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158 A. Oweidat et al.
10 Central Sensitization
As a result of a peripheral lesion that consistently generates pain impulses to the
spinal cord, inhibitory interneurons involved in modulating painful nerve transmis-
sion impulses may die. Furthermore, glial cells may remodel neuronal synapses
to intensify nociceptive transmission. The loss of inhibitory neuron function and
enhancement of aberrant signaling pathways ultimately results in elevated responses
to stimulation and the development within the CNS of additional second-order
neuronal connections [12].
The spinal cord, DRG and dorsal horn neurons can be stimulated to express
several genes and proteins implicated in enhancing the propagation of continuous
nociceptive signals. The most notable change is increased mRNA coding for various
receptors and ion channels such as Na and TRPV1. This change in receptor kinetics
leads to the hyperexcitable state of chronic pain [14].
Another vital receptor type in the spinal cord is the NMDA. A tightly bound
Mg plug normally keeps this receptor inactive during acute noxious stimulation.
However, with continuous nociceptive stimulation a prolonged slow depolarization
of the neurons in the dorsal horn causes a massive influx of calcium which displaces
the Mg plug from the NMDA receptors. This then allows glutamate to bind to NMDA
receptors which results in activation of NMDA receptors and the subsequent ‘wind-
up’ phenomenon, which manifests as allodynia.
The wind-up process results in neuroplasticity.
Neuroplasticity is the physical remodeling of neuronal cytoarchitecture that from
persistent acute pain leading to the transition from acute to chronic pain.
Another factor in central sensitization is loss of inhibitory neurons in the s pinal
cord and changes in the cortex and gray matter that further reduce the inhibitory
signals coming from the brain [15–17].
11 Peripheral Nerve Injury and Its Effects on Spinal Dorsal
Horn Interneuron Neuroplasticity in Chronic Pain
The dorsal horn of the spinal cord is composed broadly of excitatory and inhibitory
neurons and is organized into six laminae. Sensory information from the peripheral
tissues is transmitted through the afferent sensory neurons to the dorsal horn. The
superficial laminae I and II receives nociceptive signals, while the deep laminae
III to VI have non-nociceptive information transmitted to them. Integrated sensory
information is then transferred to several brain regions, including the thalamus
[16, 17].
Due to the relatively close anatomic location of the structures of each lamina,
structural and functional neuroplasticity of the dorsal horn can induce pain percep-
tion alterations. When the somatosensory processing system is altered by peripheral
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Pain and the Transition from Acute to Chronic 159
injury, the information can be incorrectly sensed, often leading to normally non-
noxious stimuli evoking pain sensation. This pain caused by non-noxious stimuli is
called allodynia, and is a characteristic of neuropathic and nociplastic pain [16, 17].
An example of this neuroplastic change associated with allodynia can be seen
with neuropeptide Y promoter (Npy) inhibitory interneurons. Outer lamina II Npy
inhibitory interneurons send inhibitory gamma-aminobutyric acid (GABA) signals to
projection neurons in lamina I. Additionally, the axons of Npy neurons also project
to lamina III/IV cells, where the subtypes of interneurons are closely associated
with noxious stimuli. After a peripheral nerve injury stimulus, there is a decreased
Npy neuronal excitability resulting in pain like behavior with touch; This touch
evoked pain is improved when the Npy interneuron excitability is increased.The
synaptic modifications of the circuits in the spinal cord dorsal horn cause balanced
changes in the neuronal projections to the brain in lamina 1 with regards to excitation
and inhibition. This at least partially accounts for chronic pain development and
maintenance [14, 17].
In the brain:
A pain matrix has been identified by radiological evidence. Functional magnetic
resonance imaging and positron emission tomography scans have identified several
essential pain centers and various changes in the pain matrix when sensitiza-
tion occurs: the thalamus where the spinothalamic tract terminates (somatosensory
discrimination), mid/anterior insula, anterior cingulated cortex and prefrontal cortex
(affective and motivational components of pain), periaqueductal gray (PAG) and
rostral ventromedial medulla (RVM) (fight-or-flight responses and stress-induced
analgesia), reticular formation (regulating descending pathways), spinoparabrachial
pathway to the hypothalamus and the amygdala (autonomic and sensory coordina-
tion). There is a strong correlation between chronic pain and mental status reflected
in pathophysiologic changes in the pain matrix [14].
12 Endogenous Pain Inhibitory System
Top-down modulation of pain signals has long been observed. Physicians in WWII
often noted soldiers with significant battlefield injuries who reported minimal
pain. The endogenous pain inhibitory system is now widely accepted. It involves
descending inputs from the hypothalamus, amygdala, and cingulate cortex that
communicate with the thalamus and midbrain (periaqueductal gray) and then to
the medulla—neurons within the medulla project to the spinal cord dorsal horn.
The inhibitory modulating pathways are sensitive to opioids and other agents,
including cannabinoids serotonin and norepinephrine. The precise mechanism by
which drugs interact with the inhibitory system is still incompletely understood, but
activation of the inhibitory pathways is the end result. Activation of these pathways
may be an important mechanism to decrease the development of chronic pain [17].
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160 A. Oweidat et al.
Epigenetics
Epigenetics refers to modifications in gene expression that do not require a change in
genetic sequence; rather, changes in the environment alter gene expression. Despite
in-depth evaluations examining the impact of pain modulation genetics and epige-
netics, a paucity of valid, evidence-based information limits the clinical applicability
of these pathways [2].
In contrast to the genetic determinism inherent in genomic studies, the field of
epigenetics strives to understand environmental control over gene expression [3].
Epigenetic mechanisms of genetic pain associations reveal specific biological mech-
anisms that, with the presence or lack of specific gene(s), contribute to a delivered
pain response and explain the difference in pain physiology. Epigenetic alterations,
including DNA methylation, histone acetylation, and RNAi, are necessary for normal
tissue specialization and neurologic development. However, these same modifica-
tions play a significant role in the induction of the chronic pain phenotype following
neurologic injury [4].
Significant evidence highlights epigenetics’s ability to modify general pain types,
including inflammatory, neuropathic, visceral, and cancer-related pain. Each of these
pain types may benefit from future therapeutics that utilize epigenetic targeting to
maximize potential analgesic benefits, decrease chronic pain development, and limit
side effects [5].
Preventing Acute Pain from Becoming Chronic
Unlearning’ by the nervous system could be an important concept for unraveling the
development of chronic pain in the future; however, currently, treating acute pain
aggressively is an important strategy in pain management to prevent chronic pain.
It is reasonable to assume that severe and persistent preoperative pain can lead to
chronic pain development, so it is crucial to focus on aggressive pain management
in the perioperative period. However, to date, the effectiveness of this approach has
been equivocal [6].
It is not a surprise that chronic pain frequently develops after surgery. All of the
aforementioned factors leading to peripheral and central sensitization are present
during many surgical procedures, including an intense noxious input and secondary
inflammation. There are limited studies that investigate how psychological factors
influence chronic post-surgical pain, and the results are often contradictory. Some
experts suggest that being in a hypervigilant state can cause chronic post-surgical
pain. Fear of surgery and anxiety could also be contributing factors. It is known
that certain regions of the brain, known as limbic regions, can influence the RVM.
This area has descending projections that modulate the activity of the dorsal horn,
which is involved in maintaining nerve injury-induced pain, mainly through a 5-HT3
mechanism. Therefore, emotional factors related to pain may have a neuroanatomic
basis in humans [6].
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Pain and the Transition from Acute to Chronic 161
A structured approach to blunting the development of chronic pain might include:
1. Predicting which patients might be at risk for elevated postoperative pain: Early
recognition of patients with a high risk of developing chronic pain is imperative.
Preoperative quantitative sensory testing (QST) has shown potential as a clinical
tool to predict postoperative pain. It can be used to identify patient populations at
high risk of developing acute postoperative pain and guide the use of pre-emptive,
intraoperative, and postoperative analgesia [6].
The degree of acute pain is predictive of the development of chronic pain, and
surgical types associated with significant postoperative pain are consistently found
to simultaneously suffer more frequently from the development of chronic pain. In
a study by Visser et al., amputation, sternotomy, and thoracotomy were the surgical
procedures most likely to be associated with the development of chronic pain.
2. Implement appropriate preventative analgesia that aims to target receptors at
various levels of the pain pathway to reduce overall neuronal excitability and
improve analgesia. The principle of utilizing a multimodal analgesic approach
is to provide synergistic pain control and minimize the therapeutic risks of any
individual modality.
In the periphery:
Consider how the extent of tissue damage helps determine the severity of nociceptive
stimulation, the length of the tissue healing process, the magnitude of inflamma-
tion, and how these factors can impact the risk of chronic pain development. This
notion that links peripheral injury to chronic pain development reinforces the need
to handle tissues carefully, avoid injuring nerves, and further the development of
minimally invasive surgical techniques as a pathway to reducing the risk of chronic
pain development.
Within the spinal cord:
The activation of NMDA receptors and wind-up phenomenon are important changes
in the spinal cord that foster the transition from acute to chronic. The perioper-
ative administration of NMDA receptor antagonists, including ketamine, nitrous
oxide, magnesium, and methadone, should simultaneously reduce perioperative pain
intensity, wind-up, and chronic pain [25].
These agents may also be beneficial in treating intractable pain and as adjuncts to
multimodal pharmacological treatment plans. Unfortunately, treatment is frequently
limited to short courses due to the development of side effects and addictive potential.
Adjuvants such as a-2-delta ligands binding to voltage-dependent calcium
channels (gabapentin and pregabalin) are anti-neuropathic agents with probable
preventative effects.
Local and regional anesthesia block the afferent transmission of pain signals,
reducing pain sensitivity. In theory, reducing acute pain should reduce central neuro-
plasticity and, therefore, minimize the risk of the development of chronic pain
[12].
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162 A. Oweidat et al.
In the brain matrix:
There is a strong link between individual preoperative expectations, psychological
status, and postoperative pain intensity. Functional MRI studies have demonstrated
changes in the centers of the brain matrix of patients with chronic pain. These centers
are mainly responsible for mood, affect, and behavior. Predicting which patients
with significant psychosocial stressors are more prone to chronic pain develop-
ment appears reasonable [19–22].
.
Therefore, a biopsychosocial approach should
be utilized in treating patients with a high risk of developing chronic pain.
13 Preventing Neuroplastic Changes
There are some exciting possibilities for preventing changes in the dorsal
horn’s neuroplasticity. One such possibility is the use of drugs that block 5-
hydroxytryptamine-3 (5-HT3) receptors. Studies have shown that this method can
have anti-nociceptive effects in humans by blocking the descending serotonergic
facilitatory drive to the dorsal horn laminae. Additionally, while gabapentin interacts
with the auxiliary α2δ subunit of voltage-gated Ca2 + channels, there is evidence
that its actions also depend on the 5-HT3 receptor [6].
14 Prevention of Microglial Activation
There are drugs available that can modify or inhibit microglia, such as fluoracitrate,
acetyl-l-carnitine, monocycline, and propentofylline. These drugs have been found
to alleviate pain sensitivity. In diabetic peripheral neuropathy, microglial cells appear
to play a significant role, as evidenced by an increased density of these cells in the
dorsal spinal cord and thalamic nuclei of diabetic mice.
Cannabidiol has been found to have anti-nociceptive effects in mice. Specifically,
when given at the same time as the onset of diabetic neuropathy,it was associated with
reduced microglial density in the dorsal spinal cord and blunted elevation in phospho-
rylated p38 MAPK. Reducing microglial accumulation and activation in the spinal
cord can limit neuropathic pain development, even after cannabidiol withdrawal.
CB1 and CB2 agonists show anti-nociceptive effects until discontinued in estab-
lished neuropathic pain. Early treatment to inhibit microglia in the CNS can prevent
neuropathic pain in diabetic patients who commonly experience it. Microglial acti-
vation can be regulated through receptor modulation. P2X7 and P2X4 receptors are
upregulated during nerve injury, and their deletion can attenuate neuropathic pain.
CCR2 gene deletion blocks glial cell recruitment. An NF-κB inhibitor can prevent
neuropathic pain development. ERK activation is also involved in neuroplasticity
and maintains microglial expression of the pain phenotype [6].
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Pain and the Transition from Acute to Chronic 163
In order to prevent chronic pain, it may be necessary to institute a program
of preventive analgesia that encompasses the entire perioperative period from
before the incision until final wound healing. Unfortunately, it is not known to
what extent and for how long the blockade of pain signals would be required to
prevent the establishment of chronic pain [23]. In addition, we cannot forget the
effects of local and systemic inflammatory mediators in developing chronic pain.
Again, it remains unclear if blocking pain signaling pathways without addressing
inflammation provides meaningful reductions in chronic pain intensity or duration.
Approximately 7% of all major surgical interventions result in a pain disability
problem one year later. This substantial pain burden requires a consideration of how
the chronicity of this pain and the ongoing need for opioids might impact the recovery
narrative for surgical patients. Building transitional pain services that employ a multi-
faceted approach to monitoring opioid use after discharge from surgery and aiming
to safely wean patients from opioids while maintaining effective pain management
may ultimately be the solution that provides an encompassing approach for those
patients who experience chronic pain.
The services offered by the TPS are broken down into three categories:
A) Introduction and optimization of multimodal analgesia to both improve pain
management and facilitate weaning from opioids [24].
B) Leveraging non-pharmacologic interventions including physiotherapy and
acupuncture.
C) Deploying psychological interventions by a trained pain psychology team
around an acceptance and commitment therapy (ACT) model.
The TPS treats two types of patients: opioid-naïve patients without a preexisting
pain condition and patients presenting with a preexisting pain condition or on preop-
erative opioid medications. The care of these patients is managed and coordinated
by an interdisciplinary team composed of anesthesiologists, acute pain nurse practi-
tioners, clinical psychologists, palliative care specialists, exercise physiologists, and
patient-care coordinators.
Multiple pharmacologic interventions have been proposed to interfere with the
development of chronic pain by modulating pain pathways at multiple locations.
Continued research will be necessary to determine the effectiveness of these compo-
nents and multi-modal approaches in reducing the development and severity of
chronic pain.
Key Points:
•
Nociceptors have free nerve endings in the skin and other tissues, mediating the
transduction of external or internal chemical or physical stimuli into generator
potentials. They transform generator potentials into action potentials that propa-
gate toward the central nervous system and cause the release of neurotransmit-
ters and neuromodulators into the superficial dorsal horn of the spinal cord or
brainstem.
•
Ectopic signaling (antegrade and retrograde) can be seen in pathology and
contributes to neurogenic inflammation.
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164 A. Oweidat et al.
•
Tissue insult leads to increased sensitivity of nociceptive terminals through
increased density of several transducers and posttranslational modifications
(phosphorylation).
•
This is mediated by inflammatory mediators such as ATP, PGE2, NGF, and TNF-α
from epithelial cells, resident (mast) cells, and recruited (macrophages) immune
cells.
•
Neuronal changes (neuroplasticity) in threshold and excitability increase noci-
ceptors’ sensitivity and ectopic activity (peripheral sensitization).
•
Tissue insult can also affect potential action thresholds and spike initiation/
propagation through modifications in membrane ion channels. All of these sites
represent current and potential therapeutic targets.
•
•Transitional pain service models employ a multi-faceted approach to monitoring
opioid use after discharge from surgery and aim to wean patients from opioids
while maintaining effective pain management safely.
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Transitional Pain Clinic
Marianne Tanios, Maher Kodsy, Emma Fu, Vipul Dhumak, Brendan Astley,
and Hesham Elsharkawy
Abstract Transition pain clinic are growing in importance in several parts of the
world due to the need for an organized approach for treating pain. Those clinics can
help transition patient from chronic pain to care in the acute setting and vice versa.
This allows for continuity of care without interruption of pain treatment at any phase
of management.
Keywords Chronic post-surgical pain
· Transitional pain clinic · Multimodal
pre-emptive analgesia
· Acute pain management · Chronic pain management ·
Closing the gap
M. Tanios (
B
) · E. Fu · V. Dhumak · B. Astley · H. Elsharkawy
Department of Anesthesiology, Case Western Reserve University—MetroHealth Medical Center,
2500 MetroHealth Drive, Cleveland, Ohio 44109, USA
e-mail: mtanios@metrohealth.org
E. Fu
e-mail: efu@metrohealth.org
V. Dhumak
e-mail: vdhumak1@metrohealth.org
B. Astley
e-mail: bastely@metrohealth.org
H. Elsharkawy
e-mail: helsharkawy@metrohealth.org
M. Kodsy
Department of Anesthesiology, Perioperative Services, Elyria Anesthesia Services, Inc.,
University Hospitals Elyria Medical Center, 630 East River Street, Elyria, OH 44035, USA
e-mail: maher.kodsy@UHospitals.org
© 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_12
167
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168 M. Tanios et al.
1 Introduction
The development of Chronic Postsurgical Pain (CPSP) is currently a major concern
after surgery. Patients with CPSP utilize a disproportionate amount of healthcare
resources, driving up costs and potentially leading to poor quality of life. Patients
suffering from CPSP have limited treatment options and often are overly reliant on
opioids.
Many patients are not overly burdened by pain in the early perioperative period
when they are closely attended to by hospital clinicians or have undergone a proce-
dure intended to alleviate pain. However, many patients experience a worsening of
pain symptomatology when they are discharged from the hospital and have fewer
options and resources available to address the pain that they are experiencing. Poorly
controlled chronic postoperative pain is a concerning situation for those patients with
preexisting pain, anxiety, depression, opioid tolerance, addiction, alcohol abuse and
pain catastrophizing [1–4].
Pain is defined by the World Health Organization (WHO) as an unpleasant
sensory and emotional experience associated with actual or potential tissue damage
or described in terms of such damage. Multiple factors affect the pain experience
of a given patient and this makes tackling the trajectory of pain challenging. Team
collaboration between surgeons and anesthesia caregivers is of paramount impor-
tance to target postoperative pain from different perspectives and improve outcomes.
In high-risk patients, a referral plan to a transitional pain clinic may be required to
mitigate acute pain before it proceeds to chronic pain [5].
In most cases, recovery from surgery and the pain associated with the procedure
progresses quickly as patients return to their baseline level of function. Despite the
typically limited duration of recovery period, subjecting patients to poorly controlled
pain is no longer acceptable and there is a need to implement proactivecomprehensive
approaches for pain management rather than utilizing reactive acute care only [6].
The main goal of the “Transitional Pain Clinic” is to focus on implementing predic-
tive models to enhance care effectiveness in practice settings, decrease postoperative
opioid use, and decrease healthcare costs.
2 Definition of CPSP
Our understanding of CPSP is growing and the complications that can arise from it
can be life changing, often negatively affecting the patient’s daily living activities.
CPSP appears to be far more common in recent years than in the past. Recently, the
WHO along with the International Association of the Study of Pain (IASP) thought
to include chronic pain in the new International Classification of Diseases Eleventh
Revision (ICD-11), and defined CPSP as pain that occurs after surgery/traumatic
tissue injury and stays with the individual for a long time (at least 3 months) [7, 8].
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