Chapter 83
Pain Management
Didier Demesmin, MD, MBA
Lynne M. Dunphy, PhD, APRN, FNP-BC, FAAN, FAANP
Brian Oscar Porter, MD, PhD, MPH, MBA
The ongoing opioid crisis lies at the intersection of substantial public
health challenges—reducing the burden of suffering from pain and
containing the toll of the harms that can result from the use of opioid
medications.
—Pain Management and the Opioid Epidemic:
Balancing Societal and Individual Benefits
and Risks of Prescription Opioid Use;
National Academies of Sciences,
Engineering, and Medicine, 2017
INTRODUCTION
The above statement, cited in a Pain Management Best Practices Inter-
Agency Task Force Report (2019), remains even truer today. The ravages of
the COVID-19 epidemic have only accelerated and heightened the ongoing
opioid epidemic, even though the root causes are better understood. Pain
continues to be a multifaceted complex public health concern globally and
nationally. It is estimated that 100 million Americans suffer from chronic,
noncancer pain, and according to Healthy People 2030, one in 12 Americans
live with high-impact chronic pain. Many Americans experience acute pain
for a variety of reasons, such as trauma, burns, injuries, and surgeries, many
of which are short-term and self-limiting. However, improperly managed
,acute pain can lead to high-impact chronic pain. The economic burden of
chronic pain accounts for more than $600 billion annually in direct medical
costs and lost productivity. In fact, general pain—both acute and chronic—is
one of the most common reasons that patients seek help from a primary care
provider, accounting for as many as 50% of physician visits per year in the
United States.
There are many definitions of pain. The International Association for the
Study of Pain (IASP) defines pain as “an aversive sensory and emotional
experience typically caused by, or resembling that caused by, actual or
potential tissue injury” (IASP Pain Task Force, 2021). This new definition of
pain emphasizes that a person’s experience of pain is not always supported
by evidence of tissue damage, and as such, the experience of pain cannot be
reduced to the activity of sensory neurons. It also reinforces that nonverbal
pain indicators should be considered and a patient’s report of pain should be
accepted (see Fig. 83.1). Many patients may experience pain in the absence
of noxious stimuli, and this definition supports a view of pain as a complex
biopsychosocial phenomenon that involves an interplay of sensory-
physiological, cognitive-affective, and behavioral processes. Pain can also be
thought of as a motivational state that engenders goal-directed action.
PAIN MECHANISMS: PATHOPhYSIOLOGY
An important concept central to a thorough understanding of pain
mechanisms, pathophysiology, and treatments is the concept of
somatosensation. Somatosensation is the activation of physical stimuli by
neural substrate, resulting in the perception of touch, pressure, and pain.
Nociceptors are sensory receptors that respond to noxious stimuli; they are
specialized neurons that detect a noxious stimulus and then conduct it to the
central nervous system (CNS). Nociceptors transduce mechanical, chemical,
and thermal stimuli into electrical activity to the CNS where it is processed
and interpreted as pain. Nociceptors have been identified in all tissues and
organs throughout the body except the nervous system. Noxious stimuli are
transmitted from the injured tissue such as skin, muscle, or viscera to the
cerebral cortex. This information is projected to higher cortical levels to the
thalamus and to the somatosensory cortex of the cerebral cortex where pain
perception occurs.
A basic understanding of the anatomy and physiology of pain transmission
is essential in evaluating different pain states and associated pharmacological
,and interventional treatments. The nervous system can transmit and modulate
various nociceptive stimuli. Pain stimuli are transmitted via nociceptors,
which are peripheral afferent nerve fibers that detect noxious stimuli—
thermal, mechanical, or chemical. These stimuli are conducted from these
first-order neurons peripherally to the spinal cord via spinal roots at each
cervical, thoracic, lumbar, and sacral level. These first-order neurons may
ascend two to four spinal cord segments in Lissauer’s tract before synapsing
with second-order neurons in the gray matter of the ipsilateral dorsal horn.
These second-order neurons then cross to the contralateral side of the spinal
cord and ascend via the spinothalamic tract to the thalamus, where third-order
neurons project to the cerebral cortex.
Peripheral nociceptors have their cell bodies residing in the dorsal root
ganglion, which lies within the intervertebral foramina at each spinal level.
Nociceptors are pseudounipolar, and they travel in a bidirectional fashion
from the periphery to the spinal cord and from the spinal cord to the
peripheral organs and tissues. Thus, their axons travel both centrally to the
spinal cord and higher brain centers and transmit impulses peripherally to the
skin and other organs. There are two major classes of pain-transmitting
fibers: A delta fibers, which are of medium diameter and thinly myelinated,
and C fibers, which are of small diameter and unmyelinated. The A delta and
C fibers can detect thermal, mechanical, or chemical stimuli. The A delta and
C fiber nociceptors encode and transmit information to the CNS concerning
the intensity, location, and duration of noxious stimuli. A delta fibers mediate
acute and precisely localized pain, whereas C fibers mediate poorly localized
and delayed pain.
, Figure 83.1 Pain cloud. Source: U.S. Department of Health
and Human Services (2019, May). Pain Management Best
Practices Inter-Agency Task Force Report: Updates, Gaps,
Inconsistencies, and Recommendations.
Somatosensory perception of pain involves four processes: transduction,
transmission, modulation, and perception (see Fig. 83.2). Transduction is the
basis of creating a chemical event that progresses to an electrical event.
Transduction occurs in the peripheral terminals of primary afferent neurons.
These primary afferent first-order neurons respond to mechanical, chemical,
and thermal stimuli. The axonal membrane of these primary afferent neurons
has transduction channels that once an action potential is sufficient to
depolarize the axon will generate potentials that are then transmitted through
the nervous system. Noxious substances that facilitate pain production
include bradykinin, tumor necrosis factor (TNF), histamine, prostaglandins,
hydrogen ions, and potassium ions. Transmission is the process by which, as
this stimulus progresses, the action potential depolarizes the neuron, allowing
for the release of chemicals that facilitate the pain stimulus of the afferent
primary neuron to the dorsal horn of the spinal cord. Modulation of pain from
the higher CNS occurs via the descending inhibitory tracts and can occur at
Pain Management
Didier Demesmin, MD, MBA
Lynne M. Dunphy, PhD, APRN, FNP-BC, FAAN, FAANP
Brian Oscar Porter, MD, PhD, MPH, MBA
The ongoing opioid crisis lies at the intersection of substantial public
health challenges—reducing the burden of suffering from pain and
containing the toll of the harms that can result from the use of opioid
medications.
—Pain Management and the Opioid Epidemic:
Balancing Societal and Individual Benefits
and Risks of Prescription Opioid Use;
National Academies of Sciences,
Engineering, and Medicine, 2017
INTRODUCTION
The above statement, cited in a Pain Management Best Practices Inter-
Agency Task Force Report (2019), remains even truer today. The ravages of
the COVID-19 epidemic have only accelerated and heightened the ongoing
opioid epidemic, even though the root causes are better understood. Pain
continues to be a multifaceted complex public health concern globally and
nationally. It is estimated that 100 million Americans suffer from chronic,
noncancer pain, and according to Healthy People 2030, one in 12 Americans
live with high-impact chronic pain. Many Americans experience acute pain
for a variety of reasons, such as trauma, burns, injuries, and surgeries, many
of which are short-term and self-limiting. However, improperly managed
,acute pain can lead to high-impact chronic pain. The economic burden of
chronic pain accounts for more than $600 billion annually in direct medical
costs and lost productivity. In fact, general pain—both acute and chronic—is
one of the most common reasons that patients seek help from a primary care
provider, accounting for as many as 50% of physician visits per year in the
United States.
There are many definitions of pain. The International Association for the
Study of Pain (IASP) defines pain as “an aversive sensory and emotional
experience typically caused by, or resembling that caused by, actual or
potential tissue injury” (IASP Pain Task Force, 2021). This new definition of
pain emphasizes that a person’s experience of pain is not always supported
by evidence of tissue damage, and as such, the experience of pain cannot be
reduced to the activity of sensory neurons. It also reinforces that nonverbal
pain indicators should be considered and a patient’s report of pain should be
accepted (see Fig. 83.1). Many patients may experience pain in the absence
of noxious stimuli, and this definition supports a view of pain as a complex
biopsychosocial phenomenon that involves an interplay of sensory-
physiological, cognitive-affective, and behavioral processes. Pain can also be
thought of as a motivational state that engenders goal-directed action.
PAIN MECHANISMS: PATHOPhYSIOLOGY
An important concept central to a thorough understanding of pain
mechanisms, pathophysiology, and treatments is the concept of
somatosensation. Somatosensation is the activation of physical stimuli by
neural substrate, resulting in the perception of touch, pressure, and pain.
Nociceptors are sensory receptors that respond to noxious stimuli; they are
specialized neurons that detect a noxious stimulus and then conduct it to the
central nervous system (CNS). Nociceptors transduce mechanical, chemical,
and thermal stimuli into electrical activity to the CNS where it is processed
and interpreted as pain. Nociceptors have been identified in all tissues and
organs throughout the body except the nervous system. Noxious stimuli are
transmitted from the injured tissue such as skin, muscle, or viscera to the
cerebral cortex. This information is projected to higher cortical levels to the
thalamus and to the somatosensory cortex of the cerebral cortex where pain
perception occurs.
A basic understanding of the anatomy and physiology of pain transmission
is essential in evaluating different pain states and associated pharmacological
,and interventional treatments. The nervous system can transmit and modulate
various nociceptive stimuli. Pain stimuli are transmitted via nociceptors,
which are peripheral afferent nerve fibers that detect noxious stimuli—
thermal, mechanical, or chemical. These stimuli are conducted from these
first-order neurons peripherally to the spinal cord via spinal roots at each
cervical, thoracic, lumbar, and sacral level. These first-order neurons may
ascend two to four spinal cord segments in Lissauer’s tract before synapsing
with second-order neurons in the gray matter of the ipsilateral dorsal horn.
These second-order neurons then cross to the contralateral side of the spinal
cord and ascend via the spinothalamic tract to the thalamus, where third-order
neurons project to the cerebral cortex.
Peripheral nociceptors have their cell bodies residing in the dorsal root
ganglion, which lies within the intervertebral foramina at each spinal level.
Nociceptors are pseudounipolar, and they travel in a bidirectional fashion
from the periphery to the spinal cord and from the spinal cord to the
peripheral organs and tissues. Thus, their axons travel both centrally to the
spinal cord and higher brain centers and transmit impulses peripherally to the
skin and other organs. There are two major classes of pain-transmitting
fibers: A delta fibers, which are of medium diameter and thinly myelinated,
and C fibers, which are of small diameter and unmyelinated. The A delta and
C fibers can detect thermal, mechanical, or chemical stimuli. The A delta and
C fiber nociceptors encode and transmit information to the CNS concerning
the intensity, location, and duration of noxious stimuli. A delta fibers mediate
acute and precisely localized pain, whereas C fibers mediate poorly localized
and delayed pain.
, Figure 83.1 Pain cloud. Source: U.S. Department of Health
and Human Services (2019, May). Pain Management Best
Practices Inter-Agency Task Force Report: Updates, Gaps,
Inconsistencies, and Recommendations.
Somatosensory perception of pain involves four processes: transduction,
transmission, modulation, and perception (see Fig. 83.2). Transduction is the
basis of creating a chemical event that progresses to an electrical event.
Transduction occurs in the peripheral terminals of primary afferent neurons.
These primary afferent first-order neurons respond to mechanical, chemical,
and thermal stimuli. The axonal membrane of these primary afferent neurons
has transduction channels that once an action potential is sufficient to
depolarize the axon will generate potentials that are then transmitted through
the nervous system. Noxious substances that facilitate pain production
include bradykinin, tumor necrosis factor (TNF), histamine, prostaglandins,
hydrogen ions, and potassium ions. Transmission is the process by which, as
this stimulus progresses, the action potential depolarizes the neuron, allowing
for the release of chemicals that facilitate the pain stimulus of the afferent
primary neuron to the dorsal horn of the spinal cord. Modulation of pain from
the higher CNS occurs via the descending inhibitory tracts and can occur at
