CPSP is a new emerging disease but can be a silent epidemic. Optimal perioperative management may reduce the incidence of CPSP. Minimal invasive surgical techniques Agressive perioperative multimodal analgesia, inluding epidural or nerve blocks. Appropriate management of acute pain is therefore not only a humane obligation, but also may prevent of chronic pain!

1. CURRICULUM VITAE

2. Andi Husni Tanra
Chairman of ISAPM
(Indonesia Society of Anesthesiology for Pain Management)
1 st National meeting “Indonesian Society of Anesthesiology for Pain management” (ISAPM)

3. INTRODUCTION
*Good Pain, is an alarm symptom, tell us
that something wrong in our body Acute Pain
or Inflammation pain. Pain with nociception
*Bad pain, is a disease entity  is a disease of
nervous system  Chronic Pain. Pain without
nociception
Chronic pain is a pain that persists beyond
normal tissue healing time, which is assumed to
be three – six months.

4. What is Chronic Pain After Surgery?
1) Chronic Pain After Surgery or Chronic Post
Surgical Pain is a new emerging disease  “a
disease of nervous system”
 Intractable pain after surgery
 Persistent pain after surgery
2) Is a common disease after surgery but under
recognized ( about 1% of total surgery)
3) Affects million patients world wide  a “silent
epidemic” disease. (in us 40 million surgical
cases/year)  incidence in US = 400.000 pts

5. Pain Clinics in UK, See a Lot of Chronic Pain
After Surgery and Trauma!
 5130 chronic pain patients
in 10 pain clinics in the UK
 post surgery: 22.5%
 post trauma: 18.7%
 So, about 2000 chronic pain patients, due to surgery
and trauma, in UK.
(Crombie et al. Pain Clin 1992; 5: 436-7)

6. Definition for CPSP (Chronic Post-Surgical
Pain).
 Based on four criteria, namely:
1. Pain developed after surgical procedure.
2. It was at least 2 months duration.
3. Other causes for the pain had been
excluded.(e.g. continuing malignancy, infection, etc )
4. An attemp had been made to explore and
exclude the possibility that the pain was
cotinuing from a pre-existing problem.
(Macrae and Davies 1999)

7. Predisposing factors to
develope CPSP.
1. The type of surgery.
2. Postoperative pain intesity.
(under-treatment of postoperative pain).
3. Psychological factor.
4. Genetic factors.

8. 1. The Type of Surgery,
Common surgeries which may develope to
CPSP are:
1. Limb amputation
2. Thoracic surgery
3. Breast surgery
4. Herniorrhapy
5. Cholicystectomy

9. 1. CPSP; After limb amputation
Two type of pain syndrome
 Stump pain
 Phantom pain
 The incidence of phantom pain
varies from 50% - 85%
 About 40% of amputees having
severe phantom pain
 Prevalence of phantom pain
 After trauma was 12%
 Due to cancer was 48%

10. Phantom Limb Pain is a ‘Pain
Memory’!
 In 57% of subjects with phantom pain,
this resembled preamputation pain.
 “… somatosensory inputs of sufficient
intensity and duration can produce
long-lasting changes in central neural
structures”
Katz&Melzack, Pain 1990;43:319

11. 2. CPSP; After thoracic surgery
 Pain after thoracotomy is fairly common.
 Incidence up to 50%
 Damage to intercostal nerve has been assumed
to be the main cause of chronic pain.
 Sternotomy also showed almost similar results,
the incidence was 28 %.
 This suggest a more comlicated aethiology of
chronic pain after post thoracotomy.
 Even endoscopic surgery may not able to
prevent CPSP.

14. 3. CPSP; After breast surgery
 Several type of pain syndrome;
Phantom pain (13-24%
Pain in the scar ( 11-57%)
Pain in the arm (12- 51%)
 Incidence of pain at one or more
these sites is 50 %
 Damage to intercostobrachial
nerve is considered the main
cause.
 Carpenter ‘s found only a
lumpectomy developed chronic
pain.

15. 4. CPSP; After herniorrhapy
 Incidence of chronic pain after hernia repair was
0- 37%.
Cunningham* et al found that
 Pain at 12 months was 65%
 12% moderate to severe pain
 Pain at 2 years was 54%
 11% moderate to severe pain
 Incidence of chronic pain after transperitoneal
laparascopic hermorrhapy  15% at 9 m follow-up
* Cunningham et al. Pain in the post-repair patient. Ann Surg 1999;224:598-602

16. 5. CPSP After Cholecystectomy
 Difficult to investigate because most patient
have pain before surgery and persist after
cholecystectomy.
 Arround 40% of patients complain pain -related
after cholecystectomy.
 Incidence of chronic pain varying from 3% =20%
 Laparascopic cholecystectomy.
 Incidence of chronic pain is lower than open
cholecystectomy.

17. The incidence of CPSP varies with
the surgical procedures.
 Limb amputation 0 – 81 %
 Thoracotomy 0 – 50 %
 Mastectomy 13 – 24 %
 Herniorrhaphy 0 – 37 %
 Cholecystectomy 3 – 56 %
H. Kehlet world congress on pain 2005

18. CPSP; After other surgeries
 Symphatectomy
 Total hip replacement 28% (Nikolajsen)
 Cardiac surgery
 Rectal amputation
 Vasectomy
 Dental extraction
 Histerectomy 14 % (Brandsborg)
 Cesarian Section 12% (Nikolajsen)
 Etc.

19. Predisposing factors to
develope CPSP.
1. The type of surgery.
2. Postoperative pain intesity.
(under-treatment of postoperative pain).
3. Psychological factor.
4. Genetic factors.

20. Postoperative pain intensity
 Clinical studies have demonstrated that the
development of chronic pain postoperatively is
associated with the intensity of acute pain
experienced.
 Laboratory research showed that neuropathic pain
may appear within hours of nerve injury and
persist for weeks to months thereafter.
• Kalso E, et al Pain after thoracic surgery . Acta Anesthesiolo Scand 1992; 36:
96-100.
• Peter , et al Somatic and psychosocial predicts long term outcome after
surgical inetrvetion. Ann Surg 2007; 245: 487- 94.

21. 2. Postoerative pain intensity
 After surgery some changes in the NS
may occur:
1. Peripheral sensitization
2. Constant bombardment of the CNS
with noxious input.
3. Central Sensitization, what we called
“wind-up” “Recruitment”

22. ASIC/BNC
1.Peripheral sensitization

23. 2. Constant Bombardment of the CNS
TO BRAIN
Dorsal Horn
Pain Neuron + +
+
C
IN
A-delta
+
Mediated in part by
NMDA receptor on the
dorsal horn pain neuron
A-beta
_ _
0
IN
IN = interneuron; NMDA = N-methyl-D-aspartate.
Woolf CJ, et al. Science. 2000;288:1765-1769.

24. 3. Central Sensitization
 Central sensitization refers to enhanced excitability of
dorsal horn neurons and is characterized by:
1. increased spontaneous activity
2. An increase in responses evoked by C fibers
3. Enlarged receptive field area
 Windup is progressive increase in the magnitude of C-
fiber evoked responses of dorsal horn neurons
produced by repetitive activation of C-fibers.
 Recruitment During ongoing activation after
injury, the receptive fields of these neurons
expand, leading to spread of pain.

25. progressive increase in
response of second
order neurons to
repetitive C-fiber input
4. “Wind-Up”
Mendel and Wall, 1965
Now is appreciated that
“wind-up” is a crucial
factor for chronic pain
after surgery
NMDA unblocked
NMDA blocked (AP5)
Stimulus frequency applied to
C-fiber nerve endings
Actionpotentialdischargein
Secondorderspinalneurons
60
50
40
30
20
10
0
2 4 6 8 10 12 14

26. Ongoing activation after injury,
the receptive fields of these
neurons expand, leading to
spread of pain.
Recruitment

27. Even Peripheral Changes of CRPS are Result of
Central Sensitization!

28. So, the main cause neuro-plasticity
after surgery or trauma are
 Tissue damage
 Nerve damage

29. PERIPHERAL
ACTIVITY
CENTRAL
SENSITIZATION
Decreased
threshold to
peripheral
stimuli
Increased
spontaneous
activityExpansion of
receptive
field
Hyperalgesia
Allodynia
Tissue damage
Primary Hyperalgesia
Nerve damage
Spontaneous
pain
Secondary Hyperalgesia

30. Consequences of Unrelieved of
Postoperative Pain
Myocardial
ischaemia
Increased
sympathetic
activity
Myocardial
O2
consumption
GI effects
Shallow
breathing
Increased
catabolic
demands
Anxiety
and fear
Peripheral/
central
sensitisation
GI motility
Atelectasis
hypoxaemia
hypercarbia
Poor wound
healing/muscle
breakdown
Sleeplessness,
helplessness
Neuro-
plasticity
Delayed
recovery Pneumonia
Weakness
and impaired
rehab.
Psycho-
logical
distress
Chronic
pain
GI = gastrointestinal

31. Predisposing factors to
develope CPSP.
1. The type of surgery.
2. Postoperative pain intesity.
(under-treatment of postoperative pain).
3. Psychological factor.
4. Genetic factors.

32. 3.Psychological factors
 There are consistent relationship between
preoperative anxiety and acute postoperative
pain.
 Psycholocical factors include:
 anxiety
 extroversion
 depression
 educational level
 attitudes to medication, ect.
 Postoperative pain is influenced by
exaggerated negative beliefs and responses.
 Postoperative pain is consistenly found to be
the risk factor for CPSP across many study.

33. Patient education
Information influences the pain experience
after surgery.
In one study, that good preoperative
information resulted in;
 post-operative pain declining rapidly
 lower pre-operative anxiety and
 more satisfaction with post-operative
pain management.
* (Burke, S and Shorten, G.D. when pain after surgery doesn’t go away.
Biochemical Society transactions 2009. vol 37, part 1 )

34. Predisposing factors to
develope CPSP.
1. The type of surgery.
2. Postoperative pain intesity.
(under-treatment of postoperative pain).
3. Psychological factor.
4. Genetic factors.

35. 4. Genetic factors
 Some diseases may be markers for developing
CPSP, include ;
1. Fibromyalgia Syndrome
2. Migraine/headache
3. Irritable Bowel Syndrome
4. Irritable Bladder Syndrome
5. Raynaud’s Syndrome
 We must be warning the possibility for
developing CSPS in these patients.
 2 Studies on CPSP found many patients with a
history of IBS, backpain or headache.

36. How to prevent CPSP ?
Since Chronic Post Surgical Pain;
 is common
 cause suffering
 reduced Quality of Life
 difficult to treat
 Prevention is very important

37. Preventing chronic pain after surgery
Possible strategies for
1. Avoid unnecessary surgery,
Avoid to wish to have surgery for reasons other than
ilness or disability ( cosmetic surgery, sterilization).
2. Modify surgical technique
Minimal invasive technique, laparascopic or
endoscopic surgery or nerve sparing.
3. Aggressive multimodal analgesia or
Aggressive treatment of early inflammatory pain.

38. If surgery can not be avoided
2 things can be done for preventing
 Using minimal invasive surgical
techniques . (the role of surgeon)
 Agressive Perioperative
multimodal Analgesia ( the role of
anesthesiologist)

39. Agressive Multimodal Analgesias
Jin et al. J Clin Anesth;13:524, 2001
Kehlet et al. Anesth Analg;77:1048. 1998
Woolf CJ, Science, 288:1765-1768, 2000
Optimal effect can be
achieved when combined
with LA - Epidural
- Nerve block
- Infiltration
Cox-2 agents
Opioids
Multimodal
NSAIDs
Gabapentinoid
NorAdr &
5HT antagonists
NMDA
antagonists
Parecoxib
Ibuprofen
Ketamine
Tramadol
Pain free and
Stress free
iv
iv
iv
iv
iv
iv

40. Clinical evidence
Multimodal analgesia using a continuous
paravertebral block + acetaminophen and parecoxib has
less pain during the first 96 h post-operatively, and had a
lesser incidence of CPSP 10 weeks after breast surgery.
(Iohom, G., Abdallah, H,. Et al. (2006) Anesth. Analg. 103, 995-1000)
 The peri-operative use of anti-neuropathic agents,
such as gabapentin and prgabaalin, has also been
associated with improved long-term outcomes
following mastectomy.
 Fassoulaki A, et al. – Anesth Analg 2002;95(4):985-91.
 Reuben SS, et al. J Pain Symptom Manage 2004;27(2):133-9.

41. Clinical evidence
* A Single dose of gabapentin administered
to patients before mastectomy decreases
post-operative morphine consumption
and pain during movement.
* Gabapentin, as part of a multimodal
analgesic regimen, decreased the incident
of CPSP at 10 weeks after breast surgery.
* (Burke, S and Shorten, G.D. when pain after surgery doesn’t go away.
Biochemical Society transactions 2009. vol 37, part 1 )

42. Clinical evidence
 Studies have shown that effective peri-operative
analgesia using epidural analgesia reduces acute and
chronic pain in thoracotomy and major abdominal
surgery.
Obata H, et al. –Can J. Anaesth 1999;46(12):1127-32
Senturk M, et al. – Anesth Analg 2002;94(1):11-5
Lavand’homme P, et al. – Anesthesiology 2005;103(4):813-20
For thoracic  insertion at Th 4-5-6
For upper abdominal  at Th 8-9-10
For lower abdominal  at Th 11-12-L1

43. 1Kehlet H et al. Anesth Analog. 1993;77:1048-1056.
+
Local Anesthetic
-Epidural
-Nerve Block
-Infiltration
Opioids
Paracetamol,
NSAID, COXIB,
Gabapentinoid,
2 agonist
Optimal
Analgesia
May
Prevent
CPSP

44. Treatment of CPSP
depend on the symptoms
 Neurophatic pain
Tricyclic anti depressants
Anti-epileptic drugs;
 Gabapentin and pregabalin are efficacious in the
treatment of PHN and DPN but also may play a
big role the treatment CPSP, particularly after
mastectomy.
 Nociceptive pain
 Paracetamol
 NSAIDs
 Opioid if necessary

45. conclusion
 CPSP is a new emerging disease but can be a
silent epidemic.
 Optimal perioperative management may reduce
the incidence of CPSP.
 Minimal invasive surgical techniques
 Agressive perioperative multimodal
analgesia, inluding epidural or nerve
blocks.
 Appropriate management of acute pain is
therefore not only a humane obligation, but also
may prevent of chronic pain!

46. This Concept is Not New
GW Crile proposed in 1913,
that pain can cause ‘scars’ in the central
nervous system, if the noxious stimuli of
surgery have unsuppressed access to this
system.
Crile, Lancet 1913;185:7

47. Some chronic pain patients after
surgery and trauma.
in
Pain clinic at Hiroshima
University Hospital, Japan