ACUTE PAIN MANAGEMENT

Harry Isbagio, Jakarta

 Definition of Pain

An unpleasant sensory or
emotional experience associated
with actual or potential tissue
damage; or described in such
terms.
 Time-based classification of pain

• Acute: short-term; usually due to nociception

(tissue damage); resolves with healing.
• In back pain, Acute = < 4 wks
Sub-acute = 4-12 weeks
Chronic = > 12 weeks
• Chronic pain: pain lasting > 3-6 months
• Persisting pain (NHMRC: acute pain guidelines)
The role of general
practitioners
Early and appropriate interventions by
general practitioners (GPs) :

- Can have a major impact in improving the

assessment and treatment of pain
- Preventing the development of chronic pain.
Consequences of poorly managed acute pain

 The Patient suffers

 CVS: MI, dysrhythmias
 Resp: atelectasis, pneumonia
 GI: ileus, anastamosis failure
 Endocrine: “stress hormones”
 Hypercoagulable state: DVT, PE
 Impaired immunological state
 Infection, cancer, wound healing
 Psychological:
 Anxiety, Depression, Fatigue

 Chronic Post-surgery/trauma Pain

GP : Area opportunities for
improved assessment & treatment
strategies
 Acute back pain
 Acute peripheral musculoskeletal pain

 Acute herpes zoster infection

 Acute abdominal pain

 Acute headache

 Acute orofacial pain

 Acute pain in patients with

haemophilia/ haemarthrosis
 Acute pain in patients with cancer

 Acute pain in patients with

HIV/AIDS.
General principles of pain management

 Unrelieved severe pain has adverse physiological and

psychological effects.
 Proper assessment and control of pain require patient
involvement.
 Effective pain relief requires flexibility and tailoring of
treatment to the individual.
 Pain is best treated early, because established, severe pain is
more difficult to treat.
 While it is not always possible to completely alleviate pain,
it should be possible to reduce pain to a tolerable or
comfortable level.
Assessment of pain and pain history
Visual Analogue Scale (VAS)

Careful assessment of pain should occur initially

and then regularly throughout treatment, using
self-reporting techniques.
 As pain varies so markedly between individuals,

patient involvement in the initial and continuing

assessment of their pain is essential.
 Assessment of pain and pain history
Visual Analogue Scale (VAS)

Pain should be assessed both at rest and during

activity
Pain relief assessed as to its adequacy, to allow

appropriate function.
Unexpected levels of pain or pain that suddenly

increases, especially when associated with changes in

other vital signs, may signal the development of a
new surgical or medical diagnosis
 Taking a pain history
 Circumstances associated with
pain onset
 Primary site of pain
 Radiation of pain
 Character of pain (eg is pain
throbbing, sharp, aching etc)
 Intensity of pain (eg on visual
analogue scale)
— at rest
— on movement
— at present
— during last week
— highest level
 Factors altering pain
 — what makes it worse?
 — what makes it better?
 Associated symptoms (eg nausea)
 Temporal factors
 — is pain present continuously or
otherwise?
 Effect of pain on activities
 Effect of pain on sleep
 Medications taken for pain
 Other treatments used for pain
 Health professionals consulted
for pain treatment
Pain history information of significance
for symptomatic treatment of pain
 Expectations of outcome of
pain treatment
 Patient’s belief concerning
the causes of pain
 Reduction in pain required
to resume ‘reasonable
activities’
 Patient’s typical coping
response for stress or pain,
including presence of
anxiety or psychiatric
disorders
 Family expectations
and beliefs about pain,
stress and postoperative
course
 Ways the patient
describes or shows pain
 Patient knowledge,
expec tations and
preferences for pain
management
Acute Pain Management Modalities

 Pharmacologic :
 Cyclo-oxygenase inhibitors
 Non-specific COX inhibitors(classical NSAIDs)
 Selective COX-2 inhibitors, the “coxibs”
 Acetaminophen is probably COX-3

 Opioids

 Local Anesthetics
 Adjuvant agents
 WHO Pain Ladder

http://erlewinedesign.com/end-of-life-care/gfx/who_ladder.gif
 Opioids
 Binding to opioid receptors both within and outside
the central nervous system
 Receptor type for clinical analgesia is named ‘mu
 Other commonly used mu opioid agonists codeine,
pethidine, oxycodone, methadone, fentanyl.
tramadol.
 Side effects —All mu opioids have the potential to
cause constipation, urinary retention, sedation,
respiratory depression, nausea and vomiting.
 Titration of opioids should be based on the patient’s
analgesic response and side effects.
 Opioids
 A true allergy to opioids is very uncommon.
 No evidence use of opioids for treatment of severe
pain leads to opioid dependence or addiction.
 Different methods of opioid administration each have
advantages and disadvantages in different groups of
patients
 Effective when the dosage regimen is tailored to the
individual.
 The patient’s need for pain relief as more important
than strict adherence to a dose interval.
Non-steroidal anti-inflammatory drugs

 Effective in the management of mild to moderate pain

 The concurrent use of opioids and NSAIDs often
provides more effective analgesia than either of the
drug classes alone.
 NSAIDs have a significant opioid dose-sparing effect
and can be useful in reducing opioid side effects.
 Their efficacy as components of multimodal analgesia
has been confirmed by clinical trials.
Non-steroidal anti-inflammatory drugs

 NSAIDs produce a risk of platelet dysfunction that

may impair blood clotting,
 Risk of gastro-intestinal bleeding and renal
dysfunction (particularly in the older age group)
 Risk of NSAID induced asthma.
 The adverse effects of NSAIDs are potentially
serious and they cannot be used in all patients.
 Paracetamol
 Paracetamol is effective for mild to moderate pain,
 Adjunct to opioids in more severe pain.
 The recommended dose is 0.5 to 1 gr every 3-6 hours
 Maximum daily dose of 6 g a day in divided doses
 Fewer side effects than NSAIDs,
 Used if NSAID contraindicated (asthma, peptic ulcers).
 Should not be used in patients with liver dysfunction
 Risk of liver damage with the combination of alcohol
and paracetamol.
 Local anesthetic
 Block generation & conduction of nerve impulse in
peripheral & central nervous systems

Myelinated fibers Function

A-alpha(Aα) Motor, proprioception
A- beta(Aβ) Touch, pressure
A-gamma(Aγ) Muscle spindle tone
A-delta(Aδ) Pain, temperature, touch
B Sympathetic (preganglion)
Myelinated fibers
C Pain, temperature
 Technique for administering
local anesthesia
Peripheral nerve blocks
Ilioinguinal/hypogastric : herniorrhaphy
Paracervical : F&C, D&C, cone biopsy
Penile : circumcision
Brachial plexus : arm, hand
Intercostal/paravertebral : breast
Peribulbar/retrobulbar :eye

REVIEW ARTICLE WHITE ANESTH ANALG

NON-OPIOID ANALGESICS AND ACUTE POSTOPERATIVE PAIN 2005;101:S5–S22
Technique for administering
local anesthesia
Tissue infiltration wound instillation
Topical analgesia
EMLA : skin lesion
Lidocaine spray : bronchoscopy, endoscopy
Lidocaine gel /cream: uro,oral surgery
Cocaine paste : nasal ,endosinus surgery

REVIEW ARTICLE WHITE ANESTH ANALG

NON-OPIOID ANALGESICS AND ACUTE POSTOPERATIVE PAIN 2005;101:S5–S22
 Local anesthetic
Agents % solution Duration(h) Max dose
Lidocaine
-infiltration 0.5-1 1-2
-epidural 1-2 1-2 7mg/kg
-plexus or nerve 0.75-1.5 1-3
Bupivacaine
-infiltrate 0.125-0.25 1.5-6
-epidural 0.25-0.75 1.5-6
-plexus or nerve 0.25-0.5 8-24+ 3.5mg/kg
 Corticosteroid
 Reduce pain in several ways
 Reduce inflammation
 Relieve nerve compression
 Decrease spontaneous firing of sodium channels
in neuromas
 Effective in
 Pain secondary to edema (CNS ds.)
 Prostglandin-mediated pain (arthritis, bone
metastasis)
 Not recommend for long term
What is the “Best Way” to manage
pain?
 FIRST, DO NO HARM
Therefore, the “best way” is a BALANCE

Patient Effective
Safety Analgesic
Modalities
 KEY POINTS
 “Emphasis is placed on the utilization of a multimodal
analgesic approach to maximize analgesia while
minimizing side-effects.”
 Transduction

 Transmission

 Modulation

 Perception

 There is as of yet no single silver bullet!!

Pain Pathways
Multimodal analgesia

Opioid
Anti inflammatory agents
Alpha 2 agonist

Local anesthetics
Opioid
Anti inflammatory agents
Alpha 2 agonist

Local anesthetics
Opioid
Anti inflammatory agents
 Analgesia with Opioids alone
 The harder we “push” with single mode analgesia,
the greater the degree of side-effects

Side effects

Analgesia
 Multi-modal Analgesia
 “With the multimodal analgesic approach there is
additive or even synergistic analgesia, while the side-
effects profiles are different and of small degree.”

Side-
Analgesia effects
The rationale for COX-Inhibitors in
acute pain management
 The problem with the “Little Pain – Little Gun,
Big Pain – Big Gun Approach”
– With opioids, analgesic efficacy is limited by side-
effects
– “Optimal” analgesia is often difficult to titrate
• >10 – fold variability in opioid dose:response for
analgesia in opioid naïve patients!
• factors add to the difficulty
– Opioid tolerance, anxiety, obstructive sleep apnea, sleep
deprivation, concomitantly administered sedative drugs
The rationale for COX-Inhibitors in
acute pain management
 The problem with the “Little Pain – Little Gun,
Big Pain – Big Gun Approach”

– Patient Safety!! If the “Big Gun” is failing due to

dose limiting sedation/respiratory depression, the
addition at that time of the “Little Gun” may kill the
patient.
 Analgesia with Opioids alone
 The harder we “push” with single mode analgesia,
the greater the degree of side-effects
Pain

Opioid
Side-effects
Resp Depression

Analgesia

Opioid
The rationale for COX-Inhibitors
in acute pain management
 Opioid dose sparing of 30 – 50%
– Less c/o opioid S/E

 Dose:response is quite uniform from

patient to patient
– S/E and contra-indications well described
The rationale for COX-Inhibitors
in acute pain management
Improved pain scores, especially with
activity
Greater patient satisfaction
Safer for the patient
Why a Selective COX-2 inhibitor?

 Equivalent analgesic efficacy with non-

selective COX-inhibitors
 No effects on platelets! 0, ZIPPO
 Much reduced incidence of upper GI
S/E compared to non-selective
 Duration of action about 24 hr.
 Formation of Prostaglandins
Phospholipids
(in cell membrane) Stimulus
(cell injury/damage)

Phospholipase A2 Ca++

Arachidonic Acid

Lipoxygenase Cyclooxygenase

Leukotrienes Prostaglandins G2
(LTD4 & LTC4)

PGI2 PGE2 PGF2a

PGD2
Prostaglandins H2
Thromboxane (TXA2)
 Mechanism of Action of NSAIDs
Normal condition Inflammation
Arachidonic acid
COX-1 COX-2 COXIBs (ACX, CEL)
(constitutive)
X T-NSAIDs
VOL, MOV) X
(CAT, (inducible)

PGH2 PGH2

PGE2 PGI2 TXA2 PGE2 PGI2 TXA2

Stomach Stomach Platelets Synovial membrane,

Kidney Kidney endothelium, vascular
Brain Endothelium smooth muscle, WBCs, brain

• GI protection • platelet • inflammation

• vasodilation aggregation • pain
• vasoconstriction • fever
• renal perfusion
• inhibit platelet
aggregation
Postorthopedic Surgical Pain
Etoricoxib in Knee or Hip Replacement Surgery:
Pain Relief Scores* over 24 Hours
Etoricoxib provided pain relief superior to placebo and similar
to naproxen sodium (controlled-release)
2.0
Mean PR scores (± SE)

**
1.5
Naproxen sodium (controlled-
release) 1100 mg (n=73)
1.0
Etoricoxib 120 mg (n=80)

0.5
Placebo (n=75)

0.0
0 1 2 3 4 5 6 7 8 9 10 11 12 20 24
Time (hour) postdose
*PR rated on a 0- to 4-point scale (0 = none, 1 = a little, 2 = some, 3 = a lot, 4
=complete); **p<0.001 for etoricoxib 120 mg and naproxen sodium (controlled-
release) 1100 mg vs. placebo over eight hours; p=0.721 for etoricoxib 120 mg vs.
naproxen sodium (controlled-release) 1100 mg over eight hours.
SE = standard error
 Acute
Acute Gouty
Gouty Arthritis
Arthritis
Etoricoxib
Etoricoxib vs.
vs. Indomethacin
Indomethacina (Phase III)::
(Phase III)
Patient
Patient Assessment
Assessment of
of Pain
Paina
Etoricoxib produced substantial improvement vs. baseline at 4 hours
0.0 0.0
Study 1 b,c
Study 2d,e
LS mean change from

–0.5 –0.5
baseline ( SE)

–1.0 –1.0

–1.5 –1.5

–2.0 –2.0

–2.5 –2.5

–3.0 –3.0
R 4 hr 2 3 4 5 6 7 8 R 4 hr 2 3 4 5 6 7 8
Day in study Day in study
Etoricoxib 120 mg Indomethacin 150 mgf
(n=72 study 1, n=101 study 2) (n=71 study 1, n=83 study 2)
LS = least squares; SE = standard error; R = randomization; CI = confidence interval
a
0- to 4-point Likert scale (0 = none, 1 = mild, 2 = moderate, 3 = severe, 4 = extreme); bLS mean change from baseline four hours after
initial
dose = –0.94; 95% CI, –1.11, –0.76; cLS mean difference from indomethacin = 0.09 (–0.14, 0.33) over days 2 to 8; dLS mean change from
baseline four hours after initial dose = –1.04, 95% CI, –1.22, –0.86; eLS mean difference from indomethacin = –0.07 (–0.27, 0.14); f50 mg
three times daily
Adapted from Schumacher HR Jr et al BMJ 2002;324:1488–1492; Rubin BR et al Arthritis Rheum 2004;50:598–606.
Acute
Acute Gouty
Gouty Arthritis
Arthritis
Etoricoxib
Etoricoxib vs.
vs. Indomethacin
Indomethacin (Phase III)::
(Phase III)
Joint
Joint Swelling*
Swelling*
Etoricoxib as effective as indomethacin in reducing swelling
0.0 0.0
Study 1 Study 2
LS mean change from

–0.5 –0.5
baseline ( SE)

–1.0 –1.0

–1.5 –1.5

–2.0 –2.0

–2.5 –2.5

R 2 5 8 R 2 5 8 Improved
Day in study Day in study
response

Etoricoxib 120 mg Indomethacin 150 mg**

(n=74 study 1, n=101 study 2) (n=73 study 1, n=86 study 2)
*Investigator assessment; 0- to 3-point Likert scale (0 = none, 1 = palpable, 2 = visible, 3 = bulging beyond joint
margins); **50 mg three times daily
Adapted from Boice JA et al. Poster presented at EULAR, 2002; Navarra S et al. Poster presented at APLAR,
2002; Schumacher HR Jr et al BMJ 2002;324:1488–1492; Rubin BR et al Arthritis Rheum 2004;50:598–606.
Summary
Terima Kasih
Specific areas of pain management

Acute musculoskeletal pain:

 Back and neck pain

 Peripheral musculoskeletal pain (Gout, RA, Seronegative, Septic)

 Sporting injuries

Acute herpes zoster infection

Acute abdominal pain
Acute Headache
Acute pain in patients with cancer
Acute pain in haemophilia/haemarthrosis
Acute pain in HIV/AIDS
Acute dental/Orofacial pain
Acute obstetrical pain
Agents used to manage acute pain