Clinical Article

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

PRIME POINTS
• Learn about how pain is
unique for each person.
• Do patients with
chronic pain exhibit objec-
tive physiological indica-
tions 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 experi-
ence pain and how should
they be treated if they can-
not verbalize their pain
experience?
• Do elderly patients
experience pain differently
compared with younger
persons or do they just
respond more slowly to
pain?
P
ain often occurs in criti-
cal 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 posttrau-
matic wounds, invasive monitoring
devices, prolonged immobilization,
mechanical ventilation, and routine
nursing procedures such as suction-
ing and dressing changes.1-5 In addi-
tion, patients may have a preexisting
chronic pain condition, complicat-
ing the assessment and treatment of
acute pain. Pain is a problem in crit-
ical care that has not been adequately
addressed.6 Strategies for changing
pain management practices include
providing documentation, imple-
menting pain guidelines, using algo-
rithms, and increasing education in
pain management for acute and
critical care nurses.6 A review of
pain physiology is essential to fully
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
understand the principles of pain
management.
The pain experience can be func-
tionally 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 eld-
erly persons have both subtle and
sharp differences in the perception of
pain. Much of the nursing literature
on pain is focused on common inter-
ventions 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 mani-
festations. To provide the best possible
care for patients experiencing pain,
nurses must understand the physiol-
ogy of pain, the different types of pain
and their varied manifestations, the
diversity of patients’ responses, and
the rationale for choices of pain con-
trol methods.
Evolution of Pain Theories
As early as 1644, Descartes pro-
posed a theory of pain, that a straight-
line 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 cen-
tral mechanism of pain in the brain.
However, although receptors are spe- Brain
cialized, 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 Spinal cord
pain proposed in the late 19th century,
Gate
pain is the result of stimulation of cer- closed
Gate
tain nerve impulses that form a pattern open Substantia
and are then combined and dumped gelatinosa
into the spinal cord as a lump sum of
pain, a process called “central summa-
tion.”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 place- Small-diameter
fibers
bos on pain.
In 1965, Melzack and Wall8 pub-
Pain sensation
lished the well-known gate control the-
Small-diameter fibers
ory of pain, the theory most familiar
to nurses. According to this theory, a
Figure 1 The gate control theory of pain.
mechanism in the brain acts as a gate
Reprinted from Ignatavicius and Workman,9(p67) with permission. Copyright Elsevier 2006.
to increase or decrease the flow of nerve
impulses from the peripheral fibers to
the CNS. An “open” gate allows the not allow flow of nerve impulses, theory has been widely accepted since
flow of nerve impulses, and the brain decreasing the perception of pain the 1970s, it leaves unanswered ques-
can perceive pain. A “closed” gate does (Figure 1). Although the gate control tions, including chronic pain issues,
sex-based differences, stress effects, and
Authors the effects of previous pain experiences.
Jennifer E. Helms is an associate professor of nursing at Arkansas Tech University, Russell-
In 1999, Melzack and Wall10 pre-
ville, Arkansas. sented a newer theory of pain, consis-
Claudia P. Barone is professor and dean, College of Nursing, University of Arkansas for tent with the idea of gate control, that
Medical Sciences, and a registered nurse II at University Hospital, PRN, Little Rock, addresses some of these unanswered
Arkansas.
questions. This “new and improved”
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). theory, the neuromatrix theory, says
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
that each person has a genetically
Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org. built-in network of neurons called the

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“body-self neuromatrix.” Just as each
person is unique in physical appear-
ance, each person’s matrix of neurons
is unique and is affected by all facets
of the person’s 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 tis-
sue damage and pain.
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 biologi-
cal, electrical, thermal, mechanical,
and chemical stimuli. Pain perception
occurs when these stimuli are trans-
mitted 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,” typi-
cally stimulated by a cut, an electrical
shock, or a physical blow. Transmission
through the A fibers is so fast that the
body’s 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
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Primary sensory cortex
• Location of pain
Limbic forebrain
• Emotional reaction
to pain
Thalamus
Axons project
to other areas
of brain
Brainstem
Anterolateral
tract
Spinal cord
Nociceptors
Noxious stimulus
(may be chemical,
thermal, or mechanical)
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 abil-
ity 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 trans-
mission and duration of pain impulses.
This capacity has implications for the
use of touch and massage for some
patients in pain.
Cortical association area
• Interpretation of pain
Dorsal horn
Release of
substance P
Peripheral
transmission
Peripheral activity
• Vasodilation
• Edema
• Hyperalgesia
• Release of
chemicals
Regulators of Pain
Chemical substances that modu-
late the transmission of pain are
released into the extracellular tissue
when tissue damage occurs. They
activate the pain receptors by irritat-
ing nerve endings. These chemical
mediators include histamine, sub-
stance 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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 Table Physiologic sources of pain
Physiologic structure
Nociceptive pain
Somatic pain
Clutaneous or superfi-
cial: skin and subcuta-
neous 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
Sharp, burning
Dull, aching, cramping
Poorly localized
Diffuse, deep cramping or
splitting, sharp, stabbing
Poorly localized
Shooting, burning, fiery,
shocklike, sharp, painful
numbness
Sources of acute
postoperative pain
Incisional pain, pain at insertion
sites of tubes and drains,
wound complications,
orthopaedic procedures, skele-
tal muscle spasms
Chest tubes, abdominal tubes
and drains, bladder distention
or spasms, intestinal distention
Phantom limb pain, postmastec-
tomy pain, nerve compression
Sources of chronic pain syndromes
Bony metastases, osteoarthritis and
rheumatoid arthritis, low back pain,
peripheral vascular disease
Pancreatitis, liver metastases, colitis,
appendicitis
HIV-related pain, diabetic neuropathy,
postherpetic neuralgia, chemotherapy-
induced 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 Con-
sequently, 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 neuro-
modulators, known as endogenous
opioids, that inhibit the action of
neurons that transmit pain impulses.14
β-Endorphins and dynorphins are the
types of natural opioidlike substances
released, and they are responsible for
pain relief. Endorphins are the modu-
lators 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 mecha-
nism 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 anal-
gesic response in many persons.15
Placebo analgesia can affect nocicep-
tive 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 alter-
ing pain mechanisms in the spinal
cord. For example, psychological fac-
tors 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 pur-
pose by providing a warning that ill-
ness 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 subcuta-
neous 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 Inter-
national Association for the Study of
Pain. The term chronic is still widely

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Lung and Liver
diaphragm
Liver
Heart
Small
Pancreas
intestine
Stomach
Ovary
Kidney
Kidney
Colon
Bladder
Appendix
Ureter
A B
Figure 3 Sites of referred pain.
Reprinted from Huether and McCance,22(p333) with permission. Copyright Elsevier 2004.
used, although many pain experts now stimulation of peripheral nerves winds
think that all forms of chronic pain up the CNS, leading to intensified
are variations of the same phenome- stimulation of nerve fibers that is
non and should be labeled specifically, referred to as nonnociceptive pain.
such as neuropathic pain.23 Chronic The concept of windup is crucial to
pain can be continuous (eg, arthritis) understanding chronic pain.24 Windup
or intermittent (eg, migraines). is the reason pain can continue long
Chronic pain is poorly understood after the expected recovery time for
and is more complex and difficult to an injury or a pain-initiating event.
manage than is acute pain. Under- Patients with chronic pain may
standing chronic pain requires recog- not have the behaviors associated
nizing that the nervous system is not with acute pain.12 Additionally,
hardwired. If it were hardwired, each autonomic nervous system responses
noxious stimulus, such as a needle (eg, nausea, vomiting, pallor, sweat-
stick, would elicit exactly the same ing) decrease with prolonged pain.
nervous system response at the same The body’s fight-or-flight reaction,
intensity every time. But pain is much which normally occurs with acute
more complex, involving affective and pain, does not occur because the
cognitive traits of the person who sympathetic nervous system has
experiences it. Melzack and Wall8 adapted to persistent pain impulses.
showed that repeated stimulation of Understanding chronic pain, there-
C fibers results in progressive buildup fore, requires listening to the per-
of electrical response in the CNS, a son’s description of it, because
phenomenon called windup, some- expected physical symptoms may
what analogous to the effect of wind- not be present. Unfortunately,
ing up a child’s windup toy. The more because of the lack of objective evi-
the toy is wound up, the faster and dence of pain, many patients who
longer the toy will run. This persistent report chronic pain are viewed as
42 CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008
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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 norepineph-
rine, thereby altering neurotransmis-
sion along pain pathways.27 Patients
should be educated that the onset of
analgesia with these medications dif-
fers from the onset of the antidepres-
sant 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 com-
plaints of pain are viewed as an indi-
cation of depression or hypochondria.
Health care professionals therefore
should explain to patients that anti-
depressants, 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 tele-
phone wire leaves the phone line
dead, but the opposite occurs in
neuropathic pain. Injury to the
peripheral nerves can cause sponta-
neous paresthesias, numbness, pain
with movement, tenderness of a
partly denervated body part, and
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pain that is electric shock–like, burn-
ing, shooting, or tingling.
Abnormally amplified signals in
the CNS due to windup result in cen-
tral 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 stim-
ulation is used as an adjuvant therapy
for some patients with neuropathic
pain.29 With this technique, stimulat-
ing the large-diameter nerve fibers
closes the gate in the spinal cord dor-
sal 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 antide-
pressants, 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 sensa-
tions 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 sen-
sations, which are typically intermittent,
are described as shooting, stabbing,
pricking, squeezing, throbbing, and
burning. The missing limb may feel
twisted or cramped. Often preampu-
tation 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
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theories have been proposed to
explain the pathophysiology of phan-
tom 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 interac-
tions 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), β-blockers,
and opioids have been used success-
fully 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 cen-
tral 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
CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 43
treatment is universally effective.
Usually combinations of various treat-
ments 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. Treat-
ment includes pharmacotherapy,
transcutaneous electrical nerve stimu-
lation, and neurosurgery. Antidepres-
sants, antiepileptics, antiarrhythmics,
local anesthetics, analgesics, and a
wide variety of other medications have
been used for central pain, all with
varying success. Neurosurgical proce-
dures, such as cordotomy (interrupt-
ing the pathways that carry pain
through the spinal cord) and thalam-
otomy (destroying cells in the thala-
mus), may be tried in patients with
central pain that do not respond to
other treatments, but even these meas-
ures 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 thresh-
olds and tolerance to painful stim-
uli.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.
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 Interest-
ingly, researchers have found that brain
activity in men and women differs
during a pain experience. Silverman
et al47 used positron emission tomog-
raphy 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 condi-
tion. The brain patterns of the men
and women experiencing pain dif-
fered significantly, but no sex-based
differences were detected in the con-
trol group. This finding suggests that
pain is processed differently depend-
ing 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 com-
mon. All nerve pathways necessary
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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 anesthe-
sia during circumcision later had
greater behavioral and physiological
disturbances during immunization.
Furthermore, a lack of adequate post-
operative analgesia in children can
increase morbidity. In a study by
Anand and Hickey,49 compared with
postoperative infants who received
high-dose opioid analgesia, postoper-
ative infants who did not had a signif-
icantly higher risk for death.
Another common myth is that
children do not experience chronic
pain. Indeed, children do experience
chronic pain syndromes, such as com-
plex 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 sensa-
tion, perception, and behavior are not
well established.59 Findings from stud-
ies on pain in human aging are con-
flicting, 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 inten-
sity lessens with age. Pain as a sensory
process does not mimic other senses,
such as hearing and sight, which grad-
ually 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. Addi-
tionally, 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 physiologi-
cal effects can ensue, including
inadequate sleep, exhaustion, dis-
orientation, 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 0 1 2 3 4 5
treatments, such NO HURT HURTS HURTS HURTS HURTS HURTS
LITTLE BIT LITTLE MORE EVEN MORE WHOLE LOT WORST
as incisions, Alternate
drains, ischemia, coding 0 2 4 6 8 10

inflammation,
edema, and
indwelling inva-
sive and nonin-
vasive catheters,
and by a patient’s
previous experi-
ences with
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 doesn’t 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 don’t 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

painful stimuli. April 2005

Assessment Figure 4 Wong-Baker FACES Pain Rating Scale.

Pain is an Reprinted from Hockenberry MJ, Wilson D, Winkelstein ML. Wong’s Essentials of Pediatric Nursing. 7th ed. St Louis, MO, 2005, p 1259.
70

important prob- Used with permission. Copyright, Mosby.

lem in critical
care, and the assessment of pain scales are the numeric rating scale critically ill patients and is used to
should be a priority. The Joint Com- and the FACES scale. Scores on the evaluate behaviors that may indicate
67
mission developed a pain assess- numeric rating scale range from 0 pain, including facial expression,
ment and management program to 10, with 10 being the worst pain upper limb movement, and ventila-
that hospitals must implement to ever experienced and 0 being no tor compliance. Use of the scale is
fulfill accreditation requirements. pain sensation at all. The difficulty limited to patients who can demon-
Unfortunately, even with pain assess- with using this scale is that critically strate the behaviors being assessed.72
ment guidelines and mandates in ill patients often cannot speak
place, clinicians often underrate because of endotracheal intubation. Treatment
68,69
pain. Critically ill patients’ self- The second pain scale is the FACES Once pain has been assessed,
70
reports of pain can be inaccurate or pain-rating scale, which may be interventions directed toward pain
inconclusive because of endotracheal more useful in critical care. This relief must be implemented. Pain
intubation, use of sedatives, or an scale includes 6 faces with indica- management can be divided into
unconscious state. As a result, health tions of increasing pain intensity pharmacological and nonpharmaco-
care providers must rely on sensory, (Figure 4); a patient points to the logical interventions. In a study by
physiological, and behavioral appropriate face to indicate the Gelinas et al,73 nonpharmacological
parameters to assess the presence patient’s pain level. interventions were used in 22% of the
of painful stimuli. These parameters Some patients cannot provide a pain episodes evaluated. A variety of
include increases in heart rate and self-report because they are sedated comfort-producing measures were
blood pressure, anxiety, and difficulty or have cognitive impairment. Assess- implemented, including endotracheal
in providing mechanical ventilation. ment of these patients requires use tube suctioning, repositioning in bed,
Pain scales can be used to deter- of a tool that relies on evidence of massage, oral care, and reassurance.
mine the degree of pain a patient is pain behaviors. The Behavioral Pain Other nonpharmacological measures
71
experiencing. Two commonly used Scale was developed for use in for critically ill patients include

46 CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 http://ccn.aacnjournals.org

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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 them-
selves 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 interven-
tion, rather than just timing, may be
the most important factors for treat-
ing pain and preventing hyperalge-
sia after surgical intervention.
For acute pain episodes, anal-
gesics should be administered intra-
venously for the quickest onset of
action. Importantly, not only the
onset of action but also the expected
duration of action of pain medica-
tions must be understood so that
the medication schedule can maxi-
mize pain control efforts.78 Around-
the-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
Céline Gélinas et al in the American Journal
of Critical Care, 2006;15:420-427.
Available at www.ajcconline.org.
http://ccn.aacnjournals.org
Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018
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, harm-
ful physiological effects can ensue,
including inadequate sleep, exhaus-
tion, disorientation, anxiety, tachy-
cardia, 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 pain-
relieving 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 anti-
inflammatory drugs in certain circum-
stances may augment a patient’s
response to pain and provide relief.
Personal beliefs of each patient and
the patient’s family should also be
CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 47
considered useful when deemed
appropriate. These beliefs might
include prayer, meditation, relaxation
techniques, and acupuncture.
Conclusion
The experience of pain is unique
for each person and encompasses a
person’s physical, psychological, cog-
nitive, 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 dif-
ferent manifestations. A patient with
chronic pain will not have objective
physiological indications expected of
patients with pain, such as pallor,
sweating, tachycardia, and facial gri-
macing. Additionally, differences in
sex and age may play a role in a patient’s
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 ver-
bally 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 ade-
quately 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 con-
tribute to the pain experience. CCN
eLetters
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Financial Disclosures
None reported.
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http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 49

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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? 8. Which of the following is a source of neuropathic pain?
a. Acute and chronic pain have different physiological mechanisms. a. Bladder distention
b. Treatments for acute and chronic pain are the same. b. Incisional pain
c. Children and adults share the same perceptions of acute and chronic pain. c. Phantom limb pain
d. Physiologic indicators of acute and chronic pain are identical. d. Skeletal muscle spasms

2. Which of the following pain theories includes the process of “central 9. What is the reason pain can continue long after the expected recovery
summation”? time for an injury?
a. Gate control theory c. Neuromatrix theory a. Windup
b. Specificity theory d. Pattern theory b. Open gate
c. Body-self neuromatrix
4. Where is pain interpreted? d. Somatosensory “memory”
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
4. Surgical patients exhibit malignant hyperthermia when exposed to b. Women have a higher pain threshold.
which classes of drugs? c. Women report pain less frequently
a. Neuromuscular blocking agents and volatile inhalation agents d. Women have a higher pain tolerance
b. Neuromuscular blocking agents and antibiotics
c. Antibiotics and sedating agents 11. Which of the following statements is correct about pain in children?
d. Steroids and antibiotics a. Children do not experience chronic pain
b. Inadequate postoperative analgesia in children can increase morbidity
5. Compared with A fibers, which one of the following is correct about C fibers? c. Children do not experience pain to the same extent as adults
a. C fibers are larger d. Children do not feel pain because of an immature nervous system
b. C fibers have a myelin sheath
c. C fibers produce “fast pain.” 12. Which of the following statements is correct about pain in older
d. C fibers produce constant pain adults?
a. Older adults rely more on first pain than second pain
6. What modulator allows an athlete to continue an athletic event after b. Pain intensity lessens with aging
sustaining an injury? c. Older adults have a faster response time to pain
a. Leukotrienes c. Prostaglandins d. Pain may be manifested as delirium
b. Endorphins d. Bradykinin
13. Which of the following terms describes pain from a stimulus that
7. Which of the following statements is correct about visceral pain? does not normally produce pain?
a. Visceral pain is superficial a. Hypesthesia c. Hyperesthesia
b. Visceral pain is described as sharp and burning b. Allodynia d. Hyperalgesia
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.

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Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc Kc
Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd Kd
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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Physiology and Treatment of Pain
Jennifer E. Helms and Claudia P. Barone
Crit Care Nurse 2008;28 38-49
American Association of Critical-Care Nurses
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Critical Care Nurse is an official peer-reviewed journal of the American Association of Critical-Care Nurses (AACN) published
bimonthly by AACN, 101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949)
362-2049. Copyright ©2016 by AACN. All rights reserved.

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