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The Role of Inpatient/Acute Pain Services for Perioperative Pain … 147
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https://t.me/med1917
Pain and the Transition from Acute
to Chronic
Adeeb Oweidat, Rofayda Gad, Yair Rubin, Alain Harb,
Nour El Hage Chehade, and Amro Khalili
Abstract Chronic post-surgical pain reduces quality of life, challenging to treat, and
has economic impact. Factors that predispose patients to development of chronic post-
surgical pain may be potential targets for identification and prevention of transition
from acute to chronic pain. This involves a multidisciplinary perioperative plan that
begins at the preoperative clinic and continues beyond healing phase of surgery.
Keywords Types of pain
· Neuroplasticity · Epigenetics
A. Oweidat (
B
)
Associate Program Director for Regional Anesthesia and Acute Pain, University of Iowa Hospital
and Clinic, Iowa City, USA
e-mail: adeeb.oweidat@gmail.com
R. Gad
Instructor of Anesthesiology NYU Hospital, Iowa City, USA
e-mail: Rofayda.Y.Gad@gmail.com
Y. Rubin
Clinical Associate Professor of Anesthesia, Medical Director, Non OR Anesthesia Services,
University of Iowa Hospital and Clinic, Iowa City, USA
e-mail: yair-rubin@uiowa.edu
A. Harb
Assistant Professor of Anesthesiology, University of Miami, Miller School of Medicine, Miami,
Florida, USA
e-mail: alain.ch.harb@gmail.com
N. El Hage Chehade
Assistant Professor of Anesthesiology, Cleveland Clinic, Cleveland, USA
e-mail: ELHAGEN2@ccf.org
A. Khalili
Instructor of Clinical Anesthesiology, Division of Cardiovascular Anesthesia, American
University of Beirut Medical Center, Beirut, Lebanon
e-mail: amero.kh@hotmail.com
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024
A. Abd-Elsayed and K. Schroeder (eds.), Perioperative Pain Management,
https://doi.org/10.1007/978-3-031-67648-2_11
149
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150 A. Oweidat et al.
1 Introduction
The International Association for the Study of Pain (IASP) defines pain as the
unpleasant sensory and emotional experience associated with actual or potential
tissue damage. Though it is most often related to tissue damage, perception of the
damage varies due to many factors: attitudes, beliefs, personality, social factors,
non-modifying factors like gender and ethnicity, and underlying conditions such as
comorbidities, mental stress, and substance abuse. Moreover, genetic associations
affect a person’s pain perception by orchestrating the entire mechanism [1].
2 Theories of Pain
•
Gate Control theory (1965): This is the first theory of pain, which presented pain
as a mind–body experience. The theory states that a stimulus must synapse at
three different locations within the spinal cord: the fibers of the dorsal column
and in the dorsal horn, the Substantia Gelatinosa, and the transmission cell. The
Substantia Gelatinosa regulates the signals from the periphery; It will either block
pain signals or allow them to enter the spinal cord’s “neurological gate.” The gate
will open if the pain in the periphery is more intense than the non-painful positive
stimuli. The signal is then transmitted in the spinal cord, ascends to the thalamus,
where it is integrated, and then registered within the primary somatosensory cortex
of the parietal lobe. A real-life example is demonstrated within pediatric medical
care. Suppose a positive, non-painful stimulus (game or play) of high enough
intensity and distraction is administered to the child simultaneously as a painful
procedure. In that case, it closes the pain gate in the spinal cord, preventing the
ascending propagation of the pain nerve signal from the procedure [2].
•
Neuro-matrix Model: The neuro-matrix model was developed 30 years after the
gate control theory following observations of amputees suffering from phantom
limb pain. This model suggests that painful sensations originate in t he central
nervous system (CNS) rather than the periphery. The neuro-matrix consists
of various areas within the CNS that contribute to pain perception signaling.
Locations include the spinal cord, brainstem, thalamus, somatosensory cortex,
motor cortex, prefrontal cortex, insular cortex, and limbic system. This model
acknowledges that pain can be affected by cognitive and emotional factors [2].
•
Biopsychosocial: This model hypothesizes that pain results from intricate biolog-
ical, psychological, and sociological interactions. It supports the notion that the
human body cannot be categorized when considering management options for
pain. John D. Loeser, an anesthesiologist, was the first to implement this model.
He proposed that four parts need to be taken into consideration in the treat-
ment of pain: nociception (perceptive component), pain (sensory-discriminatory
component), suffering (motivo-affective component), and pain behaviors (cogni-
tive behavioral component). The biopsychosocial model of pain is also the closest
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Pain and the Transition from Acute to Chronic 151
to incorporating genetic factors. The way we approach pain management today
is based mainly on Loeser’s four elements of pain, and failure to consider these
elements can be viewed as an inadequate assessment of care [2].
Pain is a protective mechanism that serves an important role. However,if it persists
long after resolving the triggering event, it loses its intended function. Typically, after
cessation of nociceptive stimuli and tissue recovery, the body returns to its normal
state, and pain is no longer experienced. If the pain does not diminish and instead
continues beyond the expected healing timeline, the patient now has developed
chronic pain [26]. Factors differentiating between acute and chronic pain include
the cause, the duration, and the treatment approach (Table 1). The term transitional
pain service has gained attention in recent years. Transitional pain services focus on
trying to help surgical patients who are felt to be at risk of their acute pain evolving
into chronic pain. This will be the main focus of the next section of this chapter [6,
7].
In 2016, The International Association for the Study of Pain further classified pain
into three broad descriptive categories: nociceptive, neuropathic, and nociplastic.
These categories are intended to provide information about the mechanisms under-
lying the pain, which can serve as targets for drug or non-drug treatments and facilitate
communication between stakeholders (e.g., clinicians, patients, and researchers) [8].
– Nociceptive pain: Adaptive transient pain in response to a noxious stimulus (like an
alarm that announces the presence of a potentially damaging stimulus). Nocicep-
tive pain is caused by neural activity responding to potentially damaging stimuli
such as postoperative tissue damage, post-exercise injuries, mechanical low back
pain, and sickle cell crisis. Nociceptive pain is further divided into visceral and
somatic pain [6].
– Neuropathic pain: Is initiated or caused by a primary lesion or damage of the
somatosensory nervous system, including the peripheral and central neural struc-
tures, causing spontaneous pain and hyperalgesia (like an alarm that is constantly
on even though there is no emergency or gives repeated false alarms). Proposed
mechanisms associated with the initiation of neuropathic pain may include trauma,
stroke, autoimmune diseases, and responses to toxic element exposure. Typical
neuropathic pain includes postherpetic neuralgia, trigeminal neuralgia, complex
Table 1 Description of pain
Characteristic of pain Cause Duration of pain Treatment strategy
Acute pain Known Short, Resolves after
healing < 3 months
Self-limiting. Resolves
after removing the
underlying cause
Chronic pain Mostly
unknown—Related to
Neuroplasticity of the
CNS
Persists past healing
for > 3 months
Attempt to accomplish
pain control rather than
cure
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152 A. Oweidat et al.
regional pain syndrome type II, central pain syndromes, and distal polyneuropathy
due to various causes such as diabetes, HIV, and alcohol [6, 7].
– Nociplastic pain: the underlying mechanism is considered augmented CNS pain,
sensory processing, and altered pain modulation [28]. It represents hypersensi-
tivity to pain resulting from abnormal central processing of normal input (e.g.,
fibromyalgia, irritable bowel syndrome, tension-type headache, noncardiac chest
pain) [6, 7]. This type of pain can occur in isolation, as often occurs in conditions
such as fibromyalgia or tension-type headache, or as part of a mixed-pain state
in combination with ongoing nociceptive or neuropathic pain, as might occur in
chronic low back pain [9].
Furthermore, Pain can also be categorized into two broad categories: adaptive and
maladaptive. Adaptive pain protects the organism from injury or promotes healing
when damage has occurred. Maladaptive pain, in contrast, is a pathologic operation of
the nervous system; it is a disease where pain is uncoupled from a noxious stimulus or
healing tissue. Such pain may occur due to damage to the nervous system (neuropathic
pain) or abnormal nervous system operation (functional pain). It is usually persistent
or recurrent [6, 7].
3 Mechanism of Pain
Noxious stimuli are transduced to the dorsal horn of the spinal cord, where amino
acid and peptide transmitters activate second-order neurons. Spinal neurons then
transmit signals to the brain. The resultant actions by the individual involve sensory-
discriminative, motivational-affective, and modulatory processes in an attempt to
limit or stop the painful process. As we said, this is in normal conditions; however,
Persistent, intense pain activates secondary mechanisms at the periphery and within
the central nervous system that cause allodynia, hyperalgesia, and hyperpathia,
which can diminish normal functioning [6].
Multiple mechanisms that can produce pain have been identified; they include
nociception, peripheral sensitization, phenotypic switches, central sensitization,
ectopic excitability, structural reorganization, and decreased inhibition.
Nociception: Represents the sole mechanism responsible for nociceptive pain and
comprises the processes of transduction, conduction, transmission, and perception.
Nociceptors have unmyelinated (C-fiber) or t hinly myelinated (A- fiber) axons. The
pathways and mechanisms involved in mediating nociceptive pain signals include
four stages.
Transduction: It is the process by which painful mechanical, thermal, or chemical
stimuli are encoded to generate electrical signals—the generator potentials. Pain or
noxious stimuli are converted into electrical activity following activation of recep-
tors sensitive to heat, cold, mechanical, or chemical stimuli in the unmyelinated C-
fiber, thinly myelinated A-delta fiber, and myelinated A-beta fiber of the peripheral
nociceptors. Depending on the neuron type, each group of neurons responds with
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Pain and the Transition from Acute to Chronic 153
slow, intermediate, or rapid velocity to different stimuli and pain thresholds. Once a
generator potential reaches a threshold, an action potential is fired.
Conduction: The process by which an action potential is conducted along a nerve
fibers membrane to reach the presynaptic membrane of synapsis between neurons in
the spinal cord or brain. Pain or noxious stimuli are converted into electrical activity
following activation of receptors sensitive to heat, cold, mechanical, or chemical
stimuli in the unmyelinated C- fiber, thinly myelinated A-delta -fiber, and myelinated
A-beta fiber of the peripheral nociceptors. Depending on the neuron type, each group
of neurons responds with slow, intermediate, or rapid velocity to different stimuli
and pain thresholds.
Transmission is when the action potential is passed from one nerve cell to another
through a chemical or electrical synaptic connection. In the pain processing pathway,
synaptic transmission from the first order to the second-order neurons occurs at the
spinal cord’s dorsal horn or the brainstem’s sensory nucleus. The transmission from
second to third-order neurons occurs in the brainstem’s thalamus or the parabrachial
nucleus.
Perception: Perception of pain is formed at the cortical level and usually serves
as a warning. Normally, the threshold for pain should be sensitive enough to prevent
damage but not hypersensitive to the extent of interfering with normal activi-
ties. Responses to pain include reflex withdrawal through a reflex pathway in the
spinal cord or brainstem, purposeful pain avoidance and emotional reaction, cortical
processing, and learning and memory that involve the hippocampus and other neural
structures [6, 7].
It is worth noting that the transmission of pain signaling from the periphery to the
central nervous system and cortex is plastic and can change over time in response
to repeated stimuli. For example, the neuroplasticity of peripheral nociceptors can
result in peripheral sensitization to stimuli, and this transition will be addressed in
the next section [10, 11].
•
Aβ fibers: are considered rapidly conducting and respond to mechanical stimuli
with a low threshold.
•
Aδ fibers: respond to heat, cold, and high-intensity mechanical stimuli and conduct
with intermediate velocity.
•
C fibers: conduct slowly and can respond to heat, mechanical or chemical stimuli.
•
The interface between primary afferents and the spinal cord occurs in the laminae.
•
Aβ fibers make synaptic connections with PKC + neurons in Laminae III-IV and
ϒ wide dynamic range neurons (WDR) in lamina V.
•
Aδ fibers make synaptic connections with spinothalamic projection neurons in
outer lamina II and wide dynamic range (WDR) neurons in Lamina V. The WDR
neurons are important as they have been implicated in “wind up” or sensitization
of the spinal cord because the intensity of their response increases as the frequency
of the incoming stimulus increases [6–9].
•
C fibers make synaptic contacts with spinothalamic projection neurons in lamina
I and Inner lamina II.
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154 A. Oweidat et al.
Visceral organs may also create pain symptomology. Visceral pain is mediated
by visceral nerves that include sympathetic nerves (cervical, thoracic, and lumbar)
and parasympathetic nerves (cranial nerve X and spinal nerves S2-4), with their cell
bodies residing in the dorsal root ganglion (DRG) or visceral nerve ganglion (Nodose
ganglion). The second-order neurons are localized in laminae I and II of the spinal
cord or in the brainstem (Nucleus solitarius).
Electrical signals (action potentials) are transmitted to the dorsal horn of the spinal
cord and then relayed via two primary ascending pathways, the spinothalamic (pain
and temperature) and spinoparabrachial (likely mediates affective pain) tracts. The
spinothalamic pathway projects into the thalamus and somatosensory cortex, while
the spinoparabrachial pathway connects to the hippocampus’s ventral medial nucleus
and the amygdala’s central nucleus [6, 7, 10, 11].
4 Nociceptors: Anatomy, Physiology, and Peripheral
Sensitization
In some pathological circumstances, action potentials can be generated in locations
other than the peripheral nerve endings. This phenomenon is called ectopic activity/
discharge. Ectopically generated spikes can be conducted to the spinal cord and
the peripheral nerve ending, where Substance P is released and has been related to
neurogenic inflammation.
The sensory neuron cell body is a site critical for integrating neural activity.
Proteins and signaling molecules are delivered to the soma via axonal transport
mechanisms, possibly contributing to aberrant or ectopic activity under pathological
conditions. Many of the proteins responsible for these processes have been identified
under normal and pathological conditions [6, 7, 10, 11].
There are several different types of peripheral nociceptors involved in pain
processing.
•
Thermal nociceptors detect extreme temperatures, and mechanical nociceptors
detect intensive pressure. These nociceptors comprise small diameter Aδ (Adelta)
fibers that are thinly myelinated and conduct signals at a velocity of 5–30 m/s.
•
C fibers are the primary neuronal type of polymodal nociceptors. These fibers
are unmyelinated neurons with a slower conduction velocity of approximately
one m/sec or less. These nociceptors are activated by high-intensity mechanical,
chemical, and thermal stimuli.
•
A third type of neuron involved in pain processing is the Aβ neuron. These neurons
are large-diameter sensory fibers that contribute to the normal perception of stim-
ulus quality, even though they do not respond directly to noxious stimuli. Activity
in large-diameter fiber systems can modify pain perception and is believed to
mediate allodynia in various pathological circumstances.
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Pain and the Transition from Acute to Chronic 155
Both C and Aδ fibers can release glutamate and substance P (a neuropeptide).
Substance P is thought to enhance and prolong the actions of glutamate. Substance
P may activate more post-synaptic neurons as there is no reuptake mechanism.
5 Specific verus Diverse Nociceptors
Diverse nociceptors in the body respond to specific stimulation through the
expression and activation of specific receptors/channels. For example.
•
Mechano-transduction is mediated by TRPV4, ASIC-3, and the low threshold
voltage-gated calcium channel (VGCC) CaV3.2.
•
Thermo-transduction is mediated by TRPM8 (melastatin type 8) for cool, TRPV4
for warm, and TRPV1 (vanilloid type 1) for hot sensations.
•
Chemoreceptors, through specific receptors/channels, can sense tissue acidosis
(TRPV1 and ASIC-3), noxious organic compounds (e.g., aldehydes at TRPA1)
and endogenous chemicals (e.g., ATP at P2X3).
In addition to specific nociceptors, some nociceptors express diverse channels/
receptors that can respond to different stimulations, i.e. mechanical, thermal and
chemical. These nociceptors are called polymodal nociceptors [6, 7, 10, 11].
Enhancing our collective understanding of how pain is signaled has become a
target of much research in the first part of this century. This enhanced research activity
has frequently focused on subtypes of the capsaicin receptor, which are cationic
channels that form the “pain” receptors. The Transient Receptor Potential (TRP) is
a family of receptor subtypes. Some respond to mechanical stimuli (mechanotrans-
ducer), whereas others are thermo-transducers (e.g., TRPV1 and TRPA1 subtype).
TRPV1 agonists, agonists, and target destruction of TRPV1-expressing neurons
are under investigation. Also note that the G Protein-coupled receptors (GPCR),
tropomyosin-receptor-kinase (TRK), and Cytokine receptors are essential for modu-
lating the sensitivity of nociceptors. Further understanding of these channels may
lead to new targeted therapies [12, 13].
6 Transduction of the Painful Stimulus
Following the process of converting a stimulus to an electrical stimulus, the process of
transduction propagates the signal from the periphery to the central nervous system.
Any understanding of this process is crucial because it represents an additional area
that may be impacted by either plasticity/remodeling and therapeutics [12, 13].
Generator Potential:
In the normal or naïve state, the stimulus activates multiple potential recep-
tors. These mechanical, thermal, and/or chemical stimuli are transduced by specific
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156 A. Oweidat et al.
receptors/channels into a membrane potential depolarization, called the “generator
potential” in the nerve endings [6, 12].
Spike initiation:
Spike initiation is the next step in the pathway after the stimulus has interacted with
a pain receptor to trigger a generator potential. Numerous ion channels play a role in
the spike initiation and upstroke of the spike. The Na1.7, Nav1.8, and Nav1.9 are the
most important sodium channels for spike initiation. It is important to understand
that the anatomical distribution of the ion channels is critical to producing action
potential generation and propagation. Several voltage-gated channels regulate the
action potential threshold. All of these ion channels are potential therapeutic targets
[6, 12, 13].
Spike propagation:
The ion channels underlying action potential propagation, such as Nav1.6, are
distinct from those underlying spike initiation. Following an insult, similar to the
pain receptors and spike initiation, the pattern of channel expression can change,
including redistribution of NaV1.7 and/or NaV1.8 to the cell membrane. Therapies
directed at sodium channel-blocking compounds, such as local anesthetics, TCAs,
and some COX inhibitors, have been used to treat pain [ 6, 12, 13].
Cell body:
The cell body (soma) serves as the supply depot for the rest of the neuron, synthe-
sizing and packaging the proteins, transmitters, and lipids. In nociceptive afferents,
the VGSC NaV1.8 is the primary sodium channel in the cell for action potential
generation [6, 12, 13].
7 Pro- and Anti-inflammatory Mediators and Receptors
•
GPCRs (G-protein coupled receptors) are responsive to E-type prostaglandins
(EP), bradykinin (B) types 1 and 2, and serotonin (5HT) types 1A, 2, and 7.
•
Tyrosine receptor kinases (TRK) are responsive to trophic factors such as nerve
growth factor (NGF) and artemin
•
There are receptors for inflammatory cytokines such as TNF-α, interleukin 1-β,
and IL-6.
•
These inflammatory mediators and their receptors are up-regulated or phospho-
rylated, leading to increased excitability of nociceptive neurons [6, 12, 13].
8 How Acute Pain Turns into Chronic
According to the CDC, chronic pain is the leading cause of disability in the United
States. In most circumstances, terminating acute nociception and full tissue recovery
restores normal homeostasis and ends the pain process. However, repetitive noci-
ceptive stimulation may result in a prolonged inflammatory process by activating
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Pain and the Transition from Acute to Chronic 157
lymphocytes and releasing TNF-a and interleukins. Chronic inflammation leads
to a series of changes in the periphery, such as reduction of pain threshold in the
primary afferent neurons, phosphorylation of protein kinases A and C, up-regulation
of voltage-gated sodium channels and TRPV1 receptors in DRG, and increased
production of substance P and CGRP in both the periphery and the spinal cord.
This process is known as peripheral sensitization and involves complex maladaptive
neuroplastic mechanisms at all levels of pain processing, from the periphery to the
brain, that ultimately culminate in a chronic pain state [14].
Chronic pain After Surgery: [15]
Patient-specific
•
Genotype
•
Medical history, preoperative chronic pain, opioid use
•
Psychological factors
•
Past experiences
Medical/Surgical
•
Type of surgery, reoperation, and related therapies
•
Anesthesia and analgesia
•
Severity/duration of acute post-operative pain
Predictors for Poor Postoperative Pain [15]:
•
Age
•
Depression
•
Catastrophizing
•
Preexisting pain
•
Preoperative use of opioids
•
Prior surgery at same site
•
Type of surgery
•
Preexisting chronic pain
9 Peripheral Sensitization
In the periphery, sensitivity and maladaptive processes can spread beyond the site
of the initial injury and result in secondary hyperalgesia. In addition, spinal cord
neuronal excitability can produce an exaggerated response to non-painful stimuli
(allodynia). Hyperalgesia and allodynia may have a biological protective role in that
they cause the organism to protect and reduce movement of the affected area, thus
limiting further tissue injury and allowing for healing. However, when sensitization
extends far beyond the initial physical or temporal boundaries of the acute event,
maladaptive chronic pain conditions can result in significant negative impacts on a
patient’s ability to function and manage their pain symptomology [14, 18].
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