Vous êtes sur la page 1sur 13

Clinical Article

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

ain often occurs in criti- understand the principles of pain
cal care patients and is management.
one of the most clinically The pain experience can be func-
challenging problems tionally divided into acute and chronic
PRIME POINTS for critical care nurses. types. Acute and chronic pain are due
Pain and discomfort in these patients to different physiological mechanisms
• Learn about how pain is can be due to surgical and posttrau- and thus require different treatments.
unique for each person. matic wounds, invasive monitoring In addition, children, adults, and eld-
devices, prolonged immobilization, erly persons have both subtle and
mechanical ventilation, and routine sharp differences in the perception of
• Do patients with nursing procedures such as suction- pain. Much of the nursing literature
chronic pain exhibit objec-
ing and dressing changes.1-5 In addi- on pain is focused on common inter-
tive physiological indica- ventions but does not explain the
tion, patients may have a preexisting
tions expected of patients chronic pain condition, complicat- physiological mechanisms of pain and
with pain, such as pallor, ing the assessment and treatment of the vastly different types of pain that
sweating, tachycardia, and acute pain. Pain is a problem in crit- patients may have. Thus, in this article,
facial grimacing? ical care that has not been adequately we review theories of pain and examine
addressed.6 Strategies for changing the physiology of pain, with emphasis
• Is there a difference in pain management practices include on the types of pain and their mani-
how women and men providing documentation, imple- festations. To provide the best possible
experience pain ? menting pain guidelines, using algo- care for patients experiencing pain,
rithms, and increasing education in nurses must understand the physiol-
pain management for acute and ogy of pain, the different types of pain
• How do children experi- critical care nurses.6 A review of and their varied manifestations, the
ence pain and how should
pain physiology is essential to fully diversity of patients’ responses, and
they be treated if they can-
the rationale for choices of pain con-
not verbalize their pain
trol methods.
experience? CEContinuing Education
Evolution of Pain Theories
• Do elderly patients This article has been designated for CE credit.
A closed-book, multiple-choice examination As early as 1644, Descartes pro-
experience pain differently follows this article, which tests your knowledge posed a theory of pain, that a straight-
of the following objectives:
compared with younger line channel of pain exists from skin
1. Describe the different types of pain
persons or do they just 2. Recognize the diversity of patients’ to brain.7 During the 19th century,
respond more slowly to responses to pain
3. Understand the physiology of pain
von Frey theorized that pain pathways
pain? move from specialized receptors in

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

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

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,
pain is the result of stimulation of cer- closed
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
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
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

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 39

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018
“body-self neuromatrix.” Just as each
person is unique in physical appear- Primary sensory cortex
• Location of pain
ance, each person’s matrix of neurons Limbic forebrain
• Emotional reaction Cortical association area
is unique and is affected by all facets • Interpretation of pain
to pain
of the person’s physical, psychological,
and cognitive makeup, as well as his Thalamus
Axons project
or her experience. Thus, the pain to other areas
experience does not reflect a simple of brain
one-to-one relationship between tis-
sue damage and pain.

Pathways of Pain
Nociceptors, or pain receptors, Anterolateral
tract Dorsal horn
are free nerve endings that respond to
painful stimuli. Nociceptors are found
throughout all tissues except the brain, Release of
and they transmit information to the Spinal cord substance P
brain. They are stimulated by biologi- Peripheral
cal, electrical, thermal, mechanical, transmission
Peripheral activity
and chemical stimuli. Pain perception • Vasodilation
occurs when these stimuli are trans- • Edema
mitted to the spinal cord and then to Nociceptors • Hyperalgesia
Noxious stimulus • Release of
the central areas of the brain. Pain (may be chemical, chemicals
impulses travel to the dorsal horn of thermal, or mechanical)
the spine, where they synapse with
dorsal horn neurons in the substantia Figure 2 Pathways of pain.
Reprinted from Copstead and Banasik,11(p1174) with permission. Copyright Elsevier 2005.
gelatinosa and then ascend to the
brain. The basic sensation of pain
occurs at the thalamus. It continues to slowly than the A fibers do because Regulators of Pain
the limbic system (emotional center) the C fibers are smaller and lack a Chemical substances that modu-
and the cerebral cortex, where pain is myelin sheath. The C fibers are the late the transmission of pain are
perceived and interpreted (Figure 2). ones that produce constant pain. released into the extracellular tissue
Two types of fibers are involved in According to the gate control when tissue damage occurs. They
pain transmission. The large A delta theory, stimulation of the fibers that activate the pain receptors by irritat-
fibers produce sharp well-defined pain, transmit nonpainful stimuli can block ing nerve endings. These chemical
called “fast pain” or “first pain,” typi- pain impulses at the gate in the dorsal mediators include histamine, sub-
cally stimulated by a cut, an electrical horn. For example, if touch receptors stance P, bradykinin, acetylcholine,
shock, or a physical blow. Transmission (A beta fibers) are stimulated, they leukotrienes, and prostaglandins.
through the A fibers is so fast that the dominate and close the gate. This abil- The mediators can produce other
body’s reflexes can actually respond ity to block pain impulses is the reason reactions at the site of injury, such
faster than the pain stimulus, resulting a person is prone to immediately grab as vasoconstriction, vasodilatation,
in retraction of the affected body part and massage the foot when he or she or altered capillary permeability.
even before the person perceives the stubs a toe. The touch blocks the trans- For example, prostaglandins induce
pain. After this first pain, the smaller mission and duration of pain impulses. inflammation and potentiate other
C fibers transmit dull burning or aching This capacity has implications for the inflammatory mediators. Aspirin,
sensations, known as “second pain.” use of touch and massage for some nonsteroidal anti-inflammatory
The C fibers transmit pain more patients in pain. medications, and the new COX-2

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

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

Table Physiologic sources of pain
Sources of acute
Physiologic structure Characterictics of pain postoperative pain Sources of chronic pain syndromes
Nociceptive pain
Somatic pain
Clutaneous or superfi- Sharp, burning Incisional pain, pain at insertion Bony metastases, osteoarthritis and
cial: skin and subcuta- Dull, aching, cramping sites of tubes and drains, rheumatoid arthritis, low back pain,
neous tissues wound complications, peripheral vascular disease
Deep somatic: bone, orthopaedic procedures, skele-
muscle blood vessels, tal muscle spasms
connective tissues
Visceral pain
Organs and the linings Poorly localized Chest tubes, abdominal tubes Pancreatitis, liver metastases, colitis,
of the body cavities Diffuse, deep cramping or and drains, bladder distention appendicitis
splitting, sharp, stabbing or spasms, intestinal distention
Neuropathic pain Poorly localized Phantom limb pain, postmastec- HIV-related pain, diabetic neuropathy,
Nerve fibers, spinal Shooting, burning, fiery, tomy pain, nerve compression postherpetic neuralgia, chemotherapy-
cord, and central shocklike, sharp, painful induced neuropathies, cancer-related
nervous system numbness nerve injury, radiculopathies

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

inhibitors block cyclooxygenase 2, efficacy of the treatment under study. sweating, dilated pupils, restlessness,
the enzyme needed for prostaglandin Despite the lack of any intrinsic value, and apprehension.
synthesis, thus reducing pain.12,13 Con- placebos can and do produce an anal- Types of acute pain include
sequently, these medications are often gesic response in many persons.15 somatic, visceral, and referred9 (see
prescribed for painful conditions due Placebo analgesia can affect nocicep- Table). Somatic pain is superficial,
to inflammation. tive mechanisms in the cortex of the coming from the skin or subcuta-
The body also has a built-in brain and descending pathways of the neous tissues; visceral pain originates
chemical mechanism to manage pain. spinal cord.16-19 Matre et al20 found that in the internal organs and the linings
Fibers in the dorsal horn, brain stem, expectations about pain and analgesia of the body cavities. Referred pain is
and peripheral tissues release neuro- can modify pain perception by alter- felt in an area distant from the site of
modulators, known as endogenous ing pain mechanisms in the spinal the stimulus; it occurs because the
opioids, that inhibit the action of cord. For example, psychological fac- area of referred pain is supplied by
neurons that transmit pain impulses.14 tors such as the threat of pain and the same spinal segment as the site of
β-Endorphins and dynorphins are the expectations about analgesia modify the stimulus21 (Figure 3). Referred
types of natural opioidlike substances spinal pain transmission, thereby pain often occurs with visceral pain.
released, and they are responsible for modifying pain. Examples include shoulder pain from
pain relief. Endorphins are the modu- myocardial infarction, back pain
lators that allow an athlete to continue Acute and Chronic Pain from pancreatitis, and right shoulder
an athletic event after sustaining an Acute Pain pain from gallbladder disease.
injury. Endorphin levels vary from Acute pain serves a biologic pur-
person to person, so different persons pose by providing a warning that ill- Chronic Pain
experience different levels of pain. ness or injury has occurred. The pain Chronic pain is prolonged pain,
This endogenous opioid mecha- is usually confined to the affected area persisting beyond the expected normal
nism may play an important role in and is limited over time. Acute pain healing time.23 This characterization
the placebo effect. A placebo is an stimulates the sympathetic nervous was previously the official definition
inactive substance or treatment used system, resulting in “fight or flight” of chronic pain according to the Inter-
for comparison with “real” treatment response symptoms, including national Association for the Study of
in controlled studies to determine the increased heart and respiratory rates, Pain. The term chronic is still widely

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 41

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018
hypochondriacs and malingerers by
health care professionals.
Lung and Liver Some evidence indicates that
Liver chronic pain and depression share
Heart the same physiological pathway.25,26
Pancreas Tricyclic antidepressants and selective
Stomach serotonin reuptake inhibitors have
Ovary been used successfully for relief of
Kidney many chronic pain syndromes such
as neuropathic pain, low back pain,
and fibromyalgia. These medications
Appendix block the reuptake of neurotransmitters
Ureter such as epinephrine and norepineph-
rine, thereby altering neurotransmis-
A B sion along pain pathways.27 Patients
should be educated that the onset of
Figure 3 Sites of referred pain. analgesia with these medications dif-
Reprinted from Huether and McCance,22(p333) with permission. Copyright Elsevier 2004. fers from the onset of the antidepres-
sant effect; analgesia will occur sooner
used, although many pain experts now stimulation of peripheral nerves winds than the expected antidepressant effect
think that all forms of chronic pain up the CNS, leading to intensified will. Some patients prescribed an
are variations of the same phenome- stimulation of nerve fibers that is antidepressant as therapy for pain
non and should be labeled specifically, referred to as nonnociceptive pain. may misunderstand the purpose of
such as neuropathic pain.23 Chronic The concept of windup is crucial to the drug and assume that their com-
pain can be continuous (eg, arthritis) understanding chronic pain.24 Windup plaints of pain are viewed as an indi-
or intermittent (eg, migraines). is the reason pain can continue long cation of depression or hypochondria.
Chronic pain is poorly understood after the expected recovery time for Health care professionals therefore
and is more complex and difficult to an injury or a pain-initiating event. should explain to patients that anti-
manage than is acute pain. Under- Patients with chronic pain may depressants, in lay terms, help block
standing chronic pain requires recog- not have the behaviors associated pain impulses.
nizing that the nervous system is not with acute pain.12 Additionally,
hardwired. If it were hardwired, each autonomic nervous system responses Special Types of Pain
noxious stimulus, such as a needle (eg, nausea, vomiting, pallor, sweat- Neuropathic Pain
stick, would elicit exactly the same ing) decrease with prolonged pain. Chronic, often intractable pain
nervous system response at the same The body’s fight-or-flight reaction, due to injury to the peripheral nerves
intensity every time. But pain is much which normally occurs with acute is known as neuropathic pain.
more complex, involving affective and pain, does not occur because the According to Devor and Seltzer,28
cognitive traits of the person who sympathetic nervous system has this pain is a paradox. Injury to
experiences it. Melzack and Wall8 adapted to persistent pain impulses. peripheral nerves should deaden
showed that repeated stimulation of Understanding chronic pain, there- sensation, much as cutting a tele-
C fibers results in progressive buildup fore, requires listening to the per- phone wire leaves the phone line
of electrical response in the CNS, a son’s description of it, because dead, but the opposite occurs in
phenomenon called windup, some- expected physical symptoms may neuropathic pain. Injury to the
what analogous to the effect of wind- not be present. Unfortunately, peripheral nerves can cause sponta-
ing up a child’s windup toy. The more because of the lack of objective evi- neous paresthesias, numbness, pain
the toy is wound up, the faster and dence of pain, many patients who with movement, tenderness of a
longer the toy will run. This persistent report chronic pain are viewed as partly denervated body part, and

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

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

pain that is electric shock–like, burn- theories have been proposed to treatment is universally effective.
ing, shooting, or tingling. explain the pathophysiology of phan- Usually combinations of various treat-
Abnormally amplified signals in tom pain, the exact etiology remains ments have the best results. However,
the CNS due to windup result in cen- unknown. The origin of phantom treatments typically only reduce the
tral sensitization, which is an increased pain is thought to be in the CNS and pain, rather than eliminating it, so
sensitivity of spinal neurons. Central may be a somatosensory “memory” patients should be warned that relief
sensitization causes allodynia (pain that involves complex neural interac- probably will not be complete. Treat-
from a stimulus that does not normally tions in the brain.34 ment includes pharmacotherapy,
produce pain, such as touch) and Treatment for phantom pain is transcutaneous electrical nerve stimu-
hyperalgesia (a heightened pain challenging and often unsuccessful. No lation, and neurosurgery. Antidepres-
response to a stimulus that is painful). medications are specifically indicated sants, antiepileptics, antiarrhythmics,
Transcutaneous electrical nerve stim- for phantom pain, but anticonvulsants local anesthetics, analgesics, and a
ulation is used as an adjuvant therapy (carbamazapine), antidepressants wide variety of other medications have
for some patients with neuropathic (clomipramine, doxepin), β-blockers, been used for central pain, all with
pain.29 With this technique, stimulat- and opioids have been used success- varying success. Neurosurgical proce-
ing the large-diameter nerve fibers fully to relieve phantom pain in some dures, such as cordotomy (interrupt-
closes the gate in the spinal cord dor- patients. Transcutaneous electrical ing the pathways that carry pain
sal horns. The mainstay of treatment nerve stimulation and sympathetic through the spinal cord) and thalam-
for neuropathic pain, however, is blocks have had limited success.35 otomy (destroying cells in the thala-
pharmacotherapy with antiepileptics mus), may be tried in patients with
and antidepressants. Antiepileptic Central Pain central pain that do not respond to
drugs inhibit discharges on damaged Central pain is a form of chronic other treatments, but even these meas-
nerves, and antidepressants enhance pain caused by a lesion or dysfunction ures have had only limited success.36
dorsal horn inhibition (ie, they help in the CNS. Causative lesions include
close the gate). The tricyclic antide- infarction, hemorrhage, abscess, Differences in Populations
pressants, despite their poor side effect degeneration, tumors, and traumatic Sex-Based Differences
profile, are more effective in treating injury in the brain or spinal cord. For An abundance of research has
neuropathic pain than are the newer example, stroke, multiple sclerosis, indicated sex-based differences in
serotonin selective reuptake inhibitors. and spinal cord injury can all result in the experience of pain. Women report
central pain.36 The term thalamic pain pain with greater frequency than
Phantom Pain is often used synonymously with cen- men do37-41 and have lower thresh-
After amputation of a limb, a tral pain, although thalamic pain is olds and tolerance to painful stim-
patient may experience painful sensa- specifically caused by lesions in the uli.42-45 Differences also exist in the
tions in the missing limb. As many as thalamus. The intensity of the pain types of painful conditions that are
70% of amputees report this phantom ranges from mild to excruciating, but prevalent in women and men. For
limb pain,30 usually within the first the pain is constant and irritating, example, headaches occur in both
week after amputation.31 Painful sen- causing the patient much suffering. sexes, but women experience more
sations, which are typically intermittent, Patients with central pain often report tension headaches and migraines
are described as shooting, stabbing, burning, aching, lancing (“cutting”), with aura, whereas men report more
pricking, squeezing, throbbing, and pricking, lacerating, and pressing cluster headaches and migraines
burning. The missing limb may feel sensations. The location of the pain without aura.46 Musculoskeletal
twisted or cramped. Often preampu- depends on the lesion involved; the conditions (eg, fibromyalgia) and
tation pain and phantom pain are pain may occur in an entire half of autoimmune diseases are reported
similar.32,33 Most patients report a the body or in only a small area, such much more often by women than
decrease in the degree and incidence as a hand. by men.
of phantom pain in months to years The specific mechanisms of central The reason for these sex-based
after the amputation. Although several pain are poorly understood, and no differences is a matter of debate.

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 43

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018
Potential mechanisms in pain include for pain transmission and perception second pain (C fiber) than on first pain
sex hormones, differences in the brain are present and functioning by 24 (A fiber). This difference means that
and spinal cord in men and women, weeks’ gestation.48 Research49-54 in both older adults are more likely to describe
genetics, sociocultural roles, stress, animal models and human newborns a painful injury or stimulus as burning
and neuroactive agents.41,43,45 Interest- confirms that a lack of analgesia for (slower C fiber second pain) rather
ingly, researchers have found that brain pain causes “rewiring” in the nerve than as sharp or pricking (faster A fiber
activity in men and women differs pathways involved in the transmission first pain).61,62 Another well-documented
during a pain experience. Silverman of pain. Consequently, an infant or finding in the elderly is a slower
et al47 used positron emission tomog- child who experiences pain once will response time to pain.58,59,63
raphy to examine brain activation have greater pain perception during No evidence exists that pain inten-
patterns in healthy men and women later painful experiences. For example, sity lessens with age. Pain as a sensory
who were not in pain and compared Taddio et al54 found that babies who process does not mimic other senses,
the patterns with those of men and did not receive analgesia or anesthe- such as hearing and sight, which grad-
women experiencing a painful condi- sia during circumcision later had ually diminish with normal aging.56
tion. The brain patterns of the men greater behavioral and physiological Altered reactions to painful events
and women experiencing pain dif- disturbances during immunization. may be due to loss of communications
fered significantly, but no sex-based Furthermore, a lack of adequate post- skills, cognitive abilities, or the failure
differences were detected in the con- operative analgesia in children can of basic reflexes due to aging. Addi-
trol group. This finding suggests that increase morbidity. In a study by tionally, pain in the elderly may be
pain is processed differently depend- Anand and Hickey,49 compared with manifested as something other than
ing on sex. postoperative infants who received pain, such as delirium. Referred
high-dose opioid analgesia, postoper- pain may be atypical in the elderly,
Pain in Children ative infants who did not had a signif- as in silent (painless) myocardial
Until the 1970s, pain in children icantly higher risk for death. infarction. Although this lack of
was ignored in health care research.48 Another common myth is that referred pain is a clinical problem,
The common assumption was that children do not experience chronic no definitive evidence exists of the
children did not experience pain to pain. Indeed, children do experience relationship between age and silent
the extent that adults do, because of chronic pain syndromes, such as com- myocardial infarction.
the immature nervous system, or that plex regional pain syndrome, as well
children would not remember the pain. as acute forms of pain related to chronic Assessment and Treatment
Consequently, children were often conditions such as sickle cell anemia.55-57 of Pain
undermedicated or not medicated at They also experience various forms of Pain management in critically
all for pain. This practice continued recurrent pain, most commonly ill patients can be challenging. For
until the late 1980s, when changes headache, abdominal pain, back pain, a variety of reasons, critically ill
began to occur in pain management chest pain, and limb pain.48,56,58 patients may be unable to verbalize,
in infants and children as a result of or they may not fully communicate
research, consumer demands, and Pain in the Elderly the nature of their pain. Patients and
legislation to promote development The effects of aging on pain sensa- health care providers may assume
of drugs for these patients. Substantial tion, perception, and behavior are not that treatment with opioid analgesics
evidence now indicates not only that well established.59 Findings from stud- can lead to addiction. Despite efforts
children experience pain but that the ies on pain in human aging are con- to relieve pain, harmful physiologi-
pain experience may have long-term flicting, partly because of inconsistent cal effects can ensue, including
adverse consequences. research methods and ambiguous inadequate sleep, exhaustion, dis-
The misperception that infants research definitions of pain.60 Some orientation, anxiety, tachycardia,
have immature nervous systems and notable consistencies have been found, increased myocardial oxygen demand,
therefore do not feel pain is still com- however. Compared with younger immunosuppression, and increased
mon. All nerve pathways necessary adults, elderly persons rely more on catabolism.64-67 Recognition of pain

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

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

in critically ill
patients is crucial.
Painful stimuli
can be triggered
by a variety of
conditions or 0 1 2 3 4 5
as incisions, Alternate
drains, ischemia, coding 0 2 4 6 8 10

inflammation, Brief word instructions: Point to each face using the words to describe the pain intensity. Ask the child to
edema, and choose face that best describes own pain and record the appropriate number.
indwelling inva- Original instructions: Explain to the person that each face is for a person who feels happy because he has
sive and nonin- 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
vasive catheters, whole lot. Face 5 hurts as much as you can imagine, although you don’t have to be crying to feel this bad.
and by a patient’s Ask the person to choose the face that best describes how he is feeling.
previous experi- Rating scale is recommended for persons age 3 years and older.
ences with 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.

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
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
pain. Critically ill patients’ self- The second pain scale is the FACES Once pain has been assessed,
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
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

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

application of heat or cold, massage, helps prevent pain and maintain a considered useful when deemed
therapeutic touch, guided imagery, pain rating that is satisfactory or appropriate. These beliefs might
and relaxation techniques. tolerable to the patient and helps include prayer, meditation, relaxation
Principles of pharmacological prevent the physiological changes techniques, and acupuncture.
management begin with preemptive due to poor pain management.
analgesia (before the pain begins) or Despite efforts to relieve pain, harm- Conclusion
as soon as possible after the pain ful physiological effects can ensue, The experience of pain is unique
begins. Preemptive analgesia not only including inadequate sleep, exhaus- for each person and encompasses a
reduces the pain response but also tion, disorientation, anxiety, tachy- person’s physical, psychological, cog-
can reduce the chance of long-term cardia, increased myocardial oxygen nitive, and emotional network. The
sequelae. As previously described, demand, immunosuppression, and first step in effectively dealing with
painful experiences can imprint them- increased catabolism.64-66 Expectations pain is determining the specific type
selves on the nervous system.54,74,75 of patients regarding pain can radically of pain a patient is experiencing.
Preemptive analgesia can prevent change the strength of pain responses Acute pain and chronic pain have dif-
noxious signals from reaching the in the spine. Research79 has shown that ferent manifestations. A patient with
CNS, thereby reducing the chance pain relief, to a large degree, depends chronic pain will not have objective
that spinal neurons will become on what the patient expects from a physiological indications expected of
sensitized and lead to heightened pain relief intervention. More recent patients with pain, such as pallor,
pain responses (hyperalgesia) or pain research80 confirmed the converse of sweating, tachycardia, and facial gri-
experiences from typically painless this phenomenon, that antianalgesic macing. Additionally, differences in
sensations (allodynia).76 Continuous expectations can dramatically reduce sex and age may play a role in a patient’s
pain management is essential. Recent the effect of analgesic treatments by pain experience. Women and men
evidence77 suggests that duration blocking the action of the drugs. In can experience pain differently because
and efficacy of analgesic interven- other words, if a patient expects little of mechanisms not yet understood.
tion, rather than just timing, may be or no pain relief from an analgesic or Children do experience pain and
the most important factors for treat- a pain relief measure, then the action should be treated accordingly even
ing pain and preventing hyperalge- of that drug or measure can be blocked though they may not be able to ver-
sia after surgical intervention. in the spine, and the drug or measure bally express their pain experience.
For acute pain episodes, anal- will be ineffective. Elderly patients may describe their
gesics should be administered intra- Pain can be a severe and frequent pain differently than younger persons
venously for the quickest onset of symptom in intensive care unit patients. do and often respond more slowly to
action. Importantly, not only the Many patients report dissatisfaction pain. This difference in description of
onset of action but also the expected with inconsistent pain relief and the pain does not mean that elderly
duration of action of pain medica- inability to acquire restful sleep as a patients experience less pain. Pain
tions must be understood so that result of painful stimuli. Pain control should be treated promptly and ade-
the medication schedule can maxi- in intensive care unit patients should quately in all patients. To provide the
mize pain control efforts.78 Around- encompass use of a variety of pain- best care for patients in pain, nurses
the-clock dosing is appropriate for relieving approaches. These may include must be alert to the different types
critically ill patients. Such dosing options such as traditional opioids and manifestations of pain and the
and nonopioid analgesics as well as differences of each patient that con-
narcotics and synthetic narcotics. In tribute to the pain experience. CCN

d tmore
To learn more about pain management,
read “Validation of the Critical-Care Pain
addition, the use of nonsteroidal anti-
inflammatory drugs in certain circum-
stances may augment a patient’s eLetters
Observation Tool in Adult Patients” by Now that you’ve read the article, create or con-
response to pain and provide relief. tribute to an online discussion about this topic
Céline Gélinas et al in the American Journal using eLetters. Just visit http://ccn.aacnjournals
of Critical Care, 2006;15:420-427. Personal beliefs of each patient and .org and click “Respond to This Article” in either
Available at www.ajcconline.org. the patient’s family should also be the full-text or PDF view of the article.

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 47

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018
Financial Disclosures Placebo-induced changes in FMRI in the 40. Rajala U, Keinanen-Kiukaanniemi S, Uusi-
None reported. anticipation and experience of pain. Science. maki A, Kivela SL. Musculoskeletal pains
2004;303(5661):1162-1167. and depression in a middle-aged Finnish
20. Matre D, Casey KL, Knardahl S. Placebo- population. Pain. 1995;61:451-457.
References induced changes in spinal cord processing. 41. Unruh AM. Gender variations in clinical
1. Pasero C, McCaffrey M. Pain in the criti- J Neurosci. 2006;26(2):559-563. pain experience. Pain. 1996;65:123-167.
cally ill: new information reveals that one 21. Heuther S, Leo J. Pain, temperature regula- 42. Riley JL, Robinson ME, Wise EA, Myers
of the simplest procedures—turning—can tion, sleep, and sensory function. In: CD, Fillingham RB. Sex differences in the
be the most painful one. Am J Nurs. 2002; McCance KL, Heuther SE, eds. Pathophysi- perception of noxious experimental stimuli:
102(1):59-60. ology: The Biologic Basis for Disease in Adults a meta-analysis. Pain. 1998;74:181-187.
2. Puntillo KA, White C, Morris AB, et al. and Children. 4th ed. St Louis, MO: Mosby; 43. Fillingim RB, Edwards RR, Powell T. The
Patients’ perceptions and responses to pro- 2002:401-437. relationship of sex and clinical pain to
cedural pain: results from Thunder Project 22. Huether SE, McCance KL. Understanding experimental pain responses. Pain. 1999;
II. Am J Crit Care. 2001;10(4):238-251. Pathophysiology. 3rd ed. St Louis, MO: 83(3):419-425.
3. Stanik-Hutt JA, Soeken KL, Belcher AE, Mosby; 2004:333. 44. Rollman GB, Lautenbacher S, Johnes KS.
Fontaine DK, Gift AG. Pain experiences of 23. Grichnik KP, Ferrante FM. The difference Sex and gender differences in responses to
traumatically injured patients in a critical care between acute and chronic pain. Mt Sinai J experimentally induced pain in humans.
setting. Am J Crit Care. 2001;10(4):252-259. Med. 1991;58(3):217-220. In: Fillingim RB, ed. Sex, Gender, and Pain.
4. Jacobi J, Fraser GL, Coursin DB, et al; Task 24. Bennett R. Emerging concepts in the neuro- Seattle, WA: IASP Press; 2000:165-190.
Force of the American College of Critical biology of chronic pain: evidence of abnor- 45. Keogh E, Herdenfeldt M. Gender, coping,
Care Medicine (ACCM) of the Society of mal sensory processing in fibromyalgia. and the perception of pain. Pain. 2002;97:
Critical Care Medicine (SCCM), American Mayo Clin Proc. 1999;74(4):385-398. 195-201.
Society of Health-System Pharmacists (ASHP), 25. Ressler KJ, Nemeroff CB. Role of serotonergic 46. Berkley KJ, Holdcroft A. Sex and gender dif-
American College of Chest Physicians. Clin- and noradrenergic systems in the pathophys- ferences in pain. In: Wall P, Melzack R, eds.
ical practice guidelines for the sustained use iology of depression and anxiety disorders. Textbook of Pain. 4th ed. New York, NY:
of sedatives and analgesics in the critically Depression Anxiety. 2000;12(suppl 1):2-19. Churchill Livingstone; 1999:951-965.
ill adult [published correction appears in 26. Juhl JH. Fibromyalgia and the serotonin 47. Silverman DH, Munakata JA, Ennes H,
Crit Care Med. 2002;30(3):726]. Crit Care pathway. Altern Med Rev. 1998;3(5):367-375. Mandelkern MA, Hoh CK, Mayer EA.
Med. 2002;30(1)1:119-141. 27. Thiessen B, Portenoy R. Adjuvant anal- Regional cerebral activity in normal and
5. Jodka P, Heard SO. Management of acute gesics. In: Kanner R, ed. Pain Management pathological perception of visceral pain.
pain in the intensive care unit. In: Fink MP, Secrets. 2nd ed. Philadelphia, PA: Hanley & Gastroenterology. 1997;112(1):64-72.
Abraham E, Vincent J, Patrick PM, eds. Belfus; 2002:220-230. 48. Schechter NL, Berde CB, Yaster M. Pain in
Textbook of Critical Care. 5th ed. Philadel- 28. Devor M, Seltzer Z. Pathophysiology of infants, children, and adolescents: an
phia, PA: Elsevier Saunders; 2005:13-16. damaged nerves in relation to chronic pain. overview. In: Schechter NL, Berde CB,
6. Shannon K, Bucknall R. Pain assessment In: Wall P, Melzack R, ed. Textbook of Pain. Yaster M, eds. Pain in Infants, Children, and
in critical care: what we have learnt from 4th ed. New York, NY: Churchill Livingstone; Adolescents. 2nd ed. Philadelphia, PA: Lip-
research. Intensive Crit Care Nurs. 2003; 1999:129-164. pincott; 2003:3-18.
19(3):154-162. 29. Chong MS, Bajwa ZH. Diagnosis and treat- 49. Anand KJ, Hickey PR. Halothane-morphine
7. Melzack R. The Puzzle of Pain. New York, ment of neuropathic pain. J Pain Symptom compared with high-dose sufentanil for
NY: Basic Books Inc; 1973. Manage. 2003;25(5 suppl):S4-S11. anesthesia and postoperative analgesia in
8. Melzack R, Wall P. Pain mechanisms: a new 30. Melzack R. Phantom limbs. Sci Am. 1992; neonatal cardiac surgery. N Engl J Med.
theory. Science. 1965;150:171-179. 266(4):120-126. 1992;326:1-9.
9. Ignatavicius DA, Workman ML. Medical- 31. Jensen TS, Krebs B, Nielson J, Rasmussen P. 50. Coggeshall RE, Jennings EA, Fitzgerald M.
Surgical Nursing/Critical Thinking for Collab- Phantom limb, phantom pain and stump Evidence that large myelinated primary
orative Care. 5th ed. Philadelphia, PA: Saun- pain in amputees during the first 6 months afferent fibers make synaptic contacts in
ders; 2006:66-67. following limb amputation. Pain. 1985; lamina II of neonatal rats. Brain Res Dev
10. Melzack R, Wall P, eds. Textbook of Pain. 4th ed. 17:243-256. Brain Res. 1996;92:81-90.
New York, NY: Churchill Livingstone; 1999. 32. Hill A, Niven C, Knussen C. Pain memories 51. Fitzgerald M, Shaw A, MacIntosh N. Post-
11. Copstead LC, Banasik JL. Pathophysiology. 3rd in phantom limbs: a case story. Pain. 1996; natal development of the cutaneous flexor
ed. Philadelphia, PA: Saunders; 2005:1174. 66:381-384. reflex: comparative study of preterm
12. Devine EC. Somatosensory function, pain 33. Katz J, Melzack R. Pain ‘memories’ in phan- infants and newborn rat pups. Dev Med
and headache. In: Porth CM, ed. Pathophys- tom limbs: review and clinical observations. Child Neurol. 1988;30(4):520-526.
iology: Concepts of Altered Health Status. Pain. 1990;43(3):319-336. 52. Porter FL, Grunau RE, Anand KJ. Long-
Philadelphia, PA: Lippincott; 2005:1159-1191. 34. Portenoy RK. Neuropathic pain. In: Kanner term effects of pain in infants. J Dev Behav
13. Besson J. The neurobiology of pain. Lancet. R, ed. Pain Management Secrets. 2nd ed. Pediatr. 1992;20:253-261.
1999;353:1610-1615. Philadelphia, PA: Hanley & Belfus; 2003: 53. Porter FL, Wolf CM, Miller JP. Procedural
14. Jett L. Pain management. In: Urden LS, Stacy 147-170. pain in newborn infants: the influence of
KM, Lough ME, ed. Priorities in Critical Care 35. Jensen T, Nikolajsen L. Phantom pain and intensity and development. Pediatrics.
Nursing. St Louis, MO: Mosby; 2005:79-92. other phenomena after amputation. In: 1999;104(1):e13.
15. Wall P. The placebo and placebo response. Wall P, Melzack R, eds. Textbook of Pain. 4th 54. Taddio A, Katz J, Ilersich AL. Effect of
In: Wall P, Melzack R, eds. Textbook of Pain. ed. New York, NY: Churchill Livingstone; neonatal circumcision on pain response
New York, NY: Churchill Livingstone; 1999:799-814. during subsequent routine vaccination.
1999:799-814. 36. Boivie J. Central pain. In: Wall P, Melzack Lancet. 1997;349:599-603.
16. Rainville P, Hofbauer RK, Paus T, Duncan R, eds. Textbook of Pain. 4th ed. New York, 55. McGrath PA, Brown SC. Pain in children.
GH, Bushnell MC, Price DD. Cerebral NY: Churchill Livingstone; 1999:879-914. In: Kanner R, ed. Pain Management Secrets.
mechanisms of hypnotic induction and sug- 37. Andersson H, Ejlertsson G, Leden I, Rosen- 2nd ed. Philadelphia, PA: Hanley & Belfus;
gestion. J Cogn Neurosci. 1999;11(1):110-125. berg C. Chronic pain in a geographically 2003:180-194.
17. Petrovic P, Kalso E, Petersson KM, Ingvar defined general population: studies of dif- 56. Malleson P, Jacqui C. Pain syndromes in
M. Placebo and opioid analgesia—imaging ferences in age, gender, social class, and children. Curr Opin Rheumatol. 2003;
a shared neuronal network. Science. 2002; pain localization. Clin J Pain. 1993;8:174-182. 15(5):572-580.
295(5560):1737-1740. 38. Forgays DG, Rzewbuccjum R, Ober AJ, For- 57. National Pain Foundation. Pediatric pain:
18. Kringelbach ML, Rolls ET. The functional gays DK. Headache in college students: a psychological factors related to chronic
neuroanatomy of the human orbitofrontal comparison of four populations. Headache. pain in children and adolescents. http://
cortex: evidence from neuroimaging and 1993;33:182-190. www.nationalpainfoundation.org/MyTreat
neuropsychology. Prog Neurobiol. 2004; 39. Lester N, Lefebvre JC, Keefe FJ. Pain in ment/articles/Pediatric_General_Pain.asp.
72:341-372. young adults, I: relationship to gender and Updated May 21, 2008. Accessed August
19. Wager TD, Rilling JK, Smith EE, et al. family history. Clin J Pain. 1994;10:282-289. 21, 2008.

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

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

58. Goodman JE, McGrath PA. The epidemiol- 77. Pogatzki-Zahn EM, Zahn PK. From pre-
ogy of pain in children and adolescents: a emptive to preventive analgesia. Curr Opin
review. Pain. 1991;46:247-264. Anaesthesiol. 2006;19(5):551-555.
59. Harkins SW. Aging and pain. In: Loeser JD, 78. Ruppert SD, Kernicki JG, Dolan JT. Dolan’s
Butler SH, Chapman CR, Turk DC, eds. Critical Care Nursing. 2nd ed. Philadelphia
Bonica’s Management of Pain. 3rd ed. PA: FA Davis; 1996.
Philadelphia, PA: Lippincott; 2001:813-823. 79. Charron J, Rainville P, Marchand S. Direct
60. Harkins SW. What is unique about the comparison of placebo effects on clinical
older adult’s pain experience? In: Weiner and experimental pain. Clin J Pain. 2006;
DF, Herr K, Rudy TE, eds. Persistent Pain in 22:204-211.
Older Adults. New York, NY: Springer Pub- 80. Goffaux P, Redmond WJ, Rainville P, Marc-
lishing; 2002:4-17. hand S. Descending analgesia—when the
61. Chakour MC, Gibson SJ, Bradbeer M, Helme spine echoes what the brain expects. Pain.
RD. The effect of age on A delta-and C-fibre 2007;130(1-2):137-143.
thermal pain perception. Pain. 1996;64(1):
62. Harkins SW, Davis MD, Bush FM, Kasberger
J. Suppression of first pain and slow tempo-
ral summation of second pain in relation to
age. J Gerontol A Biol Sci Med Sci. 1996;51(5):
63. Harkins SW, Nowlin J, Ramm D, et al.
Effects of age, sex, and time-on-watch on a
brief continuous performance task. In: Pal-
more E, ed. Normal Aging II. Durham, NC:
Duke University Press; 1974:140-50.
64. Stanik-Hutt JA. Pain management in the crit-
ically ill. Crit Care Nurse. 2003;23(2):99-103.
65. Epstein J, Breslow MJ. The stress response
of critical illness. Critical Care Clin. 1999;
66. Kress JP, Pohlman AS, Hall JB. Sedation
and analgesia in the intensive care unit. Am
J Respir Crit Care Med. 2002;166:1024-1028.
67. Joint Commission on Accreditation of
Healthcare Organizations. 2005 Hospital
Accreditation Standards. Oakbrook Terrace,
IL: Joint Commission on Accreditation of
Healthcare Organizations; 2005.
68. Whelan CT, Lei Jin MS, Meltzer D. Pain and
satisfaction with pain control in hospital-
ized medical patients: no such thing as low
risk. Arch Intern Med. 2004;164:175-180.
69. Gordon DB, Dahl JL, Miaskowski C, et al.
American Pain Society recommendations
for improving the quality of acute and can-
cer pain management: American Pain Soci-
ety Quality of Care Task Force. Arch Intern
Med. 2005;165(14):1574-1580.
70. Hockenberry MJ, Wilson D, Winkelstein
ML. Wong’s Essentials of Pediatric Nursing.
7th ed. St Louis, MO: Mosby; 2005:1259.
71. Payen JF, Bru O, Bosson JL, et al. Assessing
pain in critically ill sedated patients by
using a behavioral pain scale. Crit Care Med.
72. Pasero C, McCaffrey M. No self-report
means no pain-intensity rating: assessing
pain in patients who cannot provide a self-
report. Am J Nurs. 2005;105(10):50-53.
73. Gelinas C, Fortier M, Viens C, Fillion L,
Puntillo KA. Pain assessment and manage-
ment in critically ill intubated patients: a
retrospective study. Am J Crit Care. 2004;
74. Bachiocco V, Scesi M, Morselli AM, Carli G.
Individual pain history and familial pain
tolerance models: relationships to post-sur-
gical pain. Clin J Pain. 1993;9(4):266-271.
75. Taddio A, Goldbach M, Ipp M, Stevens B,
Koren G. Effect of neonatal circumcision on
pain responses during vaccination in boys.
Lancet. 1995;345:291-292.
76. Woolf CJ, Chong MS. Preemptive analgesia
—treating postoperative pain by preventing
the establishment of central sensitization.
Anesth Analg. 1993;77(2):362-379.

http://ccn.aacnjournals.org CRITICALCARENURSE Vol 28, No. 6, DECEMBER 2008 49

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018
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.

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

Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb Kb
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
Program evaluation Name Member #
Yes No
Objective 1 was met K K Address
Objective 2 was met K K City State ZIP
Objective 3 was met K K
Content was relevant to my Country Phone
For faster processing, take
nursing practice K K
this CE test online at My expectations were met K K E-mail
http://ccn.aacnjournals.org This method of CE is effective RN Lic. 1/St RN Lic. 2/St
(“CE Articles in this issue”) for this content K K
or mail this entire page to: The level of difficulty of this test was: Payment by: K Visa K M/C K AMEX K Discover K Check
K easy K medium K difficult
AACN, 101 Columbia To complete this program, Card # Expiration Date
Aliso Viejo, CA 92656. it took me hours/minutes. Signature

The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation.
AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN
programming meets the standards for most other states requiring mandatory continuing education credit for relicensure.

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018

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
Published online http://ccn.aacnjournals.org/
Personal use only. For copyright permission information:

Subscription Information
Information for authors

Submit a manuscript

Email alerts

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.

Downloaded from http://ccn.aacnjournals.org/ by AACN on July 18, 2018