Anesthesia

Lecture Title: Acute Pain Management









Lecturer name: Osama Ibraheim

MD,SOB.

Lecture date:

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. HEAT

2. COLD

3. CHEMICAL

4. MECHANICAL

TORSION STRETCH CUT PINCH PRICK

COMPRESS CRUSH

TYPOLOGY OF PAIN



1. Acute

2. Chronic benign

3. 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. Cardiovascular 1. Extremities

2. Pulmonary 2. Endocrine

3. Gastrointestinal 3. CNS

4. Renal 4. Immunologic

Adverse Effects of Pain

Cardiovascular: 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 Pain

Extremities: 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 POTASSIUM

HISTAMINE ACETLYCHOLINE

BRADYKININS LEUKOTRIENES

PROSTAGLANDINS 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 FIBER

PAIN CLASSIFICATION

A FIBER……..SHARP-STABBING-LOCAL

“ FIRST PAIN”



B FIBER....PHYSIOLOGIAL REACTION



C FIBER....DULL-ACHE-BURN-THROB

NONLOCALIZED-RADIATE

“SECOND PAIN”

NERVE FIBER CLASSIFCATION

TYPE 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 Delta

1. 1 - 4 micrometers diameter

2. Myelinated, Rapid conduction

3. Sharp, localized

4. Heat, cold

5. “First pain”

B myelinated

preganglionic autonomic



C non-myelinated

pain-temperature

C Fibers



1. Small

2. Slow Conduction

3. Unmyelinated

4. Postganglionic autonomic

C Fibers

1. Dull pain, burning, Aching throbbing

2. Nonlocalized - radiating - diffused

3. Temperature,Touch,Mechanical

4. “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 membranes

2. Periosteum

3. Deep fascia

4. Ligaments

5. Joint capsules

6. Cornea

7. Subcutaneous tissue

Areas of Moderate Nociceptor

Concentration

1. Skeletal muscle

2. Cardiac muscle

3. Smooth muscle

Areas of Minimal Nociceptor

Concentration

1. Bone

2. Cartilage

3. Marrow

Physiologic Processes of

Nociception

1. Detection

2. Transduction

3. Transmission

4. Modulation

5. 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 ANALGESIA

2. NEUROENDOCRINE ANALGESIA

3. CNS/PNS ANALGESIA

4. OPIOID ANALGESIA

5. SITUATION

6. PATHOLOGY

7. PHYSIOLOGY

Modulation – Excitatory Substances

1. Peripheral

Prostaglandins, bradykinins, histamine, K,

substance P, serotonin (5HT2)

2. Spinal

Glutamate, 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 Pain

Dorsal horn to thalamic

Third Neuron Pain

Thalamus 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:

• a: Motor , Proprioception (afferent)

• b: Motor, Touch (afferent)

• g: Muscle spindles (efferent)

• d: Pain, Temperature (afferent)



B. Myelinated B-Fibers:

• Pre-ganglionic Sympathetic Fibers



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

Nociceptive pathways: peripheral

sensory nerves

Dorsal horn of Spinothalamic

spinal cord tract Nociceptive

Dorsal Root sensory fibres are

Ganglion C-fibres and Ad

fibres

Peripheral

nerve Sympathetic ganglion C-fibres

Viscera umyelinated

Ad myelinated

Slow conduction

Blood vessels velocity

Skeletal Signal variety of

Tendon muscle

bundle

noxious stimuli -

C and Ad polymodal

Muscle and skin Nociceptive fibres

receptors terminals

Ascending Pain Pathways

Cortex

Topographic

representation

Thalamus maintained

Sites for pain

modulation are

Mesencephalon

spinal cord and

Pons thalamus





Medulla

oblongata





Spinal

cord

• Segmental reflex • Suprasegmental

responses: • reflex responses:



Increased skeletal muscle Increased Sympathetic

tone , Increased oxygen tone , Hypothalamic

consumption , Lactic acid stimulation.

production

Chemical Mediators

Membrane 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 pain

Recognize patient:

• Askthe patient

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

• Find the source

Quantify 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 analgesia

Reassess

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

DRUGS

NSAID’s

COX-1 Minor – Moderate pain

COX-2 rofecoxib, parecoxib-inj Severe pain

Actions:

Inhibit synthesis of PG-E

Direct analgesic effect on higher centers

Modify nociceptive responses-bradykinins

Antiplatelet

Hypothrombinaemia

Lowers body temp

Hypoglycemia

Lower doses

only

Metabolic acidosis

Adverse gastrointestinal effects

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 Intravenous

Sublingual/buccal Epidural (opioid)

Oral transmucosal Intrathecal (opiod)

Intranasal Intra articular (opioid)

Transdermal Topical - EMLA cream

Rectal Intradermal

Inhalational Peripheral N block

Subcutaneous 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

dose

2. A rapid onset of action

3. Avoidance of first-pass hepatic metabolism

4. Maintenance of a steady-state concentration

of drug

5. 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 feeling

2. Immobilize MOTOR responses

3. Obtund REFLEXES

4. wipe out MEMORY

5. Control VC and CTZ

6. Not permanent

7. Cause sense of well-being

REGIONAL ANESTHESIA

SEGMENTAL LOSS OF SENSATION

BY BLOCKING NERVE CONDUCTION

REGIONAL

1. SPINAL

2. EPIDURAL

4. 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 ANESTHETICS

Local 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- a, b1& b 2

• a has I- IV homologous domains

• Each domain has 6 transmembrane domains

• Bind with S6 transmembrane domain.

CONTRAINDICATIONS

 RELATIVE

–Patient Appropriateness

–Local Infection near injection site

–Hypovolemia

–CNS Disease

–Chronic Back Pain or Prior Lami

–Prior 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.

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

Required



T-4 to T-6

T-4

IntraAbdominal

T-6

T-6 to T-8

T-10

GU, Low

Abdominal

T-8 to T-10

GU, A/R, Legs

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: • Delayed:

• Between 6 and 12

• In the first two hrs.

hrs. • Consequent of

• Is the result of rostral spread of

vascular uptake opioid in CSF to

respiratory center in

and the floor of 4th.

redistribution. 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



populations .

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

relevant page numbers..

Thank You 

Dr.



Date: