Lecturer name:Lecturer name: Osama IbraheimOsama Ibraheim MD,SOB.MD,SOB.Lecture date:Lecture date:

Lecture Title:Lecture Title: Acute Pain Management

Lecture Objectives..Lecture Objectives..

Fundamental Considerations

• Millions of patients worldwide undergo surgery.

Although developing more effective techniques for postoperative analgesia, many patients experience pain.

PAIN

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

IASP, Subcommittee on Taxonomy, 1979

ETIOLGY OF PAIN

1. HEAT2. COLD3. CHEMICAL4. MECHANICAL TORSION STRETCH CUT PINCH PRICK

COMPRESS CRUSH

TYPOLOGY OF PAIN

1. Acute2. Chronic benign3. Chronic cancer

Chronic Pain vs Acute Pain

Acute: A Symptom of Injury or Disease

Chronic Benign: Pain itself is the disease

Chronic Cancer: Actual Tissue destruction

Adverse Effects of Pain

1. Cardiovascular2. Pulmonary3. Gastrointestinal4. Renal

1. Extremities2. Endocrine3. CNS4. Immunologic

Adverse Effects of PainCardiovascular: Tachycardia, hypertension, increased

SVR, increased cardiac work, increased myocardial O2 demand.

Pulmonary: Hypoxia, hypercarbia, atelectasis, decreased cough, decreased vital capacity and function residual capacity, V/Q mismatch.

Gastrointestinal: Nausea, vomiting, ileus, intolerance for oral intake.

Renal: Oliguria, urinary retention.

Adverse Effects of PainExtremities: Skeletal muscle spasm, limited

mobility, thromboembolism.Endocrine: Excessive adrenergic activity, vagal

inhibition, catabolic metabolism, increased O2 consumption.

CNS: Sedation, fatigue, anxiety, and fear cause central sympathetic stimulation.

Immunologic: Inhibited cellular immunity, increased risk of infection, ?? impaired wound healing ??

FREE NERVE ENDINGS ARE PRESENT IN ESSENTIALLY

ALL BODY TISSUES IN VARYING AMOUNTS

IN RESPONSE TO A PAINFUL STIMULUS, SUBSTANCES ARE

EXCRETED.

ALGOGENIC(substances released by pain)

SEROTONIN POTASSIUMHISTAMINE ACETLYCHOLINEBRADYKININS LEUKOTRIENESPROSTAGLANDINS SUBSTANCE P29

NOREPINEPHRINE

THE RECEPTORS IN THE FREE NERVE ENDINGS RESPOND TO THE

SUBSTANCES BY BECOMING CHARGED ELECTROCHEMICALY

RECEPTORS THEN PROPAGATE AN ELECTROCHEMICAL STIMULUS TO

DIFFERING NERVE FIBERS

NOCICEPTION

This electrochemical event that occurs between the site of tissue damage or injury sets off a series of neural transmissions that eventually results in the perception of pain……Collectively this known as nociception

NERVE FIBERPAIN CLASSIFICATION

A FIBER……..SHARP-STABBING-LOCAL “ FIRST PAIN”

B FIBER....PHYSIOLOGIAL REACTION

C FIBER....DULL-ACHE-BURN-THROB NONLOCALIZED-RADIATE “SECOND PAIN”

NERVE FIBER CLASSIFCATIONTYPE FUNCTION A a myelinated motor A alpha myelinated touch-pressure A beta myelinated touch-pressure A delta myelinated pain-temperature A gamma myelinated proprioception

A Delta1. 1 - 4 micrometers diameter2. Myelinated, Rapid conduction3. Sharp, localized4. Heat, cold5. “First pain”

B myelinated preganglionic autonomic

C non-myelinated pain-temperature

C Fibers

1. Small2. Slow Conduction3. Unmyelinated4. Postganglionic autonomic

C Fibers1. Dull pain, burning, Aching throbbing2. Nonlocalized - radiating - diffused3. Temperature,Touch,Mechanical4. “Second pain”

Gate Theory Balance between A delta and C fibers to

dorsal horn determines the intensity of the stimulus that is passed to higher brain center

Area of High Nociceptor Concentration

1. Mucosal membranes2. Periosteum3. Deep fascia4. Ligaments5. Joint capsules6. Cornea7. Subcutaneous tissue

Areas of Moderate Nociceptor Concentration

1. Skeletal muscle2. Cardiac muscle3. Smooth muscle

Areas of Minimal Nociceptor Concentration

1. Bone2. Cartilage3. Marrow

Physiologic Processes of Nociception

1. Detection2. Transduction3. Transmission4. Modulation5. Perception

Detection

1. “First pain”

2. “Second pain”

TRANSDUCTION

NOXIOUS STIMULI TRANSLATED INTO ELECTRICAL FIRING AT THE SENSORY NERVE ENDINGS

TRANSMISSION

1. PROPAGATION OF IMPULSE TRAVELS VIA NEURAL PATHWAYS.

2. SENSORY AFFERENT NEURONS PROJECT INTO THE SPINAL CORD

3. ASCENDING NEURONS RELAY TO BRAINSTEM AND THALAMUS

4. THALAMUS RELAYS TO CEREBRAL CORTEX

MODULATION

INTRINIC PAIN MODIFICATION 1.DIFFERENT IN INDIVIDUALS 2.DEPENDS ON..... PAST EXPERIENCES CULTURE PSYCHIC

MODULATION-CONT

1. STIMULUS PRODUCED ANALGESIA2. NEUROENDOCRINE ANALGESIA3. CNS/PNS ANALGESIA 4. OPIOID ANALGESIA5. SITUATION6. PATHOLOGY7. PHYSIOLOGY

Modulation – Excitatory Substances1. Peripheral

Prostaglandins, bradykinins, histamine, K, substance P, serotonin (5HT2)

2. SpinalGlutamate, aspartate, amino acids, substance

P, norepinephrine (alpha 1)

Modulation - Inhibitory

Supraspinal – Endorphins, enkephalins, dynorphins,

norepinephrine (alpha 2), GABA, somatostatin (5HT1), neurotensin

First Neuron Pain

Peripheral afferent fibers to dorsal horn

Second Neuron PainDorsal horn to thalamic

Third Neuron PainThalamus to cortex

Pain Pathways:• Tissue damage>>>Algesic substanses

release>>>Noxious stimuli>>>A delta and C fibers>>>to the Neuraxis>>>Many to Ant. and Anterolat.Horns>>>Segmenal reflex responses , and others via the Spinothalamic and Spinoreticular tracts>>>Suprasegmental and cortical responses.

Classification & Function of Peripheral Nerve Fibers

A. Myelinated A- Fibers:• : Motor , Proprioception (afferent)• Motor, Touch (afferent)• Muscle spindles (efferent)• Pain, Temperature (afferent)

B. Myelinated B-Fibers:• Pre-ganglionic Sympathetic Fibers

C. Non-Myelinated C- Fibers: Pain, Temperature.

Nociceptive pathways: peripheral

sensory nerves

Dorsal Root Ganglion

Blood vessels

Skeletal muscle

Muscle and skin receptors

Tendon bundle

Peripheral nerve Sympathetic ganglion

Viscera

Spinothalamic tract

Dorsal horn of spinal cord

Nociceptive terminals

C and A fibres

Nociceptive sensory fibres are C-fibres and A fibresC-fibres umyelinatedA myelinatedSlow conduction velocitySignal variety of noxious stimuli - polymodal

Spinal cord

Medulla oblongata

Mesencephalon

Thalamus

Cortex

Ascending Pain Pathways

Pons

Topographic representation maintainedSites for pain modulation are spinal cord and thalamus

• Segmental reflex responses:

Increased skeletal muscle tone , Increased oxygen consumption , Lactic acid production

• Suprasegmental

• reflex responses:

Increased Sympathetic tone , Hypothalamic stimulation.

Chemical MediatorsMembrane ion channels of Nociceptive neurons

Directly coupling to membrane receptors• Hydrogen• ATP• Serotonin• 5HT3

Indirectly (more commonly) mediating intracellular secondary messages

• Bradykinins B1, B2

• Cytokines• Prostanoids• Histamine H1

• Serotonin• 5HT1

Factors that modify perioperative pain :

• 1- Site ,nature and duration of surgery.• 2- Type and extent of incision.• 3- Physiologic and psychologic makeup of the

patient.• 4- Pre operative preparation of the patient.• 5- Presence of complications of surgery.• 6- Anesthetic management.• 7- Quality of perioperative care.• 8- Preoperative treatment of painful stimuli .

Preemptive Analgesia :

• Antinociceptive treatment of that prevents the establishment of altered central prossesing, which amplifies postop. Pain.

• Windup:functional changes in the dorsal horn because of pain .

• This type of therapy ,in addition to reducing acute pain ,attenuates chronic postop. Pain.

Principles of Pain Management

Anticipate painRecognize patient:

• Ask the patient• Look for signs (HR, BP, facial grimacing, tears, sweating, etc)

• Find the sourceQuantify pain (mild, moderate, severe)

Treat:• Quantify the patients perception of pain

• Correct the cause where possible• Give appropriate analgesics regularly as required

Remember most sedative agents do not provide analgesiaReassess

Modalities of Pain Relief Non-opioid analgesics+opioid analgesics

Regular injections of opioids Continuous IV or SC infusion of opioids

Patient controlled analgesia (PCA) Extradural opioids & or local anesthetics Combined exrtadural + spinal analgesia

Long acting oral opioids Long acting regional blocks

Ketamine (S+)

Modalities of Pain Relief

Pharmacological Non-pharmacological

DRUGSNSAID’s

COX-1 Minor – Moderate pain COX-2 rofecoxib, parecoxib-inj Severe pain

Actions:Inhibit synthesis of PG-E

Direct analgesic effect on higher centersModify nociceptive responses-bradykinins

AntiplateletHypothrombinaemia

Lowers body temp Hypoglycemia Metabolic acidosis

Adverse gastrointestinal effects

Lower doses only

Systemic Opioids :Analgesic effects of opioids : via receptors in the

CNS.Roots of administeration :I.M. ,I.V. ,Transdermal

,Oral ,Topical ,I.V. regional ,Perineural ,etc.I.M. root is the most treatment choice after

surgery.The” As Needed” part of the order is often

interpreted to mean “As little as possible” .No relation exists between Gender and opioid

requirement.

Analgesic Opiates

• Morphine• Pethidine• Fentanyl• Sufentanil• Alfentanil• Remifentani• ANTIDOTE : Naloxone

Routes of administration of analgesics

Oral IntravenousSublingual/buccal Epidural (opioid)

Oral transmucosal Intrathecal (opiod)Intranasal Intra articular (opioid)

Transdermal Topical - EMLA creamRectal Intradermal

Inhalational Peripheral N blockSubcutaneous Nerve plexus block

Intramuscular Intravenous regional

Modalities of Pain Relief

Non-pharmacological• Transcut. Electrostimulation

• Cryoanalgesia(obselete)

• Acupuncture

• Hypnosis

New Modalities Of Systemic Drug Administration

The goals of new methods are:1. Precise,controlled delivery of the prescribed

dose2. A rapid onset of action 3. Avoidance of first-pass hepatic metabolism 4. Maintenance of a steady-state concentration

of drug5. An improved side-effect profile and 6. Improved patient compliance

Transdermal Route Advantages

1. Decreased first-pass hepatic metabolism

2. Decreased gastrointestinal degradation

3. Stable plasma concentrations,and

4. Improved patient compliance

Treatment methods :• 1-Systemic opiods. • 2-Patient-controlled analgesia.• 3-Regional anesthetic techniques .• . a : Intraspinal analgesia.• b :Patient-controlled epidural analgesia.• c :Combined spinal-epidural technique.

• 4-intraarticular analgesia.• 5-Nonopioid analgesics.• 6-Cryoanalgesia.• 7-T.E.N.S.• 8-Psychologic and other methods.

Patient-Controlled Analgesia:

PCA was originally developed to minimize the effects of pharmacokinetic and

Pharmacodynamic variability among patients.A negative feedback loop exists: experiencing

pain>>>Medication demanded>>>Reducing pain >>>No further demand .

• If Nurses, Relatives,or Parents assume responsibility for drug administration,or if using this device by the patient is for reasons other than pain relief ,this loop fails.

• Cases of respiratory depression during PCA use have been reported.

• Causes :advanced age, hypovolemia, large doses, use of background continuous-infusion mode.

• No difference in respiratory mechanics between PCA and IM opioids (FEV1,FRC,PFR)is seen.

Side effects of PCA:

• Nausea ,Vomiting ,Itching.

• Treated by changing opioid or using drugs that provide symptomatic relief.

• A pre printed set of standard orders can facilitate a uniform standard of care.

Regional Anesthetic Techniques:

• Advantages:

• Positive respiratory, cardiovascular and neuroendocrine effects; reduced thromboembolic complications and blood loss; and reduced convalescence

IDEAL COMPONENTS

1. Block SENSORY feeling2. Immobilize MOTOR responses3. Obtund REFLEXES4. wipe out MEMORY5. Control VC and CTZ6. Not permanent7. Cause sense of well-being

REGIONAL ANESTHESIA

SEGMENTAL LOSS OF SENSATIONBY BLOCKING NERVE CONDUCTION

REGIONAL

1. SPINAL2. EPIDURAL4. INTRAVENOUS ( BIER )5. AXILLARY (INFILTRATION)6. RETROBULBAR

LOCAL ANESTHETICS

AMIDES MAX / DOSE• BUPIVACAINE 2 MG/KG• LIDOCAINE 7 MG/KG • ROPIVACAINE 4 MG/KG• MEPIVACAINE 7 MG/KG• PRILOCAINE 6MG/KG

LOCAL ANESTHETICS

ESTERS MAX /DOSE CHLOROPROCAINE 20 MG/KG COCAINE 3 MG/KG NOVOCAINE 12 MG/KG TETRACAINE 3 MG/KG

LOCAL ANESTHETICSLocal anesthetics are

the drugs, which reversibly block the generation, propagation and oscillations of electrical impulses in the excitable tissues.

MECHENISM OF ACTION

• Block nerve fiber conduction by acting directly on nerve membranes to inhibit sodium ion from crossing the membrane– Nerves cannot depolarize– Conduction of impulses is blocked

Mechanism of Action

• Decrease or prevent transient increase in the permeability of excitable membranes to Na+ ions

• Direct interaction with voltage gated Na+

channels• Increase in threshold• Decrease in the rate of rise of A.P. • Slows down the conduction

Mechanism of Action

• Site of action - Inside the membrane• Binding sites within the Na+ channel• Heterotrimeric complexes of glycosylated

proteins ( 300 k Da)• 3 sub units- 1& 2

• has I- IV homologous domains• Each domain has 6 transmembrane domains• Bind with S6 transmembrane domain.

CONTRAINDICATIONSCONTRAINDICATIONS

RELATIVERELATIVE

–Patient AppropriatenessPatient Appropriateness

–Local Infection near injection siteLocal Infection near injection site

–HypovolemiaHypovolemia

–CNS DiseaseCNS Disease

–Chronic Back Pain or Prior LamiChronic Back Pain or Prior Lami

–Prior SAB with difficultyPrior SAB with difficulty

Nerve Fiber and Local Anesthetic Setup

Sequence of clinical anesthesia

1. Sympathetic block (vasodilate & skin T0)

2. Loss of pain and temperature sensation

3. Loss of proprioception

4. Loss of touch and pressure sensation

5. Loss of motor function

Interscalene brachial plexus blocks :analgesia for 12-24 hrs.

Sciatic and Femoral n. blocks :similar results.Intercostal n. blocks : 6-12 hrs. analgesia.Administration of long acting L.A.s from a

catheter into pleural cavity :unilat. Analgesia with little or no sensory block.

L.A. infusion into Axillary sheath, Femoral sheath, and the vicinity of the Sciatic n.:analgesia and particularly useful to facilitate perfusion after extensive revascularization.

Interscalene

L.A. boluses or infusions :

• Advantages over parenteral opioids:• Early ambulation, improve bowel function,

higher arterial O2 tension, fewer pulmonary complications.

• For optimal results, the catheter tip should be near the segments innervating the insicision.

PLUXES BLOCK

BRACHEAL PLUXEX BLOCK

Segmental Level of Block Segmental Level of Block RequiredRequired

T-4 to T-6T-4 to T-6

IntraAbdominalIntraAbdominalT-6 to T-8T-6 to T-8

GU, Low GU, Low AbdominalAbdominal

T-8 to T-10T-8 to T-10

GU, A/R, LegsGU, A/R, Legs

T-4

T-6

T-10

IVRA (BIER’S BLOCK)

SPINAL ANESTHESIA

Intraspinal analgesia:

With:

• Opioids

• Opioid-L.A. mixture

• Ketamine

• Clonidine

• Neostigmine

Opioids:

• Initial reports in 1979.

• Single injection of intrathecal Morphin provides about 24 hrs. analgesia.

• Epidural root uses more, because:

• Popularity of technique during surgery, ability to leave catheter in place, familiarity with technique, no risk of PDPH.

• Elderly patients require remarkably small doses of epidural morphine.

• Fentanyl is useful when rapid onset of epidural analgesia is important.

• Epidural meperidine is widely used in some parts of the world and as with other opioids, respiratory depression can occure.

Respiratory depression

• early:• In the first two

hrs.

• Is the result of vascular uptake and redistribution.

• Delayed:• Between 6 and 12

hrs. • Consequent of rostral

spread of opioid in CSF to respiratory center in the floor of 4th. Ventricle.

• Pruritus is a common side effect and is seen more in obstetrics patients.

• Face is a common site of itching.

• Although it is not due to histamine release, antihistamines provide symptom relief.

• Nalbuphine is also of value.

• Naloxone is consistently effective (repeated doses or infusion).

• Urinary retention is higher in volunteers than in patients and in men than in women.

• Naloxone prevents or reverses it but may require doses that antagonizes analgesia.

• Most patients are able to void spontaneously when the catheters are removed.

• Nausea and vomiting: due to rostral spread of opioid in CSF to the vomiting center and the CTZ .

• Treatment:

• first line: antiemetics (may produce unwanted sedation and resp. depression ) , Scopolamine patches.

• Second line: I.V. droperidol, Ondansetrone.

• Sedation produced by intraspinal opioids may be the result of spread of the drug in CSF to receptors in the thalamus, limbic system or cortex and hypercarbia can augment it.

• Epidural buprenorphine 0.15 mg. produces prolonged depression of the CO2 response that lasts 8-12 hrs.

Ketamine:• Produces analgesia via interaction with

cholinergic, adrenergic, and serotonergic systems.

• Side effects: sedation, blurred vision, tachycardia, hypertension, and hallucinations.

• In some studies on baboons : neurotoxic changes.

• The routine use of intrathecal ketamine in humans is not recommended.

Clonidine:

• If administered by the oral route can augment spinally mediated opioid analgesia.

• Epidural or intrathecal clonidine can provide effective analgesia alone.

• Intrathecal clonidine does not provide surgical anesthesia.

Intra-Articular analgesia

• Following arthroscopic surgery, a combination of systemic Ketorolac and intra-articular bupivacaine decreased analgesic requirement and pain.

Nitrous oxide:

• Useful, especially for painful experiences of short duration (dressing changes, debridements).

• Rapid onset of analgesia and rapid recovery.• In concentrations of 30-50% is as potent as 10 mg.

I.M. morphine.• “Anesthesia” may occur>>>risk of aspiration.

• Long term administration: causes bone marrow suppression and leukopenia (reversible when detected early).

• Entonox:50%mixture of N2O with oxygen.

Cryoanalgesia:

• Temp.s between -5 and -20`causes disintegration of axons and breakdown of myelin sheaths while the perinurium and epinurium remain intact.

• Is used most common for thoracotomy pain and hernia repair pain.

• Residual neuropathic pain has been seen following cryoanalgesia.

Transcutaneous electrical nerve stimulation(T.E.N.S.)

• Uses both for chronic pain and acute perioperative pain.

• Advantages: absence of opioids side effects (resp. depression, sedation, nausea and vomiting, urinary retention)

• It is simple, noninvasive and free of toxicity.

• The mechanism of analgesia by TENS is not known and it may be by:

• Modulation of nociceptive impulses in the spinal cord (gate control theory).

• Activation of inhibitory area in the brain stem.

• Stimulation of the release of endorphins, or a combination of these mechanisms.

• A placebo effect may play a role.

Psychologic and other methods:

• After surgery patients may suffer ”discomfort” due to headache, NG tubes, drains, IV catheters, or anxiety, fear, and insomnia.

• Therapy of these problems may result in reporting of less “pain”.

• Preoperative discussion, reassurance and provision information results in less anxiety, less opioid use and shorter hospital stay.

• Relaxation tapes prior to surgery results in less analgesic use and a smoother recovery.

Perioperative analgesia in special Perioperative analgesia in special

populationspopulations..

Pediatric patients:

• Misconceptions about pain in children are common (e.g. children don’t feel pain, or if it is felt it is not remembered.

• Pain causes suffering and psychologic abnormalities in children of all age.

• Special scales are available for young children (self reporting of pain).

• In preverbal children, the interpretation of behavior must be used to estimate intensity of pain.

• Because of fear of IM injections alternatives are: sublingual, rectal and transdermal routs.

• I.V. PCA is effective in children.• Caudal opioid analgesia can be used in children.• Regional techniques: dorsal nerve block of the

penis, or lidocaine jelly, or EMLA creams for circumcision, ilioinguinal and iliohypogastric nerve blocks for pains after orchiopexy and herniorrhaphy, etc.

• NSAID,s are considered as adjuncts rather than as primary agents.

Elderly patients:

• The average age of surgical patients will increase in the future.

• Older patients have more complex cases than younger.

• PCA & PCEA is ineffective in some elderly patients because of their reluctance.

• Treatment of perioperative pain in elderly remains inadequate because:

• Fear of complications associated with treatment of pain.

• Pain is reported less in elderly.

• NSAID,s may have benefits in elderly because:

• Different site of action that may be more effective.

• Opioid sparing.• An additional anti-inflammatory effect.• But they have increased risk of side effects

because of decreased renal clearance>>>they doses must be decreased.

Advantages of regional anesthesia:

• Minimizing physiologic trespass.• Pharmacologic simplicity.• Reduced blood loss.• Fewer thromboembolic complications.• Reduced stress response.• Less confusion.• Less postoperative pain.

Patients with chronic pain and /or chronic opioid use

• General principles:• 1-expect high self-reported pain scores.• 2-base treatment decision on objective

pain assessment (deep breathing, coughing, etc.).

• 3-recognize and treat nonnociceptive sources of suffering.

• Continue opioids for as long as is appropriate for acute pain.

Addiction:

• A chronic disorder characterized by compulsive use of a substance resulting in physical, psychologic, or social harm to the user and continued use despite that harm.

Clinical triad suggestive of addiction:

• 1-high self-reported pain scores.• 2-high opioid use compared with other

patients having similar procedures.• 3-a relative absence of opioid-induced side

effects.

• PCA is not good for providing basal opioid replacement.

• PCA is good for extra opioids needed for postoperative pain.

ROLE OF THE ANESTHESIOLOGIST IN PERIOPERATIVE PAIN

MANAGEMENT

Anesthesiologists are a logical choice to provide periop. Pain relief, because they are:

1-familiar with the pharmacology of analgesics and L.A.s.

2-aware of short- and long-term effects of drugs given intraoperatively.

3-knowledgeable about pain pathways and their interruption.

4-are skilled in techniques available to provide superior pain control.

EPIDURAL ANESTHESIA

EPIDURAL DRUG ADMINISTRATION

FIXATION OF CATHETER

FINAL SKIN FIXATION AND DRESSING

LEST YOU FORGET

Discomfort from: • Full bladder/bowel/gasses

• Noise• Alarms• Visitors

• Painful IV site• Multiple lines

• Repeated disturbance from medical personnel

• Complications of analgesic drugs• Other pathological complications

Reference book and the Reference book and the relevant page numbers..relevant page numbers..

DrDr. .

Date: Date:

TThank You hank You