Acute pain management & preemptive analgesia (3)

ACUTE PAIN MANAGEMENT & PRE-EMPTIVE ANALGESIA

SHADAB KAMAL

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.

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)

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,

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.

FORMS OF ACUTE PAIN

Post-traumaticPost-operativeObstetric painPain a/w acute medical illnesses (eg.

myocardial infarction , pancreatitis, renal calculi etc…)

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.

PHYSIOLOGIC RESPONSEPHYSIOLOGIC RESPONSECardiovascular

: HR, BP ,PVR, Myocardial O2 consumption

MI, DVT, pulmonary embolismRespiratory

:⇩ 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

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)

TARGETS OF A PREVENTIVE APPROACH TO ACUTE PAIN MANAGEMENT

Perioperative periodPreoperative (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

HISTORY AND PROGRESS IN PRE-EMPTIVE ANALGESIAPre-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

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)

PREEMPTIVE ANALGESIA

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

patientincluding preoperative treatment

of painful stimuli.5- Presence of complications of surgery.6- Anesthetic management.7- Quality of perioperative care.

INFLAMMATORY PAIN MEDIATORSNeurotransmitter 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

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

RATIONALE FOR MULTIMODAL ANALGESIA

GoalProviding effective pain relief,

reducing opioid-related side effects and surgical stress response, and improve clinical outcome

ConceptCombination various analgesic

techniques and different classes of drugs

Failure reasonInappropriate timing of administration

of analgesic

TREATMENT1-Systemic opiods.2-Nonopioid analgesics3-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.

OPIOIDSESSENTIAL 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

OPIOIDS:BACKBONE OF ANALGESIA

Pure Agonists Morphine, oxymorphone, meperidine,

hydromorphone, fentanyl Partial agonists, mixed agonist-antagonists

Buprenorphine Butorphanol

Pure Antagonists (reversal of agonists) Naloxone

OPIOID ADMINISTRATION

Systemic: IV, SC, IM, oral Intra-articular injection Local injection Epidural or intrathecal injection Transdermal fentanyl patch (patient-

activated electrically facilitated delivery)

OPIOIDS

1.Agonists : stimulate receptor : no ceiling effect ( no limit mg/kg)

: moderate to severe pain : Codiene, morphine, pethidine,

fentanyl, methadone

OPIOIDS

2. Partial agonists ceiling effects eg.buprenorphine, butorphanol can be used as adjuvants in

neuraxial anelgesia

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

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

MEPERIDINE

: atropine like effect : tachycardia ,dry mouth

: metabolism liver

Normeperidine CNS excitation

: shivering treatment

: interaction with MAOI hyperpyrexia, convulsion ,hypertension ,coma

FENTANYL

: rapid onset & short duration

: inactive metabolite

: no histamine release

:100X potent than morphine

DOSE: 1-2 mics/kg iv

CODEINE

: weak opioids: orally plus with paracetamol : mild to moderate pain.: Doses 15-60 mg4 hourly (with a maximum of 300 mg daily)

POTENTIAL SIDE EFFECTS OF OPIOIDS

- Respiratory & cardiovascular depression - Nausea, vomiting, ileus , Constipation

- Urinary hesitency & retention

- Pruritus

- Sedation dizziness ,delirium

-Myoclonus/seizure

- Tolerance , dependence

NALOXONE: Rx opioid intoxicationDoses: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

TRAMADOL

Multiple mechanismWeak µ-receptor agonistInhibit serotonin & NE reuptake

Dose : 50-100 mg PO q 4-6 hr.Max. 400 mg/di.v. :1-2 mg/kg

NON-OPIODSACETAMINOPHEN 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

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

NSAID

Side effects Therapeutic effectsTXA2

PGE2

PGI2 PGI2

NSAID

Drug Drug Dosage Dosage Maximum Maximum daily dosedaily dose

Nonselective Nonselective inhibitorinhibitorDiclofenacDiclofenacIndomethaciIndomethacinnIbuprofen Ibuprofen

50 mg PO bid-tid50 mg PO bid-tid

75 mg PO bid75 mg PO bid

200-800 mg q 6 200-800 mg q 6 hr.hr.

200 mg200 mg

150 mg150 mg

3200 mg3200 mg

Cox-2 Cox-2 inhibitorinhibitorCelecoxib Celecoxib

100-200 mg PO 100-200 mg PO bidbid2-4mg/kg iv

400 mg400 mg

KETAMINE

An antagonist at NMDA receptorAn opioid sparing effect and improved

analgesia in opioid-resistant painInitial 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

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

EPIDURAL ANALGESIAProvides 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

BF

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.

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.

COMBINED SPINAL EPIDURALHas become popular in obstetrics

and in operating room.Advantage: rapid onset of surgical

anesthesia with availability to continue analgesia for post op. period.

REGIONAL ANESTHETIC TECHNIQUES:• Anelgesia superior to opioids• Positive respiratory, cardiovascular and

neuroendocrine effects• reduced thromboembolic complications and

blood loss; and reduced convalescenceBrachial plexus blocks :analgesia for upto 12

hrs.Sciatic and Femoral n. blocks :similar results.Paravertebral Blocks: equal to thoracic epiduralIntercostal n. blocks : 6-12 hrs. analgesia.Interpleural blockCryoanelgesia Intra-articular Anelgesia: upto 24 hours

WOUND INFILTRATION WITH LOCAL WOUND INFILTRATION WITH LOCAL ANAESTHETICSANAESTHETICS

It’s commonly perfomed to achieve wound analgesia

The routine use of adjuvants in wound infiltration is currently not recommanded

NONPHARMACOLOGICAL OPTIONS

TRANSCUTANEOUS ELECTRICAL TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION (TENS)NERVE STIMULATION (TENS)

Used widely in chronic painEvidence 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

OTHERS

Relaxation techniquesMusic therapyAcuputureHypnosis

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

CONCLUSION

Multimodal pain therapyLess post-op complicationsReduced duration of hospital stayImprovement in post-op painBetter clinical outcomes

The analgesic techniques used should be individualised to the patient and the type of surgery

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.

THANKS