CPSP

Question 1

By reading this article, you should be able to:

Answer 1

1. Define chronic post-surgical pain (CPSP) according to the ICD-11 (International Classification of Diseases, Eleventh Revision) classification and describe its impact on surgical patients.
2. Specify typical risk factors for the development of CPSP to identify patients at risk and initiate adequate preventative strategies.
3. Discuss possible treatment strategies and anaesthetic techniques to reduce the risk of CPSP.

Question 2

Key

Answer 2

1. CPSP is one of the most common complications of surgery.
2. Risk factors for CPSP occur before, during and after surgery.
3. Anaesthetic techniques, particularly the reduction of opioid use and regional anaesthesia may reduce the incidence of CPSP.

Question 3

CPSP

Answer 3

Chronic post-surgical pain (CPSP)
is one of the most frequent complications after surgery,

at 6–12 months after surgery is 20–30% with a slight decrease over time

increasing number of surgeries worldwide

Obesity, inflammatory disease and increased life expectancy have resulted in an increasing volume of surgeries such as hip and knee arthroplasty that are associated with a high risk of CPSP.

Question 4

1Incidences of CPSP for different types of surgery. Data adapted from several studies

Answer 4

1. Amputation
2. Abdominal surgery (bowel and colorectal)1
3. C section
4. Cholecystectomy
5. Craniotomy
6. Hip Arthroplasty
7. Mastectomy
8. Sternotomy

Question 5

Definition of CPSP

Answer 5

1. Pain develops or increases in intensity
   after a surgical procedure or a tissue injury.
2. Pain persists beyond the healing process, that is ≥3 months after the triggering event.
3. Localisation
   Surgical area
   Projected innervation of nerve
   Head’s zone (after surgery or injury to deep somatic and visceral tissue)
4. Other causes of pain (e.g. pre-existing pain conditions, infection, malignancy) are excluded.
5. Chronic post-surgical pain can often show characteristics of neuropathic pain.

The inclusion of CPSP in the ICD-11

Question 6

Mechanisms and characteristics

Answer 6

1. includes peripheral (at the site of injury) as well as central (spinal and supraspinal) sensitisation
2. Inflammatory and immune response to axonal and tissue damage,:

including the release of neurotransmitters peripherally
as well as in the spinal cord
ectopic neural activity
and altered activity in the dorsal horn

3. There are also changes in the supraspinal processing
   including brain network connectivity
   and changes in endogenous, descending pain modulation.

Question 7

Symptoms

Answer 7

Developing CPSP often report typical clinical symptoms

such as

1. hyperalgesia (increased painful sensation caused by a noxious stimulus),
2. allodynia (painful sensation caused by a usually non-painful stimulus),
3. dysaesthesia (unpleasant touch perception or tingling) indicating nerve damage and central sensitisation very early after surgery

quantitative sensory testing (QST)
Hyperalgesia detected early after surgery might predict prolonged,

signs of neuropathic
Incidence for different surgeries varies widely and is highest after thoracotomy, mastectomy and amputationain

injury to the subcostal nerves during thoracic surgery and injury to the brachial nerve/axillary plexus during mastectomy

Question 8

Risk factors

Answer 8

The early identification of risk factors can allow risk stratification and the implementation of preventative treatment strategies.

1. Surgical risk factors
2. Acute postoperative pain

3.Preoperative chronic pain

4. Psychoscoial
5. Patient related

Question 9

prevention

Answer 9

ID those at high risk
QST

Prevention of CPSP

1. Ketamine
   Perioperative ketamine may reduce opioid consumption and acute postoperative pain;
   it is one of the most promising drugs available for reducing the prevalence of CPSP
2. Gabapentinoids
   Can reduce neuropathic pain
   Certain procedures - spine surgey
3. IV Lidocaine
   Breast surgery
4. Others
   Duloxetine
   Enhanced pain sensitivity - may reduce

Question 10

Prevention

Answer 10

RA

Reduces risk in most types studies so far
Blocking
nociceptive input
Central sensitisation reduced

Epi - thoracotomy
PVB -

Question 10

Prevention

Answer 10

RA

Reduces risk in most types studies so far
Blocking
nociceptive input
Central sensitisation reduced

Epi - thoracotomy
PVB - Thoracotomy + Breast

2. Reduction of opioid use
   Preoperative opioid consumption including chronic opioid use is a risk factor for persistent postoperative pain

Potential mechanisms include induction of opioid tolerance, changes in the central reward system, facilitated central sensitisation and altered descending inhibition

Activation of N-methyl-d-aspartate (NMDA) receptors and (micro-)glia are some of the molecular mechanisms and might explain the effect of ketamine in patients with preoperative chronic pain

There are some indications for high intraoperative remifentanil dosage being associated with a higher incidence of CPSP; however, compared with sevoflurane-based anaesthesia, a TIVA with propofol and lower dosed remifentanil led to lower incidences of CPSP

ds by using multimodal analgesia, regional analgesia techniques or by using ketamine could potentially reduce the incidence of CPSP

Question 11

Non-pharmacological intervention and transitional pain services
Chronification of pain

Answer 11

Non-pharmacological intervention and transitional pain services
Chronification of pain a biological but also a highly individual process involving psychosocial and temporal aspects

A multidisciplinary approach, including non-pharmaceutical therapies such as physiotherapy and psychological support might be far more effective

atient at risk not only perioperatively but also for several weeks after surgery. These ‘transitional pain services’ aim to close the gap between acute postoperative pain management and pain management after discharge from hospital

Question 12

Conclusions

Answer 12

CPSP is an important clinical and socioeconomic challenge that is now included in the new ICD-11.

Procedure-specific incidence rates and surgery,

as well as patient-related risk factors,
have been identified,
and some prediction models have been developed.

The evidence for most pharmacological and non-pharmacological interventions is limited.

However, it makes intuitive sense to reduce the intensity of acute pain by adopting multimodal strategies and regional techniques and limiting the use of pre- and perioperative opioids.

Multidisciplinary concepts targeting the biopsychosocial aspects of the pain chronification process are promising but warrant further evaluation before integrating them routinely into clinical practise.