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Patient/Surgical Risk Factors for Chronic
Pain and Opioid Dependency
Whitney Carter, Chelsea-Ann Patry, Andrew Mendelson, and Lynn Kohan
Abstract Post operative pain is a primary concern for patients undergoing surgery.
Acute post-surgical pain can lead to the development of chronic post-surgical pain.
While opioids were, at one point, overwhelmingly and exclusively utilized in the
treatment of acute pain, it is now recognized that exposure to opioids may increase
the risk of opioid dependence and opioid use disorder. Multimodal analgesia now
represents the mainstay of analgesic treatment that seems to address acute surgical
pain, chronic post-surgical pain, and minimize the development of opioid depen-
dence. In this chapter, we discuss development risk factors, prevention strategies, and
the treatment of chronic postsurgical pain while considering how pain management
interventions might decrease the risk of opioid dependence/opioid use disorder.
Keywords Chronic post-surgical pain
· Opioid dependence · Opioid use disorder
1 Introduction
It is estimated that approximately 15 million patients undergo surgeries each year
in the United States (U.S) [1]. Health care costs associated with surgeries continue
to rise; accounting for 40% of total health care expenditures [2]. A national survey
reports that “pain after surgery” is most frequently listed by patients as their primary
W. C arter · C.-A. Patry · A. Mendelson · L. Kohan (
B
)
Department of Anesthesiology, University of Virginia School of Medicine, Charlottesville, VA,
USA
e-mail: LRK9G@UVAHealth.org; lrk9g@hscmail.mcc.virginia.edu
University of Virginia Hospital, Charlottesville, VA, USA
W. C arter
e-mail: QHM7QR@UVAHealth.org
C.-A. Patry
e-mail: CAP6Q@UVAHealth.org
A. Mendelson
e-mail: HAV4PM@UVAHealth.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_3
37
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38 W. Carter et al.
concern when undergoing a surgical procedure [3]. Additionally, patients often report
moderate to severe pain following surgery resulting in decreased functional status
and delayed hospital discharge [4]. Opioids have traditionally been the primary anal-
gesic for post operative pain [5, 6]. While potentially effective analgesics, opioids are
associated with numerous risks including respiratory depression, hyperalgesia, toler-
ance, and the development of persistent long term opioid use or opioid use disorder
[7, 8]. The Centers for Disease Control (CDC) Guidelines on opioids helped to
curtail excessive prescribing for chronic pain but offered limited guidance for those
patients seeking analgesia in the perioperative period [9, 10]. As a potential corollary,
there continues to be large variation in post-operative opioid prescribing, often to
excess, regardless of the extent of the surgery [11, 12]. Studies suggest persistent
post-surgical opioid use (6–10%) can develop even after short exposure to opioids
[13, 14]. Opioid use disorder (OUD) may also be a consequence after even short
term exposure, with a prevalence of approximately 1–5% following surgery [15,
16]. While clinicians may have concerns regarding patient satisfaction if opioids
are limited post operatively, studies suggest similar clinical and patient reported
outcomes whether they were prescribed opioids or not [17]. Additionally, it has been
demonstrated that patients frequently stop taking opioids prior to the resolution of
post-surgical pain, thus high doses and long durations of opioids may not be neces-
sary following surgery [18, 19]. Limiting opioid prescribing may help to decrease the
risk of long-term opioid use as well as the development of OUD. Anesthesiologists,
surgeons, and other healthcare professionals all play a key role in recognizing risk
factors for the development of chronic post-surgical pain (CPSP), long-term opioid
therapy (LTOT), and OUD.
2 Chronic Post-surgical Pain
Chronic post-surgical pain (CPSP) is pain t hat develops or increases in intensity
after a surgical procedure or injury and persists for at least 3 months following the
surgery and typical healing process. Other causes of pain, whether it be infection,
malignancy, or a pre-existing condition, need to be ruled out [20].Thelocationof
the pain is important for a CPSP diagnosis; the pain is located at the surgical site or
the area of injury, it affects the nerves that innervate the surgical area, or it is related
to the dermatomes in the area of injury. Additionally, it is i mportant to distinguish
whether the tissue trauma develops from a controlled procedure (surgery) or uncon-
trolled damage (accidental traumas) [20]. Although the exact mechanism of CPSP is
not known, the development of CPSP is thought to be related to immune and inflam-
matory responses to trauma [20]. The pathophysiology involves both peripheral and
central sensitization and symptoms typically include hyperalgesia, allodynia, and
dysesthesia [19]. Approximately 35–57% of patients with CPSP demonstrate signs
of neuropathic pain, but it appears that visceral, inflammatory, and neuroplastic pain
might also play a role depending on the surgical procedure [20].
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Patient/Surgical Risk Factors for Chronic Pain and Opioid Dependency 39
CPSP is unfortunately a common complication after surgery and while it can
negatively impact quality of life and activities of daily living, it also results in an
economic and healthcare resource utilization burden. While the exact incidence of
CPSP is unknown, studies have reported it to be approximately 11.8% at 12 months
[21]. This figure varies with the type of surgery as a higher incidence of CPSP was
noted among patients undergoing orthopedic surgeries [21].
3 CPSP Risk Factors
While predicting the development of CPSP is extremely difficult, there appears to
be a number of modifiable and non-modifiable risk factors. Severe preoperative and
acute surgical pain appear to positively correlate with the development of CPSP [22].
Psychological factors are also predictors of CPSP with anxiety, catastrophizing and
depression the most likely linked [23]. Younger age, higher BMI and female sex have
been reported to increase the risk of CPSP [20]. Surgical technique can also influence
the development of CPSP; laparoscopic approaches have been shown to decrease the
development of CPSP for cholecystectomy and herniorrhaphy [24, 25]. Orthopedic
surgeries have also been shown to have a higher incidence of CPSP development
[21].
4 CPSP Prevention/CPSP Treatment
CPSP is a complex and unwanted adverse condition occurring after surgical proce-
dures that leads to functional limitations and psychological trauma for patients [26].
Thus, the importance of developing preventivemeasures becomes imminent. Preven-
tion of CPSP can vary from limiting nerve injury via modifying surgical techniques,
utilizing local/regional anesthetics, and implementing ketamine IV treatments [27].
While managing CPSP, physicians can utilize pharmacologic treatments like topicals,
NSAIDS, acetaminophen, antidepressants, corticosteroids, regional/local anesthesia,
anticonvulsants, NMDA antagonist, and opioids [28].
Modification of Surgical Technique
One of the risks of CPSP occurring in patients is related to the extent of nerve
and tissue injury during s urgical procedures. Modifying surgical techniques is one
possible way to help prevent the occurrence of chronic pain in post-operative settings
[26]. A prospective, multicentric study by Alfieri demonstrated that the lack of nerve
identification in the setting of hernioplasty was significantly correlated with the
developmentof chronic pain [29]. In this study,surgeons were asked to report whether
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40 W. Carter et al.
or not each nerve had been identified and preserved or divided and the primary
endpoint of the study then sought to determine the presence of moderate and severe
chronic pain at 6 months and 1 year post-op [29]. Statistical analysis demonstrated
that patients in whom all nerves were identified had a significantly diminished risk
of developing moderate to severe chronic pain compared to patients with only 1 or
2 nerves identified or patients whose nerves were not identified during surgery [29].
Thus the identification and preservation of nerves during open inguinal hernia repair
reduced chronic groin pain.
Local/Regional Anesthesia
Local anesthetics aim to suppress and prevent sensitization with the goal of reducing
pain and analgesic requirements in acute and chronic pain settings [30]. Periopera-
tive lidocaine may suppress many pathways that are known to contribute to persistent
post-surgical pain [31]. Local anesthetics have potent anti-inflammatory properties
and have been found to reduce circulating levels of IL-1, IL-6, and TNF-alpha [32].
Local anesthetics have also demonstrated NMDA receptor antagonism in ex-vivo
human models [33]. In addition, lidocaine reduces peripheral nociceptive input via
blockade of sodium channels as well as other peripheral signal transduction path-
ways [34]. Local anesthetics are an important adjunct used to decrease pain, opioid
consumptions and opioid-related adverse effects [30] and have been found to provide
analgesia in the setting of acute and chronic pain [35, 36].
Multiple independent studies have sought to determine the effect of several
different local anesthetic administration regimens on the development of CPSP.
Patients who underwent breast cancer surgery receiving IV lidocaine demonstrated
a lower incidence of CPSP 3 months following surgery [37]. A randomized, double
blind, parallel-group, placebo- controlled study by Albi-Feldzer et al. looked at 236
patients scheduled for breast cancer surgery who were randomized to receive ropi-
vacaine or placebo infiltration to the wound [38]. It was found that ropivacaine
infiltration significantly decreased immediate post-operative pain for the first 90 min
but did not decrease chronic pain at 3, 6, or 12 months postoperatively [38]. Addi-
tionally, 40 patients with ischemic heart disease scheduled for elective CABG were
prospectively randomized to receive either general anesthesia or thoracic epidural
anesthesia to evaluate the effects on postoperative pain [39]. The differences in pain
scores were decreased at rest during 6, 12 and 24 hours in the thoracic epidural anes-
thesia group. Pain scores among the epidural group continued to remain decreased
at one-month follow-up [39].
A recent systematic review of perioperative lidocaine infusion efficacy that
included 420 patients in 6 trials found a reduction in the development of CPSP,
however no significant differences were found on the McGill Pain Questionnaire
[31]. Furthermore, clear data on systematic safety is lacking [31]. In conclusion,
lidocaine infusions may offer some benefit in the prevention of CPSP, however more
information on efficacy and safety is warranted. Wound infiltration data related to the
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Patient/Surgical Risk Factors for Chronic Pain and Opioid Dependency 41
prevention of CPSP is similarly lacking but the safety profile of this practice makes
it something generally worth considering if other regional anesthesia techniques are
contraindicated.
Regional anesthesia including peripheral nerve blocks and neuraxial anesthesia
have been investigated in the prevention of CPSP. Peripheral nerve blocks may reduce
neuronal inflammation and glial cell activation resulting in decreased CPSP [28].
However, results have been somewhat inconsistent. At least one study suggests the
relationship between peripheral nerve blocks and reduced CPSP may depend on the
type of block and that some blocks may even increase the risk of CPSP [40]. Other
studies suggest that while peripheral nerve blocks result in short term reduction of
postoperative pain, the long term impact is less substantial. Ilfield et al. found that the
use of peripheral nerve blocks (PNB) helped to reduce the occurrence of phantom
limb pain up to 4 weeks post-surgery but had no impact at 12 weeks when compared
to placebo [41].
The evidence for neuraxial anesthesia is also mixed. Richebé et al. found that
epidural analgesia reduced the incidence of CPSP at 1 year in thoracotomy,abdominal
surgery, and breast surgery, however the optimal dosing and duration needed was
unclear and there was no reduction in opioid use found [28]. A recent Cochrane
review reported that epidural analgesia resulted in reduced CPSP after thoracotomy
[42]. In addition, a recent meta-analysis found low quality evidence that pre-emptive
epidural analgesia reduced chronic pain after thoracotomy [43].
Unfortunately, the use of paravertebral blocks did not show a beneficial impact on
the prevention of CPSP. A large multicenter international study found no difference
in CPSP assessed at 6 and 12 months in 2108 women with breast cancer who received
paravertebral block plus propofol versus general anesthesia and opioids [44].
Overall, the evidence for the use of epidural anesthesia is moderate for the preven-
tion of CPSP, while the evidence for the use of PNBs is unknown, with limited to no
evidence for the use of paravertebral nerve blocks in the prevention of CPSP [41].
Ketamine
Ketamine is a N-methyl-D-aspartate (NMDA) receptor antagonist that has shown
to have anesthesia, analgesic, anti-hyperalgesic, and also anti-inflammatory prop-
erties [45]. NMDA receptors are important for understanding the pathophysiology
of central sensitization after surgery and blocking this receptor has been shown
to prevent the development and reduce both acute postoperative pain intensity
and opioid consumption [45]. Ketamine can be administered intranasally, orally,
subcutaneously, intravenously and epidurally in a perioperative setting [46].
A recent randomized, blinded clinical trial examined if intra-operative low-dose
ketamine would reduce postoperative opioid consumption and acute pain in 147
patients that underwent lumbar fusion surgery when compared to a placebo group.
In this study, perioperative ketamine administration was associated with a significant
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42 W. Carter et al.
decrease in morphine consumption at 0–24 hours following surgery [47]. Addition-
ally,six months post-operatively, patients in the ketamine group reported significantly
more improvement of their back pain compared to the placebo group, improvement
in ambulation was noted as well [47]. A 2014 meta-analysis reported a reduction
in CPSP symptoms at 3 and 6 months after surgery when intravenous ketamine
was administered. However, significant variability in timing and dosing of ketamine
resulted in the authors being unable to provide an optimal regimen [46]. Additionally,
Kang et al. found a reduction in CPSP at 3 months after breast surgery in patients
receiving ketamine but the clinical importance was minimal [48].
In conclusion, ketamine may reduce the incidence of CPSP but the overall strength
of evidence is low [48].
Non-steroidal Anti-inflammatory Drugs (NSAIDs)
and Acetaminophen
NSAIDs are potent anti-inflammatory agents that prevent prostaglandin synthesis by
inhibiting cyclooxygenase enzymes. While acetaminophen also inhibits cyclooxy-
genase enzymes, its therapeutic mechanism remains unknown [49]. While there
is strong evidence that both NSAIDs and Acetaminophen are effective for acute
post-surgical pain, there is minimal evidence to support the use of NSAIDs and
Acetaminophen in the prevention of CPSP [30]. Multiple prospective studies have
shown NSAIDs have little or no effect on the development on CPSP [50, 51].
Antidepressants
Tricyclic antidepressants and selective serotonin-norepinephrine reuptake inhibitors
are becoming a common treatment for chronic pain, especially since these medi-
cations are effective in reducing neuropathic pain and depression [26]. 150 patients
who were scheduled for a partial or radical mastectomy with axillary dissection were
involved in a randomized, double-blind study. The study consisted of the patients
falling into three groups taking either venlafaxine, gabapentin, or placebo medication
for 10 days starting the night before their operation. Results suggest that venlafaxine
or gabapentin have an equipotent effect in reducing analgesic requirements [52].
Venlafaxine was found to significantly reduce the incidence of post-mastectomy
pain syndrome 6 months in women having breast cancer surgery [52].
A systematic review across fifteen studies (total of 985 participants) evaluated
the efficacy of antidepressants at reducing post-operative pain. Unfortunately, the
evidence currently does not support the clinical use of antidepressants beyond
controlled investigations for the treatment of acute, or prevention of chronic, post-
operative pain [53]. However, there are multiple positive trials suggesting potential
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