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Physiology and Treatment of Pain

Jennifer E. Helms and Claudia P. Barone

Crit Care Nurse. 2008;28: 38-49
2008 American Association of Critical-Care Nurses
Published online http://ccn.aacnjournals.org
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Critical Care Nurse is the official peer-reviewed clinical journal of the American
Association of Critical-Care Nurses, published bi-monthly by The InnoVision Group,
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Clinical Article

Physiology and
Treatment of Pain
Jennifer E. Helms, RN, PhD
Claudia P. Barone, RN, EdD, LNC, CPC, CCNS-BC, APN


Learn about how pain is

unique for each person.

Do patients with

chronic pain exhibit objective physiological indications expected of patients

with pain, such as pallor,
sweating, tachycardia, and
facial grimacing?

Is there a difference in
how women and men
experience pain ?

How do children experience pain and how should

they be treated if they cannot verbalize their pain

Do elderly patients

experience pain differently

compared with younger
persons or do they just
respond more slowly to

ain often occurs in critical care patients and is

one of the most clinically
challenging problems
for critical care nurses.
Pain and discomfort in these patients
can be due to surgical and posttraumatic wounds, invasive monitoring
devices, prolonged immobilization,
mechanical ventilation, and routine
nursing procedures such as suctioning and dressing changes.1-5 In addition, patients may have a preexisting
chronic pain condition, complicating the assessment and treatment of
acute pain. Pain is a problem in critical care that has not been adequately
addressed.6 Strategies for changing
pain management practices include
providing documentation, implementing pain guidelines, using algorithms, and increasing education in
pain management for acute and
critical care nurses.6 A review of
pain physiology is essential to fully

understand the principles of pain

The pain experience can be functionally divided into acute and chronic
types. Acute and chronic pain are due
to different physiological mechanisms
and thus require different treatments.
In addition, children, adults, and elderly persons have both subtle and
sharp differences in the perception of
pain. Much of the nursing literature
on pain is focused on common interventions but does not explain the
physiological mechanisms of pain and
the vastly different types of pain that
patients may have. Thus, in this article,
we review theories of pain and examine
the physiology of pain, with emphasis
on the types of pain and their manifestations. To provide the best possible
care for patients experiencing pain,
nurses must understand the physiology of pain, the different types of pain
and their varied manifestations, the
diversity of patients responses, and
the rationale for choices of pain control methods.

CEContinuing Education
This article has been designated for CE credit.
A closed-book, multiple-choice examination
follows this article, which tests your knowledge
of the following objectives:
1. Describe the different types of pain
2. Recognize the diversity of patients
responses to pain
3. Understand the physiology of pain

Evolution of Pain Theories

As early as 1644, Descartes proposed a theory of pain, that a straightline channel of pain exists from skin
to brain.7 During the 19th century,
von Frey theorized that pain pathways
move from specialized receptors in


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body tissues to a pain center in the

brain. The focus of this theory, known
as the specificity theory, is specialized
peripheral receptors rather than a central mechanism of pain in the brain.
However, although receptors are specialized, a focus on peripheral receptors
does not explain how an amputee can
feel pain in the amputated limb (a
phenomenon known as phantom limb
pain) when the peripheral receptors
no longer exist.
According to the pattern theory of
pain proposed in the late 19th century,
pain is the result of stimulation of certain nerve impulses that form a pattern
and are then combined and dumped
into the spinal cord as a lump sum of
pain, a process called central summation.7 This theory can better account
for the phantom limb phenomenon,
because the focus is on what occurs in
the brain rather than on peripheral
receptors. However, the theory does
not account for other factors in pain
perception, such as the effect of placebos on pain.
In 1965, Melzack and Wall8 published the well-known gate control theory of pain, the theory most familiar
to nurses. According to this theory, a
mechanism in the brain acts as a gate
to increase or decrease the flow of nerve
impulses from the peripheral fibers to
the CNS. An open gate allows the
flow of nerve impulses, and the brain
can perceive pain. A closed gate does


Spinal cord



Pain sensation
Small-diameter fibers

Figure 1 The gate control theory of pain.

Reprinted from Ignatavicius and Workman,9(p67) with permission. Copyright Elsevier 2006.

not allow flow of nerve impulses,

decreasing the perception of pain
(Figure 1). Although the gate control

Jennifer E. Helms is an associate professor of nursing at Arkansas Tech University, Russellville, Arkansas.
Claudia P. Barone is professor and dean, College of Nursing, University of Arkansas for
Medical Sciences, and a registered nurse II at University Hospital, PRN, Little Rock,
Corresponding author: Jennifer E. Helms, RN, PhD, Associate Professor of Nursing, Arkansas Tech University,
Dean Hall, 402 W O St, Russellville, AR 72801 (e-mail: jhelms@atu.edu).
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.


theory has been widely accepted since

the 1970s, it leaves unanswered questions, including chronic pain issues,
sex-based differences, stress effects, and
the effects of previous pain experiences.
In 1999, Melzack and Wall10 presented a newer theory of pain, consistent with the idea of gate control, that
addresses some of these unanswered
questions. This new and improved
theory, the neuromatrix theory, says
that each person has a genetically
built-in network of neurons called the


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body-self neuromatrix. Just as each

person is unique in physical appearance, each persons matrix of neurons
is unique and is affected by all facets
of the persons physical, psychological,
and cognitive makeup, as well as his
or her experience. Thus, the pain
experience does not reflect a simple
one-to-one relationship between tissue damage and pain.

Primary sensory cortex

Location of pain
Limbic forebrain
Cortical association area
Emotional reaction
Interpretation of pain
to pain
Axons project
to other areas
of brain

Pathways of Pain
Nociceptors, or pain receptors,
are free nerve endings that respond to
painful stimuli. Nociceptors are found
throughout all tissues except the brain,
and they transmit information to the
brain. They are stimulated by biological, electrical, thermal, mechanical,
and chemical stimuli. Pain perception
occurs when these stimuli are transmitted to the spinal cord and then to
the central areas of the brain. Pain
impulses travel to the dorsal horn of
the spine, where they synapse with
dorsal horn neurons in the substantia
gelatinosa and then ascend to the
brain. The basic sensation of pain
occurs at the thalamus. It continues to
the limbic system (emotional center)
and the cerebral cortex, where pain is
perceived and interpreted (Figure 2).
Two types of fibers are involved in
pain transmission. The large A delta
fibers produce sharp well-defined pain,
called fast pain or first pain, typically stimulated by a cut, an electrical
shock, or a physical blow. Transmission
through the A fibers is so fast that the
bodys reflexes can actually respond
faster than the pain stimulus, resulting
in retraction of the affected body part
even before the person perceives the
pain. After this first pain, the smaller
C fibers transmit dull burning or aching
sensations, known as second pain.
The C fibers transmit pain more


Dorsal horn

Release of
substance P

Spinal cord

Noxious stimulus
(may be chemical,
thermal, or mechanical)

Peripheral activity
Release of

Figure 2 Pathways of pain.

Reprinted from Copstead and Banasik,11(p1174) with permission. Copyright Elsevier 2005.

slowly than the A fibers do because

the C fibers are smaller and lack a
myelin sheath. The C fibers are the
ones that produce constant pain.
According to the gate control
theory, stimulation of the fibers that
transmit nonpainful stimuli can block
pain impulses at the gate in the dorsal
horn. For example, if touch receptors
(A beta fibers) are stimulated, they
dominate and close the gate. This ability to block pain impulses is the reason
a person is prone to immediately grab
and massage the foot when he or she
stubs a toe. The touch blocks the transmission and duration of pain impulses.
This capacity has implications for the
use of touch and massage for some
patients in pain.

Regulators of Pain
Chemical substances that modulate the transmission of pain are
released into the extracellular tissue
when tissue damage occurs. They
activate the pain receptors by irritating nerve endings. These chemical
mediators include histamine, substance P, bradykinin, acetylcholine,
leukotrienes, and prostaglandins.
The mediators can produce other
reactions at the site of injury, such
as vasoconstriction, vasodilatation,
or altered capillary permeability.
For example, prostaglandins induce
inflammation and potentiate other
inflammatory mediators. Aspirin,
nonsteroidal anti-inflammatory
medications, and the new COX-2


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Physiologic sources of pain

Physiologic structure
Nociceptive pain
Somatic pain
Clutaneous or superficial: skin and subcutaneous tissues
Deep somatic: bone,
muscle blood vessels,
connective tissues

Visceral pain
Organs and the linings
of the body cavities
Neuropathic pain
Nerve fibers, spinal
cord, and central
nervous system

Characterictics of pain

Sources of acute
postoperative pain

Sources of chronic pain syndromes

Sharp, burning
Dull, aching, cramping

Incisional pain, pain at insertion

sites of tubes and drains,
wound complications,
orthopaedic procedures, skeletal muscle spasms

Bony metastases, osteoarthritis and

rheumatoid arthritis, low back pain,
peripheral vascular disease

Poorly localized
Diffuse, deep cramping or
splitting, sharp, stabbing

Chest tubes, abdominal tubes

and drains, bladder distention
or spasms, intestinal distention

Pancreatitis, liver metastases, colitis,


Poorly localized
Shooting, burning, fiery,
shocklike, sharp, painful

Phantom limb pain, postmastectomy pain, nerve compression

HIV-related pain, diabetic neuropathy,

postherpetic neuralgia, chemotherapyinduced neuropathies, cancer-related
nerve injury, radiculopathies

Reprinted from Ignatavicius and Workman,9(p67) with permission. Copyright Elsevier 2006.

inhibitors block cyclooxygenase 2,

the enzyme needed for prostaglandin
synthesis, thus reducing pain.12,13 Consequently, these medications are often
prescribed for painful conditions due
to inflammation.
The body also has a built-in
chemical mechanism to manage pain.
Fibers in the dorsal horn, brain stem,
and peripheral tissues release neuromodulators, known as endogenous
opioids, that inhibit the action of
neurons that transmit pain impulses.14
-Endorphins and dynorphins are the
types of natural opioidlike substances
released, and they are responsible for
pain relief. Endorphins are the modulators that allow an athlete to continue
an athletic event after sustaining an
injury. Endorphin levels vary from
person to person, so different persons
experience different levels of pain.
This endogenous opioid mechanism may play an important role in
the placebo effect. A placebo is an
inactive substance or treatment used
for comparison with real treatment
in controlled studies to determine the


efficacy of the treatment under study.

Despite the lack of any intrinsic value,
placebos can and do produce an analgesic response in many persons.15
Placebo analgesia can affect nociceptive mechanisms in the cortex of the
brain and descending pathways of the
spinal cord.16-19 Matre et al20 found that
expectations about pain and analgesia
can modify pain perception by altering pain mechanisms in the spinal
cord. For example, psychological factors such as the threat of pain and
expectations about analgesia modify
spinal pain transmission, thereby
modifying pain.

Acute and Chronic Pain

Acute Pain

Acute pain serves a biologic purpose by providing a warning that illness or injury has occurred. The pain
is usually confined to the affected area
and is limited over time. Acute pain
stimulates the sympathetic nervous
system, resulting in fight or flight
response symptoms, including
increased heart and respiratory rates,

sweating, dilated pupils, restlessness,

and apprehension.
Types of acute pain include
somatic, visceral, and referred9 (see
Table). Somatic pain is superficial,
coming from the skin or subcutaneous tissues; visceral pain originates
in the internal organs and the linings
of the body cavities. Referred pain is
felt in an area distant from the site of
the stimulus; it occurs because the
area of referred pain is supplied by
the same spinal segment as the site of
the stimulus21 (Figure 3). Referred
pain often occurs with visceral pain.
Examples include shoulder pain from
myocardial infarction, back pain
from pancreatitis, and right shoulder
pain from gallbladder disease.
Chronic Pain

Chronic pain is prolonged pain,

persisting beyond the expected normal
healing time.23 This characterization
was previously the official definition
of chronic pain according to the International Association for the Study of
Pain. The term chronic is still widely


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Lung and






Figure 3 Sites of referred pain.

Reprinted from Huether and McCance,22(p333) with permission. Copyright Elsevier 2004.

used, although many pain experts now

think that all forms of chronic pain
are variations of the same phenomenon and should be labeled specifically,
such as neuropathic pain.23 Chronic
pain can be continuous (eg, arthritis)
or intermittent (eg, migraines).
Chronic pain is poorly understood
and is more complex and difficult to
manage than is acute pain. Understanding chronic pain requires recognizing that the nervous system is not
hardwired. If it were hardwired, each
noxious stimulus, such as a needle
stick, would elicit exactly the same
nervous system response at the same
intensity every time. But pain is much
more complex, involving affective and
cognitive traits of the person who
experiences it. Melzack and Wall8
showed that repeated stimulation of
C fibers results in progressive buildup
of electrical response in the CNS, a
phenomenon called windup, somewhat analogous to the effect of winding up a childs windup toy. The more
the toy is wound up, the faster and
longer the toy will run. This persistent

stimulation of peripheral nerves winds

up the CNS, leading to intensified
stimulation of nerve fibers that is
referred to as nonnociceptive pain.
The concept of windup is crucial to
understanding chronic pain.24 Windup
is the reason pain can continue long
after the expected recovery time for
an injury or a pain-initiating event.
Patients with chronic pain may
not have the behaviors associated
with acute pain.12 Additionally,
autonomic nervous system responses
(eg, nausea, vomiting, pallor, sweating) decrease with prolonged pain.
The bodys fight-or-flight reaction,
which normally occurs with acute
pain, does not occur because the
sympathetic nervous system has
adapted to persistent pain impulses.
Understanding chronic pain, therefore, requires listening to the persons description of it, because
expected physical symptoms may
not be present. Unfortunately,
because of the lack of objective evidence of pain, many patients who
report chronic pain are viewed as

hypochondriacs and malingerers by

health care professionals.
Some evidence indicates that
chronic pain and depression share
the same physiological pathway.25,26
Tricyclic antidepressants and selective
serotonin reuptake inhibitors have
been used successfully for relief of
many chronic pain syndromes such
as neuropathic pain, low back pain,
and fibromyalgia. These medications
block the reuptake of neurotransmitters
such as epinephrine and norepinephrine, thereby altering neurotransmission along pain pathways.27 Patients
should be educated that the onset of
analgesia with these medications differs from the onset of the antidepressant effect; analgesia will occur sooner
than the expected antidepressant effect
will. Some patients prescribed an
antidepressant as therapy for pain
may misunderstand the purpose of
the drug and assume that their complaints of pain are viewed as an indication of depression or hypochondria.
Health care professionals therefore
should explain to patients that antidepressants, in lay terms, help block
pain impulses.

Special Types of Pain

Neuropathic Pain

Chronic, often intractable pain

due to injury to the peripheral nerves
is known as neuropathic pain.
According to Devor and Seltzer,28
this pain is a paradox. Injury to
peripheral nerves should deaden
sensation, much as cutting a telephone wire leaves the phone line
dead, but the opposite occurs in
neuropathic pain. Injury to the
peripheral nerves can cause spontaneous paresthesias, numbness, pain
with movement, tenderness of a
partly denervated body part, and


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pain that is electric shocklike, burning, shooting, or tingling.

Abnormally amplified signals in
the CNS due to windup result in central sensitization, which is an increased
sensitivity of spinal neurons. Central
sensitization causes allodynia (pain
from a stimulus that does not normally
produce pain, such as touch) and
hyperalgesia (a heightened pain
response to a stimulus that is painful).
Transcutaneous electrical nerve stimulation is used as an adjuvant therapy
for some patients with neuropathic
pain.29 With this technique, stimulating the large-diameter nerve fibers
closes the gate in the spinal cord dorsal horns. The mainstay of treatment
for neuropathic pain, however, is
pharmacotherapy with antiepileptics
and antidepressants. Antiepileptic
drugs inhibit discharges on damaged
nerves, and antidepressants enhance
dorsal horn inhibition (ie, they help
close the gate). The tricyclic antidepressants, despite their poor side effect
profile, are more effective in treating
neuropathic pain than are the newer
serotonin selective reuptake inhibitors.
Phantom Pain

After amputation of a limb, a

patient may experience painful sensations in the missing limb. As many as
70% of amputees report this phantom
limb pain,30 usually within the first
week after amputation.31 Painful sensations, which are typically intermittent,
are described as shooting, stabbing,
pricking, squeezing, throbbing, and
burning. The missing limb may feel
twisted or cramped. Often preamputation pain and phantom pain are
similar.32,33 Most patients report a
decrease in the degree and incidence
of phantom pain in months to years
after the amputation. Although several


theories have been proposed to

explain the pathophysiology of phantom pain, the exact etiology remains
unknown. The origin of phantom
pain is thought to be in the CNS and
may be a somatosensory memory
that involves complex neural interactions in the brain.34
Treatment for phantom pain is
challenging and often unsuccessful. No
medications are specifically indicated
for phantom pain, but anticonvulsants
(carbamazapine), antidepressants
(clomipramine, doxepin), -blockers,
and opioids have been used successfully to relieve phantom pain in some
patients. Transcutaneous electrical
nerve stimulation and sympathetic
blocks have had limited success.35
Central Pain

Central pain is a form of chronic

pain caused by a lesion or dysfunction
in the CNS. Causative lesions include
infarction, hemorrhage, abscess,
degeneration, tumors, and traumatic
injury in the brain or spinal cord. For
example, stroke, multiple sclerosis,
and spinal cord injury can all result in
central pain.36 The term thalamic pain
is often used synonymously with central pain, although thalamic pain is
specifically caused by lesions in the
thalamus. The intensity of the pain
ranges from mild to excruciating, but
the pain is constant and irritating,
causing the patient much suffering.
Patients with central pain often report
burning, aching, lancing (cutting),
pricking, lacerating, and pressing
sensations. The location of the pain
depends on the lesion involved; the
pain may occur in an entire half of
the body or in only a small area, such
as a hand.
The specific mechanisms of central
pain are poorly understood, and no

treatment is universally effective.

Usually combinations of various treatments have the best results. However,
treatments typically only reduce the
pain, rather than eliminating it, so
patients should be warned that relief
probably will not be complete. Treatment includes pharmacotherapy,
transcutaneous electrical nerve stimulation, and neurosurgery. Antidepressants, antiepileptics, antiarrhythmics,
local anesthetics, analgesics, and a
wide variety of other medications have
been used for central pain, all with
varying success. Neurosurgical procedures, such as cordotomy (interrupting the pathways that carry pain
through the spinal cord) and thalamotomy (destroying cells in the thalamus), may be tried in patients with
central pain that do not respond to
other treatments, but even these measures have had only limited success.36

Differences in Populations
Sex-Based Differences

An abundance of research has

indicated sex-based differences in
the experience of pain. Women report
pain with greater frequency than
men do37-41 and have lower thresholds and tolerance to painful stimuli.42-45 Differences also exist in the
types of painful conditions that are
prevalent in women and men. For
example, headaches occur in both
sexes, but women experience more
tension headaches and migraines
with aura, whereas men report more
cluster headaches and migraines
without aura.46 Musculoskeletal
conditions (eg, fibromyalgia) and
autoimmune diseases are reported
much more often by women than
by men.
The reason for these sex-based
differences is a matter of debate.


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Potential mechanisms in pain include

sex hormones, differences in the brain
and spinal cord in men and women,
genetics, sociocultural roles, stress,
and neuroactive agents.41,43,45 Interestingly, researchers have found that brain
activity in men and women differs
during a pain experience. Silverman
et al47 used positron emission tomography to examine brain activation
patterns in healthy men and women
who were not in pain and compared
the patterns with those of men and
women experiencing a painful condition. The brain patterns of the men
and women experiencing pain differed significantly, but no sex-based
differences were detected in the control group. This finding suggests that
pain is processed differently depending on sex.
Pain in Children

Until the 1970s, pain in children

was ignored in health care research.48
The common assumption was that
children did not experience pain to
the extent that adults do, because of
the immature nervous system, or that
children would not remember the pain.
Consequently, children were often
undermedicated or not medicated at
all for pain. This practice continued
until the late 1980s, when changes
began to occur in pain management
in infants and children as a result of
research, consumer demands, and
legislation to promote development
of drugs for these patients. Substantial
evidence now indicates not only that
children experience pain but that the
pain experience may have long-term
adverse consequences.
The misperception that infants
have immature nervous systems and
therefore do not feel pain is still common. All nerve pathways necessary

for pain transmission and perception

are present and functioning by 24
weeks gestation.48 Research49-54 in both
animal models and human newborns
confirms that a lack of analgesia for
pain causes rewiring in the nerve
pathways involved in the transmission
of pain. Consequently, an infant or
child who experiences pain once will
have greater pain perception during
later painful experiences. For example,
Taddio et al54 found that babies who
did not receive analgesia or anesthesia during circumcision later had
greater behavioral and physiological
disturbances during immunization.
Furthermore, a lack of adequate postoperative analgesia in children can
increase morbidity. In a study by
Anand and Hickey,49 compared with
postoperative infants who received
high-dose opioid analgesia, postoperative infants who did not had a significantly higher risk for death.
Another common myth is that
children do not experience chronic
pain. Indeed, children do experience
chronic pain syndromes, such as complex regional pain syndrome, as well
as acute forms of pain related to chronic
conditions such as sickle cell anemia.55-57
They also experience various forms of
recurrent pain, most commonly
headache, abdominal pain, back pain,
chest pain, and limb pain.48,56,58
Pain in the Elderly

The effects of aging on pain sensation, perception, and behavior are not
well established.59 Findings from studies on pain in human aging are conflicting, partly because of inconsistent
research methods and ambiguous
research definitions of pain.60 Some
notable consistencies have been found,
however. Compared with younger
adults, elderly persons rely more on

second pain (C fiber) than on first pain

(A fiber). This difference means that
older adults are more likely to describe
a painful injury or stimulus as burning
(slower C fiber second pain) rather
than as sharp or pricking (faster A fiber
first pain).61,62 Another well-documented
finding in the elderly is a slower
response time to pain.58,59,63
No evidence exists that pain intensity lessens with age. Pain as a sensory
process does not mimic other senses,
such as hearing and sight, which gradually diminish with normal aging.56
Altered reactions to painful events
may be due to loss of communications
skills, cognitive abilities, or the failure
of basic reflexes due to aging. Additionally, pain in the elderly may be
manifested as something other than
pain, such as delirium. Referred
pain may be atypical in the elderly,
as in silent (painless) myocardial
infarction. Although this lack of
referred pain is a clinical problem,
no definitive evidence exists of the
relationship between age and silent
myocardial infarction.

Assessment and Treatment

of Pain
Pain management in critically
ill patients can be challenging. For
a variety of reasons, critically ill
patients may be unable to verbalize,
or they may not fully communicate
the nature of their pain. Patients and
health care providers may assume
that treatment with opioid analgesics
can lead to addiction. Despite efforts
to relieve pain, harmful physiological effects can ensue, including
inadequate sleep, exhaustion, disorientation, anxiety, tachycardia,
increased myocardial oxygen demand,
immunosuppression, and increased
catabolism.64-67 Recognition of pain


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in critically ill
patients is crucial.
Painful stimuli
can be triggered
by a variety of
conditions or
treatments, such
as incisions,
drains, ischemia,
edema, and
indwelling invasive and noninvasive catheters,
and by a patients
previous experiences with
painful stimuli.









Brief word instructions: Point to each face using the words to describe the pain intensity. Ask the child to
choose face that best describes own pain and record the appropriate number.
Original instructions: Explain to the person that each face is for a person who feels happy because he has
no pain (hurt) or sad because he has some or a lot of pain. Face 0 is very happy because he doesnt hurt
at all. Face 1 hurts just a little bit. Face 2 hurts a little more. Face 3 hurts even more. Face 4 hurts a
whole lot. Face 5 hurts as much as you can imagine, although you dont have to be crying to feel this bad.
Ask the person to choose the face that best describes how he is feeling.
Rating scale is recommended for persons age 3 years and older.
Download FACES scale
April 2005

Figure 4 Wong-Baker FACES Pain Rating Scale.

Pain is an
Reprinted from Hockenberry MJ, Wilson D, Winkelstein ML. Wongs Essentials of Pediatric Nursing. 7th ed. St Louis, MO, 2005, p 1259.
important prob- Used with permission. Copyright, Mosby.
lem in critical
critically ill patients and is used to
scales are the numeric rating scale
care, and the assessment of pain
evaluate behaviors that may indicate
and the FACES scale. Scores on the
should be a priority. The Joint Com67
pain, including facial expression,
mission developed a pain assessupper limb movement, and ventilato 10, with 10 being the worst pain
ment and management program
tor compliance. Use of the scale is
that hospitals must implement to
limited to patients who can demonpain sensation at all. The difficulty
fulfill accreditation requirements.
strate the behaviors being assessed.72
Unfortunately, even with pain assessill patients often cannot speak
ment guidelines and mandates in
because of endotracheal intubation.
place, clinicians often underrate
Once pain has been assessed,
The second pain scale is the FACES
pain. Critically ill patients self70
directed toward pain
reports of pain can be inaccurate or
more useful in critical care. This
relief must be implemented. Pain
inconclusive because of endotracheal
indicamanagement can be divided into
intubation, use of sedatives, or an
tions of increasing pain intensity
pharmacological and nonpharmacounconscious state. As a result, health
logical interventions. In a study by
care providers must rely on sensory,
appropriate face to indicate the
Gelinas et al,73 nonpharmacological
physiological, and behavioral
interventions were used in 22% of the
patients pain level.
parameters to assess the presence
pain episodes evaluated. A variety of
Some patients cannot provide a
of painful stimuli. These parameters
comfort-producing measures were
include increases in heart rate and
implemented, including endotracheal
or have cognitive impairment. Assessblood pressure, anxiety, and difficulty
tube suctioning, repositioning in bed,
in providing mechanical ventilation.
massage, oral care, and reassurance.
of a tool that relies on evidence of
Pain scales can be used to deterOther nonpharmacological measures
mine the degree of pain a patient is
for critically ill patients include
Scale was developed for use in
experiencing. Two commonly used


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application of heat or cold, massage,

therapeutic touch, guided imagery,
and relaxation techniques.
Principles of pharmacological
management begin with preemptive
analgesia (before the pain begins) or
as soon as possible after the pain
begins. Preemptive analgesia not only
reduces the pain response but also
can reduce the chance of long-term
sequelae. As previously described,
painful experiences can imprint themselves on the nervous system.54,74,75
Preemptive analgesia can prevent
noxious signals from reaching the
CNS, thereby reducing the chance
that spinal neurons will become
sensitized and lead to heightened
pain responses (hyperalgesia) or pain
experiences from typically painless
sensations (allodynia).76 Continuous
pain management is essential. Recent
evidence77 suggests that duration
and efficacy of analgesic intervention, rather than just timing, may be
the most important factors for treating pain and preventing hyperalgesia after surgical intervention.
For acute pain episodes, analgesics should be administered intravenously for the quickest onset of
action. Importantly, not only the
onset of action but also the expected
duration of action of pain medications must be understood so that
the medication schedule can maximize pain control efforts.78 Aroundthe-clock dosing is appropriate for
critically ill patients. Such dosing

d tmore
To learn more about pain management,
read Validation of the Critical-Care Pain
Observation Tool in Adult Patients by
Cline Glinas et al in the American Journal
of Critical Care, 2006;15:420-427.
Available at www.ajcconline.org.


helps prevent pain and maintain a

pain rating that is satisfactory or
tolerable to the patient and helps
prevent the physiological changes
due to poor pain management.
Despite efforts to relieve pain, harmful physiological effects can ensue,
including inadequate sleep, exhaustion, disorientation, anxiety, tachycardia, increased myocardial oxygen
demand, immunosuppression, and
increased catabolism.64-66 Expectations
of patients regarding pain can radically
change the strength of pain responses
in the spine. Research79 has shown that
pain relief, to a large degree, depends
on what the patient expects from a
pain relief intervention. More recent
research80 confirmed the converse of
this phenomenon, that antianalgesic
expectations can dramatically reduce
the effect of analgesic treatments by
blocking the action of the drugs. In
other words, if a patient expects little
or no pain relief from an analgesic or
a pain relief measure, then the action
of that drug or measure can be blocked
in the spine, and the drug or measure
will be ineffective.
Pain can be a severe and frequent
symptom in intensive care unit patients.
Many patients report dissatisfaction
with inconsistent pain relief and the
inability to acquire restful sleep as a
result of painful stimuli. Pain control
in intensive care unit patients should
encompass use of a variety of painrelieving approaches. These may include
options such as traditional opioids
and nonopioid analgesics as well as
narcotics and synthetic narcotics. In
addition, the use of nonsteroidal antiinflammatory drugs in certain circumstances may augment a patients
response to pain and provide relief.
Personal beliefs of each patient and
the patients family should also be

considered useful when deemed

appropriate. These beliefs might
include prayer, meditation, relaxation
techniques, and acupuncture.

The experience of pain is unique
for each person and encompasses a
persons physical, psychological, cognitive, and emotional network. The
first step in effectively dealing with
pain is determining the specific type
of pain a patient is experiencing.
Acute pain and chronic pain have different manifestations. A patient with
chronic pain will not have objective
physiological indications expected of
patients with pain, such as pallor,
sweating, tachycardia, and facial grimacing. Additionally, differences in
sex and age may play a role in a patients
pain experience. Women and men
can experience pain differently because
of mechanisms not yet understood.
Children do experience pain and
should be treated accordingly even
though they may not be able to verbally express their pain experience.
Elderly patients may describe their
pain differently than younger persons
do and often respond more slowly to
pain. This difference in description of
pain does not mean that elderly
patients experience less pain. Pain
should be treated promptly and adequately in all patients. To provide the
best care for patients in pain, nurses
must be alert to the different types
and manifestations of pain and the
differences of each patient that contribute to the pain experience. CCN

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Financial Disclosures
None reported.

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CE Test

Test ID C0863: Physiology and Treatment of Pain

Learning objectives: 1. Describe the different types of pain 2. Recognize the diversity of patients responses to pain 3. Understand the physiology of pain

1. Which of the following statements is correct about acute and chronic pain?
a. Acute and chronic pain have different physiological mechanisms.
b. Treatments for acute and chronic pain are the same.
c. Children and adults share the same perceptions of acute and chronic pain.
d. Physiologic indicators of acute and chronic pain are identical.

8. Which of the following is a source of neuropathic pain?

a. Bladder distention
b. Incisional pain
c. Phantom limb pain
d. Skeletal muscle spasms

2. Which of the following pain theories includes the process of central

a. Gate control theory
c. Neuromatrix theory
b. Specificity theory
d. Pattern theory

9. What is the reason pain can continue long after the expected recovery
time for an injury?
a. Windup
b. Open gate
c. Body-self neuromatrix
d. Somatosensory memory

4. Where is pain interpreted?

a. Substantia gelatinosa
c. Cerebral cortex
b. Nociceptors
d. Limbic forebrain

10. Compared with men, which is correct about the pain experience in women?
a. Women experience more migraines with aura
b. Women have a higher pain threshold.
c. Women report pain less frequently
d. Women have a higher pain tolerance

4. Surgical patients exhibit malignant hyperthermia when exposed to

which classes of drugs?
a. Neuromuscular blocking agents and volatile inhalation agents
b. Neuromuscular blocking agents and antibiotics
c. Antibiotics and sedating agents
d. Steroids and antibiotics
5. Compared with A fibers, which one of the following is correct about C fibers?
a. C fibers are larger
b. C fibers have a myelin sheath
c. C fibers produce fast pain.
d. C fibers produce constant pain
6. What modulator allows an athlete to continue an athletic event after
sustaining an injury?
a. Leukotrienes
c. Prostaglandins
b. Endorphins
d. Bradykinin

11. Which of the following statements is correct about pain in children?

a. Children do not experience chronic pain
b. Inadequate postoperative analgesia in children can increase morbidity
c. Children do not experience pain to the same extent as adults
d. Children do not feel pain because of an immature nervous system
12. Which of the following statements is correct about pain in older
a. Older adults rely more on first pain than second pain
b. Pain intensity lessens with aging
c. Older adults have a faster response time to pain
d. Pain may be manifested as delirium
13. Which of the following terms describes pain from a stimulus that
does not normally produce pain?
a. Hypesthesia
c. Hyperesthesia
b. Allodynia
d. Hyperalgesia

7. Which of the following statements is correct about visceral pain?

a. Visceral pain is superficial
b. Visceral pain is described as sharp and burning
c. Visceral pain is poorly localized
d. Visceral pain is described as painful numbness.

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

1. K a

2. K a

3. K a

4. K a

5. K a

6. K a

7. K a

8. K a

9. K a

10. K a

11. K a

12. K a

13. K a

Test ID: C0863 Form expires: December 1, 2010 Contact hours: 1.5 Fee: AACN members, $0; nonmembers, $11 Passing score: 10 correct (77%) Category: A Synergy CERP A
Test writer: Denise Hayes, RN, MSN, CRNP

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