X
Drowsiness XX X Restlessness X X X
Dry/Sore Eyes X X X Seizures XXX XXX
Dry Nose X X Shortness of Breath XXX XXX XXX
Dry Mouth/Throat X X X X X Sore Throat X
Diarrhea X X Sweating XX X X
Dizziness XX XX XXX X X X Tachycardia XX X
Dysrhythmia XX Thrombocytopenia XX
Dysuria X Tinnitus XX
Facial Flushing XX Tremors X XX X
Fatigue XX XX X Urinary Freq. Changes XX XXX X
Fever X XX X X XXX Vomiting X X X X X
GI Bleeding or Pain X Weakness X
Hallucinations XXX XXX Wheezing XX XX XX
AH: Antihistamines, BD: Bronchodilators, CS: Cromolyn Sodium, AT: Antitussives,

DC: Decongestants, EX: Expectorants


Quick Guide to Respiratory System Case History Taking
Compromise of the respiratory system results in reduced availability of oxygen and poor
removal of carbon dioxide, both of which can adversely affect the health of all the tissues and
systems of the body. It is especially important to note that diminished oxygen delivery to body
cells and resistance to blood entering the lungs place greatly increased stress on the heart.
Congestive heart failure is a common co-finding in long-term respiratory disorders.
Questions
1. Identify the respiratory disorder(s) for which the client is being treated. Time frame since
diagnosis? Progression of the condition?
2. How is the condition managed? Generally well stabilized? Medications, herbal
remedies, lifestyle changes, exercise regimen, etc.
3. If asthma or allergies, is it clear what the triggers/antigens are? Be thorough in asking
about allergies or sensitivities to oils, aromas, or other elements present in your clinic
environment.
4. Have there been any recent crises or hospitalizations? If yes, get details. Discuss how to
proceed if such an occurrence were to take place.
5. Is a pharmaceutical delivery device like an inhaler being utilized? Does the client need
to keep it handy during treatments? How is it used?
6. Other means of pharmaceutical delivery, e.g., skin patch?
7. Health of other body systems? Ask in particular about the heart (see Quick Guide in
Chapter 7) and blood pressure. Any other systemic disorders? How managed?
Medications for other disorders? Any drug combining issues?
8. Regular medical monitoring? When was the last physician visit?
9. Activity and energy levels? Exercise tolerance? Breathlessness episodes?
10. Have any restrictions been placed on exercise or hydrotherapy?
11. Smoking and drinking habits? (These can be aggravating factors.)
12. Sleep habits? Apnea? Any positions that are not comfortable to lie in?
13. Does stress have an impact on the condition?
14. Tissue health, especially in the extremities? Is healing time slower for cuts or injuries? Any
numbness or sensory impairment?
15. Aches and pains related to the condition? Postural problems?
Observations
1. Observe thoracic posture for hyperkyphosis, barrel chest, pigeon chest. Is there spinal
immobility, head forward posture?
2. Status of the muscles of respiration and spinal and thoracic joints - do the muscles look
tight or prominent? Does the person move stiffly? Is breathing visible, effortful?
3. Breathing patterns – apical, diaphragmatic, shallow, rapid? Mouth or nose breather?
Listen for wheezing sounds, watch for shortness of breath.
4. Observe for coughing, runny eyes, nose, etc.
5. Tissue health – look for bruises, varicosities, edema, etc. Skin and nail beds – pallor,
cyanosis, and fingernail clubbing are signs of hypoxia.

Quick Guide to Working with Clients with Compromised Respiratory Systems
Treating clients with respiratory complaints is not uncommon for the massage therapist. Massage
can be helpful in addressing musculoskeletal concerns, in promoting relaxation, and sometimes
in reducing congestion. Keep drinking water and Kleenex handy.
• Massage is not appropriate during an acute episode like an asthma attack, or if there is an
infection with fever.
• Consider the client’s cardiovascular status and adapt massage and hydrotherapy approaches
accordingly. The combination of a chronic respiratory disorder and a weakened heart can
‘double up’ on causes of dyspnea, high blood pressure, fatigue, and so on.
• Consider the integrity of the body tissues. With any long-term respiratory disorder the tissues
will tend to be more fragile and more easily injured; when injured they will heal more slowly
and with a poorer quality of repair.
• Shorter treatments are suggested at first to give both therapist and client an opportunity to
monitor responses to therapy. If unsure about how best to design a treatment plan given the
person’s health status, consult with the physician.
Client Positioning
• Nasal stuffiness, sinusitis, and other types of upper respiratory congestion are most compatible
with semi-supine or seated positions.
• Asthmatics may have difficulty lying flat in either prone or supine position because of a feeling
of not being able to get enough breath.
• Sidelying position is useful for treating the intercostals and abdominal oblique muscles and is
sometimes a preferred position for asthmatics.
• Towel rolls/small bolsters can be used to stretch
thoracic structures during massage treatment.
Place a comfortably sized ‘roll’ widthwise across
the table so that when the client lies back onto it
the positioning will be just below the inferior angles
of the scapulae (head level should not be lower
than the sternum). If the client finds this position too
uncomfortable, adjust the roll to a smaller size or try
a rolled towel laid lengthwise under the spine.
• Clients will generally benefit from specific work to the muscles of respiration and the joints ot
the thoracic spine. Direct manual techniques may need to be modified if there is significant
tissue fragility. Used appropriately, rib springing and joint play can also be highly effective in
mobilizing stiff joints.
• Tapotement on the back can reflexly trigger coughing episodes; it also appears to promote
bronchospasm, so it is not a good technique to employ with asthmatics. Clients with lower
respiratory tract congestion, for example from bronchitis or emphysema, can benefit from the
use of heavy tapotement to promote clearance, although intense coughing may be
triggered. This work is generally done in prone position with a large number of pillows under
the body and torso (the head is tilted somewhat downward) to promote drainage. This
specialized technique is usually performed by physical therapists – massage practitioners must
refer clients out for this work or consult carefully before proceeding. Note that both the
position and the technique are not appropriate if there is significant cardiovascular disease.
• Drainage techniques, including specialized lymphatic drainage if the therapist has been
trained, can be very useful in treating sinusitis or other types of upper respiratory congestion.

Muscle strains, nerve impingement syndromes, and rib fractures and dislocations can
severely restrict respiratory function. In many instances the client will benefit from
massage therapy. It is important to keep in mind that such clients are often taking anti-
inflammatories, cough suppressants, analgesics, and possibly other types of medications
to manage pain and inflammation.
Massage Guidelines – Clients Taking Medications for Respiratory Disorders
General Guidelines
1. Keep in mind that clients with respiratory disorders are often taking pharmaceuticals
in addition to respiratory medications, especially if they have cardiovascular
problems. Also, preparations geared to respiratory complaints may contain a number
of drugs that can influence massage treatment planning.
2. NSAID medications can intensify asthma. A client may use an OTC aspirin or
ibuprofen product for a musculoskeletal complaint, experience more breathing
difficulty, and as a result increase asthma medication use. Such situations should be
referred to the physician for further evaluation.
3. Side effects of dizziness, lightheadedness, and postural hypotension are common to

most of the medications discussed in this chapter. Monitor the client and be prepared
to shorten the treatment. Give specific post-treatment instructions to move slowly and
carefully when sitting up and getting off the massage table.
4. The drugs discussed in this chapter all have the potential to create or add to breathing
difficulties like shortness of breath, wheezing, and bronchospasm. Position the client
comfortably and allocate more time to work on the muscles of respiration. If the client
complains that breathing difficulty is increasingly becoming a problem, suggest
medical follow-up.
5. Dryness of the respiratory passages and mouth can cause episodes of throat irritation
and coughing during treatments. Keep some drinking water handy.
Specific Guidelines
1. Antihistamines
Central nervous system depression can compromise the normal responses of
connective tissues to manual techniques that involve deep pressure and stretching.
Inquire about the degree of drowsiness or fatigue present from the antihistamine use –
this information is your guide to determine the degree of CNS depression. If the client

is experiencing considerable fatigue or sleepiness you will probably need to give
shorter treatments with a more stimulating rather than relaxing focus.
Paresthesias, neuritis, and muscle weakness may occur. These require the practitioner
to modify depth of technique. Keep in mind that client feedback might be misleading.
Hypersensitive tissue areas should not be treated locally until the sensitivity has
decreased.
If anemia is present as a side effect of antihistamine use the client may bruise more easily.
2. Cromolyn Sodium
Angioedema reactions and skin rashes may be symptoms of a systemic allergic
response to this drug. The affected tissues become edematous and painful. Depending
on the intensity of the reaction the massage appointment may need to be rescheduled
until the situation is stabilized. If massage treatment is possible, ensure that the client
is positioned comfortably and avoid direct contact with the sensitive areas. Keep in
mind that nearby tissues may also be tender to pressure.
Client complaints of joint pain and muscle weakness may be related to side effects of
this drug. Assess/consult to determine if such complaints are actually drug side effects.
Changes in urinary function often occur. The client may need to interrupt the treatment
to use the washroom.
3. Bronchodilators
Cardiovascular and respiratory problems such as blood pressure changes, chest pain,
irregular heart beat, wheezing, and bronchospasm need to be monitored carefully. If
the doctor has evaluated these side effects and the client is okay for massage, adapt the
treatment to avoid causing additional stresses. Do not use tapotement, especially on
the back, since it can trigger exaggerated cardiovascular and respiratory reactions.
Numbness and vascular changes like increased bleeding time can occur with
bronchodilator use. Observe for signs of bruising and modify depth of technique.
Occasionally bronchodilator medications cause seizure disorders. Determine how the

situation is being managed and ensure that massage therapy is appropriate. If yes,
schedule your treatments to maximize medical stability.
4. Decongestants
Elevated heart rate and changes in blood pressure are the main concerns with
decongestant use. Stay informed about any cardiovascular system reactions the client
may be having and take blood pressure routinely. Review the guidelines in Chapter 7.
Seizures are also an occasional complication of decongestant use.

5. Antitussives and Expectorants
Dextromethorpham can cause altered sensory perception. The client may not give
accurate feedback about technique depth or hydrotherapy temperatures, and may be
prone to episodes of lightheadedness and disorientation. When such symptoms are
present to a significant degree, massage treatment can be an additional stress on the
body. Postpone massaging until after the physician has evaluated the medication use.
Since corticosteroids and narcotic analgesics can be utilized for their decongestant and
antitussive effects, refer to the information in Chapter 6 about these drugs. Their use
can have a number of implications for massage treatment design.
Before treating clients with respiratory conditions, make sure you are aware of any medically
indicated hydrotherapy restrictions. These may be related to a number of factors, including
cardiovascular status, medications being used, and asthma sensitivities.
Identify any sensitivities to essential oils and bath additives before beginning hydrotherapy
treatments. If unsure, start with water modalities only and introduce additives gradually.
Keep in mind that people with breathing difficulties may find the more intense hydrotherapy
modalities overwhelming.
If the client has medication-induced hypotension, systemic heat treatments are not
appropriate. This issue is discussed in more detail in Chapter 5.
Decongestant medications raise a concern about the use of heat treatments like steams and
saunas. Normal heat dissipation responses to temperature can be compromised, and the heart
may react in an erratic manner (palpitations, dysrhythmias, rising blood pressure). Monitor
blood pressure during any hydrotherapy modalities used.
Decongestant nose drops and sprays have more localized effects, but these should also
be taken into account in hydrotherapy decision-making. For example, facial steams can be
very effective in relieving upper
respiratory tract congestion, but
when a local decongestant is being
used, blood vessels in the nasal
passages will not vasodilate normally
in response to the heat stimulus.
Cough suppressant medications like

dextromethorpham and codeine can
alter temperature perception. All
hydrotherapy treatments should be
modified and the client should be
carefully monitored throughout the
treatment.

Mustard poultices are often used on the chest to reduce respiratory tract congestion,
especially with chronic bronchitis.
Several of the drugs prescribed for respiratory conditions can cause side effects like muscle
cramps and joint pain. Exercise can intensify these complaints without the client or
practitioner making the connection to a medication side effect. It is important to be aware of
the profiles of the drugs being taken before recommending exercises.
Antihistamines and decongestants can increase perspiration during exercise. Confirm that the
client understands the need to drink enough fluids and avoid becoming overheated.
Cardiovascular and respiratory problems like heart palpitations, hypertension, shortness of

breath, and bronchospasm can be worsened by exercise. Determine what the client’s normal
activity levels are and plan a program that is compatible.
Exercise prescription for the seriously compromised respiratory patient is a specialized field.
When a client has advanced emphysema, bronchitis, or asthma it is best to work with a health
care team that provides the services of a qualified exercise therapist.
1. American Lung Association, Trends in Asthma Morbidity and Mortality, January 2001
www.lungusa.org/data/asthma/asthmach_1.html#economic
2. United States Environmental Protection Agency, Asthma and Upper Respiratory Illness
www.epa.gov/children/asthma.htm
3. American Lung Association, “Estimated Prevalence of Lung Disease,” Lung Association Report
April 2001 www.lungusa.org/data/lae_01/lae.html#bronchitis

CHAPTER 10
Drugs for Managing

Mood and Emotional Disorders
The Canadian Mental Health Association describes mental illness as “the single largest
category of disease affecting Canadians.” According to a study published in Chronic
Diseases in Canada1 in 1998, depression and distress cost Canadians at least $14.4 billion
per year in treatment, medication, lost productivity, and premature death.
Mood and emotional disorders are also referred to as affective disorders, which are
sub-categorized into several distinct medical conditions. For the purposes of this text the
focus will be on anxiety, depression, and psychosis.
Everyone experiences episodes of anxiety and depression that arise from life situations,
for example:
• before a major exam

• having to give a speech to one’s peers
• following the death of a loved one
• after losing a job
These bouts of altered mood are usually normal and short-lived. They are part of change
and personal growth processes. During such times medications are sometimes used on a
short-term basis. However, when mood disturbances have a serious affect on health and
well-being, psychotherapy and ongoing medication treatment may become necessary.
Research suggests that biochemical imbalances in the brain contribute to disturbances of

mood and emotion. Chiefly involved are the neurotransmitters, which are molecules
produced in and released from nerve cells (neurons). They cross the synaptic gaps
between neurons in order to transmit signals from cell to cell. When these transmitters are
available as needed and in balance with each other, they play an important role in normal
expression and stabilization of emotion. Alterations in the actions, influence, and
availability of several neurotransmitters have been associated with specific mood
disorders. The neurotransmitters most commonly involved appear to be gamma-
aminobutyric acid (GABA), serotonin, norepinephrine, and dopamine.

NEUROTRANSMITTERS COMMONLY IMPLICATED
IN MOOD AND EMOTIONAL DISORDERS
Gamma-Aminobutyric Acid (GABA)

GABA is present in all parts of the CNS. There are two types of receptors for GABA:
GABA-A and GABA-B. Stimulation of the A type of receptor causes an increase in
intracellular chloride ion concentration; when the B receptors are stimulated cell
membrane permeability to potassium is altered. GABA’s effects are inhibitory – it is
considered the CNS’s primary inhibitory neurotransmitter. Anti-anxiety drugs such as the
benzodiazepines mimic the inhibitory actions of GABA through acting on the A receptors.
Serotonin (5-hydroxytryptamine or 5 HT)

Serotonin is found in three major body areas: in blood vessels, in the intestinal wall, and in
the central nervous system. Within the CNS, serotonin functions as an inhibitory
neurotransmitter and is involved in the regulation of mood, appetite, body temperature,
sleep, and sexual function. It also plays a role in pain control and suppression. Fourteen
main sub-types of serotonergic receptors have being identified. Reduced serotonin levels
have been correlated with aggressive behavior, irritability, sleep disorders, depression, and
eating disorders. Antidepressant drugs such as Prozac enhance serotonin functions.
Dopamine
Dopamine, synthesized in various areas of the CNS including the hypothalamus, the basal
ganglia (primarily in the substantia nigra), the frontal lobes, and the limbic system,
influences mood by producing the pleasurable sensations that accompany behaviors like
sex, eating, and being in control. It increases secretion of the hormones corticotropin and
growth hormone and inhibits the release of prolactin. Many chronic diseases result from
overproduction or underproduction of dopamine. Parkinson’s Disease, for example, is a
condition of dopamine underproduction. Symptoms of schizophrenia can occur when
dopamine flow throughout the nervous system is compromised. There are at least five
types of dopamine receptors. Several pharmaceuticals are used to improve dopamine
function in the CNS, including the anti-psychotic drug Thorazine.
Norepinephrine
Norepinephrine is also known as noradrenaline. It is a neurotransmitter found in the
autonomic nervous system (ANS) and generally in the CNS. A portion of the body’s
norepinephrine supply is produced from dopamine and released from areas located in
the pons and medulla of the brainstem. The supply for the ANS is largely manufactured in
the adrenal medulla. There are about eleven subtypes of norepinephrine receptors.
Depending on the type of receptor being stimulated, norepinephrine can have inhibitory
or excitatory effects. It is believed to play a role in regulation of several functions including
mood, arousal, focus, alertness, and blood pressure control. It may be responsible for some
symptoms of depression.

synapse
pre-synaptic post-synaptic
neuron neuron
neurotransmitter
receptor sites on
neurotransmitter post-synaptic
stored in vesicles membrane
Each neuron produces its own neurotransmitter, which it stores in specialized vesicles.
Stimulation of the pre-synaptic neuron results in the neurotransmitter substance being
released into the synapse. It traverses the ‘gap’ to the post-synaptic neuron where it
occupies its receptor sites. Depending on whether the transmitter is an inhibitory or
excitatory chemical, the post-synaptic neuron is either inhibited or excited. Once the
neurotransmitter has relayed its message it is removed from the synapse.
The drugs used to treat anxiety, depression, and psychosis produce their therapeutic effects by
targeting neurons, their receptors, and neurotransmitter activity in a variety of ways.
Medications used to manage mood and emotional disorders fall into three main categories:
• anxiolytic or anti-anxiety agents

• antidepressants
• antipsychotic drugs
1. THE ANTI-ANXIETY MEDICATIONS

Results of a 1999 study sponsored by the Anxiety Disorders Association of America showed
that the total cost of anxiety disorders in the United States, including misdiagnosis and
undertreatment, is more than $42 billion a year.2 More than 19 million Americans suffer from
one or more anxiety disorders, making them the most common of all mental illnesses.
According to the National Institute of Mental Health,3 there are several classifications of
anxiety. The table on the next page outlines the general signs and symptoms of each.

Anxiety Disorder Characteristics
Classification
Episodes of intense fear that strike often and without

warning. Physical symptoms include chest pain, heart
Panic Disorder
palpitations, shortness of breath, dizziness, abdominal
distress, feelings of unreality, and fear of dying.
Obsessive-Compulsive Repeated unwanted thoughts or compulsive behaviors

Disorder that seem impossible to stop or control.
Persistent symptoms that occur after a traumatic event

Post-Traumatic Stress such as a rape or other criminal assault, war, child
abuse, a natural disaster, or a crash. Symptoms include
Disorder
nightmares, flashbacks, numbing of emotions, depression,
anger, irritability, distraction, and being easily startled.
Specific Experience of extreme, disabling, and irrational fear of

Phobia something that poses little or no actual danger.
PHOBIAS
Social An overwhelming and disabling fear of scrutiny,
Phobia embarrassment, or humiliation in social situations.
Constant and exaggerated worrisome thoughts and

tension about routine life events and activities, lasting at
Generalized Anxiety least six months. The person tends to anticipate the worst
Disorder even though there is little reason to expect it. Physical
symptoms include fatigue, trembling, muscle tension,
headache, and nausea.
Clients complaining of anxiety related symptoms such as tension headaches, backache,

insomnia, and fatigue often use a combination of medications and massage therapy to help
control their anxiety.

The medications most commonly used to reduce anxiety include:
• the benzodiazepines
• buspirone HCl (BuSpar)
In the past, drugs such as the barbiturates and chloral hydrate were used extensively in
the management of mood disorders, including anxiety. The barbiturates can produce
serious side effects like respiratory depression and cardiovascular shock, while chloral
hydrate creates dependency with long-term use. These drugs are now largely replaced
by the much safer benzodiazepines for mood disorder treatment. The barbiturates are
presently used in the management of various forms of epilepsy and as an adjunct to
general anaesthesia.
Benzodiazpines
Commonly prescribed drugs in this category include: diazepam (Valium), lorazepam
(Ativan), alprazolam (Xanax), and ketazolam (Loftran).
Uses
The benzodiazepines are used in the management of:
• short-term anxiety related conditions
• insomnia
• tension headaches
• stress related muscle tension, spasms, and pain
• various medical disorders characterized by seizures or convulsions
Mechanism of Action
The benzodiazepines depress all areas of the central nervous system to produce effects
ranging from muscle relaxation and mild sedation to deep sleep. In very large doses coma
and even death can result.
The precise mechanism of action of these drugs is not completely understood, but they appear
to enhance the inhibitory actions of GABA. When GABA binds to its receptor sites on the
neuron membrane it initiates a series of reactions to increase chloride ion influx into the cell.
Higher intracellular chloride concentration causes neurons to become hyperpolarized,
meaning that they are more difficult to activate. GABA is believed to act in this manner on
both pre- and post-synaptic neurons in all areas of the brain to depress CNS discharge levels.
The benzodiazepines stimulate GABA receptors to produce the same effect.
Buspirone HCl
Buspirone HCl (BuSpar) is different chemically and pharmacologically from the
benzodiazepines. It reportedly has fewer CNS side effects, does not exert anticonvulsant,
sedative, or muscle relaxant effects, and has less abuse potential than the benzodiazepine
group.
Uses
Buspirone HCl is indicated for:
• generalized anxiety disorders
• short-term relief of anxiety related symptoms
Mechanism of Action
Buspirone is a relatively new drug whose mechanism of action is not known. It does not
affect GABA receptors but instead appears to have:
• a high affinity for serotonin (5-HT1A) receptors
• a moderate affinity for brain dopamine receptors
Its anti-anxiety effects begin to be felt after about two weeks.
Benzodiazepines
Act on neuronal GABA
receptors to mimic and
enhance its effects.
GABA
Increases chloride influx
Anxiety is
into neurons, causing them
to hyperpolarize; CNS firing
reduced
is reduced in a
generalized manner.
Buspirone HCl
Influences serotonin
and dopamine receptors
in the brain.
2. THE ANTIDEPRESSANTS
The World Health Organization (WHO) estimates that by the year 2020 depression will be the
number two cause, second only to ischemic heart disease, of “lost years of healthy life”
worldwide. It is currently estimated that 340 million people suffer from depression globally,
of whom 17-20 million are in the U.S. population.4
Studies indicate that the cost of clinical depression exceeds $47.3 billion annually in the
United States. One out of every five adults will experience a depression episode at some time,
and women are twice as likely as men to suffer from bouts of depression. Everyone including
children can be affected.5

GENERAL SIGNS AND SYMPTOMS OF DEPRESSION
Persistent sad mood

Loss of interest in ordinary activities
Loss of interest in sex
Decreased energy, fatigue
Sleep disturbances
Eating disturbances (loss of appetite and weight, or weight gain)
Difficulty concentrating and remembering
Poor self confidence
Difficulty making decisions
Feelings of guilt, worthlessness, helplessness
Thoughts of death and/or suicide
Suicide attempts
Irritability
Excessive crying
Chronic aches and pains that do not respond to treatment
Decreased productivity
Absenteeism
Alcohol and drug abuse
Type of Depression Characteristics
Major Depression Most common type of depression. At least five of

(clinical depression) the major symptoms of depression are present.
Second most common type of depression. A

Dysthymia milder form – sufferers may present with only two
or three symptoms and are often undiagnosed
and undertreated. Can last two years or more.
The depressive phase of a manic-depressive
Bipolar Depression mood disorder, in which the person experiences
extreme highs and lows. Symptoms are very
similar to major depression.
Usually occurs in the winter months and is
associated with absence of sunlight. Tends to
Seasonal Affective Disorder resolve in the spring and summer months. Typical
symptoms include loss of energy, decreased
activity, sadness, and excessive eating and
sleeping.
Post-partum, drug induced, pain induced,
Other
endogenous, and reactive types.

More information about the types of depression can be obtained through the Internet or local
mental health support groups.
The following groups of medications are used alone or in combination in the management of
depression:
• antidepressants
• anti-anxiety medications (see previous section)
• lithium carbonate
• antipsychotic drugs (discussed in the next section)
The commonly prescribed antidepressants include:

• the tricyclic antidepressants
• the selective serotonin re-uptake inhibitors (SSRIs)
The Tricyclic Antidepressants

The most common drugs in this group are: amitriptyline (Elavil), imipramine (Tofranil), and
doxepin (Sinequan).
Uses
The tricyclic antidepressants are used in the management of:
• depression
• anxiety related conditions
• various compulsive or obsessive disorders
• migraines and chronic muscle tension
headaches
• sources of neurogenic pain, such as
cancer pain and peripheral neuropathy
• attention disorders, hyperactivity, and
enuresis (bed wetting) in children 6+
• other conditions: peptic ulcers,
narcolepsy, bulimia nervosa, cocaine
withdrawal
Mechanism of Action
The biochemical model of depression in use until recently suggested that concentrations of
serotonin and norepinephrine were low and therefore post-synaptic neuroreceptors were not
being sufficiently activated. The current belief is that post-synaptic neurons seem to create
more serotonin and norepinephrine receptors, making them supersensitive to these molecules.
It is this supersensitivity that leads to the symptoms of depression.

The tricyclic antidepressants produce their effects by inhibiting re-uptake of norepinephrine
and serotonin molecules that have been released into synapses. This increases the volume of
these transmitters in the synaptic gaps. With more neurotransmitter substance in their
synapses post-synaptic neurons are even further stimulated. This super-stimulation causes
their membranes to ‘down-regulate.’ Restoration of normal sensitivity of post-synaptic
neurons improves the quality of signals traveling among the different parts of the brain, and
balances and normalizes the reactions of the neuroreceptors to their neurotransmitters.
pre-synaptic post-synaptic
neuron neuron
Normal activity at
the synapse.
In depression, the
post-synaptic
membrane becomes
more sensitive to
neurotransmitter
stimulation.
The tricyclic
antidepressants
prevent uptake of
neurotransmitter
molecules from the
synapse.
The post-synaptic
membrane
down-regulates to
return to normal
sensitivity.
The tricyclic antidepressant mechanism of action

The therapeutic effect of the tricyclic antidepressants, that is reduction of depression
symptoms, begins to occur after a minimum of 2-3 weeks. This lag is believed to correspond
with the time it takes the post-synaptic neuromembranes to down-regulate.
Serotonin Selective Re-Uptake Inhibitors (SSRIs)

This is a relatively new but already extensively used group of drugs that includes: fluoxetine
(Prozac), paroxetine (Paxil), and sertraline (Zoloft).
The SSRI mechanism of action is similar to that of the tricyclic antidepressants except that
SSRIs selectively inhibit the re-uptake of serotonin. The effects of these drugs also become
apparent 2-3 weeks after the start of therapy. The SSRIs are credited with a safer profile than
the tricyclic drugs.
Recent Developments
Two new medications, called venlafaxine (Effexor) and nefazodone (Nefadar, Serzone,
Serzonil), have been introduced into the marketplace recently and are being increasingly
used in depression management. Although their exact mechanisms of action are still
unclear, venlafaxine appears to be a potent re-uptake inhibitor of serotonin and
norepinephrine and a weak inhibitor of dopamine re-uptake. Nefazodone displays
re-uptake inhibition of both serotonin and norepinephrine but not dopamine. Although
the end result is similar to that of the tricyclic antidepressants, these drugs appear to have
a safer profile, comparable to the SSRIs.
Lithium Carbonate
Lithium carbonate, manufactured as Carbolith, Duralith, Eskalith, Lithane, and Lithizine, is a
more specialized type of antidepressant.
Uses
Lithium is used either alone or in combination with other medications to manage:
• manic depressive (bipolar) depression

• vascular headaches
Mechanism of Action
Lithium is the drug of choice in managing bipolar depressive syndromes, but its actions are
not fully understood. Several theories6 exist regarding its mechanism of action. One suggests
that lithium ions accumulate inside neurons by entering via their sodium channels. The cells
have difficulty removing them, and increased intracellular lithium concentrations result in
decreased neuron excitation. Another theory is that lithium serves as a second messenger to

engage processes that reduce the excitability of neurons. It is also suggested that lithium may
affect synaptic serotonin concentrations. Whatever the mechanism, lithium helps normalize
the production, concentration, and metabolism of serotonin and norepinephrine. The resulting
stabilizing effect on the patient occurs in about three weeks.
Lithium Toxicity
Lithium dosage has to be carefully monitored medically because of the close
relationship between therapeutic and toxic doses. There are a number of symptoms of
lithium toxicity: diarrhea, drowsiness, loss of appetite, muscle weakness, nausea and
vomiting, slurred speech, confusion, clumsiness, blurred vision, dizziness, severe trembling,
and increased urination.
Lithium is reabsorbed in the kidneys in a manner very similar to sodium. When less sodium
is passing through the kidney tubules, such as during heavy sweating, lithium reabsorption
will actually increase. This can lead to toxic levels of lithium if sodium is not actively
replaced.
3. THE ANTIPSYCHOTIC MEDICATIONS

Psychosis is a major emotional disorder characterized by personality disintegration and loss
of contact with reality.7,8 The cause is somewhat unclear, although several contributing
factors have been identified. These include genetic inheritance, environmental factors, CNS
biochemical imbalances, viral infections, and social predisposition. Most researchers believe
that psychotic behavior is related to an imbalance of the neurotransmitter dopamine.
Schizophrenia is the most common type of mental illness involving psychotic behavior.
Some of the symptoms of schizophrenia include delusions, hallucinations, unusual movement
patterns, and disorganized thinking and actions. The 1996 total cost of treating schizophrenia
in the United States, including direct treatment and societal and family costs, was about $65
billion. Schizophrenia affects one percent of the population, consumes a fourth of all mental
health costs, and accounts for one in three psychiatric hospital bed occupancies.9
Dopamine Theory of Psychosis

The dopamine theory of psychosis postulates that too much dopamine is being produced
in the limbic system and in other areas of the CNS. This excess dopamine is absorbed by
the post-synaptic neurons, and the symptoms of schizophrenia result for reasons that are
not entirely clear. The role of antipsychotic medication is to prevent excess dopamine
from entering these neurons.

Types of
Schizophrenia Characteristics
Preoccupation with one or more delusions or frequent

Paranoid auditory hallucinations
Feelings of persecution
Lack of initiative, motivation, social interest, enjoyment,

Negative or Deficit
emotional responsiveness
Immobility, stupor
Catatonic
Excessive motor activity
(must have at least Extreme negativism
two symptoms)
Mutism
Peculiarities of voluntary movement
(voluntary assumption of inappropriate or bizarre postures)
Stereotyped movements
Prominent mannerisms, grimacing
Echolalia
(compulsive repetition of words spoken by someone else)
Echopraxia
(compulsive imitation of the actions of others)
Grossly disorganized or catatonic behavior
Residual Absence of prominent delusions, hallucinations,
disorganized speech
Disorganized behavior, disorganized speech, flat affect
Disturbance in behavior, communication, and thought
Disorganized
Lack of any consistent theme
Unusual mannerisms and facial expressions
This section will focus on two categories of drugs used to manage psychosis:
• the typical antipsychotic drugs
• the atypical antipsychotic drugs
Antipsychotics are often used in combination with other CNS medications, for example
anti-anxiety drugs or lithium.
Typical Antipsychotic Drugs

This drug group is known as the phenothiazines. They are among the oldest antipsychotic
medications and are still widely used today. The most commonly prescribed include:
chloropromazine (Largactil, Thorazine), haloperidol (Haldol), and trifluoperazine (Stelazine).
Uses
The phenothiazines are used in the management of:

• psychotic disorders, for example schizophrenia, or for patients with explosive
or hyper-excitable behavior
• short-term management of severe psychotic depression with anxiety
• elderly patients with multiple symptoms such as anxiety, agitation, tension,
fears, depressed mood, and sleep disturbances
• severe nausea and vomiting
• intractable hiccups
Mechanism of Action
These drugs act at all levels of the central nervous system to interfere with the effects of
dopamine. They occupy and block dopamine receptor sites on post-synaptic neurons. Their
effects include altering responses to dopamine in parts of the brain like the mesolimbic area,
which is important to emotions and mood.
Two main effects are achieved with the phenothiazines:

• a tranquilizing effect that occurs soon after the drug is administered,
characterized by profound quiet and calm
• an anti-psychotic effect that takes 2-3 weeks to develop, characterized by
normalization of thought, mood, and behavior
The sedative, anti-anxiety, and antiemetic (control of vomiting) properties of the
phenothiazines are related to their global inhibitory impact on the CNS, including on the
reticular activating system and the chemoreceptor trigger zone.
HYDROTHERAPY ALERT
The phenothiazines suppress the hypothalamic centers that regulate central and
peripheral temperatures. Regulation of both hot and cold are affected. In hot and humid
conditions the sweating mechanism is compromised and the person can develop heat
stroke. In cold environments, hypothermia can develop.7 These effects pose serious
concerns related to the use of hydrotherapy, as will be discussed later in the chapter.
Atypical Antipsychotic Drugs

In 1989, clozapine (Clozaril) became the first of this group of drugs to receive FDA approval
as an antipsychotic medication. Subsequently, risperidone (Risperdal), olanzapine (Zyprexa),
and sertindole (Serlect) have also come onto the market.
Mechanism of Action
The antipsychotic effects of these drugs seem to be produced more selectively at specific CNS
locations. For example, clozapine acts on dopamine receptors in the limbic areas of the brain.
Risperidone and olanzapine influence specific dopamine and serotonin sites. The actions and
effects of the atypical antipsychotic drugs give them a generally safer drug profile than the
traditional phenothiazines.

SIDE EFFECTS – Drugs for Mood and Emotional Disorders
BZD: Benzodiapines, BUS: Buspirone, TCAD: Tricyclic Antidepressants, LI: Lithium, PHZ:
Phenothiazines, SSRI: Selective Serotonin Reuptake Inhibitors, ATAP: Atypical Antipsychotic
Side Effects BZD BUS TCAD LI PHZ SSRI ATAP

Abdominal Cramps X X
Acne X XX
Agranulocytosis XXX
Allergic Reactions XXX
Alopecia X XX
Akathisia* XXX
Angina XX
Anorexia X X
Anxiety X X XX
Asthma XX
Ataxia XX X X
Appetite Changes X XX XX
Arthritis XX X
Blood Dyscrasias XXX XXX XXX
Blurred Vision XX X XXX XXX XX XX
Bone Pain XX
Bradycardia XXX XXX XX
Breast Pain XX X
Breathing Difficulty XX XXX XX
Bronchitis XX
Bursitis X X
Cardiac Arrest XXX
Cramps X X
Chest Pains & Congestion XX
Chills X X
Cough X
Cold Extremities XXX XX
Confusion XXX X XXX XXX X
Constipation XX X XXX X
Convulsions XXX XXX
Decreased Sweating XXX
Depression XXX X
Dreams –Vivid XX
Diarrhea XX X X XXX XX
Dizziness XX X XX X XX
Drowsiness XX XX XXX X XX
Dry/Sore Eyes XX X XX

Dry Mouth X X XX X X XX
Dry Skin X X
Dry Throat XX
Dystonia* XXX
Dyspnea X X
Edema X XX XX X
Euphoria XX
Eye Pain XXX X X
Fatigue X X XX
Fever XXX X X X
GI Discomfort X XX
Hallucination XXX XX
Headaches X X XX X X X
Heat Stroke XXX
Hepatitis XXX XXX
Hypertension XXX XX
Hypotension X XXX XX XX XX
Increased Appetite X XX
Increased Sweating X X X
Increased Salivation X
Insomnia XX X X XXX
Irregular Heartbeat XX X XX X
Joint Pain XX
Laryngospasm XXX
Libido Changes X X XXX X XXX X
Lightheadedness XX XX XX X
Liver Dysfunction+ XXX XXX
Memory Impairment XXX
Menstrual Pain, Cycle Chgs X X XX X
Migraine X
Mood Changes XX
Muscle Cramps X X X X
Muscle Weakness XXX XX XXX X XXX X
Myocardial Infarction XXX XX
Nausea X X XX X X
Nasal Stuffiness X X
Neck Pain X X
Nervousness XX
Nosebleeds X X
Numbness XX XX
Palpitations X X XX X
Paresthesia XX
Photosensitivity X XX X
Postural Hypotension XX X X XX XXX
Pruritus X X XX
Pseudoparkinsonism* XXX
Psychosis XX
Pupil Dilation X X
Rashes XXX X X XX

Respiratory Depression XXX
Respiratory Infection X
Restlessness XXX XX
Sedation X XX XXX
Seizures XXX XX XXX
Slurred Speech XXX
Sore Throat XXX X
Stroke XXX
Tachycardia X XXX XXX XXX XX
Tardive Dyskinesia* XXX X
Taste Changes X XX X X X
Thrombocythemia X
Thrombophlebitis (inj) X
Thirst X X
Thyroid Function Chgs XXX
Tinnitus X X X X
Tiredness (unusual) XXX XXX XXX XX
Tremors X X XXX XXX XX
Uncontrolled Movements XXX XXX
Unusual Bleeding XXX XXX
Urinary Frequency Chgs XX XXX XXX XX XX
Viral Infection XX
Vomiting X X XXX XX X
Weakness (unusual) XXX XX XXX XXX XX
Weight Gain X XX XXX X XX
Weight Loss XX X
BZD: Benzodiapines, BUS: Buspirone, TCAD: Tricyclic Antidepressants, LI: Lithium, PHZ:
Phenothiazines, SSRI: Selective Serotonin Reuptake Inhibitors, ATAP: Atypical Antipsychotic
+ liver dysfunction: jaundice-like symptoms including yellow eyes and skin

* akathisia: restlessness, need to keep moving
dystonia: muscle spasms of the face, neck and back, tic-like or twitching movements, twisting movements of
the body, inability to move the eyes, weakness of arms and legs
pseudoparkinsonism: difficulty speaking and swallowing, loss of balance, shuffling walk, mask-like face,
stiffness of arms and/or legs, trembling of hands and fingers
tardive dyskinesia: lip smacking or puckering, puffing of cheeks, rapid or worm-like movements of the
tongue, uncontrolled chewing movements, uncontrolled arm and leg movements


Quick Guide to Case History Taking
Clients will not always be open about mental health problems they are experiencing.
Recognition of medications and symptom presentations can help the practitioner identify
areas needing diplomatic exploration. Therapists must be able to define the fine line
between obtaining necessary treatment planning data and prying into personal
information.
Questions
1. Identify the mood disorder(s) for which the client is being treated.
2. When was the diagnosis made?
3. Is the cause known? Are current life stressors a factor?
4. Clarify the medications being taken. Is the condition well stabilized on these
medications?
5. If the client has musculoskeletal complaints, could they be related to the condition
or to medication use? Has this been evaluated medically?
6. Inquire about organ system health. For example, the cardiovascular system can be
stressed by emotional disorders and by several of the medications used to manage
them.
7. Does the client have a good support system?
8. What are the goals of the client in seeking massage treatment?
9. Any past experience with massage therapy? What was the response to it? Any
concerns or reservations about receiving massage?
10. Inquire about where the client “holds stress.” Try in a diplomatic way to identify
sensitive areas that might be difficult for the client to have touched.
11. Inquire about destabilizing factors like lack of sleep, poor diet, work stress, and
alcohol consumption.
Observations
1. Is the client cooperative when answering your questions? Can you establish rapport
and get the information you need to proceed?
2. How focused or attentive is the client?
3. Pay attention to postural holding patterns. They can give clues about specific areas
of tension, past experience of trauma, and overall emotional state.
4. Observe how the client breathes – shallow rapid breathing often signals stress.
5. Inquire about any visible bruises and scars. These may be related or unrelated to the
mental health problem; bruises may reflect medication side effects.

Quick Guide to Working with Clients Who Have Mood Disorders
Working with clients with mood disorders can be challenging. It is important to mutually
agree on the nature of the therapeutic relationship being entered into and the scope of
massage therapy practice as it applies in each case. Ideally, the massage therapist will
be only one of a team of health care practitioners the client is seeing. The massage
therapist needs to show sensitivity and acceptance, and to maintain good professional
boundaries to avoid dependency or issues arising from unrealistic expectations of
massage therapy. The guidelines for working with clients with mood disorders are not
necessarily different from other scenarios, but additional awareness, sensitivity, and
diplomacy are called for.
1. The client must understand the treatment plan and feel informed about the
techniques you are going to use and on what body areas. If the client specifically
indicates not wanting a part touched, always respect this request. Focus your efforts
on developing trust and ease in the therapeutic relationship. When the client is ready
to evolve the treatment he or she will let you know.
2. Be a good listener, but do not exceed your scope of practice or your personal
comfort zone. Work in concert with the other health care practitioners involved with
the client’s case.
3. Shorter treatments are suggested for first time clients – this gives everyone an
opportunity to monitor the response to therapy. Progress the treatment plan slowly
and in frequent communication with the client. Be prepared to stop treatments
before the scheduled time if the client is feeling emotionally overwhelmed by the
massage work. If unsure about appropriate treatment plan design, consult with the
attending physician.
4. Ensure the treatment room is warm and comfortable and external noises are
eliminated or reduced to a minimum. Encourage relaxing breathing techniques,
beginning with diaphragmatic breathing. Pillow for comfort, keeping any
musculoskeletal complaints or medication effects in mind.
5. Show sensitivity to the client’s requests or feelings of vulnerability. Be clear that it is the
client’s decision to disrobe for treatment at his or her level of comfort. You may want to
treat in supine position (or other position preferred by the client) until he or she is more
at ease with massage. It is important for the client to feel in control of such options.
1. Avoid use of techniques that are deep and aggressive. Such techniques, in addition
to the medication-related bruising risk, can jeopardize the client’s feeling of safety
and cause increased anxiety.
2. The overall effect of your choice of techniques should be nurturing and relaxing. Be
especially careful when working on areas you know to be sensitive ones – the
techniques used, whether very gentle or more standard, need to have the qualities
that feel appropriate to the client.
3. Be mindful of how you handle or hold the client’s limbs. Certain manners of treatment
or specific positions may trigger negative responses. Always inform the client about
what you are going to do.

Massage Guidelines - Clients Taking Medications for Mood and Emotional Disorders
General Guidelines
1. Check the side effects profile for each drug the client is taking. Toxicity or other
adverse reactions are a concern with several of the drugs used to manage mood and
emotional disorders. Stay aware of all the medications being taken and be alert for
unexpected symptoms or known adverse indicators.
2. Complaints of headaches or muscle and joint pain are typical with most of the drugs
discussed in this chapter. If you have been asked to address such complaints but after
a few treatments there is no improvement, consult with the medical doctor. You may
be trying to treat a side effect.
3. Side effects of dizziness, drowsiness, and lightheadedness in varying degrees of

intensity are common to most of the medications used to treat mood disorders.
Massage treatment can heighten these symptoms. Be prepared to shorten your
treatment time. Give the client specific instructions about getting on and off the table,
especially to move slowly after the treatment.
4. Changes in heart rate and blood pressure, and chest pains, strokes, and heart attacks
can be related to side effects of several of the mood disorder drugs. Monitor the blood
pressure and be alert to changes in skin color, breathing, or pulse that could indicate
increasing stress on the heart. When the client is vulnerable cardiovascularly, assess
the impact of CV medications being used and avoid treatment approaches that could
add to the heart’s workload (reference Chapter 7).
5. Mood disorder medications are frequently administered by injection. If your client

receives ‘shots,’ review the appropriate section in Chapter 5.

Specific Guidelines
1. Benzodiazepines
Unusual bleeding can occur with these medications. Modify your depth of pressure to
avoid causing bruising. Keep in mind that the client may not give accurate feedback
about technique depth due to the benzodiazapine CNS depressing effect.
Exercise caution when stretching muscles and mobilizing joints. Stretch receptor
responses will be compromised and the muscles more easily injured. They may also
go into reflex spasms more readily.
Feeling unusually tired or weak can be a side effect of the benzodiazapines. Before
treating, inquire about whether the physician has evaluated these symptoms. If not, it
is probably better to re-schedule the appointment. If yes, you may need to shorten your
treatment time or adjust to a ‘lighter’ treatment design.
2. Tricyclic Antidepressants and SSRIs

The client may appear restless during the massage. Be prepared for more frequent
position changes and perhaps more conversation than is customary.
Complaints of muscle cramps and spasms can be related to electrolyte loss from
diarrhea. In this situation, aggressive manual work or stretching techniques may cause
tissue trauma.
Paresthesias and unusual bleeding can occur with the SSRIs. Modify your depth of
pressure and observe for signs of bruising. Client feedback may be misleading.
3. Phenothiazines
Some clients experience muscle spasms, dystonia, and various types of movement
incoordination. Working deeply into affected muscles or stretching muscle spasms
may not be appropriate. Do not use strong heat applications to relax the tissues since
these drugs alter responsiveness to temperature stimuli. Soothing relaxation work is
most helpful.
Laryngospasm and/or tight feelings in the throat and anterior neck can also occur with
phenothiazine use. Attempting to ‘loosen’ the neck directly may cause more anxiety
and increase the discomfort.
4. Atypical Antipsychotics
Low blood pressure and orthostatic hypotension are a particular concern with this
pharmaceutical group. Give appropriate instructions concerning getting up after the
massage session – the client may need assistance.
There can be complaints of shortness of breath. If the client is comfortable with the
idea, spend focused time treating the muscles of respiration.

A side effect of these medications, called agranulocytosis (a drop in the white blood cell
count), can result in immune system compromise. The client will likely complain of
fatigue and weakness, and will be at increased risk of developing infections. The client
might present in a weakened state of health, with the muscles, joints, and other
connective tissues feeling more sensitive. Modify your depth of pressure, and be
prepared to shorten your treatment. Avoid treating such clients when you yourself are ill.
Some people experience seizures when taking the atypical antipsychotics. If this is the
case, determine how the seizure disorder is being managed and whether the client’s
condition is stable enough for massage. If so, decide on a treatment schedule that is
best suited to the medical stability of the client.
5. Lithium
Be alert for signs or complaints that suggest lithium toxicity. This is a serious concern
and presence of such symptoms requires immediate medical evaluation. If you suspect
lithium toxicity is occurring, do not massage until the physician gives the ‘all clear.’
Inquire whether the client has been given any condition or medication related temperature
restrictions; ask about daily bath/shower tolerances and if there are areas of sensory
impairment. Many of the drugs discussed in this chapter affect the health of the cardiovascular
system in some way. Take blood pressure readings before and after hydrotherapy treatments
and monitor the client closely during the application. When unsure, discuss the proposed
procedure with the physician.
The benzodiazepines depress all areas of the CNS. With CNS depression vascular responses
to hydrotherapy modalities can be altered. Using modified temperatures and local versus
systemic treatments is recommended.
The tricyclic antidepressants and SSRIs cause increased sweating. This can be a particular
concern if the client is also experiencing bouts of diarrhea. Dehydration and low electrolyte
levels can result. Modify temperatures and application times and monitor the client closely,
making sure he or she is sipping water during the treatment.
Lithium can approach toxic levels under conditions that cause heavy sweating. Systemic
hydrotherapy modalities like steams, saunas, hot baths, and sweating herbal wraps are not
recommended.9 Review the signs and symptoms of lithium toxicity presented earlier.
The phenothiazines impair the body’s temperature regulating mechanisms. Systemic hot and
cold hydrotherapy modalities are contraindicated. Do not use intense heat to relax muscle
tension – the client may be unable to give accurate feedback and is at risk for burning at lower
than expected temperatures. Local cold applications like cryotherapy can also cause tissue
damage.

A progressive aerobic exercise program can be very helpful in managing the effects of anxiety
and depression. Improved circulatory and aerobic capacities aid in increasing energy and
appetite, and in improving the quality and quantity of sleep.
Some degree of muscle weakness is a side effect of virtually all the drugs discussed in this
chapter, especially the benzodiazepines and lithium. Adjust the intensity, frequency, and
duration of the exercises prescribed. Encourage the client not to overexercise.
Low electrolyte levels and dehydration can be a concern with the tricyclic antidepressants and
SSRIs. Make sure the client knows the importance of being adequately hydrated and properly
nourished for exercise, as well as not becoming overheated.
Vigorous exercise, especially in hot conditions, is not recommended for clients using lithium.
Increased sweating and dehydration can lead to lithium toxicity.
When phenothiazine use is producing spasmodic or dystonic symptoms in the client’s

muscles, it is important to be cautious about recommending strengthening exercises,
especially those incorporating weights.
Because the phenothiazines affect temperature control mechanisms in the hypothalamus,

vigorous exercise, especially in hot environments, is not recommended. As well, clients
taking the phenothiazines must pay particular attention to spending too long in direct sunlight.
The metabolites from these medications accumulate in the skin and can react with sunlight to
produce a deep blue-black discoloration.
Ensure your client’s exercise program has medical approval.
1. Stephens, T. & Joubert, N., “The Economic Burden of Mental Health Problems in Canada,” Chronic
Diseases in Canada, 22(1), Mental Health Promotion Unit of Health Canada, 2001
www.hc-sc.gc.ca/hpb/lcdc/publicat/cdic/cdic221/cd221d_e.html
2. Anxiety Disorders Association of America, “Misdiagnosis of Anxiety Disorders Costs U.S. Billions,” 1999
panicdisorder.about.com/gi/dynamic/offsite.htm?site=http://www.adaa.org/dyna/view.cfm%3FID=5
3. National Institute of Mental Health www.nimh.nih.gov/anxiety/anxiety/idx_fax.htm#top
4. “Depression: A Global, National and Personal Burden”
www.depressionresources.ofinterest.com/depression/article.htm
5. National Mental Illness Screening Project www.nmisp.org/dep/depfaq.htm
6. United States Pharmacopeial Convention Inc., USP DI, Drug Information for the Health Care
Professional, Volume1B, 12th ed., 1992
7. Tabers Cyclopedic Medical Dictionary, 16th ed., F.A. Davis Company, Philadelphia, 1989
8. Freeman Clarke, J.B. et al., Pharmacologic Basis of Nursing Practice, 4th ed., Mosby Year Book Inc.
Missouri, 1993
9. “U.S. Health Official Puts Schizophrenia Costs at $65 Billion,” The Schizophrenia Homepage
www.schizophrenia.com/news/costs1.html

CHAPTER 11
Drugs for Managing Cancer
The diagnosis of cancer is among the most feared of all diagnoses. Cancer affects everyone’s
life in some way and places a tremendous burden on society. According to the National
Cancer Institute of Canada,1 there will be an estimated 134,100 new cases and 65,300 cancer
deaths in 2001. The most frequently diagnosed cancers are breast cancer for women and
prostate cancer for men. The leading cause of cancer death is lung cancer; the most common
childhood cancer is leukemia.
In the United States, cancer is second only to cardiovascular disease as a cause of death.
Cancer costs for the year 2000, including health care expenditures and lost productivity, are
estimated at $107 billion.2 It is projected that in 2001 over 1.2 million Americans will be
diagnosed with cancer and as many as 552,000 will lose their lives to it. The number of new
cancer cases is expected to increase by 29% by the year 2010.3
Defining Cancer
Cancer is a generic term used to describe over 2004 malignant diseases whose common
characteristic is uncontrolled tissue growth and spread of abnormal cells.
During normal cell life, cells grow, divide, perform their functions, and eventually die. This
cycle is directed by genes, hormones, and specific intercellular communications that dictate
cell sizes and numbers consistent with their tissue functions. When these controls are
disrupted, whether by environmental, genetic, or lifestyle influences, cells can become
renegades. Acting outside normal constraints, they begin to multiply rapidly to form new
tissue masses called neoplasms or tumors. Tumors can arise from any cell type and are
broadly grouped into two categories: benign and malignant.
Benign tumors are not classified as cancer. They do not invade tissues or spread to other body
parts. They are usually successfully removed surgically, or if located in a difficult spot, with
laser treatment. Malignant, or cancerous, tumors are much more dangerous. Cancer tissues
do not respect tissue boundaries. They invade neighboring structures and shed cells that can
migrate to distant sites to form new cancers.

Distinguishing Features of Benign and Malignant Neoplasms
Benign Malignant
Have an expansile growth Have an invasive growth pattern, overrunning host

pattern, enlarging locally stroma and other tissue structures.
within their host structure.
Are usually contained within Can invade body cavities and blood and lymph
a capsule. channels, leading to spread to secondary sites
Do not spread to distant sites. (metastasis).
Cell turnover is slower. Cell replication is rapid and frequently abnormal.
Cells are usually fairly well Poor differentiation and maturation of cells is typical,
differentiated. including a tendency to regress to pre-differentiated
or ancestor cell types (anaplasia).
Reprinted with permission from Massage Therapy and Cancer, Curties-Overzet Publications Inc., 1999.
Naming Cancerous Neoplasms

Malignancies that originate from epithelial tissues like skin and glandular membranes are
referred to as carcinomas, while those associated with mesenchymal tissues such as
bone, muscle, and some organs are called sarcomas. Cancers arising from the blood
have names ending in the suffix ‘emia’ as in leukemia, while those that derive from lymph
cells are called lymphomas. Cancers are also sometimes named after individuals, for
example Kaposi’s sarcoma.
Treatment of Cancer
There are many approaches to treating and managing cancer, some of which are contentious
or experimental. The current standard medical approach involves:
• surgery
• radiation
• drug therapy
While only one or two of these therapies may be utilized for some cancers, cancer treatment
protocols often incorporate a combination of all three.
Surgery is considered the most effective of the three treatments. If the malignancy is operable
and diagnosed early enough, surgery can remove all of the cancerous tissue and result in a cure.
However, surgery becomes less effective when there are a number of disseminated tumors.
Radiation is the second most effective cancer therapy. Cells that are rapidly dividing are very
sensitive to radiation, and cancerous growths contain continually replicating cells.

Radiation therapy is best suited to cancers that are not disseminated and small in size. It is
primarily used to ‘clean up’ any remaining cancer cells after surgery, to shrink tumors to make
them more operable, and to control growth of inoperable tumors. Radiation has its dangers
and is used in precise locations in controlled doses – sites are often ink-marked or tattooed for
exact future reference.
Drug Therapy
While in some cases drug therapy is the treatment of choice, usually pharmaceuticals are
employed when the cancer is less amenable to treatment by surgery and radiation, in other
words when it has spread. Drugs are also often used when there is a statistical probability that
an identified tumor may already have metastasized.
Drug therapy for cancer consists of:
• Chemotherapy
Chemotherapy is defined as the use of chemicals/pharmaceuticals to destroy cancerous cells.
It is a systemic treatment directed at disseminated cancers.
• Immunotherapy and Biological Response Modifiers (BRMs)

This category includes compounds like interferons, interleukins, and other biologic
substances that can be used to enhance the individual’s immune response. They work best in
combination with radiation and chemotherapy.
In the general scheme of cancer treatment management, drug therapies are usually
collectively referred to as chemotherapy, and that is how we will refer to them in this text.
Goals of Chemotherapy
Chemotherapy is used with various goals5 in mind, including:
• achieving a cure
• preventing or controlling cancer spread
• slowing tumor growth
• providing pain relief and otherwise improving quality of life
Depending on the type and location of the cancer, the oncologist selects the chemotherapy
approach most likely to be effective. There is a myriad of pharmaceuticals to work with.
Some drugs are designed to target rapidly replicating cells to disrupt their reproduction cycle,
while others inhibit tumor growth and viability.
For your reference, the table on the next pages, although by no means complete, lists common
cancer types and the names of drugs6 typically used singly or in combination to treat them.

Common Cancer Drugs by Cancer Type
Type of Cancer Drug
Pacis (BCG, live)

Bladder Valstar (valrubicin)
Brain Gliadel (carmustine wafer)
Aredia (pamidronate disodium) injection

Arimidex (anastrozole)
Aromasin (exemestane)
Ellence (epirubicin hydrochloride)
Fareston (toremifene citrate)
Breast Femara (letrozole)
Herceptin (trastuzumab)
Nolvadex (tamoxifen citrate)
Taxol (paclitaxel)
Taxotere (docetaxel)
Xeloda (capecitabine)
Camptosar (irinotecan hydrochloride) injection

Colorectal Celebrex (celecoxib)
Head and Neck Ethyol (amifostine) injection
Panretin (alitretinoin) gel 0.1%

Kaposi's Sarcoma DaunoXome (daunorubicin citrate liposome)
Taxol (paclitaxel) injection
Busulfex (busulfan)
Campath (alemtuzumab)
Daunorubicin HCl (daunorubicin hydrochloride)
Leukemia Gleevec (imatinib mesylate)
Neupogen (filgrastim)
Mylotarg (gemtuzumab ozogamicin)
Trisenox (arsenic trioxide)
Ethyol (amifostine)
Etopophos (etoposide phosphate)
Gemzar (gemcitabine HCl)
Hycamtin (topotecan hydrochloride)
Lung FocalSeal-L Surgical Sealant
Photofrin (porfimer sodium)
Taxol (paclitaxel)
Taxotere (docetaxel)

Type of Cancer Drug
Elliotts B Solution (calcium chloride, dextrose,

magnesium sulfate, potassium chloride, sodium
bicarbonate, sodium chloride, sodium
phosphate, dibasic)
Lymphoma Intron A (interferon alfa-2a)
Rituxan (rituximab)
Ontak (denileukin diftitox )
Targretin (bexarotene)
UVADEX (methoxsalen sterile solution, 20 mcg/ml)
Doxil (doxorubicin HCl liposome) injection

Ovarian Hycamtin (topotecan HCl)
Taxol (paclitaxel)
Pancreatic Gemzar (gemcitabine HCl)
Lupron Depot (leuprolide acetate)

Nilandron (nilutamide) tablets
Novantrone (mitoxantrone hydrochloride)
Prostate Trelstar Depot (triptorelin pamoate)
Viadur (leuprolide acetate implant)
Zoladex (goserelin acetate implant)
Actiq (fentanyl citrate) – analgesic

Anzemet (dolasetron mesylate) – antinausea
Blenoxane (bleomycin sulfate)
Ceprate SC Stem Cell Concentration System
DepoCyt (cytarabine liposome) injection
Dostinex (cabergoline)
Duraclon (clonidine hydrochloride)
Miscellaneous Products Fludeoxyglucose (F-18) injection
e.g. for: Isolex 300 and 300i Magnetic Cell Selection System
side effect control Kytril (granisetron)
immune system strengthening Levulan Kerastick (aminolevulinic acid HCl)
encouraging repair processes Neumega (oprelvekin)
Quadramet (samarium sm 153 edtmp)
Sandostatin LAR® Depot (octreotide acetate)
injection
Temodar (temozolomide)
Zofran ODT (odansetron) – antinausea
Zometa (zoledronic acid) injection
Zyloprim (allopurinol sodium)

The Cell Cycle
Before delving more deeply into the mechanisms of action of the anticancer drugs, an
overview of the cell cycle is needed.
With the exception of the permanent cells (muscle and nerve), all cells proliferate by moving
through the cell cycle. Stable cells, which make up most body structures, only reproduce when
new cells are needed. Labile cells, constituting for example the skin, hair, and membranes
lining systems like the gastrointestinal tract, reproduce constantly.
The cell cycle is divided into several phases: G1, S, G2, M, and G0. Each phase is
characterized according to the intracellular activity that occurs. The G phases are growth,
normal activity, and rest phases. With the enzyme RNA polymerase influencing DNA
structure, several important proteins and enzymes are produced. The G phases also serve as
check-in points for the cell, when the viability of newly created cellular elements is evaluated
to see if any repairs or corrections are necessary. During the S phase DNA is replicated, and
in the M phase the cell undergoes division to form two identical daughter cells.
M phase
G0 phase
If signalled to
reproduce, the
cell leaves the
The mitotic spindle pulls the G0 phase and
DNA chromosome pairs apart enters G1
to create two identical sets
G2 phase G1 phase
S phase
helicase enzyme
unzipping DNA
DNA polymerase &

Topoisomerase II assembling DNA
The cell cycle

Let’s look at the cell cycle phases in more detail:
G1 Phase (Gap 1)
During the G1 phase the cell begins to produce the components needed for two cells. It grows
in size, stores energy, and increases production of RNA and the proteins necessary for
DNA formation. This stage is also considered to be an important checkpoint. The cell
biologically monitors all of its components as well as its size and internal environment. If it
is not ready for the DNA duplication process of the next stage, the cell goes into a growth and
repair (G0) phase.
S Phase (Synthesis)
This is the phase in which the cell’s DNA is duplicated in preparation for mitosis. DNA
duplication is a very precise, complex, and energy consuming process. Specific enzymes and
proteins are involved, some already having been made in G1 and some synthesized during this
phase.
The DNA structure is a double helix – double-stranded with a helix or coiled shape. Before
the actual duplication process can begin, the DNA must untwist or unwind itself to become
two straight single strands. The enzyme helicase ‘unzips’ the DNA, following which several
other enzymes including DNA polymerase and topoisomerase II ensure that the strands
replicate properly.
At the end of DNA duplication the cell enters another G phase.
G2 Phase (Gap 2)
During G2 the cell continues to grow, produces new proteins, and stores more energy in
preparation for division. In addition to a double volume of DNA, by the end of this phase it
contains all the substances needed for two cells. This phase also serves as another important
checkpoint for the cell. The new DNA is evaluated for proper duplication and the other
cellular components are checked to ensure they are ready for the next process.
M Phase (Mitosis)
Mitosis, or cell division, occurs during this phase. Mitosis takes place over several stages that
culminate in the separation of the cellular components into two identical daughter cells.
Integral to this process is the formation of the mitotic spindle, a specialized biological
structure that only forms when cells are dividing. The spindle consists of a series of protein
(tubulin) microtubules that facilitate the separation of DNA chromosomes in opposite
directions to ensure that each new cell has its own complete set of DNA.
G0 (Zero) Phase
After cell division has occurred and two daughter cells are formed, the new cells can either
re-enter the replication cycle or go into a G0 (non-reproductive) state. Cells in G0 perform

their normal metabolic functions, but otherwise cellular activity during this phase is
considerably less than during the reproductive cycle.
Most cells in the body are in a G0 state, carrying on with normal cellular functions. However,
labile cells in structures like the GI tract, skin, bone marrow, and hair follicles are
continuously re-entering the replication cycle. In this way they are somewhat similar to the
rapidly reproducing cells of cancerous growths, and as a result they are more vulnerable to the
effects of anti-cancer drugs than other types of normal body cells.
Drugs Used in Cancer Treatment

The cancer patient is usually taking several types of medications. Some are specific cancer
fighting drugs while others are used to combat treatment side effects, pain, nutritional
deficiencies, anxiety, depression, and so on. Many of these adjunctive use medications have
been addressed in earlier chapters, for example analgesics in Chapter 6, anti-anxiety and
antidepressant drugs in Chapter 10, and medications for stabilizing cardiovascular function in
Chapter 7. The massage therapist must be prepared to investigate the diverse drug
combinations clients with cancer may be using.
In this chapter the focus is on two groups of pharmaceuticals:
• the antineoplastic drugs

• antinausea or antiemetic drugs
1. THE ANTINEOPLASTIC DRUGS

The antineoplastics work in a variety of ways to either destroy cancer cells or disrupt tumors.
They include:
• drugs that affect cell replication

• drugs that affect tumor growth
Drugs that Affect Cell Replication

This category encompasses several
different types of medications:
• alkylating drugs
• antimetabolites
• antitumor antibiotics
• drugs that affect the mitotic
spindle

• alkylating drugs
The commonly used alkylating drugs are: busulfan (Myleran), mechlorethamine (Mustargen,
Nitrogen Mustard), chlorambucil (Leukeran), cyclophosphamide (Cytoxan, Neosar), and
dacarbazine (DTIC-Dome).
Mechanism of Action
This drug group is widely used in chemotherapy. They are described as ‘cell proliferation
dependent but cell-cycle phase nonspecific,’ meaning that they can be effective during any
phase of the cell cycle.
However, the alkylating drugs are most proficient at influencing the S phase. They form
crosslinks between the two strands of the double helixed DNA and prevent it from unzipping
and unwinding. The DNA becomes unable to duplicate, and enzymes, proteins, and other
cellular components cannot be synthesized.Cellular metabolism and reproduction are
compromised and the cell eventually dies.
• antimetabolites
The most frequently prescribed drugs in this category include: fludarabine (FLUDARA),
methotrexate (Folex, Mexate), fluorouracil (Adrucil), floxuridine (FUDR), and cytarabine
(Cytosar-U).
Mechanism of Action
The antimetabolite group consists of several substances that are similar in structure to normal
intracellular elements and can compete with them in various ways. Like the alkylating drugs,
the antimetabolites can produce effects during all phases of the cell cycle but are most
effective during the S phase.
RNA and DNA synthesis are the processes primarily targeted. For example, methotrexate and
fluorouracil are directly inserted into DNA and RNA components or compete for receptor
sites on enzymes to disrupt their activities. The end result is formation of defective strands of
RNA and DNA and reduced cell replication.
Folic acid and thymidylate are examples of essential substances used by cells in the
production of DNA and RNA. Methotrexate is described as a folic acid antagonist because it
interferes with the biochemical transformation of folic acid. Fluorouracil, on the other hand,
seems to disrupt thymidylate.
The antimetabolites are quite sensitive to the most rapidly dividing cells in the body, which
include cancer cells, bone marrow, skin, intestinal mucosa, and urinary bladder cells.
• antitumor antibiotics
Names of drugs in this category include: actinomycin D (Dactinomycin), daunorubicin
(Daunomycin, Cerubidine), doxorubicin (Adriamycin), idarubicin (Idamycin), bleomycin
(Blenoxane), and plicamycin (Mithracin).

Mechanism of Action
These drugs are antibiotics that have been found to have cancer-fighting properties. They can
affect cells during any part of the cell cycle and are used either alone or in combination with
other antineoplastic drugs.
The mechanisms of action of the antitumor antibiotics are not completely understood. They
appear to interact with DNA in a variety of ways. Their methods include:
• disrupting the interaction between DNA and the enzyme RNA polymerase
• binding to DNA and preventing unwinding of the double helix
• inhibiting the function of the topoisomerase II enzyme, resulting in
production of DNA strands that are likely to cleave and break
• drugs that affect the mitotic spindle

The commonly prescribed drugs in this group are: paclitaxel (Taxol), vincristine (Oncovin,
Vincasar), and vinblastine (Velban, Velsar).
Mechanism of Action
These drugs are also known as the tubulin inhibitors. They act specifically to impair cell
division by influencing the formation and/or breakdown of the mitotic spindle during the
M phase of the cell cycle. The result is that the spindle is not effective in separating the DNA
chromosomes into two sets. Without successful completion of DNA duplication, the cell will
not reproduce.
Drugs that Affect Tumor Growth

Pharmaceuticals that perform functions to discourage tumor growth include:
• hormonal agents
• interferons
• angiogenesis inhibitors
• hormonal agents
Hormonal agents are used to address cancers whose tumor growth is dependent in some way
on hormones.
Mechanism of Action
These drugs either block hormone receptor sites on tumors or influence the body’s production
of hormones on which tumors are dependent. The hormones usually associated with tumor
growth are the male and female sex hormones testosterone and estrogen. For example,
metastatic prostate cancer is testosterone dependent and most breast cancers show estrogen

dependency. Luteinizing hormone, produced in the pituitary gland, can also play a role in
tumor growth.
Tumors that are androgen (testosterone) dependent can be treated with estrogenic hormones
to antagonize the actions of testosterone, while estrogen dependent cancers can be treated with
androgenic hormones.
Hormones like the corticosteroids are used to treat lymphoid tumors because of their specific
catabolic effect on lymphatic tissues.
Antiestrogenic Drugs: Drugs such as tamoxifen (Novaldex) and toremifene (Fareston) are
relatively new antiestrogen agents. Some cancers, for example a number of breast cancer
types, have estrogen receptors on their cells. Estrogen stimulation causes such tumors to
enlarge. Tamoxifen is believed to act by blocking these estrogen receptors. Another drug that
has an effect on estrogen is anastrozole (Arimidex). It inhibits the enzyme aromatase, which
is found in breast, muscle, liver, and adipose tissues. Aromatase plays an important role in
the formation of estrone, an estrogen precursor. Many types of breast cancer cells also contain
aromatase and therefore seem able to make their own estrogen. By inhibiting the actions of
aromatase, anastrozole is able to reduce the concentration of circulating estrogen and
discourage tumor growth.
Antiandrogenic Drugs: Antiandrogenic drugs such as flutamide (Euflex, Eulexin),

nilutamide (Nilandron), and bicalutamide (Casodex), used in the treatment of prostatic cancer,
block testosterone receptors on the prostate. Another antiandrogenic mechanism of action is
to decrease circulating levels of testosterone by affecting the biochemical chain of events
culminating in testosterone production and release.
How LHRH Analogs Affect Circulating Testosterone

The hypothalamus regulates the plasma testosterone level. If the volume of circulating
testosterone drops, the hypothalamus produces luteinizing hormone-releasing hormone
(LHRH) which stimulates the pituitary gland to release luteinizing hormone (LH) and
adrenocorticotropic hormone (ACTH). LH stimulates the testes, which produce about 90%
of circulating testosterone; ACTH stimulates the adrenal glands, which also produce and
release some testosterone. When the plasma testosterone level is high, this information is
relayed to the hypothalamus via a negative feedback loop and it decreases its
production of LHRH.
The drugs goserelin (Zoladex, Zoladex LA) and buserelin (Suprefact) are known as LHRH
analogs. These drugs mimic the actions of naturally produced LHRH. Research shows that
when LHRH is continuously released the initial result is increased LH and testosterone levels.
However, constant stimulation leads to the pituitary becoming desensitized to the effects
of LHRH and production of testosterone begins to drop. The LHRH analogs can produce
this effect.

Hypothalamus
releases LHRH
LHRH analogs
Pituitary Gland
LH ACTH
Testes Adrenal Gland

Feedback
system to the
hypothalamus
Testosterone
Antiandrogenic
Prostate agents
Gland
• interferons
Interferons are naturally occurring compounds produced by cells in response to stimuli like
viruses, tumors, and foreign substances that cause antibody production. Pharmaceutical forms
include: interferon beta-1b (Betaseron), interferon-alpha (Veldona), and interferon alfa-2a
(Intron A).
Mechanism of Action
How interferons work is still not fully understood, but immune system cells such as natural
T killers and the macrophages involved in recognizing and eliminating tumor cells seem to be
activated by them.
The human body produces three types of interferons:
• interferon alpha, produced by leukocytes and lymphoblastoid cells when

stimulated by viruses and other cell irritants
• interferon beta, primarily produced by fibroblasts
• interferon gamma, also known as immune interferon, produced by
T lymphocytes in response to antigenic and mitogenic (induces cell
mitosis) stimulation

As a group these interferons perform the following functions:
• stimulate healthy cells to resist infection
• protect cells against viral infections
• inhibit the growth of some cells, in particular cancer cells
• modify immune system responses as needed
The last two functions are particularly important in resisting tumor growth.
• angiogenesis inhibitors
The angiogenesis inhibitors are a very new category of drugs that are bringing fresh hope to
the fight against cancer. Still undergoing clinical trials (over 100 drugs are presently being
tested7), these pharmaceuticals disrupt the formation of blood vessels to tumors.
Mechanism of Action
Angiogenesis, the formation of blood vessels to match blood supply needs, is essential to the
growth and development of any tissue or organ. Tumors are no different. A solid tumor can
only grow to the size of a pinhead (1-2 cubic millimeters) before it needs to start attracting new
blood vessel branches in order to meet its nutritional requirements. Tumors produce factors
such as Tumor Angiogenesis Factor (TAF) to induce blood vessels to connect to them. The
new angiogenesis inhibitors are being designed to block or inhibit these factors in various
ways.
Blood vessel
grows branches
toward tumor Angiogenesis
inhibitor drug
TAF TAF
Cancer tumor produces Angiogenesis inhibitors

TAF to stimulate prevent the blood
blood vessel growth vessel stimulation
Because of the mechanism of action of these drugs, they are not expected to cause side effects
like the gastrointestinal irritation, bone marrow suppression, and hair loss associated with
many of the chemotherapeutic agents. It is too early to know which drugs in this category
will be the most effective and what types of side effects they may cause.

Hormonal agents
reduce hormone Drugs that alter the
stimulation of mitotic spindle
dependent cancers prevent DNA
duplication
Alkylating drugs,
antimetabolites, and
antitumor antibiotics
disrupt synthesis of
RNA and DNA and
other cell products
Angiogenesis
Cancer
inhibitors
tumor
reduce blood supply
to cancer tumors
Interferons
enhance cellular
immune responses
Tumor is less
viable
Actions of the antineoplastic drugs

2. THE ANTINAUSEA OR ANTI-EMETIC DRUGS
Commonly prescribed medications in this group include: dolasetron mesylate (Anzemet),
odansetron (Zofran ODT), granisetron hydrochloride (Kytril), dexamethasone (Decadron),
diphenhydramine (Benadryl), and prochlorperazine (Compazine).
Nausea and vomiting, sometimes quite

severe, are experienced by many cancer
patients. They result from:
• specific cancer types and

locations, e.g. stomach and
pancreatic cancers
• a number of antineoplastic
pharmaceuticals
• radiation of sites like the liver
and GI tract
The sensation of nausea and the act of vomiting are the result of a series of neural messages
and reflexes involving various systems. The final control signal comes from the vomiting
center located in the medulla of the brainstem. In addition to the vomiting center, some of the
structures involved include:
• the chemoreceptor trigger zone (CTZ)

• the vestibular apparatus (involved in motion sickness)
• the respiratory center
• receptors located in the stomach, small intestines, and pharynx
Nausea and vomiting can result in dehydration, electrolyte imbalance, and loss of interest in
eating. The patient can become very debilitated at a time when nutrition and good sleep are
important. The negative anticipation of feeling sick can be psychologically distressing in
itself for people entering cancer treatment. Management of nausea and vomiting, preferably
prophylactically, has become an important aspect of cancer care.
Drugs that are used in the treatment of nausea and vomiting act in various locations,
including:
• the vestibular apparatus (antihistamines)

• the GI tract (metoclopramide)
• the CTZ (phenothiazines, metoclopramide)
• a variety of receptor sites (antihistamines, odansetron, granisetron)

The Common Anti-Emetic Drugs
DRUG MECHANISM OF ACTION SIDE EFFECTS
Scopolamine (Transderm ScÇp) These drugs occupy histamine Refer to the information
Dimenhydrinate (Dramamine) and cholinergic receptor sites in about antihistamines in
Meclizine (Antivert, Bonine) the vestibular area. Chapter 9.
Hydroxyzine (Atarax, Vistaril)
Metoclopramide (Reglan) This drug can block dopamine Very similar to the
and serotonin receptor sites. It phenothiazines. Refer to
reduces stimulation of the CTZ Chapter 10.
and increases normal emptying of
the stomach and GI tract.
Chlorpromazine (Thorazine) These drugs act within the CTZ to Refer to the information
Prochlorperazine (Compazine) occupy/block dopamine about phenothiazines in
Thiethylperazine (Torecan) receptor sites. Chapter 10.
Perphenazine (Trilafon)
Haloperidol (Haldol)
Droperidol (Inapsine)
Dexamethasone (Decadron) This drug’s exact mechanism of Belongs to the

action in achieving its anti-emetic corticosteroid group.
effects is not known. Often used in Refer to Chapter 6.
combination with other drugs.
Ondansetron (Zofran) These drugs, called the selective Headaches, malaise,
Granisetron (Kytril) 5-HT3 inhibitors, occupy/block fatigue, constipation,
specific serotonin receptor sites in diarrhea, abdominal pain,
the stomach, on the vagus nerve, weakness, anxiety, dry
in the CTZ, and in an area called mouth, dizziness, shivers,
the solitary tract nucleus. hypotension, skin rash.
SIDE EFFECTS – Drugs for Managing Cancer

Side Effects AD AM ATA HA MSD IF Side Effects AD AM ATA HA MSD IF

Abdominal Pain X XX X X Breathing Difficulties XX
Anaphylaxis XXX Cardiotoxicity XXX XX
Anemia XX XX XXX X XXX Chest Pains XX XX
Anorexia XX XX XX XX XX XX Chills X X
Anxiety X CNS Depression XX
Blood Disorders XXX XXX XXX XXX XXX Confusion X
Blurred Vision X X Constipation X X
Bone Pain xxx(t) Convulsions XXX XXX XXX
Bradycardia X Cramps XX

Side Effects AD AM ATA HA MSD IF Side Effects AD AM ATA HA MSD IF
Cranial Nerve Paralysis XX Lightheadedness xx(t)
Cystitis xxx(f) Liver Toxicity XXX XXX XXX XXX XXX
Decreased Reflexes XX Menstrual Irregularities X X xxx(t)
Deep Vein Thrombosis xxx(t) Mood Changes X XX
Depression X X X Myalgia X X X
Dermatitis X X Myelosuppression XXX XX XXX
Diarrhea XX XX X XX XX Nausea X X X X X XX
Dizziness X X XX Nervousness X
Drowsiness X Numbness XX
Dry Skin X Orthostatic Hypertension XX
Earache X Orthostatic Hypotension XX
Ecchymosis X Paralytic Ileum XXX
Edema xx(f) Pelvic Pain xxx(t)
Endometrial Cancer xxx(t) Peripheral Edema xxx(t)
Electrolyte Changes XX Peripheral Neuropathy X XX X
Fatigue X X X Photosensitivity X xx(f) X
Fever X X X Pneumonia XX
Folliculitis X X Prickling Skin Sensation X X X
Granulocytopenia XX Pulmonary Embolism xxx(t)
Gastritis X Pulmonary Fibrosis XXX XXX XXX
GI Bleeding XXX XX Rectal Bleeding xxx(f)
Gynecomastia X xxx(f) Respiratory Congestion X
Hair Loss X X X X X X Rhinitis X
Headaches X X X X Rigors X
Hearing Loss XX Seizures XXX
Hemiparesis XX Skin Rash XX XX XX XX XX X
Hepatitis xxx(f) Spermatogenesis Chgs X
Hot Flashes X Sterility X
Hypercalcemia xxx(t) Stomach Pain X XX X
Hyperpigmentation X X Stroke xxx(t)
Hypertension XX xx(f) Tachycardia XX XX
Hypotension XX XXX X Taste Changes X X
Impotence X X Thrombocytopenia XXX XXX XXX XXX XXX XX
Insomnia XX Tinnitus X X
Irritability X Ulcers X
Irritated Injection Site xx(f) Vaginal Bleeding xxx(t)
Increased Bleeding XX Vomiting X X X X XX
Joint Pain X X Weakness XX X
Kidney Toxicity XXX XXX XXX XXX Weight Loss XX XX
Leukopenia XXX XX XXX XXX XXX XXX Wheezing XX
AD: Alkylating Drugs, AM: Antimetabolites, ATA: Antitumor Antibiotics, HA: Hormonal Agents,
MSD: Mitotic Spindle Drugs, IF: Interferons
(t) relates specifically to the antiestrogenic drugs, eg. tamoxifen

(f) relates specifically to the antiandrogenic drugs, eg. flutamide

XXX – very serious – seek medical attention as soon as possible

Quick Guide to Case History Taking for Clients Who Have Cancer
It can be challenging to put together a treatment plan that takes into account the many
factors involved in cancer scenarios. The reader is referred to Massage Therapy and
Cancer8 by Debra Curties. This text explores in more detail the clinical decision-making
issues for massage therapists working with clients who have cancer.
Questions
1. What type of cancer is it? Date diagnosed? Known metastases?
2. How has it been treated so far? Surgery? Radiation? Drug therapies? What is the present
treatment protocol? Any alternative therapies being used? (Be prepared to research.)
3. If surgery has been done, ask about:
• which tissues/organs were involved, what was removed (including lymph nodes)
• date of the procedure(s)
• post-surgical recovery – any setbacks, delayed healing, infections?
• present condition of the area, quality of repair, how well remaining tissues are
functioning; altered sensation, edema, decreased r.o.m., other complications?
• location of the scar(s) and current state (numb, hypersensitive?), client’s comfort
level with having them seen/touched
4. If radiation has been done, ascertain when and where, the current state of integrity of
the skin and underlying structures, and whether the affected area has altered sensation.
If the client is in the middle of a radiation protocol, clarify what the schedule is. Check on
the current condition of the site(s) and the presence of ‘exit’ burns. Ask about any
medical restrictions placed on touch, temperature exposure, and lubrication use.
5. Get details about drug therapy: protocol (drugs being used, schedule), side effects,
condition of skin, joints, and other connective tissues, any ongoing effects from prior
chemotherapy.
6. Inquire about body system function, blood pressure fluctuations, and presence of any
systemic disorders. If present, how are they being managed?
7. Is the client in pain? If yes, ask about the nature and behavior of the pain, severity on a
pain scale. How is the pain level affected by being touched?
8. Skin irritations, infections, or rashes? Open sores or other lesions? Easy bruising? Get
details about locations, causes. Any problems with healing delays?
9. How is the client’s energy level? How does it fluctuate with the treatment protocol?
10. Support system – family, friends, health care team, support group? Does the client feel
well supported?
11. Stress levels, stress management strategies? Problems with anxiety, depression? If yes,
how managed?
12. Experience with massage therapy? What are the client’s goals in receiving massage?
Observations
1. Assess the general posture of the client. Antalgic postures? Protective holding patterns?
Disability adjustments?
2. Observe skin color, signs of health and vitality. Observe any skin lesions present. Any
radiation marks or tattoos?
3. Check scars and treatment areas for tissue integrity, sensation status. (Proceed at the
client’s comfort level.)
4. Check for edema. If present, is it pitted?

Quick Guide to Working with Clients Who Have Cancer
Cancer symptoms, treatment protocol ‘on’ and ‘off’ phases, and medication side effects
can cause day-to-day physical and emotional state fluctuations. Before each treatment
ensure you are familiar with the client’s current health status and energy level. Be flexible in
adjusting your approach to the circumstances and the client’s goals for each session.
1. Pay particular attention to the health of the skin and underlying tissues. Radiation
treatment, chemotherapy effects, and the disease progression can alter the health
and sensitivity of all body tissue types. It is easy to cause injury with approaches that
are too aggressive. Clearly identify areas of sensory loss or impairment. Begin
cautiously, adjusting the depth, pressure, and rate and rhythm of your techniques as
appropriate. Communicate regularly to get information from the client about how
the treatment feels, but be aware that you cannot entirely rely on the accuracy of
this feedback.
2. Cancer effects and cancer therapies can greatly tax the liver, heart, and kidneys.
Keep current on the status of these systems and any therapies being used to support
their function. Modify your treatment approach accordingly.
3. Adjust your appointment schedule to be compatible with the client’s chemotherapy
and radiation protocols and the resulting fluctuations in physical health, mood, and
stamina. It is generally best to wait after ‘therapy days’ to give the client recovery
time – a day or two is typical but the time needed often gets longer as the client
proceeds with the protocol. Comply with medical directives about touch, hygiene,
and lubrication for recent radiation burns. Never blur or ‘erase’ ink markings for
radiation sites.
4. Begin with shorter, lighter treatments. Evaluate responses to therapy closely with the
client. Consult with the medical team if you need guidance in designing an
appropriate treatment plan.
5. Be prepared for the fact that massage treatment may not always be appropriate. If
the client seems too unwell or has developed new symptoms that have not yet been
medically evaluated, postpone the session. Make sure the client knows that he or she
can cancel at short notice if not feeling up to receiving massage.
6. Position for comfort. Use pillows,

towels, bolsters, and blankets to
ensure optimal ease and adequate
support, especially if the client is in
pain, has range of motion limitations,
or is very thin (cachexic). Ensure that
affected limbs or body areas are
positioned safely – do not place
undue stress on recent surgery or
radiation sites.
7. Choose approaches and techniques that focus on relaxation. Clients undergoing
cancer treatment are usually stressed, tense, and anxious. They often need to feel
nurtured and to re-experience a sense of physical enjoyment. Relaxation also helps
to increase the immune fighting ability of the body and reduce nausea. Encourage
deep breathing, however exercise caution with clients who are respiration
compromised.

Massage Guidelines – Clients Taking Medications for Cancer
General Guidelines
1. Keep track of the medications and remedies, prescribed or otherwise, that the client is
taking. Inquire routinely about medication type and dosage changes. The client will
often be using pharmaceuticals in addition to anticancer drugs. These could include,
for example, anti-anxiety medications, corticosteroids, narcotic analgesics, or
antibiotics. Many of these drug groups have been discussed in previous chapters of
this book, but others have not. Therapists are encouraged to refer to a drug reference
text or to research on the Internet to obtain needed information about client
medications.
2. Peripheral neuropathy, joint and muscle pain, and muscle atrophy and weakness are
often side effects of chemotherapy. Changes in soft tissue health, for example
inflammation, irritation, fragility, poor healing, bruising, and altered sensation are also
common. A medical opinion is often necessary to determine whether such symptoms
are related to drug side effects.
3. Chemotherapy can cause liver and kidney toxicity disorders. Accumulation of the
drugs and their metabolites can leave the client’s body in a weakened state. Normal
performance of liver and kidney functions is also affected and clients can develop
secondary symptomology like hypertension, CHF, respiratory congestion, peripheral
edema, and jaundice. Do not hesitate to postpone sessions and refer for medical
evaluation. When massage is appropriate, shorter lighter treatments are
recommended.
4. The anticancer drugs suppress the immune system in several ways, resulting in
increased susceptibility to infections and more difficulty fighting them off. Routine
hygienic practices are especially important for practitioners working with clients who
have cancer. If the person becomes ill with an infection or develops a fever, massage
is not recommended until the condition has subsided. If you yourself are ill, avoid
risking infecting the client by rescheduling for a later date.
5. Cardiovascular and blood disorder concerns such as chest pains, blood pressure
changes, cardiotoxicity, dysrhythmia, anemia, and bone marrow suppression are all
side effects of the antineoplastic drugs. Monitor the client’s blood pressure on an
ongoing basis and be alert to changes or complaints of a cardiovascular nature. Blood
disorders can predispose the client to bleeding/bruising and require modification of
manual techniques. Refer to Chapter 7 for more about CV system related guidelines.
6. Orthostatic hypotension, dizziness, and lightheadedness are side effects of several of

the medications used. These symptoms can be intensified after a massage treatment.
Give clear instructions concerning getting on and off the table – determine if the client
needs help.

7. Dehydration, poor nutritional status, and electrolyte loss from gastrointestinal
irritation are often due to the effects of chemotherapy. Such clients will have low
energy and will fatigue quickly. Be prepared to shorten your treatment time and keep
in mind that tissues can be more easily irritated or injured if aggressive manual
techniques are used. Light rhythmic stroking on the back can help reduce nausea and
gastrointestinal upset.8
8. Skin hypersensitivity, rashes, and photosensitivity reactions can occur with several of
the anticancer drugs. The skin is easily inflamed or injured. Modify technique
pressures. Do not massage on-site where there is a skin rash or local inflammation.
9. Modify appropriately around injection sites and implanted medication delivery

devices. Guidelines related to this subject are addressed in detail in Chapter 5.
Specific Guidelines
1. Alkylating Drugs
Use of these drugs often causes respiratory system compromise (pulmonary fibrosis),
increasing the workload of the muscles of respiration. It is a good idea to incorporate
more focus on these muscles, as appropriate, in your treatment plan. In addition, poor
oxygen delivery and inadequate carbon dioxide removal can weaken body tissues.
Stay alert about the depth of your manual techniques.
Convulsions and seizures can occur as central nervous system side effects of this drug
group. Consult to evaluate whether massage therapy is appropriate for the client. If
massage is approved, determine what treatment scheduling is best suited to the
stability of the condition.
Peripheral neuropathy may also occur. The symptoms can vary tremendously in
degree and intensity. Identify exactly where the areas of involvement are. If the
symptoms are severe, avoid local massage; if the problem is more mild, employ light
techniques and monitor how the client’s body responds. Keep in mind that sensory
perception may be altered.
2. Antimetabolites
These drugs are associated with a number of CV and blood disorders, including easy
bleeding, slow clotting, increased blood pressure, and anemia. It is important to adjust
the depth of your manual techniques as a matter of course when the antimetabolites
are being used. Monitor cardiovascular changes on a treatment by treatment basis.
The information about central and peripheral nervous system side effects presented in
the section above for the alkylating drugs applies as well to the antimetabolite group.
3. Antitumor Antibiotics

The antitumor antibiotics produce respiratory side effects as outlined for the alkylating
drugs, and their potential blood and cardiovascular complications are the same as
those described above for the antimetabolites.
4. Hormonal Agents
Tamoxifen use is related to increased incidence of deep vein thrombosis (DVT), which
often presents as complaints of calf and foot muscle cramping, tired feet, and swollen
ankles. Local massage where a thrombus is present can result in serious complications.
If suspicious, refer for medical evaluation before massaging the affected body part.
Irritated injection sites are typical of flutamide. Evaluate the site carefully and refer to
Chapter 5 for treatment related guidelines.
The information given about blood and cardiovascular side effects in the
antimetabolite section applies to the hormonal agents as a group. In addition,
orthostatic hypotension is very commonly reported with these drugs.
5. Drugs that Affect the Mitotic Spindle
Like the alkylating drug group and the antitumor antibiotics, mitotic spindle drugs can
cause pulmonary fibrosis. Check the information given earlier in these Specific
Guidelines. Similarly, seizures, convulsions, and peripheral neuropathies can occur
with use of drugs in this category.
Specific to this group of anticancer medications is a complication called paralytic ileus

(intestinal paralysis) that can lead to bowel obstruction. Presence of symptoms that
may be indicating this condition, such as constipation, pain, and increasing distension
should be treated as a medical emergency. Massage treatment is contraindicated.
6. Interferons
Interferon use can cause insomnia and mood changes. It is important to be sensitive
to the fact that emotional symptoms may be beyond the client’s control. Shorter
treatments may be appropriate.
Clients taking antineoplastic drugs and various adjunctive medications can pose a number of
concerns related to hydrotherapy use. Before making any hydrotherapy decisions, confirm
whether there are medically prescribed temperature or modality restrictions and check on the
presence of sensory changes or impairments. Take note of all the medications being used and
how they could influence hydrotherapy effects.
Cardiovascular Concerns: Heart and blood vessel responses are altered by many of the

drugs a client with cancer might be taking. Blood vessels may overreact to mild stimuli and
produce adverse effects like vasospasm and vascular pooling. Easy bleeding and slower
clotting can be exacerbated by hydrotherapy applications. The heart, liver, and kidneys under
stress frequently react adversely to intense stimuli like systemic hydrotherapy. Systemic
treatments should be modified or eliminated from the treatment plan altogether when the vital
organ systems are compromised.
Respiratory Concerns: Steams, saunas, and other forms of systemic hydrotherapy that
increase respiratory workload are not recommended. This is especially true for clients with
pulmonary fibrosis or who complain of shortness of breath.
General Enervation: The fatigued or debilitated client is more likely to benefit from smaller
local applications with modified temperatures.
Tissue Sensitivities: Chemotherapy and radiation treatments can make the skin and
underlying tissues fragile and either hypersensitive or hyposensitive to temperature stimuli.
As a general rule, it is contraindicated to wet rashes or other open sores or skin lesions. There
are usually specific restrictions placed on water applications at radiation sites.
Inquire about the bath or shower practices used at home or by the hospital/hospice staff – this
information is a guide to what is being well tolerated. If in doubt, seek medical advice. Where
it is considered appropriate, introduce hydrotherapy slowly and incrementally into the
treatment plan. Ensure that other members of the health care team are aware of your program
and that it is compatible with the rest of the client’s treatment schedule.
Vomiting and diarrhea stress the abdominal musculature. Cool abdominal washes support the
general health of the gastrointestinal tract and relieve muscle soreness. However, abdominal
hydrotherapy is contraindicated with gastrointestinal bleeding or severe irritation or
restriction in bowel function.
Dehydration is a common result of GI disturbances – encourage adequate hydration,

especially when using heat modalities.
Build your exercise plan around the client’s lifestyle, energy level, and body system health.
Ensure that there is medical approval for any exercise program being undertaken. Consult
with other members of the health care team if uncertain about how specific activities might
affect the medical treatment protocol or cancer progression. Monitor closely.
Make sure the client is aware of the importance of adequate hydration and nutrition before and
during exercise.
Be alert to complaints of cramps, extremity swelling, and muscle fatigue. These may be
related to a serious complaint like deep vein thrombosis. Medical evaluation is important to
assess for this complication – exercise must be suspended until the ‘all clear’ is given. These

symptoms may also be more minor medication side effects or caused by low electrolyte
levels. In this case, modified exercise may still be appropriate.
Some of the drugs used for managing cancer can predispose to photosensitivity reactions.
Instruct such clients to avoid exercising in direct sunlight.
Any respiratory or cardiovascular disorders or other major health status concerns must be
taken into account. The client’s current activity level can be a useful guide in designing an
exercise plan. However, do not exceed your scope of practice. It is important to acknowledge
when greater expertise is required.
1. The National Cancer Institute of Canada, “Current Incidence and Mortality”

www.cancer.ca/stats/highle.htm
2. Fierro, M., “How Much Does Cancer Cost?” Health Policy Studies
www.nga.org/center/divisions/1,1188,T_CEN_HES%5EC_ISSUE_BRIEF%5ED_1915,00.html
3. Margaret Foti, Ph.D, American Association for Cancer Research, “Defeating Cancer - A Sense of
Urgency and a Need for Strategic Continuity,” Testimony before the House Appropriations
Subcommittee on Labor, Health and Human Services, Education, March 21, 2000.
www.aacr.org/5000/5300/5300e.html
4. B.C. Cancer Agency, Cancer in General, revised April 2001

www.bccancer.bc.ca/pg_t_03.asp?PageID=8&ParentID=2
5. “Chemotherapy and You. A Guide to Self Help During Cancer Treatment,” NIH Publication,
revised June 1999, (99): 1136, National Cancer Institute
cancernet.nci.nih.gov/peb/chemo_you/index.html
6. Cancer Liaison Program, Office of Special Health Issues, Office of International and Constituents
Relations, U.S. Food and Drug Administration www.fda.gov/oashi/cancer/cdrugind.html
7. “Review of Anti-Angiogenesis Drugs for Lung Cancer”

www.lungcancerclaims.com/antiangiogenis%20lung%20cancer.htm
8. Curties, D., Massage Therapy & Cancer, Curties-Overzet Publications, Moncton, 1999

CHAPTER 12
Drugs for Managing HIV/AIDS
Since its discovery almost twenty years ago the human immunodeficiency virus (HIV), the
organism that causes AIDS, has challenged scientists and researchers to find a cure. The
urgency to solve the mysteries of AIDS and find a vaccine or drug that can eliminate it is
fueled by the tremendous toll this disease is taking globally:1
• As of the end of 2000, an estimated 36.1 million people worldwide
(34.7 million adults and 1.4 million children under 15) were living with
HIV/AIDS.
• Approximately 5.3 million new HIV infections (about 15,000 per day)
occurred during 2000.
• The year 2000’s global mortality rate was approximately 3 million people,
including an estimated 500,000 children under 15.
North American statistics include the following information:

• The Centers for Disease Control and Prevention (CDC) estimate that 800,000
to 900,000 U.S. residents are living with HIV, one-third of whom are
unaware of their infection.
• Approximately 40,000 new HIV infections occur each year in the United
States, 70% in men and 30% in women. Half of the newly infected people
are under 25.
• As of the end of 2000, a total of 774,467 cases of AIDS in the U.S.
population had been reported to the CDC and 448,060 deaths had been
recorded. AIDS is now the fifth leading cause of death in the United States.
• A cumulative total of 45,534 positive HIV tests were reported in Canada2 up
to December 31, 1999.
Viruses are especially difficult to counteract because they incorporate themselves into the host
body’s own cells. The majority, however, like the measles and mumps viruses, are self-
limiting in most people. The appearance of HIV has motivated researchers to focus with
greater intensity on developing effective antiviral drugs. It is a painstaking and expensive
process – the average cost of researching and developing a single drug for human use is about
$500 million. One company reportedly spent more than $1 billion over a ten-year period to
develop a protease inhibitor. There are currently 78 pharmaceutical and biotechnology
companies researching and developing over 113 antiviral medicines and vaccines.3

Despite the fact that there is still no cure for HIV/AIDS, important advances have resulted in
the development of a number of medications that significantly extend life expectancy for
people who test HIV positive. In order to understand how they work, it is necessary to
consider the structure and replication cycle of the virus.
Viral Structure
A virus is one of the smallest living
microorganisms. It consists of strands of viral glycoprotein
DNA or RNA (the viral genetic code) genetic spike
contained inside a shell called a capsid or code
nucleocapsid. A glycoprotein envelope,
actually made from a small section of the
prior host cell’s membrane, surrounds
and protects the capsid and its viral core
material. Protruding though this envelope
are spiky extensions that help the virus
detect and attach to cellular receptor
proteins.
Viruses such as the chicken pox and capsid

herpes simplex viruses contain DNA,
viral
while those with RNA strands, such as
envelope
measles and HIV, are known as
retroviruses.
Replication Cycle of a Virus

Once established in a host, a single virus can produce more than one billion new viruses per
day. This is typical production for HIV, even though each virus only lives about 1.6 days.
There are several steps or phases4 in viral replication, including:
• binding
• entry
• uncoating and reverse transcription
• nuclear entry
• integration and transcription
• translation, assembly, and budding
We will examine these steps in more detail using the specific example of the HIV retrovirus.
Phase 1: Binding
The HIV virus is attracted to T helper cells, which are immune cells that play an important
role in the body’s defense against invading organisms and foreign substances. These cells

have a marker or receptor called CD4 on their surfaces. When the virus identifies a cell with
CD4 receptors it attaches itself to the cell’s membrane.
Phase 2: Entry
The virus then penetrates the host cell and squeezes its capsid through the cell’s membrane
and into the cytoplasm. All the substances necessary for viral replication, including several
forms of its RNA and the enzymes reverse transcriptase, integrase, and protease, are included
in the material inserted into the cell.
Phase 3: Uncoating and Reverse Transcription

Once inside the cell the capsid opens and releases its contents directly into the cytoplasm.
Using the enzyme reverse transcriptase, the virus begins to transcribe its RNA genetic code
into a form that resembles the DNA of the host cell. This is necessary because the cell’s
nucleus will only allow entry to DNA.
Phase 4: Nuclear Entry

Once the virus has made its own form of DNA the strands are transported to the host cell’s
nucleus where they are allowed easy access through the nuclear membrane.
Phase 5: Integration and Transcription

Inside the nucleus the virus uses the enzyme integrase to insert its own genetic material into
the host cell’s DNA. The viral DNA, with all the mechanisms for self-replication in place, can
remain dormant within the host cell nucleus for months or years before it is activated. Once
activated, the virus takes control of the cell and begins its replication process. It starts by
re-converting its DNA into viral RNA, which leaves the nucleus and re-enters the cell’s
cytoplasm.
Phase 6: Translation, Assembly, and Budding

The viral RNA is ‘translated’ into long bands or chains of viral proteins, which are then cut
into smaller pieces by the enzyme protease. The resulting genetic parts are assembled by
messenger RNA into numerous sets of core viral material resembling the contents of the virus
that originally infected the cell.
Once assembled the viral particles migrate in groups to the cell membrane. In order to be able
to infect other cells this viral material must leave the host cell and enter the blood. Each set
of viral core material pushes into the cell membrane to form a ‘bud’ which eventually breaks
away from the cell. As it does so it takes a piece of the cell membrane with it, forming an
external envelope for the new virus.
An infected host cell can produce millions of viral copies before its resources are exhausted
and it dies.

CD4 cell
receptors membrane
T helper cell
Phase 1: attraction Phase 1: binding Phase 2: entry
viral DNA
viral RNA
reverse
transcriptase viral DNA
nucleus host cell DNA

nucleus
Phase 3: uncoating Phase 3: reverse transcription Phase 4: nuclear entry
viral RNA
integrase viral RNA translation into
replication viral proteins
viral DNA
Phase 4: integration Phase 4: transcription Phase 5: translation
protease
Phase 5: assembly Phase 6: budding Phase 6: release

1. ANTIVIRAL DRUGS
Antiviral drugs act to disrupt enzyme functions at several stages of the viral replication
process. Where possible these drugs are designed to target the specific characteristics and
behaviors of individual viruses, as is the goal with HIV. HIV pharmaceutical treatment
protocols are often referred to as ‘drug cocktails,’ since several drugs are used in combination.
This chapter will focus on the following drug groups:
• reverse transcriptase inhibitors

• nucleoside analogues reverse transcriptase inhibitors (NRTIs)
• non-nucleoside reverse transcriptase inhibitors (NNRTIs)
• protease inhibitors
• interferons
• new drugs under development
Nucleoside Analogues Reverse Transcriptase Inhibitors (NRTIs)

Drugs in this category include: AZT, zidovudine (Retrovir), acyclovir (Zovirax), ddI,
didanosine (Videx), ddC, zalcitabine (Hivid), d4T, stavudine (Zerit), and 3TC, lamivudine
(Epivir).
AZT, which was approved in 1987, was the first official anti-AIDS drug. Prior to that
acyclovir had been approved in 1982 for treating herpes infections in hospitalized patients
with compromised immune systems. These two drugs, and the other members of the NRTI
group, are now commonly used in combination with other antiviral medications in the overall
management of HIV and AIDS-related diseases.
Mechanism of Action
Nucleotides are the bases, or building blocks, of DNA and RNA. There are five nucleotides:
adenosine (adenine), cytidine (cytosine), guanosine (guanine), thymidine (thymine), and
uridine (uracil). They combine in specific pairs and with other compounds to form either
DNA (deoxyribonucleic acid), or RNA (ribonucleic acid).
During the uncoating and reverse transcription phase of viral replication, the virus converts
its own RNA structure into DNA strands. The viral DNA is accepted by the host cell’s nucleus
in part because the enzyme reverse transcriptase utilizes the cell’s own stored nucleotides to
assemble its strands.
The term analogue is used in chemistry to denote compounds that are structurally similar.
Nucleosides are components of nucleotides (a nucleoside + phosphoric acid = a nucleotide).
The NRTIs are nucleoside-like compounds that enter body cells and are incorporated by

intracellular enzymatic processes into forms that resemble normal nucleotides. Reverse
transcriptase begins to use these ‘false’ nucleotides to form viral DNA strands. The result is
defective DNA that cannot be integrated into the host cell DNA, inhibiting or slowing down
the replication process.
A serious side effect of the NRTIs is lactic acidosis.5 It is a complication that can make the
person extremely ill, but the onset is often not distinguished quickly enough from the
general AIDS-related symptom picture. The signs and symptoms of lactic acidosis include:
nausea and vomiting
abdominal pain
liver dysfunction
anorexia and weight loss
lethargy and general malaise
hyperventilation and/or dyspnea
cardiac dysrhythmia
cyanosis and cold extremities
Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)

In 1996, nevirapine (Viramune) was the first member of this drug group to be granted
accelerated approval by the Food and Drug Administration. Others include delavirdine
(Rescriptor) and efavirenz (Sustiva). The NNRTIs are also used in combination with other
antiviral drugs to control HIV/AIDS.
Mechanism of Action
The NNRTIs disrupt the formation of viral DNA, but they use a different mechanism from the
NRTIs. They inhibit the activities of reverse transcriptase by binding onto it. Without this
enzyme the virus is unable to make its DNA, and the replication process comes to a halt.
Peripheral neuropathy is a commonly experienced side effect of the NNRTIs. It occurs in

varying degrees of intensity and at its most severe is very painful. Symptoms include
numbness and tingling, reduced reflexes at the ankle, and aching/burning pain in the
legs and feet that can be intense enough to prevent walking. There may also be signs of
nerve inflammation and muscle atrophy.

Protease Inhibitors (PIs)
This group of drugs, which includes amprenavir (Agenerase), saquinavir (Fortovase),
ritonavir (Norvir), indinavir (Crixivan), nelfinavir (Viracept), and lopinavir/ritonavir
(Kaletra), was first introduced in late 1995. They are much more powerful than the reverse
transcriptase inhibitors and have been rapidly incorporated into the drug cocktails used to
manage HIV/AIDS. As of 1999 their global market value was already estimated at
approximately $2 billion.6
Mechanism of Action
The antiviral activity of the protease inhibitors occurs during the translation, assembly, and
budding phase of viral replication. They interfere with the role played by the protease enzyme,
which cuts long chains of proteins into smaller sections of viral core material.
The protease inhibitors resemble viral protein chains. They put themselves in the way of the
protease enzyme, causing it to cut the drug instead of the viral strands. The ensuing process
of assembling units of genetic material incorporates improperly cut viral strands; the new
viruses that are ultimately produced are defective and non-infectious.
Lipodystrophy, a disturbance or defect of fat metabolism, is often observed in protease

inhibitor users. Fat is typically lost from the arms, legs, and face, and appears to be
redistributed around the abdomen and at the cervicothoracic junction, where it forms a
‘buffalo hump.’ The exact cause of this metabolic change is not clear and is currently
being researched.
Interferons
Interferons are released from lymphocytes,
macrophages, fibroblasts, and certain types of
epithelia following viral exposure. Their purpose is
to stimulate non-infected cells to produce antiviral
substances to protect themselves from attack.
Interferons also assist in controlling cell growth

and replication, which has led to their role in cancer
therapy. In addition to their antiviral properties,
interferons are used in the HIV context to treat
Kaposi’s sarcoma, a blood vessel cancer closely
associated with AIDS.
For more information, the reader is referred to the

section about interferons in Chapter 11.

New Drugs Under Development
The drugs presently in use to manage viral infections all affect the virus’s replication process
once it is inside a host cell. New antiretroviral drugs currently in clinical trials, called the
‘entry inhibitors,’ seem to be able to prevent the virus from binding to and entering cells.7
Second generation protease inhibitors8 are also under investigation. They have an improved
chemical structure that allows for better antiviral activity. Laboratory testing shows encouraging
results against the HIV virus, but these drugs have not yet entered the clinical trial phase.
Protease Inhibitors
insert themselves in
place of viral protein
strands.
Translation, Assembly and Budding

The viral DNA is converted back to
RNA, re-enters the host cell’s Interferons
cytoplasm, assembles new sets of viral act to increase the
genetic material with the help of the immunity of the
protease enzyme, and leaves the cell host cells.
through a process called budding.
Binding
Integration and Transcription The virus is attracted
The virus uses the integrase to and binds to a cell
enzyme to insert its own DNA membrane receptor.
into the host cell DNA. Entry Inhibitors
These new drugs are
being designed to
prevent viruses from
Entry
entering host cells.
Nuclear Entry Viral material
Viral DNA enters the enters the host
host cell nucleus. cell.
Uncoating and
Reverse Transcriptase
The virus makes its own
form of DNA with the
assistance of the reverse
transcriptase enzyme.
NRTIs and NNRTIs
interfere with reverse
transcriptase functions.
The actions of the antiviral drugs

SIDE EFFECTS – Drugs for Managing HIV/AIDS
Side Effects PI NRTI NNRTI Side Effects PI NRTI NNRTI
Abdominal Pain X X Increased Bleeding X XXX
Anemia XX XX XX Increased Cholesterol, Triglycerides XXX XX XX
Anorexia X X Insomnia X X XXX
Anxiety X X Intense And Unusual Dreams X XX
Arthritis X X Kidney Stones X
Ataxia X Lactic Acidosis XXX
Back Pain X Leukopenia XX XX
Blood Disorders XXX XXX XXX Libido Disorders X
Blurred Vision X X Liver Disorders XXX XXX XXX
Bacterial, Viral, Fungal Infections XX Menstrual Irregularities X
Breast Enlargement X Microhemorrhages XX
Chest Pain XX Mood Changes X
Chills X X X Mouth Sores XX
CNS Depression XX XXX Muscle Atrophy X XX
Confusion X X Myalgia X X X
Convulsions XXX XXX Nausea XX XX XX
Cough X X Nervousness X X
Cramps X Neutropenia XXX XXX XXX
Decreased Concentration XX Nosebleeds X
Depression X XX Palpitations XX XX
Diarrhea XX X XXX Pancreatitis XX XXX XXX
Dizziness X X XX Peripheral Neuropathy XXX XXX XXX
Dreams – Intense, Unusual X XX Photosensitivity X
Dry Mouth X X Pneumonia XX XX
Dyspepsia X Prickling Skin Sensation XX
Edema X Psychotic Disorder X
Euphoria X Respiratory Disorder XX XX
Ear Pain X X Rhinitis X
Face, Tooth Pain X Seizures XXX XXX
Fat Redistribution XX Skin Rash XX XX XX
Fatigue, Drowsiness X X XX Skin Ulcers And Other Changes XX
Fever XX X X Splenomegaly XX
GI Distress, Constipation XX X X Sweating X X
Hair Loss X X Swollen Belly XX
Hyperesthesia XX Taste Changes X X XX
Hyperglycemia XX Thrombocytopenia XX XX
Hyper/Hyporeflexia X Vasodilation XX
Headaches XX XXX Vomiting X X
Hypertension X XX Weakness X XX X
Hypotension X Weight Increase/Loss XX
NA: Nucleoside Analogues, NNRTI: Non-Nucleoside Reverse Transcriptase Inhibitors, PI: Protease Inhibitors
x – tolerable – notify medical practitioner if bothersome
xx – serious – monitor closely and notify medical practitioner
xxx – very serious – seek medical attention

Quick Guide to Case History Questions
HIV positive clients have health statuses that range from normal health through terminal
illness, so case history taking needs to reflect the circumstances in each case. Most people
with HIV/AIDS are educated about their condition - don’t hesitate to ask questions.
Questions
1. Date of HIV diagnosis; stage and progression. History of related illness? Is the
condition presently well stabilized? If the person has active AIDS, get details of
current symptom picture, opportunistic conditions.
2. Medications: identify all pharmaceuticals and remedies being used. Is the drug
cocktail working well? Ask about medication side effects – how are they being
addressed? Have there been any episodes of drug toxicity, especially recently?
If yes, how managed?
3. Method(s) of medication administration – any injection sites or implanted devices?
4. Vital system health: Inquire about the status of the heart, liver, and kidneys in
particular, as well as presence of any systemic disorders. Any problems with blood
pressure control? If yes, how managed? Any breathing difficulties?
5. General nutritional status: Eating properly – good appetite? Taking nutritional
supplements? Ask about current or recent experience of anorexia, nausea,
vomiting, diarrhea, or constipation (contribute to dehydration, electrolyte loss,
decreased absorption of nutrients). Any recent unexplained changes in weight?
General tissue health, healing times?
6. Inquire in detail about skin health – rashes, irritated areas, locations of hypo- or
hypersensitivity, open lesions, skin cancers. Any topical medication applications?
7. Success with handling stress? Problems with anxiety, depression? If yes, how
managed?
8. Support system – family, friends, health care team, support group? Does the client
feel well supported?
9. Experience with massage? Goals in seeking out massage therapy?
Observations
1. Observe general posture, body weight/thinness, gait and mobility, breathing patterns.
2. Check the skin for:
• color and signs of vitality
• texture and moisture
• rashes, infections, lesions
• scars: identify relevance - related to lesion removal, injection sites?
• fragility, discoloration, bruising
3. Edema – if present, check for pitting.
4. Observe any locations of altered tissue sensation.
5. Check for fatty tissue redistribution.

Quick Guide to General Treatment Issues with HIV/AIDS Clients
Medication side effects and AIDS-related symptoms can vary from one session to the
next. Ensure you are familiar with the client’s current health picture before beginning
each treatment. Be flexible in adjusting your approach to the circumstances and the
client’s goals.
1. Familiarize yourself with the universal AIDS prevention guidelines, which should form
the basis of your hygienic practices with all clients. You can obtain these documents
by contacting the National AIDS Information Clearinghouse (1-800-458-5231) or the
AIDS Hotline (1-800-342-2437), or view them at the Centers for Disease Control and
Prevention website: www.cdc.gov/ncidod/hip/blood/universa.htm. A good
Canadian source is the Canadian HIV/AIDS Clearinghouse (1-877-999-7740), website:
www.clearinghouse.cpha.ca.
Find answers to any questions you may have about the spread of HIV, as well as
guidelines for health care workers.
2. Remember that clients with AIDS have compromised immune systems. If you are ill with
anything contagious, postpone the appointment. Be conscientious about infection
control in your treatment space, especially if an earlier client has had a ‘bug.’
3. Begin slowly with new clients and monitor responses to therapy closely. If unsure about
treatment plan decisions, consult with the attending physician.
4. Take the client’s blood pressure regularly. It is good clinical practice and helps to
monitor cardiovascular stress and medication side effects. Pre- and post-treatment
blood pressures can also help you evaluate the response to therapy.
5. Adapt your treatment plan around tissue fragility and sensory changes. Local
treatment is contraindicated where there are skin rashes or lesions.
6. Client position and comfort: Some HIV/AIDS clients will have painful musculoskeletal
symptoms – positioning needs to be adapted to what is comfortable. Keep the room
warm and use blankets as needed – chills and cold extremities can affect the client’s
comfort and ability to relax during the treatment. The cachexic client must be well
pillowed to avoid pressure on bony prominences.
1. Maintain a strong focus on relaxation. Encourage deep and relaxed breathing,

especially at the start of treatments (adapt if there are respiratory complications).
2. When edema is present, elevate the tissues/limbs to facilitate drainage. Exercise

appropriate precautions if the cardiovascular system is weakened (see Chapter 7).
3. Modified effleurage and petrissage, slow rhythmic techniques, passive range of

motion, and gentle joint play are usually appropriate for clients who have more
advanced AIDS illnesses.
4. Deep and aggressive techniques are not recommended where there is tissue fragility
or impaired sensation.

Massage Guidelines – Clients Taking Medications for HIV/AIDS
General Guidelines
1. Clients with HIV/AIDS can be taking several types of drugs for various reasons,
including:
• managing the HIV virus (the drug cocktail)
• controlling/preventing a variety of medication side effects
• treating AIDS-related diseases/conditions like pneumocystis carini, candidiasis,
and other fungal infections, tuberculosis, Kaposi’s sarcoma, dementia, and
cytomegalovirus infections such as hepatitis, pneumonia, retinitis, and colitis
In addition, supplements, herbs, and remedies are often used.
Some of the adjunctive medications a client with HIV can be taking will have been
discussed in previous chapters of this book while others will not. Be prepared to
research in drug reference texts or on the Internet.
Multiple medication use, especially with some of the potent pharmaceuticals in drug
cocktails, can predispose to adverse and toxic effects. Practitioners should always be
vigilant in monitoring changes in client signs and symptoms.
2. There are some severe side effects common to the drugs discussed in this chapter. The
ones that follow usually contraindicate massage therapy until they have been
medically addressed and stabilized:
• pancreatitis: Early indicators of pancreatitis can be overlooked among the

general medication side effects and symptoms of the disease. Be alert to
complaints of nausea, vomiting, and abdominal pain that refers to the back.
• blood disorders: Thrombocytopenia, leukopenia, neutropenia, and severe
anemia are examples of the more serious blood disorders that can develop.
If the person has been medically evaluated and massage is appropriate, the
practitioner must pay careful attention to the health of the tissues and to
microvasculature fragility. Deep or aggressive techniques are contraindicated.
• liver dysfunction: The liver’s normal physiologic functions are often
suppressed or impaired by medication effects, and liver dysfunction in turn
contributes to poor metabolism and excretion of drugs. Toxic metabolite
accumulation can occur and produce adverse reactions.
• skin rashes and irritations: Skin lesions of varying degrees of seriousness can
develop for a number of reasons in the AIDS client. In some cases, especially
when there is a rapid acute onset, a skin rash may be indicating a severe drug
reaction. Another possibility is the development of a secondary infection like
shingles. These can be very serious in immunocompromised individuals.

3. Be sensitive to the client’s health changes from treatment to treatment. Anorexia,
vomiting, diarrhea, and liver and blood disorders occur frequently with antiretroviral
medications. Their effects can be quite enervating, causing weakness and debilitation
that can be made worse by massage and hydrotherapy treatments that are too intense.
Make sure that the client knows it is okay to cancel appointments, even on short
notice, if he or she is feeling too unwell.
4. Musculoskeletal aches and pains are common complaints associated with taking
HIV/AIDS medications. Given all the factors, related or unrelated to HIV, that may
cause this type of symptom, it can be difficult to discern whether the complaints are
medication side effects. If massage work is not proving effective, or if the practitioner
senses that the symptoms are not ‘routine,’ medical follow-up should occur.
5. Peripheral neuropathy can be caused by progression of the AIDS condition or by an

AIDS-related infection, or it can be a drug-induced side effect. The intensity of
peripheral neuropathy symptoms varies considerably – at its most severe it may make
touch intolerable. If massage is indicated, aspects of the treatment plan like client
positioning and technique depth will need to be modified. Keep in mind that client
feedback will likely be inaccurate.
6. Facial pain, ear pain, and headaches are all common side effects of the medications
discussed in this chapter. Inquire about the most comfortable position(s) and pillow for
protection and support.
7. Because of medication effects like dizziness, fatigue, and orthostatic hypotension,

give clear instructions concerning getting on and off the massage table – help the client
if necessary.
8. Some clients will have implanted medication delivery devices. Ensure that such
devices are not compromised by the client’s position. For more detailed guidelines,
refer to Chapter 5.
Specific Guidelines
1. Nucleoside Analogues Reverse Transcriptase Inhibitors (NRTIs)
Lactic acidosis can be a serious side effect of this medication group. Massage therapy
is contraindicated until the condition is resolved. Practitioners should be vigilant for
lactic acidosis symptoms (listed earlier in this chapter). If a client appears to be
developing this condition, advise immediate medical care.
Some people develop breathing problems like asthma. Check for respiratory system
medications (refer to Chapter 9). It may be appropriate to focus additional attention
on treating the muscles of respiration.
The NRTIs are associated with easy bleeding. Observe for signs of bruising and make

sure to modify technique depth as a matter of course with clients using medications in
this group.
Vasodilation, caused by skeletal muscle atrophy (resulting in reduced vein support),

can lead to the development of extremity edema. Observe for varicosities, and
exercise caution when working around distended veins. Position the edematous tissues
to facilitate drainage. Refer to Chapters 5 and 7 for more guidelines related to
peripheral vasodilation.
The NRTIs often cause hypertension, which will be controlled medically as much as
possible by altering the antiviral drug mix and adding antihypertensives. There is the
potential, however, for chronic hypertension to stress the heart and promote a degree
of heart failure. If this is the case, the massage therapist needs to incorporate treatment
adaptations as outlined in Chapter 7.
Central nervous system depression may be present, causing generalized fatigue that
may necessitate shorter treatments. The implications of CNS depression for massage
treatment planning are discussed in more detail in Chapter 10.
Seizures and convulsions also occur in some people. If the condition has been
stabilized and massage therapy is considered appropriate, schedule your sessions in
order to maximize bioavailability of the anticonvulsant medications.
2. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Central nervous system side effects like dizziness, headaches, depression, poor
concentration, and insomnia are associated with NNRTI use. These effects tend to
occur for a few weeks following start of therapy. Clients are more easily overtaxed
physically and emotionally. It is important to be sensitive and flexible. Shift to a
shorter, less intense treatment design.
Gastrointestinal distress, especially diarrhea, can be a problem with the NNRTIs. If

not properly managed, it can lead to a degree of electrolyte loss that predisposes to
cardiac dysrhythmia. As well, muscles and their tendons can become hyper-
responsive to manual techniques, resulting in cramping and spasms. It is important for
the client to maintain hydration and good nutrition, and to seek medical assistance
with diarrhea control. The massage therapist may need to restrict technique usage to
very light, rhythmical approaches.
3. Protease Inhibitors (PIs)
Kidney stones can develop when these drugs are used. The initial symptom is usually
sharp cramping pain, often referred to as flank pain, that is experienced in the vicinity
of the kidney and down the lateral back deep into the abdomen. The pain may also
spread to the groin. A complaint of this nature should be referred to the physician.

Lipodystrophy is associated with protease inhibitor use. The client may not notice
these changes immediately, especially if they occur on the back. If this is the case,
bring it to the client’s attention and suggest medical follow up. When massaging, be
aware of the possible sensitivity of the affected tissues and modify your manual
techniques accordingly. Any aggressive approach to ‘break up’ lipid accumulations is
contraindicated.
Hyperglycemia, believed to be related to the fatty tissue redistribution, can be a

problem, especially for diabetics. If you perceive that this side effect may be
developing, suggest follow-up medical evaluation. If the client is or has become
diabetic, the massage therapy treatment design needs to be adapted to be compatible
with diabetic stability. Signs and symptoms of hyperglycemia, as well as treatment
issues and medications for diabetes, are discussed in Chapter 8.
When increased skin sensitivity or other tissue hyperesthesias are present, manual
techniques need to be carefully modified. Identify the affected tissue locations and
adjust technique rate and depth to the specific circumstance. In severe cases touch
may not be tolerable either locally or generally.
Some individuals experience microhemorrhaging when taking protease inhibitors. Be

alert for bruising and modify manual techniques around affected tissue areas.
Hydrotherapy helps strengthen the body physiologically; utilized appropriately it can be an
important part of massage treatment protocols for clients with HIV. Proceed cautiously,
beginning with mild applications that are well tolerated and monitoring reactions to treatment
carefully.
Always determine whether medical restrictions have been placed on temperature use or on the
wetting of any skin surfaces, and identify locations of altered sensation. If uncertain, discuss
the proposed procedure with the physician.
Peripheral neuropathy and tissue hyperesthesia can be aggravated by hydrotherapy

applications. Inquire about the client’s routine bath/shower temperatures and use this
information as a guide in treatment planning.
The PIs and NRTIs can cause increased sweating, especially with systemic heat exposure. If
the client is experiencing this side effect, inquire about whether he or she is drinking fluids
and replacing electrolytes. This information will help the therapist gauge the appropriateness
of heat applications. In general, hot systemic modalities are not likely to be advisable.
Systemic hot hydrotherapy can also intensify the vasodilation effects associated with NRTI
medications and adverse reactions such as dizziness and lightheadedness can occur. Systemic
heat should be avoided unless the client assures you that hot baths/showers are well tolerated.
Some local modalities, like hot footbaths, can also increase vasodilation significantly. With

local treatments, precautions would include using reduced temperatures, smaller applications,
and shortened treatment times. Always monitor the client’s reactions carefully.
Cool abdominal washes are effective in strengthening and toning the digestive tract;
warm footbaths can reduce insomnia; and cool compresses to the neck often alleviate
headaches. Used in a gentle progressive manner such modalities may help manage
drug-related side effects.
Design your exercise plan around the client’s usual activity and energy levels. Consult with
members of the health care team if unsure about how your proposed exercise program might
impact on the client’s health.
Increased sweating, a side effect of the

protease inhibitors and NRTIs, can lead to
dehydration and electrolyte imbalance. This
is a particular concern if the client is
exercising in hot/humid conditions.
Episodes of diarrhea and vomiting can also
cause dehydration and electrolyte deficiency.
Remind the client of the importance of good H 2O
nutrition and fluid replacement before and

during exercise.
Photosensitivity reactions sometimes occur

with protease inhibitor use. When exercising
outdoors the person should be well clothed
and perform activities in shaded areas.
Fatigue and weakness, peripheral neuropathy, and muscle and joint pain are all medication
side effects that can alter the HIV/AIDS client’s ability to exercise. Make sure that the
intensity, frequency, and duration of the suggested exercises are reasonable in each client’s
case. Re-evaluate the exercise plan if the client complains of symptom intensification.

1. Office of Communications and Public Liaison, National Institute of Allergy and Infectious
Diseases, National Institutes of Health, “HIV/AIDS Statistics Worldwide,” MD Public Health
Service, U.S. Department of Health and Human Services, August 2001
www.niaid.nih.gov/factsheets/aidsstat.htm
2. Division of HIV/AIDS Surveillance, Bureau of HIV/AIDS, STD and TB Laboratory Centre for
Disease Control, Health Protection Branch Health Canada, “Reported AIDS Diagnoses,” HIV and
AIDS in Canada Surveillance Report to December 31, 1999 www.avert.org/canstatg.htm
3. Pharmaceutical Research and Manufacturers of America, AIDS and The Pharmaceutical

Industry, Washington, DC
www.phrma.org/publications/backgrounders/development/aids98.phtml
4. “Retroviral Reproduction,” ARIC’s On-Line AIDS Medical Glossary

www.critpath.org/aric/gloss/body/retroviral_reproduction.htm
5. Shikuma, C., “What is Lactic Acidosis Syndrome and Mitochondrial Toxicity?” National AIDS
Treatment Advocacy Project (NATAP), University of Hawaii
www.natap.org/2000/lipo/lipo_rp4pt1whatislact092200.htm
6. HIV/AIDS, Pipeline & Products, Vertex Pharmaceuticals

www.vpharm.com/NonEnhanced/AntiviralNonE.html
7. Blakeslee, D.J., “Entry Inhibitors: The More the Better,” JAMA HIV AIDS Resource Center,
September 22, 2000 www.ama-assn.org/special/hiv/newsline/conferen/icaac00/dbentry.htm
8. “Adding to Antiretroviral Arsenal: New AIDS Drugs in Development. Resistance Repellant?”

CBS HealthWatch, February, 2001 cbshealthwatch.medscape.com/cx/viewarticle/234098_3

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Index
NOTE: Brand name medications are not anti-inflammatories, 52, 57, 70 cabergoline, 189
indexed; use generic names. antimetabolites, 193, 198, 200–1, 205 caffeine, 17, 152
antinausea drugs, 199–200 calcium channel blockers,
3TC, 213 antineoplastic drugs, 192–8 17, 51–2, 65, 105–6, 108, 118–19, 123
antipsychotics, 164, 173–5 cancer, 185–208
acarbose, 133
antithrombotics, 110–11 capecitabine, 188
ACE inhibitors, 106–8, 118–19, 123
antitumor antibiotics, captopril, 107
acetaminophen, 79, 80, 82
193–4, 198, 200–1, 206 carbamazepine, 43–4
actinomycin D, 193
antitussives, 154–5, 160 cardiac dysrhythmia, 97, 98
acyclovir, 213
antiviral drugs, 213–17 cardiac glycosides, 103–4, 118–19
adverse effects. See side effects
anxiety, 163, 165–8 cardiovascular disease, 97–124
affective disorders, 163–84
arsenic trioxide, 188 cardizen, 106
age, 19, 26
aspirin, 12–13, 24, 28, 38, 79, 82 carmustine wafer, 188
agranulocytosis, 183
effects, 19, 20, 56, 146, 158 case history taking, 47–51
AIDS/HIV, 209–25
uses, 18, 19, 50, 80, 111 cancer, 202
albumin, 39–40, 42, 142
assessment, 45–53, 66–8 cardiovascular disease, 120
albuterol, 151
asthma, diabetes, 139
alcohol, 138
63–5, 145–6, 150, 154, 157, 158, 161 HIV/AIDS, 218
alemtuzumab, 188
atherosclerosis, 97, 98 injection sites, 66–7
alitretinoin, 188
Attention Deficit Hyperactivity Disorder mood disorders, 179
alkylating drugs, 193, 198, 200–1, 205
(ADHD), 59 pain and inflammation, 91
allergic reactions, 21, 148–50
atypical antipsychotics, respiratory conditions, 156
allopathic medicine, 13
175, 176–8, 182–3 catheters, implanted; see also implant
allopurinol sodium, 189
AZT, 213 devices, 34–5, 36
alpha-glucosidase inhibitors,
celecoxib, 188
133, 134, 135, 143 barbiturates, 167
cell cycle, 190–2
alpha receptor drugs, 107–8, 118–19 BCG, live, 188
centrally acting skeletal muscle
alprazolam, 167 benzodiazepines,
relaxants, 12, 52, 56, 85
amifostine, 188 164, 167, 168, 176–8, 182, 183, 184
central venous catheter (CVC), 34–5
aminolevulinic acid HCL, 189 benzonatate, 154
cerebrovascular accident, 98
amitriptyline, 170 beta-adrenergic agonists, 151, 152
chemical drug names, 15
amprenavir, 215 beta blockers,
chemical structure, 17–18
anaesthetics, 59, 71, 167 17, 18, 101–3, 118–19, 122
chemotherapy, 187–9
analgesics; see also narcotic analgesics bexarotene, 189
chilled client, 61
57, 60, 63, 154 bicalutamide, 195
chloral hydrate, 167
anaphylaxis reactions, 21 biguanides, 132–3, 134, 135, 142
chlorambucil, 193
anastrozole, 188, 195 bile acid sequestrants, 116
chloropromazine, 174
anemia, 159, 220 bioavailability, 26
chloropropramide, 132
angina pectoris, 28–9, 97, 98, 124 biological response modifiers, 187
chlorpheniramine, 148
angiogenesis inhibitors, 197–8 bipolar depression, 169
chlorpromazine, 200
antacids, 17 bleomycin, 189, 193
cholesterol, 115–17
antiandrogenic drugs, 195–6 blood brain barrier (BBB), 40–1
chronic obstructive pulmonary disease
anti-anxiety drugs, blood coagulation, 56, 109–12, 123
(COPD), 145–6
46, 55, 56, 58, 60, 85, 164, 165–8 blood disorders, 220
chronic pain, 54
antibiotics, 62, 64, 70 blood flow, 39
client complaints, 45–6
anticholinergic drugs, 150, 152 blood pressure, 99–100
client cooperativeness, 58
anticoagulants, 12, 56, 109–10, 118–19 body tissues, 51, 56–7, 157
client feedback, 55
anticonvulsants, 43–4 brain, 39, 40–1
clonidine, 108, 189
antidepressants, 46, 55, 164, 168–73 brand names, 15–16
clozapine, 175
anti-emetic drugs, 199–200 bronchitis, 145–6, 154, 161
CNS depressants,
antiestrogenic drugs, 195 bronchodilators, 150–2, 155, 159
17, 52, 55, 60, 63, 85, 95
antihistamines, bruising, 56
CNS stimulants, 17, 59
148–9, 154, 155, 158–9, 161 buserelin, 195
codeine, 60, 81, 82, 160
antihypertensives, buspirone HC1, 167–8, 176–8
combining of therapies, 13, 43
17, 46, 55, 58–9, 65, 79, 222 busulfan, 188, 193
common flu, 50, 62

congestion, 59, 145–61, 153–4 drug distribution, 39–41 gastrointestinal disorders, 38, 41
congestive heart failure, 98, 103, 124 drug names, 15–16 gemcitabine HCL, 188, 189
constitution, 19 drug processing, 37–42 gemtuzumab ozogamicim, 188
contraceptives, 33, 73 drug pumps, 34, 35–6, 129–30 generic drugs, 15, 16, 41
corticosteroids, 12, 18, 50, 52, 60, 62, dysthymia, 169 glipizide, 132
86–9, 94, 95, 138, 153–4, 160, 195 glycosuria, 125
ear drops, 29
side effects, 46, 55, 56, 89–90 goserelin, 189, 195
efavirenz, 214
cortisone type injections, 65 granisetron, 189, 199, 200
effects; see also side effects
cough and cold medications, 154 griseofulvin, 38
17, 19–21
cough suppressants, 154–5, 160 guaifenesin, 153
elimination, 41–2
coumarin derivatives, 109
Elliotts B Solution, 189 half-life, 25
counter-irritants, 30, 93
embolus, 98 haloperidol, 174, 200
Crohn's disease, 41
emotional disorders, 163–84 heart attack, 63, 97, 98, 124
cromolyn sodium, 150, 155, 159
emotional stability, 55 heart rate, 100–1
cyclobenzaprine, 12, 85
emphysema, 145–6, 161 heavy tapotement, 157
cyclophosphamide, 193
enalapril, 107 heparin, 109, 110
cytarabine, 189, 193
enteric coated preparations, 28 histamine, 148
d4T, 213 entry inhibitors, 216 HIV/AIDS, 209–25
dacarbazine, 193 ephedrine, 59 HMG Co A reductase inhibitors, 116–17
Dantrolene, 85, 90 epidural block, 65 hormonal agents,
daunorubicin, 188, 193 epilepsy, 44, 54, 167 194–6, 198, 200–1, 206
ddC, 213 epinephrine HC1, 151 hydrocodone, 81
ddI, 213 epirubicin hydrochloride, 188 hydrotherapy, 12, 58–62, 71–2
decongestants, ergot alkaloid derivatives, 108 with cancer, 206–7
59, 153, 154, 155, 159, 160, 161 estrogen, 194–5 with cardiovascular disease, 124
deep vein thrombosis, 206 etoposide phosphate, 188 with diabetes, 143
delavirdine, 214 excipients, 37, 41 with HIV/AIDS, 223–4
denileukin diftitox, 189 exemestane, 188 with mood disorders, 175, 183
depots, 33 exercise, 63–5, 138 with pain and inflammation, 95
depression, 163, 164, 168–73 with cancer, 207–8 with respiratory conditions, 160–1
dermal administration; see skin with cardiovascular disease, 124 hydroxyzine, 200
applications with diabetes, 143–4 hyperemia, 12
dexamethasone, 12, 199, 200 with HIV/AIDS, 224 hyperglycemia, 123, 125, 136–8, 223
dextroamphetamine, 59 with mood disorders, 184 hyperlipidemia, 115–16
dextromethorpham hydrobromide (DM), with pain and inflammation, 95 hypersensitivity reactions, 21
154, 160 with respiratory conditions, 161 hypertension,
diabetes, 54, 64, 125–44 expectorants, 153, 154, 155, 160 50, 58–9, 62, 63, 64, 97, 98, 100, 222
diabetic coma, 136–7 experimental uses, 18 hypoglycemia, 136–8, 141, 142
diabetic instability, 136–8 eye drops, 29 hypotension, 59, 122, 160
diarrhea, 41, 207 hypothermia, 175
fasting, 42, 138
diazepam, 19, 20, 167
fatigue, 55 ibuprofen, 12–13, 52, 79, 158
diclofenac, 79
fenoterol hydrobromide, 151 idarubicin, 193
didanosine, 213
fentanyl citrate, 189 imatinib mesylate, 188
digitalis, 103–4, 122
fever, 70, 71, 157 immunocompromised clients; see also
digitoxin, 103
fibric acid derivatives, 116–17 HIV/AIDS, 70, 140
digoxin, 103
filgrastim, 188 immunotherapy, 187
dimenhydrinate, 200
first pass effect, 38, 39 implant devices, 65–70, 72
diphenhydramine, 148, 154, 199
floxuridine, 193 implanted catheters, 34–5, 36
dipyridamole, 111
fludarabine, 193 “indications,” 18–19
dissolving and dissociating, 37–8
fludeoxyglucose, 189 indinavir, 215
diuretics, 17, 65, 113–14, 118–19, 123
fluorouracil, 193 infants, 71
docetaxel, 188
fluoxetine, 172 inflammation, 79–90
dolasetron mesylate, 189, 199
fluphenazine decanoate, 65 injections, 32–3, 129
dopamine, 164, 168, 172, 173, 175
flutamide, 195 injection sites, 32–3, 52, 65–72, 141–2
dosage, 19, 26, 38
frequency of administration, 26 insomnia, 138
doxazosin, 108
insulin,
doxorubicin, 189, 193 gamma-aminobutyric acid (GABA),
54, 65, 72, 125, 127–31, 135, 138
droperidol, 200 164, 167, 168
insulin shock, 136–7
drug classification, 16–18 garlic, 142

interactions among medications, methotrexate, 193 ophthalmic administration, 29
19, 21, 50, 51, 79, 138, 142 methoxsalen, 189 opiates; see narcotic analgesics
interferons, methyldopa, 108 oprelvekin, 189
189, 196–7, 198, 200–1, 206, 215, 216 methylphenidate, 59 oral administration, 27–8
intestinal paralysis, 206 metoclopramide, 200 oral hypoglycemic drugs, 131–4, 142–3
intra-arterial injections, 32 metoprolol, 102 osteoporosis, clients at risk for, 57, 94
intra-articular injections, 32, 33, 69 migraine, 59 otic administration, 29
intradermal injections, 32 mitotic spindle drugs, over-the-counter medications,
intralesional injections, 32 194, 198, 200–1, 206 47, 79, 154
intramuscular injections, mitoxantrone hydrochloride, 189 oxtriphylline, 151
32, 33, 39, 69, 71 mood disorders, 163–84 oxymetazoline, 153
intrathecal injections, 32 morphine, 81
paclitaxel, 188, 189, 194
intravenous administration, mother's milk, 41
pain, 79–90
26, 32, 39, 69, 71 movement examination, 52, 68
pain perception, 52, 57
ipratropium bromide, 152 mucous membrane applications, 28–9
palpation, 52, 67
irinotecan hydrochloride, 188 multiple sclerosis, 63
pamiddronate disodium, 188
muscle pain, 30
joint pain, 30 pancreas, 125
muscle spasm, 84
pancreatitis, 220
Kaposi's sarcoma, 188, 215 mustard poultices, 161
panic disorder, 166
ketazolam, 38, 167 myocardial infarction; see heart attack
paralytic ileus, 206
kidney dysfunction, 25, 122
nadolol, 102 parenteral administration; see also
kidneys, 39, 41–2, 44, 50, 204
naproxen, 79 injections, 31–3
kidney stones, 222
narcotic analgesics, paresthesias, 124, 142, 159, 182
lactic acidosis, 214, 221–2 17, 18, 52, 81–3, 94, 95, 160 Parkinson’s Disease, 164
lamivudine, 213 side effects, 55, 56, 58, 59, 90 paroxetine, 172
letrozole, 188 nausea, 199 pathologies, 19, 26, 38
letter to medical practioner, 53 nefazodone, 172 perineural injections, 32
leukemia, 188 nelfinavir, 215 peripheral neuropathy,
leukopenia, 220 nerve block, 32 205, 214, 221, 223
leuprolide acetate, 189 neuritis, 159 perphenazine, 200
LHRH analogs, 195–6 neurological tests, 52 pethidine, 81
lipid lowering drugs, 115–19, 123 neurotransmitters, 163–4 petrissage, 12
lipid soluble drugs, 41, 65 neutropenia, 220 pharmacology, defined, 11
lipodystrophy, 215, 223 nevirapine, 214 pharmacy, vs. massage therapy, 12
lipoproteins, 115–16 niacin, 116–17 phenothiazines,
liquid oral preparations, 27, 28, 37 nicotine patch, 73 12, 60, 64, 174–5, 176–8, 182, 183, 184
lisinopril, 107 nicotinic acid, 116–17 phobias, 166
lithium, 172–3, 176–8, 183, 184 nifedipine, 106 photosensitivity reactions, 64
liver, 38, 39, 41–2, 44, 50, 204 nilutamide, 189, 195 pioglitazone, 133
liver dysfunction, 25, 220 nitroglycerine, plasma protein binding, 39–40, 42
long-term drug use, 50–1, 52, 62, 95 28–9, 31, 39, 73, 104, 123 platelet inhibitors, 56
loop diuretics, 114 non-nucleoside reverse transcriptase plicamycin, 193
lopinavir/ritonavir, 215 inhibitors (NNRTIs), 214, 216, 217, 222 post-traumatic stress disorder, 166
lorazepam, 167 non-steroidal anti-inflammatory drugs; potassium iodide, 153
lungs, 39, 41, 145 see NSAIDs potassium sparing diuretics, 114
luteinizing hormone, 195 norepinephrine, 164, 170–1, 172, 173 prazosin, 108
lymphoma, 189 NSAIDs, prochlorperazine, 199, 200
12–13, 18, 24, 28, 79–81, 94, 95, 111, 142 profimer sodium, 188
manic-depressive disorder, 169 side effects, 46, 55, 56, 90, 146, 158 propranolol, 102
manual technique selection, 56–8 nucleoside analogues reverse transcriptase protease inhibitors (PIs),
massage therapy inhibitors (NRTIs), 215, 216, 217, 222–3, 224
defined, 12 213–14, 216, 217, 221–2, 223, 224 protective responses, 56
vs. pharmacy, 12 pseudoephedrine, 59, 153
mechanisms of action, 22–5 observation, 51–2, 67
psychosis, 173–5
mechlorethamine, 193 obsessive-compulsive disorder, 166
pulmonary fibrosis, 205, 206
meclizine, 200 octreotide acetate, 189
medical stability, 54, 64–5, 140 odansetron, 189, 199 radiation therapy, 186–7, 207
metabolism, 38–9 olanzapine, 175 referrals, 46, 53
metformin, 132 ondansetron, 200 renin-angiotensin system, 106–7
onset of action, 25–6

resource texts, 13–14 thiazide diuretics, 114, 138
respiratory inflammation, 145–61 thiazolidinediones (TZDs), 133–6, 143
retroviruses, 210 thiethylperazine, 200
reverse transcriptase inhibitors, thrombocytopenia, 220
213–14, 216 thrombolytics, 112
risperidone, 175 thrombophlebitis, 71
ritonavir, 215 thrombus, 98, 111
rituximab, 189 timed release preparations, 28
rosiglitazone, 133 timolol, 102
routes of administration, 26, 27–36 tissue plasminogen activator (tPA), 112
topical applications, 29–31
samarium, 189
topotecan hydrochloride, 188, 189
saquinavir, 215
toremifene, 188, 195
schizophrenia, 173–4
toxicity, 44, 122, 173, 183, 204
scopolamine, 200
transient ischemic attack, 98
seasonal affective disorder, 169
trastuzumab, 188
selective serotonin re-uptake inhibitors
treatment guidelines; see also case
(SSRIs), 172–3, 176–8, 182, 183, 184
history taking; exercise; hydrotherapy
self care, 63
43–58, 74–5
serotonin,
for cancer, 203–8
164, 168, 170–1, 172, 173, 175
for cardiovascular disease, 121–4
sertindole, 175
for diabetes, 140–4
sertraline, 172
for HIV/AIDS, 219–25
side effects, 19–20, 21, 46
for injection sites, skin applications,
of cancer drugs, 200–1
and implant devices, 65–73
of cardiovascular drugs, 118–19
for mood disorders, 180–4
of diabetes drugs, 135
for pain and inflammation, 92–5
of HIV/AIDS drugs, 214, 215, 217
for respiratory conditions, 157–61
at injection sites, 69
treatment planning, 54–8
of mood disorder drugs, 176–8
treatment scheduling, 54–5
of pain and inflammation drugs, 90
tricyclic antidepressants,
of respiratory drugs, 155
170–2, 176–8, 182, 183, 184
sinus infection, 62
trifluoperazine, 12, 174
skeletal muscle relaxants,
triglycerides, 115–17
12, 52, 56, 63, 64, 84–6, 90, 94, 95
triptorelin pamoate, 189
skin, 39, 57, 60, 220
troglitazone, 133
skin applications, 30–1, 60, 65–70, 93
tubulin inhibitors, 194
skin patches, 31, 73
typical antipsychotics, 174–5
sleep disorders, 138, 164
solid oral preparations, 27–8, 37, 41 ulcers, 38, 41
solubility, 41
vaccinations, 71
spasticity, 84
valrubicin, 188
special tests, 52
vasoconstriction, 58–60
starch blockers; see alpha-glucosidase
vasodilation, 12, 58–60, 104–8, 222
inhibitors
vasodilators,
statins, 116–17
12, 17, 65, 104–5, 108, 118–19, 123
stavudine, 213
venlafaxine, 172
streptokinase, 112
verapamil, 106
stroke, 63, 97, 124
vinblastine, 194
subcutaneous injections, 32, 33
vincristine, 194
sublingual administration, 39
viral replication, 210–12
succinyl-choline, 85, 86
vitamin K, 109–10
sulfa drugs, 64
vomiting, 41, 199, 207
sulfonylureas, 132, 134, 135, 142, 143
sumatriptan, 59 warfarin, 109, 110
suppositories, 39
xanthine derivatives, 151, 152
tamoxifen, 188, 195, 206
temozolomide, 189 zalcitabine, 213
testosterone, 194–5 zidovudine, 213
theophylline, 151 zoledronic acid, 189

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Massage

RANDAL S. PERSAD Dip. Pharm., R.M.T.

To order copies, please contact:

To my father for his inspiration and wisdom,

There are many people who have encouraged and supported me in my

Massage Therapy & Medications 1

2 Massage Therapy & Medications

Massage Therapy and Medications represents a landmark addition to the literature

John Yates, Ph.D.

Massage Therapy & Medications 3

BASIC CONCEPTS AND GUIDELINES

COMMONLY PRESCRIBED MEDICATIONS AND

4 Massage Therapy & Medications

Massage Therapy & Medications 5

The information presented in this book will give the reader:

• a basic understanding of the concepts and principles of pharmacology

Massage Therapy & Medications 7

Why Massage Therapists Need to Know

A standard definition of pharmacology is “the study of the action of chemicals on living

Massage Therapy & Medications 11

• Centrally acting skeletal muscle relaxants (e.g. cyclobenzaprine) depress

1. The massage technique of petrissage creates hyperemia, while the application

12 Massage Therapy & Medications

To provide safe and effective treatment, massage therapists should have:

Massage Therapy & Medications 13

14 Massage Therapy & Medications

Generic name: diazepam

Official chemical name:

Massage Therapy & Medications 15

Massage practitioners are encouraged to be alert to clients changing medications between

16 Massage Therapy & Medications

The recommendation of a specific member of a drug class by a physician depends on various

Classification by Therapeutic Effect

Classification by Effect on a Specific Body System

Classification by Chemical Structure

Massage Therapy & Medications 17

Sometimes drugs are employed in an unofficial or experimental manner. An illustration of this

18 Massage Therapy & Medications

Massage Therapy & Medications 19

20 Massage Therapy & Medications

• allergic or hypersensitivity reactions

Allergic or Hypersensitivity Reactions

Massage Therapy & Medications 21

• By Combining with Specific Cellular Receptors

22 Massage Therapy & Medications

• By Chemically Altering Body Fluids

• By Chemically Altering Cell Membranes

Massage Therapy & Medications 23

A. Injury Resulting in Pain

B. The NSAID Mechanism of Action

24 Massage Therapy & Medications

TIME IN MINUTES BLOOD CONCENTRATION (mg)

Massage Therapy & Medications 25

26 Massage Therapy & Medications

How Drugs are Administered

The routes of administration discussed in this chapter include:

• oral (into the gastrointestinal tract in solid or liquid form)

Massage Therapy & Medications 27

2. APPLICATION TO MUCOUS MEMBRANES

NAME ________________________________________ AGE _ OCCUPATION _____________________________

FAMILY DOCTOR ________________________________________ PHONE _

Signature: ________________________ Date: