Acute Pain Management:

Transforming Evidence into Practice

Dr Surjya Prasad upadhyay; MD
Specialist Anaesthesiology
NMC hospital DIP
Dubai

Acute pain

There is No Pain
that can not be treated

Common myth for acute pain Treatment

Oligo-analgesia

Analgesic may mask abnormal finding

Sever pain will cause abnormal vitals signs

Patient will be addicted to narcotics

Patient will be sedate after narcotics

Some kind of pain cant be relieved

Effective pain management can be done on SOS basis .

Importance of Acute pain management

Pain control- human right

Indicator of quality of care

Untreated pain- adversely affects other systems;

Physiological and psychological upset / stress

Untreated/poorly treated pain- progress into chronic pain

Increased morbidity/ mortality/ cost/ LOS

Consequences of poorly treated pain

Pain Algorithm
Patient in Acute pain /
anticipated postoperative pain

Brief pain Assessment

Emergent use of opioid if clinical condition dictate

Comprehensive pain assessment

Appropriate Therapy
Referral

RELIEF Approach for Acute pain Treatment

R: Record Pain before and after Tx

E: Evidence based treatment

L: Look and listen to Patient: Belief your Patient

I: Inquire if Patient need Pain Medicine

E: Educate Staff

F: Facilitate/Formulate multidisciplinary APS

Assessment/ which scale?

How Acute Pain differ from Chronic

Pathology : clear Vs unclear

Duration : short

Mechanism: adaptive vs maladoptive

Prognosis: good Vs unpedictable

Treatment : simple vs complex

Acute Vs chronic pain; Hit fast and hit hard

Changing concept of pain management

Traditional

Modern concept

Palliate pain-

Prevent pain

Administered single analgesics

Multimodal analgesia

Fixed dose of opioid

Judicious use of opioid

(individualised)

PRN or SOS analgesic

Continuous / Regular
Analgesics

No protocol/ guideline for Acute

pain

Acute pain service: Advanced

pain interventions; blocks

Pain Pathway and Analgesic Actions

Treatment modalities

Non pharmacologic

Pharmacologic

1.Non-opioid
2.Opioid
3.Adjuvants

Invasive interventions
Diagnose and treat as per underlying cause

Non-pharmacologic pain management

Massage

TENS

Acupuncture

Exercise

Heat/cold massage

Neurostimulation

Scrambler therapy

Dry needling

Behavioural

Cognitive

Bio-feedback

Opioids

Best available analgesics, but not ideal

Act via different opioid receptors in brain, spinal cord

and peripheral tissue.

Classified according to potency- weak to strong

Choice of opioid- depends on patient, pain, associated

conditions

Where do opioid act ?

Weak Opioid

Codeine pro-drug;
metabolised to active drug morphine via Cytochrome
17-34% population: deficiency in converting enzyme; no action

Dihydrocodeine pro-drug, again a wide variation in patient

response.
Tramadol active drug. Dual action Mu agonist + SSNRI
Pentazocin/ butorphenol/buprenorphine- partial agonist/
agonist- antagonist- ceiling analgesic effect

Tramadol

Dual mode of action; opioid Mu agonist + selective serotonin

and noradrenaline reuptake inhibitor (SSNRI).

Effective in mild to moderate pain

Can be given IM,IV,Oral- good bioavailability

Can be combined with PCM, NSAID

Dose in adult- 50-100 mg 6-8 hrly; Max dose 400 mg in 24

Dry mouth, dizziness, sedation in high dose

Nausea vomiting- only if given fast boluses.

Strong opioid

Act directly / no need to convert into active form

Agonist at opioid receptors

Has dose dependent analgesic and other adverse effects

No ceiling effects to analgesia

Wide individual dose variation

Diverse route of administration

Morphine; pethidine, fentanyl, alfentanil, sufentanil

Morphine

Available in various form;

Consider as Reference opioid:

Initial dose 0.1-0.2 mg/kg

Metabolism- liver; 30-40% oral bio-availability

Metabolite- Morphine 3 Glucoronide- no analgesic

morhine 6 glucoronide- more analgesic than morphine

Elimination: Renal

Onset after IV-5-10 min, peak 1 hrs, Duration: 4 hrs

Meperidine/ Pethidine

Synthetic opioid

Atropine like effect-

Metabolism -liver
metabolite- normeperidine- CNS excitation,

Anti-shivering action

Interaction with antidepressant, SSRI; MAOI- serotonin

syndrome (HTN, rigidity, hyperpyrexia, seizure, Coma)

Psychiatric patients- avoid

Fentanyl

Synthetic opioid ; 100 times more potent than morphine

Short duration; suitable for PCA or continuous infusion

High fast pass metabolism

Most cardio-stable

Loading Dose-1-2 mcg/kg; onset 3-5 min, duration:30-40 min

Available in various form: lollipop, lozenge, transdermal,

intranasal spray, Injectable

Opioid precaution

Hypotension/ shock

CNS issues: head injury, delirium, dementia, psychiatric illness

Concomitant CNS depressant: Alcohol / drugs

Liver/ kidney impairment

Morbidly obese, OSA

Respiratory illness- COPD/Br Asthma

H/o- drug addiction/abuse

Opioid tolerance/ addiction/pseudoaddiction

Rarely a problem in acute setting.

Tolerance:

Pseudo addiction:

Addiction:

Opioid induced hyperalgesia:

Drawback of opioids

Nausea /vomiting--

Bladder/ bowel function

Sedation: delayed mobilisation; discharge

Respiratory: Obstructive breathing, Silent aspiration

Immuno - suppressant effects- would infection.

Cancer recurrence/ metastasis

Persistent post-op pain into chronic pain

Non-opioid Analgesics

Paracetamol

NSAIDs

Adjuvants

First line drug therapy for any pain

Effective alone for mild to moderate pain

Highly effective when combined with opioids

Acetaminophen and NSAIDS

Foundation for pain treatment protocol.

First on and last off

Sole agent in mild to moderate pain

30-60% opioid sparing effects

Analgesic efficacy- has ceiling effects- limiting factor

Opioid- add on therapy when require

Paracetamol

Mechanism similar to NSAIDs but act centrally

Analgesic, antipyretic, but no anti-inflamatory

Safest analgesic of all

Can be given oral / IV/ PR

1st line therapy in mild to moderate pain

Central part of MMA.

Max dose 4 gm in 24 hrs in adult (60-90 mg/kg in children)

NSAIDS

Most extensively used medicine in world in all age group

Analgesic, antipyretic and anti-inflammatory

NSAID- related hospital admission 7-11%

Higher the potency (less amount requirement)- more toxic

Broadly two sub class- Cox-1 and Cox-2 inhibitor.

Combination of NSAIDS: no benefit;

Paracetamol + NSAID: additive effects

NSAIDs selectivity

NSAIDs: side effects

GI side effects

Salt & water retention

Hepatotoxicity

Nephrotoxicity

Bleeding tendency

Prolongation of labour

Asthma and allergy

CV risk/ MI: coxib

Adjuvants

TCA / SSRI / SNRI - neuropathic pain with concomitant

depression

Anticonvulsant- gabapentanoid

Muscle rexant (baclofen, BZD) - relieve muscle spasm

Lidoderm- herpetic pain

Calcitonin- osteoprotic fracture pain

Corticosteroid- tissue edema, neuropathic pain

Central sympatholytic: clonidine/ dexmedetomidine

Potentiate & improve analgesia

reduce side effects

Two Most impressive Adjuvants for

acute pain management

Ketamine
Dexamethasone

Ketamine

NMDA- antagonist

Antihyperalgesic, anti-allodynic

Pre-emptive use- prevent conversion into chronic pain

Dissociative anaesthesia:( 1-2 mg/kg) the lights are on,

but no one is home

Powerful analgesia even in very low dose 0.1-0.3 mg/kg

Preserve haemodynamic/ respiration

Disadvantages:mood, cognition, salivation, nausea

Comparable analgesia with 0.3 mg /kg ketamine

Vs
0.1 mg/kg morphine for Short term pain relief in ED

When to Use Ketamine?

OSA
Dose: 0.1 mg-0.3 mg/Kg
Either as Sole agent or as Adjuvant to opioid

Dexamethasone
Anti-inflammatory/ anti emetic
IV single dose 0.1 mg/kg at the time of induction

Reduced postop pain score

Reduction in opioid consumption

Reduction in rescue analgesic

RA: Intravenous / perineural dexamethasone-

Prolonged sensory motor blockade

Prevent neurotoxicity and rebound hyperalgesia.

Reg Anesth Pain Med. 2015 Jul-Aug;40(4):321-9. Br J Anaesth. 2013;1(2):191200. Reg Anesth Pain Med. 2015 Mar-Apr;40(2):125-32.

Interventions in Acute Pain

Continuous nerve/plexus block

Epidural Analgesia (LA+/- Opioid)

Intrathecal Analgesia

PCA- Intravenous/ epidural

Newer truncal blockade: (Alternative to epidural) TAP, PVB,

QLB, fascia transversalis, Rectus sheath, PECS

Regional block for acute pain

Superior quality of analgesia

Ultrasound has revolutionised regional block

No major systemic side effects

Virtually eliminate opioid use

Can provide continued analgesia

Higher patient satisfaction

Early ambulation/ discharge

Transdermal fentanyl iontophoresis

(IONSYS)

One of the newest advancement.

Credit card size fentanyl reservoir

Can be put in arm, chest.

Programmable like PCA

Up to 6 doses per hour

Work for 24 hrs or upto 80 doses

Approved by FDA in April; 2015

Yet to be available in middle east

Liposomal encapsulated Bupivacaine

MMA / Rationale poly pharmacy

Multimodal Analgesia (MMA)

Transforming evidence into Practice

EBM- Proven and evaluated treatment Practice

EBP- transition of knowledge

Knowledge translation = 17 years

Various sources of knowledge

Why the Gap between evidence and practice

3 main cause of Gap in the quality of pain care
delivery
1.Healthcare professionals.
2.Health care system
3.Patients

Problem related to healthcare professionals

Out of date or inadequate attitudes and knowledge;

1. Pain control- mask recognition of surgical complications

2. Surgery has to be associated with pain
3. Patient complaining pain: fussy

Clinical inertia-

Incomplete knowledge

Fear of side effects/ addiction

Problem related to health care system

Regulatory impediment

Failure to capture short and long term quality outcomes-

Cost shifting to patients (eg insurers)

Inadequate equipment, manpower or drug delivery system

Practice restriction, (eg- nurse are permitted only for im, sc, no
IV; use of narcotics )

Problem related to patients

Out of date or mistaken ideas

Belief that nice patients do not complain of pain or suffering

Fear of side effects/ addictions

Lack of awareness of the importance of pain control

Tendency to be satisfied with inadequate pain control-

Acute Pain service

Comprehensive pain services

Multidisciplinary team

Anaesthesiologist based/

Nursed based anaesthesia supervised

No consensus as to be best model

Very wide variation in APS structure

Most APS initially provide postop / trauma analgesia

APS activities
Appropriate selection of analgesic regimens
Standardized protocols and Guidelines
Advanced interventional techniques
Audit and quality improvement programs
Education

Summary: Treatment modality for Acute Pain

Case 1

60 year male

RTA ;polytrauma

Multiple fracture

Brought in emergency

Agitated, restless; disoriented

Complaining of severe pain

Issues

CNS status

Haemodynamics

Unknown Comborbid illness

How to address pain

Opioid- not a good choice

Acetaminophen- safe if liver function is ok

Epidural- not a choice

NSAIDs- difficult choice even RFT is normal

Best choice- nerve/ plexus blockade, cont infusion

Case 2

75 year/ male

HTN, DM, COPD

# neck of femur in ED

Severe pain-10/10.

Splinting ,PCM, voltarin, pethidine

No relief

What next?

FICB

Conclusion

Assess pain properly

Belief your patient

Never give up

Multimodal analgesia technique

Pre-emptive analgesia

Regular analgesic

Greater use of regional analgesia

Be open to new ideas and embrace them

References
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