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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