1. ACUTE PAIN
MANAGEMENT & PRE-
EMPTIVE ANALGESIA
SHADAB KAMAL

2. INTRODUCTION
IASP define pain as an unpleasant sensory
and emotional experience associated with
actual or potential tissue damage, or
described in terms of such damage.

3. PAIN MANAGEMENT
 Applies to entire discipline of anaesthesiology, more
specifically involves management of pain throughout
the perioperative period as well as nonsurgical pain in
both inpatient and outpatient settings.
 Broadly divided into
 acute pain management (primarily deals with patient
recovering from surgery or with acute medical
conditions and mostly due to nociception) and
 chronic pain management (includes diverse groups of
patients almost always seen in outpatient setting)

4. PRACTICE OF PAIN MANAGEMENT
 The contemporary practice of pain management
is not limited to anesthesiologists but often
includes other physicians (physiatrists, surgeons,
internists, oncologists, psychiatrists, and
neurologists) and nonphysicians (psychologists,
physical therapists, acupuncturists, and
hypnotists).
 The most effective approaches are
multidisciplinary,

5. ACUTE PAIN
 Acute pain is caused by noxious stimulation due
to injury, a disease process, or the abnormal
function of muscle or viscera.
 It is usually nociceptive.
 Nociceptive pain serves to detect, localize, and
limit tissue damage.
 Four physiological processes are involved:
transduction, transmission, modulation, and
perception.
 This type of pain is typically associated with a
neuroendocrine stress response that is
proportional to the pain’s intensity.

6. FORMS OF ACUTE
PAIN
Post-traumatic
Post-operative
Obstetric pain
Pain a/w acute medical illnesses (eg.
myocardial infarction , pancreatitis, renal
calculi etc…)

7. TYPES OF ACUTE PAIN
 Two types:
 Somatic pain: can be
(1)Superficial and
(2)Deep somatic pain
 Visceral pain: four subtypes:-
(1)true localized visceral pain,
(2)Localized parietal pain,
(3)referred visceral pain, and
(4)Referred parietal pain.

8. PHYSIOLOGIC RESPONSEPHYSIOLOGIC RESPONSE
Cardiovascular
:  HR,  BP ,PVR,  Myocardial O2consumption
MI, DVT, pulmonary embolism
Respiratory
:⇩ lung volume  atelectasis
:⇩cough, sputum retention infection, hypoxemia
Gastrointestinal
: ⇩gastric & bowel motility,
:risk of bacterial transregression of bowel wall
Musculoskeletal
:Muscle spasm, immobility risk DVT
:Muscle wasting prolong recovery

9.  Central nervous
: central sensitization  CPSP/ chronic pain
 Psychological
: anxiety, fear, sleep deprivation, leading to 
pain
 Neuroendocrine
: catabolic hormone
(glucagon, growth hormone, cortisol, vasopressin,
aldosterone, renin angiotensin)
 hyperglycemia, impaired wound healing
: ⇩anabolic hormone (insulin, testosterone)

10. TARGETS OF A PREVENTIVE
APPROACH TO ACUTE PAIN
MANAGEMENT
Perioperative period
Preoperative (days before surgery and
just minutes before skin incision)
Intraoperative (after incision to those
initiated just prior to the end of surgery)
Postoperative (after the end of surgery
and may extend for days thereafter)
Specific factors within these phases
contribute to the development of acute
operative pain

11. HISTORY AND PROGRESS
IN PRE-EMPTIVE
ANALGESIA
Pre-emptive analgesia would block the
induction of central neural
sensitization brought about by the
incision and reduce the intensity of acute
postoperative pain ( proposed first by
Crile and later by Wall)
General anesthesia may attenuate the
transmission of afferent injury barrage
from the periphery to the spinal cord and
brain, but it doesn’t block the
transmission

12. PREEMPTIVE
ANALGESIA :
 It involves the introduction of an analgesic
regimen before the onset of painful stimuli,
with the goal of preventing sensitization
of the nervous system to subsequent stimuli
that could amplify pain
Windup: functional changes in the dorsal
horn because of pain.
This type of therapy, in addition to reducing
acute pain, attenuates chronic postoperative
pain/ chronic post-surgical pain (CPSP)

13. PREEMPTIVE ANALGESIA

14. FACTORS THAT MODIFY PERI-
OPERATIVE PAIN
1- Site ,nature and duration of surgery.
2- Type, location extent of incision.
3- Physiologic and psychologic makeup
of the patient.
4- Pre operative preparation of the patient
including preoperative treatment of
painful stimuli.
5- Presence of complications of surgery.
6- Anesthetic management.
7- Quality of perioperative care.

15. MEDIATORS
Neurotransmitter Effect on nociception
Substance P Excitatory
Glutamate Excitatory
Aspartate Excitatory
ATP Excitatory
Somatostatin Inhibitory
Acetylcholine Inhibitory
Endorphins Inhibitory
Enkephalins Inhibitory
Norepeinephrine Inhibitory
Adenosine Inhibitory
Serotonin Inhibitory
GABA and glycine Inhibitory
Calcitonin gene related peptide Excitatory

16. Substance P synthesized in
dorsal root ganglion,
sensitisiating the neuron to
nociceptive signals; binding
NK1, resulting Ca ion influx;
induce NO production
serotonin
released
from
platelets ,
mast cells
and excite
afferents via
5HT1-3
Ketamine is
effective NMDA
antagonist
PERIPHERAL AND CENTRAL
SENSITIZATION

17. RATIONALE FOR
MULTIMODAL ANALGESIA
Goal
Providing effective pain relief, reducing
opioid-related side effects and surgical
stress response, and improve clinical
outcome
Concept
Combination various analgesic techniques
and different classes of drugs
Failure reason
Inappropriate timing of administration of
analgesic

18. TREATMENT
1-Systemic opiods.
2-Nonopioid analgesics
3-Patient-controlled analgesia.
4-Regional anesthetic techniques .
a : Intrathecal analgesia.
b :Patient-controlled epidural analgesia.
c :Combined spinal-epidural technique.
5-intraarticular analgesia.
6-Cryoanalgesia.
7-T.E.N.S.
8-Psychologic and other methods.

21. OPIOIDS
ESSENTIAL ELEMENT OF PAIN MANAGEMENT
Receptors
Mu (μ or OP3)
μ1
μ2
Kappa (κ or OP2)
Delta (δ orOP1)
Sigma(σ)
Clinical effect
Analgesia, sedation, euphoria
Resp. depression, physical dependence
Spinal analgesia, resp. depression
Analgesia, resp. depression
Dysphoria, hallucination, tachycardia
hypertension

22. OPIOIDS:
BACKBONE OF ANALGESIA
 Pure Agonists
Morphine, oxymorphone, meperidine,
hydromorphone, fentanyl
 Partial agonists, mixed agonist-antagonists
Buprenorphine
Butorphanol
 Pure Antagonists (reversal of agonists)
Naloxone

23. OPIOID ADMINISTRATION
 Systemic: IV, SC, IM, oral
 Intra-articular injection
 Local injection
 Epidural or intrathecal injection
 Transdermal fentanyl patch (patient-
activated electrically facilitated delivery)

24. OPIOIDS
1.Agonists
: stimulate receptor
: no ceiling effect ( no limit mg/kg)
: moderate to severe pain
: Codiene, morphine, pethidine,
fentanyl, methadone

25. OPIOIDS
2. Partial agonists
 ceiling effects
eg.buprenorphine, butorphanol
 can be used as adjuvants in
neuraxial anelgesia

26. OPIOIDS
3. Agonists-antagonists
: agonist-κ or σ receptor
but antagonist to μ receptor
: can used in mild to moderate pain
: ceiling effects
: precipitate withdrawal in opioids
dependent
: pentazocine, nalbuphine

27. MORPHINE
Dose: 0.1-0.2 mg/kg iv
•metabolism : liver
M-3-Glucoronide : no analgesic property
M-6-G : more potent than morphine(2X)
• histamine release
•INCLUDE liposomal extended release
preparations for epidural administration

28. MEPERIDINE
: atropine like effect : tachycardia ,dry
mouth
: metabolism liver
Normeperidine  CNS excitation
: shivering treatment
: interaction with MAOI  hyperpyrexia,
convulsion ,hypertension ,coma

29. FENTANYL
: rapid onset & short duration
: inactive metabolite
: no histamine release
:100X potent than morphine
DOSE: 1-2 mics/kg iv

30. CODEINE
: weak opioids
: orally plus with paracetamol
: mild to moderate pain.
:Doses 15-60 mg 4 hourly
(with a maximum of 300 mg daily)

31. POTENTIAL SIDE EFFECTS OF
OPIOIDS
 - Respiratory & cardiovascular depression
 - Nausea, vomiting, ileus , Constipation
 - Urinary hesitency & retention
 - Pruritus
- Sedation dizziness ,delirium
 -Myoclonus/seizure
 - Tolerance , dependence

32. NALOXONE
: Rx opioid intoxication
Doses:
Respiratory depression & somnolence
: 1-4 mcg/kg repeat 2-3 min
: 0.5-5 mcg/kg/hr continuous infusion
Urinary retention & Pruritus
: 1-2 mcg/kg
Nausea vomitting
: 0.5-1 mcg/kg
side effects : withdrawal symptoms,
hypertension, tachycardia, pain, pulmonary
edema

33. TRAMADOL
Multiple mechanism
Weak µ-receptor agonist
Inhibit serotonin & NE reuptake
Dose : 50-100 mg PO q 4-6 hr.
Max. 400 mg/d
i.v. :1-2 mg/kg

34. NON-OPIODS
ACETAMINOPHEN
 Action
 Analgesic
 Antipyretic
 Anti-inflammatory agent
 Effective for the musculoskeletal aches,joint
stiffness
 Disadvantage
 Dose-dependent hepatotoxicity, GI upset
 Agranulocytosis
 Dosage
 650-1000 mg PO q 4 hr.
 Max. 4 g/d
 Reduce dose 50-70% in patient with significant
hepatic impairment

35. NSAIDS
 The cornerstone on the treatment of acute
pain in the early postoperative period
 Reduce local concentration of arachidonic
acid metabolites
 Combination of ibuprofen and paracetamol
reduce the need for early analgesia
 Cyclo-oxygenase-2 inhibitors(COX-2)
 Parecoxib can be administrated introp and immediately
postop before oral medicaiton toleranted

36. NSAID
Side effects Therapeutic effects
TXA2
PGE2
PGI2 PGI2

37. NSAID
DrugDrug DosageDosage Maximum daily doseMaximum daily dose
NonselectiveNonselective
inhibitorinhibitor
DiclofenacDiclofenac
IndomethacinIndomethacin
IbuprofenIbuprofen
50 mg PO bid-tid50 mg PO bid-tid
75 mg PO bid75 mg PO bid
200-800 mg q 6 hr.200-800 mg q 6 hr.
200 mg200 mg
150 mg150 mg
3200 mg3200 mg
Cox-2Cox-2
inhibitorinhibitor
CelecoxibCelecoxib
100-200 mg PO bid100-200 mg PO bid
2-4mg/kg iv
400 mg400 mg

38. KETAMINE
An antagonist at NMDA receptor
An opioid sparing effect and improved
analgesia in opioid-resistant pain
Initial bolus(0.5 mg/kg) and continuous
infusion(3 microgm/kg/min) combined
with continuous femoral nerve block in
TKR
Transdermal ketamine patch
 IM 2-4 mg/kg
iv 0.25 -0.5 mg/kg

39. CLONIDINE
An α2-adrenoceptor agonist with anti-
nociceptive activity via peripheral,
supraspinal and primary spinal cord
mechanism
Activation of postsynaptic α2-
adrenoceptors of descending
noradrenergic pathways
Epidural clonidine advantages over
epidural local anesthetics and opioids, no
adverse effects of motor block, urinary
retention, respiratory depression, and
pruritus
Dose 1-2 mics/kg

40. EPIDURAL ANALGESIA
Provides superior pain relief and
attenuate the stress response to
surgery, particularly continuous infusion
during and after surgery
Combined use of epidural local
anesthetics and adjuvants provides
introperative analgesia and postoperative
pain effectively
Associated problems: motor blockade,
incompatibility with anticoagulation,
urinary retention

42. BF

44. PATIENT-CONTROLLED ANALGESIA
(PCA)
 Patients are able to self administer precise
dose of opioid intravenously (or in epidural
space) on and as needed basis.
 The physician programs the infusion pump
to deliver a specific dose,the minimum
interval between doses (lockout
period),maximum amount of opioid that can
be given in a given period(1-4h).
 When PCA is first initiated a loading dose of
opioid must be given.

45.  Most adults require 2-3mg/h of iv morphine
in the first 24-48 hrs and 1-2mg/h in the
following 36-72 hrs
 PCA is a cost effective technique that
provides superior analgesia with high pt
satisfaction.
 Drug consumption is less
 Patients are able to adjust analgesia
according to their pain severity.

48. COMBINED SPINAL EPIDURAL
Has become popular in obstetrics and
in operating room.
Advantage: rapid onset of surgical
anesthesia with availability to continue
analgesia for post op. period.

49. REGIONAL ANESTHETIC
TECHNIQUES:
• Anelgesia superior to opioids
• Positive respiratory, cardiovascular and
neuroendocrine effects
• reduced thromboembolic complications and
blood loss; and reduced convalescence
Brachial plexus blocks :analgesia for upto 12 hrs.
Sciatic and Femoral n. blocks :similar results.
Paravertebral Blocks: equal to thoracic epidural
Intercostal n. blocks : 6-12 hrs. analgesia.
Interpleural block
Cryoanelgesia
Intra-articular Anelgesia: upto 24 hours

50. WOUND INFILTRATION WITH LOCALWOUND INFILTRATION WITH LOCAL
ANAESTHETICSANAESTHETICS
It’s commonly perfomed to achieve
wound analgesia
The routine use of adjuvants in wound
infiltration is currently not recommanded

51. NONPHARMACOLOGICAL OPTIONS

52. TRANSCUTANEOUS ELECTRICALTRANSCUTANEOUS ELECTRICAL
NERVE STIMULATION (TENS)NERVE STIMULATION (TENS)
Used widely in chronic pain
Evidence in acute pain treatment is
inconclusive, due to lack of well-
conducted RCTs
All available trials used TENS as an
adjuvant to medication, and it’s possible
the effects of TENS was masked by the
analgesic effect of medication

53. OTHERS
Relaxation techniques
Music therapy
Acuputure
Hypnosis

54. MULTIMODAL APPROACH TO
PERIOPERATIVE RECOVERY
 Principles of a multimodal strategy include
 Control of post-op pain for early mobilization
 Early enteral nutrition
 Education
 Attenuation of perioperative stress response
through regional anesthetic techniques
 Multimodal analgesia
 The use of epidural anesthesia and anelgesia
covers the last two

55. CONCLUSION
Multimodal pain therapy
Less post-op complications
Reduced duration of hospital stay
Improvement in post-op pain
Better clinical outcomes
The analgesic techniques used should be
individualised to the patient and the type
of surgery

56.  Akknaesthesiologist should work as
perioperative physician, actively participate in
the management of perioperative pain for the
enhanced outcome of the patients after surgery.
 Anaesthesia provider should practice multimodal
analgesia to control multiple perioperative
pathophysiological factor that lead to
postoperative pain and its sequelae.

57. THANKS