Acute pain & it’s management

Presenter- Dr Sudha
Moderator – Dr Mahadevaiah
Physiology of pain
• The nociceptive pathway is an afferent three-neuron dual ascending
(e.g., anterolateral and dorsal column & medial lemniscal pathways)
system, with descending modulation from the cortex, thalamus, and
brainstem
• Nociceptors are free nerve endings located in skin, muscle, bone, and
connective tissue with cell bodies located in the dorsal root ganglia
• First-order neurons - periphery as A delta & polymodal C fibres
• A delta fibers transmit “first pain”- sharp or
stinging - well localized.
• Polymodal C fibers transmit "second pain-
diffuse & is associated with the affective and
motivational aspects of pain.
• First-order neurons synapse on second-order
neurons in the dorsal horn primarily within
laminas I, II, and V, where they release excitatory
amino acids and neuropeptides.
• Axons of both nociceptive-specific
neurons ascend the spinal cord via the
dorsal column-medial lemniscus and the
anterior lateral spinothalamic tract to
synapse on third-order neurons in the
contralateral thalamus  Project to the
somatosensory cortex where nociceptive
input is perceived as pain
 Descending inhibitory pathway
• Descending modulatory neural pathways
function to reduce pain perception
• Efferent responses by inhibiting pain
transmission in the dorsal horn, PAG, brainstem,
rostroventromedial medulla(RVM)and other
regions of the CNS.
• The cerebral cortex, hypothalamus, thalamus,
PAG, nucleus raphe magnus(NRM), and locus
coeruleus (LC) all send descending axons that
synapse with and modulate pain transmission
• Components of the descending system that play critical roles in
modulating pain transmission
1. endogenous opioid system,
2. the descending noradrenergic system
3. serotonergic neurons
Elements of pain process

• Transduction- event where by noxious thermal, chemical, or

mechanical stimuli are converted into an action potential.

• Transmission-when the action potential is conducted through the

nervous system via the first,second &third-order neurons, which have
cell bodies located in the dorsal root ganglion, dorsal horn, and
thalamus
Modulation:
• Modulation of pain transmission involves altering afferent neural
transmission along the pain pathway.
• The dorsal horn of the spinal cord is the most common site for
modulation of the pain pathway.
• Modulation can involve either inhibition or augmentation of the pain
signals
Perception:
• Perception of pain is the final common pathway, which results from
the integration of painful input into the somatosensory and limbic
cortices
Neurotransmitters & receptors
• Three classes of transmitter compounds integral to pain transmission
include

1.The excitatory amino acids glutamate and aspartate

2. The excitatory neuropeptides substance P and neurokinin A
3. The inhibitory amino acids glycine and GABA.
The various receptors are

1. NMDA (N-methyl-D-aspartate)
2. AMPA (a-amino-3-hydroxy-5- methylisoxazole-4-proprionic acid)
3. Metabotropic
Gate control theory
• Ronald Melzack and Wall in 1965,suggested that nociceptive aff.
Fibres were subjected to modulating influence of GATE at the first
synaptic contact in the spinal cord.
• Large fibres tends to close the GATE ( inhibit transmission) , while
small fibres open the GATE.
• In otherwords A-beta fibre stimulation activates inhibitory neurons in
dorsal horn that inhibits the nociceptive transmission.
• Also descending pathways from cortex and midbrain, thermal and
tactile afferents profoundly influence the GATE.
• The large fibers are under cognitive control.
If they are active, they activate the
substantia gelatinosa (sg) in the spinal cord.
• If the sg is active, the activity of T-cells is
diminished.
• If the T-cells don't reach their activity
threshold, no pain is experienced.
• If small fibers are active first, sg is inhibited,
both fibers increase T-activity
Consequences of poorly managed acute pain
Assessment of acute pain
McGill pain questionnaires
• It is a checklist of words describing symptoms.
• Attempts to define the pain in 3 major dimensions
• .Sensory-discriminative
• Motivational-affective
• Cognitive-evaluative
• Contains 20 sets of words that are divided into 4 groups.
• 1- 10 sensory
• 5 affective.
• 1 evaluative.
• 4 miscellaneous.
Features of pain comply addressed during
assessment
• Onset of pain
• Pattern of pain
• Site of pain
• Radiation of pain
• Quality (character) of pain
• Intensity (severity) of pain
• Exacerbating factors (what makes the pain start or get worse?
• Relieving factors (what prevents the pain or makes it better?
• Response to analgesics (including attitudes and concerns about
opioids)
• Response to other interventions
• Associated physical symptoms
• Associated psychological symptoms
• Interference in daily routine
3 Classes of acute pain
• Breakthrough: Pain that escalates above a persistent background
pain.

• Transitory and Intermittant: Pain that is episodic in the absence of

background pain.

• Background: Pain that is persistent but may vary over time

Management of acute pain
DRUGS:
• Opiods
• Non opiods (NSAIDS)
• NMDA receptor antagoinsts
• Alpha-2 agonists
• Alpha 2 –delta subunit calcium channel ligands

Invasive Procedures :
• Neuraxial blockade – Epidural/ intrathecal
• Peripheral nerve blockade
• Transcutaneous Electrical Nerve Stimulation (TENS)
• Acupuncture
• Heat Application
• Cryoanalgesia
• Ultrasonic stim.
Opioids
• Opioids are the mainstay for the treatment of acute postoperative
pain, and morphine is the "gold- standard.“
• The three primary mechanisms of action for opioid analgesia at the
level of the spinal cord, include:

1. Inhibition of calcium influx presynaptically, which results in

depolarization of the cell membrane and decreased release of
neurotransmitters and neuropeptides into the synaptic cleft;
2.enhancing potassium efflux from the cell postsynaptically, which
results in hyperpolarization of the cell and a decrease in pain
transmission,

3. activation of a descending inhibitory pain circuit via inhibition of

GABAergic transmission
Common:
1. sedation,
2. nausea and vomiting,
3. respiratory depression,
4. constipation
Less common
1. confusion,
2. urinary retention,
3. dizziness,
4. myoclonus
Opioid induced hyperalgesia
• Relatively "rare phenomenon“
• patients who are receiving opioids, suddenly and paradoxically
become more sensitive to pain despite continued treatment with
opioids
• OIH is more likely to develop following high doses of phenanthrene
opioids such as morphine.Changing the opioid to a phenyl piperidine
derivative such as fentanyl may cause OIH.
• coadministration of an NMDA receptor antagonist can abolish opioid-
induced tolerance and OIH.
NSAIDS
• NSAIDs are among the most commonly used drugs
• It has anti-inflammatory, analgesic, and antipyretic effects
• Therapeutic benefit of NSAIDS is believed to be mediated through
the inhibition of cyclo- oxygenase (COX) enzymes, types 1 and 2,
which convert arachidonic acid to prostaglandins
• Prostaglandin E, is the key mediator of both peripheral and central
pain sensitization
• Peripherally, prostaglandins do not directly mediate pain; rather, they
contribute to hyperalgesia by sensitizing nociceptors
• Centrally, prostaglandins enhance pain transmission at the level of the
dorsal horn by
• increasing the release of substance P and glutamate from first-order
pain neurons,
• increasing the sensitivity of second-order pain neurons
• inhibiting the release of neurotransmitters from the descending pain-
modulating pathways
NMDA receptor antagoinsts
• Excitatory neurotransmitter stimulation of the NMDA receptor is
believed to be involved in the development and maintenance of
several phenomena
1. persistent postoperative pain,
2. hypersensitivity and allodynia,
3. opioid-induced tolerance,
4. Opioids induced hyperanalgesia

Ketamine & Dextromethorphan are commonly used

Ketamine :-
• Low-dose ketamine (0.25- to 0.5-mg intravenous bolus followed by an
infusion of 2 to 4 µg/kg/min) can provide significant analgesia and is
opioid- sparing
• Apart from NMDA receptor blockade, but in addition the drug
interacts with opioidergic, cholinergic, and monoaminergic receptors
and blocks sodium channels
• Ideal intravenous PCA morphine-ketamine combination ratio is 1:1
Dextromethorphan:
• Does not have a direct analgesic affect; rather, analgesia is likely
mediated by its NMDA receptor antagonism.
• It has been used for many years as an antitussive. It can be
administered orally, intravenously, and intramuscularly.
• Inhibit secondary hyperalgesia following peripheral burn injury and
cause a reduction in temporal summation of pain.
• Preoperative administration of 150 mg of oral dextromethorphan can
reduce the PCA morphine requirements
Alpha -2 adrenergic agonists

• Clonidine and dexmedetomidine

• It provide analgesia, sedation, and anxiolysis
• The presynaptic activation of a₂-receptors that results in the
decreased release of norepinephrine is believed to mediate analgesia
Clonidine
• selective partial agonist for the a2-adrenoreceptor
• Analgesia is mediated supraspinally (locus coeruleus), spinally
(substantia gelatinosa), and peripherally
• It can be administered orally, transdermally, intravenously, and
neuraxially for perioperative pain management.
• Premedication with 5 µg/kg of oral clonidine in patients decrease the
use of PCA morphine and decrease the incidence of postoperative
nausea and vomiting.
• Doses of 0.5 to 1 µg/kg may enhance the efficacy and increase the
duration of local anesthetics in peripheral nerve blockade.
• Side effects include sedation, hypotension, and bradycardia if the
dose exceeds 150 pg
Dexmedetomidine
• Highly selective a₂-agonist
• Does not interact with the GABA-mimetic system and therefore does
not depress the respiratory drive
• Analgesia, titratable sedation (e.g., “cooperative sedation”), and
anxiolysis
• The centrally mediated reduction in sympathetic tone is reported to
have a cardioprotective effect
• It is a useful adjunct to both opioid and nonopioid analgesics as part
of a multimodal analgesic protocol
• Loading dose of 1 µg/kg i.v over 10 minutes followed by an infusion of
0.2 to 0.7 mcg/kg/hr i.v
• Dexmedetomidine infusion (0.2 to 0.7 µg/kg/hr) combined with
peripheral nerve blockade may provide superb analgesia, anxiolysis,
and sedation during prolonged procedures
• Infusions as high as 5 to 10 µg/kg/hr have been reported for use as a
total intravenous anesthetic with favorable results.
• Side effects: bradycardia and hypotension, which can be treated with
atropine, ephedrine
Alpha 2 – delta Ca2+ channel ligands
• Gabapentin and pregabalin
• Effective analgesics not only for the treatment of neuropathic pain
syndromes but also for the treatment of postoperative pain.
• when these drugs are combined with an NSAID, the combination has
been shown to besynergistic in attenuating the
hyperalgesiaassociated with peripheral inflammation.
• prevents the development of central excitabilityand is
antihyperalgesic.
• Side effects - somnolence, dizziness, confusion and ataxia
Pre- emptive analgesia
• Analgesics given to patients prior to the onset of pain aiming to
prevent changes in the spinal cord that occur with repetitive painful
stimuli from the site of injury
• Benefits were shown only in animal studies but not in clinical human
studies - long term benefits may occur
• The goal of pre-emptive analgesia is to prevent NMDA receptor
activation in the dorsal horn.
• It causes wind-up, facilitation, central sensitization expansion of
receptive fields, and long-term potentiation, all of which can lead to a
chronic pain.
• "WIND UP Phenomenon"-results from repetitive C-fiber stimulation
of neurons in the dorsal horn leads to central plasticity
Patient controlled analgesia
• PCA is any technique of pain management that allows the patients to
administer their ownanalgesia on demand.
• Five variables associated with all modes of PCAinclude:
1. bolus dose,
2. Incremental (demand) dose,
3. Lockout interval,
4. Background infusion rate
5. 1- and 4-hour limits
Neuraxial analgesia
• Epidural analgesia is a critical component of
multimodal perioperative pain management
and improved patient outcome.

• Meta-analysis the efficacy of epidural

analgesia found epidural analgesia to be
superior to systemically administered opioids
• Efficacy of epidural technique is determined by numerous factors such
as
• catheter incision site congruency
• choice of analgesic drugs
• rates of infusion
• duration of epidural analgesia
• type of pain assessment (Rest vs Dynamic)
• Combining a local anesthetic plus an opioid in the epidural space is
believed to have a synergistic effect.
• Recommendations are that the infusion be continued for at least 2 to
4 days
Drugs in common use
• Local Anesthetics:
• Xylocaine: 2-0.5%
• Bupivacaine (Marcaine): 0.5, 0.25, 0.125, 0.1, 0.625 %
• Ropivacaine Hcl (Naropin): 0.75, 0.2%
• Opiates:
• Morphine: 2-4 mg
• Fentanyl : 50-200 m
• Others: As Clonidine, NSAID, Neostigmine, Ketamine,...
Peripheral nerve blockade
• Single injection peripheral nerve blockade has been shown to provide
pain control that is superior to opioids with fewer side effects
• continuous peripheral nerve block (CPNB) techniques can extend the
benefits of peripheral nerve blockade well into the postoperative
period
• CPNB has proven to be an effective technique for postoperative pain
management it is superior to opioid analgesia with fewer opioid
related side effects and rare neurologic and infectious complications
• CPNB in the ambulatory setting include prolonged postoperative
analgesia, facilitated discharge from the hospital, fewer opioid-related
side effects, and greater patient satisfaction
• Blocks commonly used are
• Brachial plexus block
• Lumbar plexus
• Femoral N.block
• Sciatic N. Block
• Popliteal n. Block
Risk factors For nerve injury
Patient :-
• Body habitus
• Pre-existing neurologic disorder (e.g., diabetes mellitus or patients
who have received chemotherapy in the recent past)
• Male gender
• Advanced age
SURGICAL :-
• Direct surgical trauma or stretch
• Prolonged tourniquet time
• Hematoma
• Infection
• Tightly applied casts or surgical dressings
• Patient positioning
ANASTHESIA :-
• Mechanical injury from the needle or catheter
• Chemical neurotoxicity from the local anesthetic
• Ischemic injury to the nerve
TENS
What is transcutaneous electrical nerve
stimulation (TENS) therapy?
• Transcutaneous electrical nerve stimulation
(TENS) is a therapy that uses low voltage electrical
current to provide pain relief.
• A TENS unit consists of a battery-powered device
that delivers electrical impulses through
electrodes placed on the surface of your skin. The
electrodes are placed at or near nerves where the
pain is located or at trigger points.
How does TENS work?

• There are two theories about how transcutaneous electrical nerve

stimulation (TENS) works.
• One theory is that the electric current stimulates nerve cells that
block the transmission of pain signals, modifying your perception of
pain.
• The other theory is that nerve stimulation raises the level of
endorphins, which are the body’s natural pain-killing chemical. The
endorphins then block the perception of pain.
Indications
• TENS therapy has been used or is being studied to relieve both
chronic (long lasting) and acute (short-term) pain. Some of the
most common conditions for which TENS has been used include:
• Osteoarthritis (disease of the joints).
• Fibromyalgia (aching and pain in muscles, tendons, and joints all
over the body, especially along the spine.
• Tendinitis (an inflammation or irritation of a tendon).
• Labor pain.
• Low back pain.
• Chronic pelvic pain.
• Diabetes-related neuropathy (damage to the nerves that connect
the brain and spinal cord to the rest of the body).
• Peripheral artery disease (“hardening of the arteries” that circulate
blood to the body).
Contraindications
• An implantable device (cardioverter/defibrillator, neurostimulators,
bone growth stimulator, indwelling blood pressure monitors). Do
not use TENS therapy over or close to the areas where an electronic
device is implanted. TENS could cause these devices to malfunction.
• Are pregnant. Do not apply TENS therapy to the abdomen; pelvic
area; lower back; or to acupuncture points at the knee, hand or
ankle. (However, TENS can be used for labor pain.)
• Cancer. Do not apply electrodes to areas of the body where there is
known or suspected cancer. Do not use TENS if you have
undiagnosed pain and a history of cancer in the last 5 years.
• Epilepsy. Do not apply electrodes to your head, neck or shoulders.
The impulses could cause seizures.
• Deep vein thrombosis or thrombophlebitis. Do not use TENS
therapy as it may increase blood circulation, which may increase the
risk of dislodging a blood clot.
• A bleeding (hemorrhagic) disorder or recent or actively bleeding
tissue. TENS therapy could increase bleeding at the tissue site or
increase the risk of bleeding in persons with bleeding disorders.
• Heart disease. Do not apply TENS therapy to the chest if you have
heart disease, heart failure or arrhythmias.
What are the parts of TENS device and how do
they work?

• The battery-powered TENS device is about the

size of a small cell phone.
• The device comes with several sets of electrode
wires and end pads. The electrodes connect to
the device at one end and are attached to
about 2 inch by 2 inch pads at the other end.
• Each pad has an adhesive backing and is
positioned on your skin in specific areas along
nerve pathways in the area to be treated.
• The device delivers pulses of electrical energy. Pulses can be
adjusted for intensity, frequency, duration, and type (burst or
continuous)
Advantages of TENS
• TENS is a non-invasive method of pain relief.
• It can be used alone or in addition to prescriptions or over-the-
counter pain-relieving medications.
• The amount of medication may be able to be reduced in some
patients who use TENS therapy.
• Another benefit of the TENS unit is that it is small and portable and
therefore can be used at home or away, anytime pain relief is
needed.
Disadvantages
• TENS therapy has few reported side effects.
• In rare cases, patients have reported burns at the sites where the
electrodes are placed.
• Some patients may be allergic to the adhesive used to affix the pad
to the skin or the materials in the pad itself (the skin may appear
red, irritated, or a rash may break out).
• Some people may be sensitive to or feel uncomfortable with the
prickling/tingling sensation generated by the TENS unit.
Interferential current therapy
• It is one of the types of electrotherapy used for the management of
pain.
• The principle of interferential therapy is to cause two medium-
frequency currents of slightly different frequencies to interfere with
one another
• This helps in Modulation of pain
Indications
• Pain Relief in conditions such as causalgia, herpes zoster, and
neuralgia.
• Cervical spondylosis.
• Osteoarthritis of the knee.
• Ankylosing spondylitis
• Rheumatoid arthritis.
• Frozen shoulder.
• Disc herniation.
• Spinal canal stenosis.
• Muscle Stimulation - prevent muscle wastage, re-education, maintain
range of motion stress incontinence
• Reduction of Edema (Condition involving the excess collection of
watery fluid in the cavities or tissues)
• Muscle injuries
• Ligamentous injuries
Effects of interferential therapy

• Reduces pain and inflammation.

• Increases blood circulation.
• Causes vasodilation.
• Removes waste substances from the affected area.
• Increases metabolic rate.
• Decreases blood pressure
• Treats chronic ligamentous lesions.
• Cures edema and hematoma.
• Improves restricted movements of joints.
• Increases muscle stimulation.
• Restores the lost movement of muscles.
Contraindications
• Infective condition
• Malignancy.
• Pacemakers.
• Loss of sensation.
• Danger of Hemorrhage
• Large open wounds.
• Dermatological Conditions.
• Arterial disease.
• Febrile condition.
• Deep vein thrombosis.
• During menstruation.
• Unreliable patient
Perioperative pain management of Children
• Acute pain management in children undergoing surgery or invasive
procedures offers several specific and unique challenges for the
anesthesiologist.
• child's parents and siblings relative to their child's responses to the
operative environment.
• unavoidable preoperative fear and anxiety in the child.
• developmental and communication issues.
• difficulties in evaluating pain and the effectivenessof treatment.
• the patient's reaction to pain, surgery, and the environment manifest
as active crying and screaming ,resistant to care.
A child's responses to pain may be variable and unpredictable because
of the
1. age and development,
2. verbal communication skills,
3. fear and anxiety,
4. prior experiences,
5. parental presence or absence6. parent's reactions to the care
Non opioid analgesics
• The use of nonopioid analgesics administered orally or by rectal
suppository are important adjuvant analgesic therapies.
• Nonparenteral administration of acetaminophen either by oral
administration (10 to 20 mg/kg) often given with oral midazolam (0.5
mg/kg) as a component of preoperative sedation or by rectal
suppository (20 to 40 mg/kg) after induction of anesthesia provides
excellent supplemental analgesia.
Opioid analgesics
• The atypical opioid tramadol (3 mg/kg) has also been used as an oral
preparation, usually in combination with midazolam (0.5 mg/kg) prior
to the induction of anesthesia in children.

• Intranasal sufentanil (0.2 µg/k) can also be used to manage

preoperative anxiety and postoperative analgesia in children and may
be more effective than oral tramadol
• epidural neuraxial analgesia either as a single-shot technique or
continuous catheter technique has become a key component of the
perioperative pain management.
• use of a single-shot "kiddy" caudal using a local anesthetic with
morphine is effective in relieving pain associated with minor
procedures in the outpatient setting
• there is serious risk associated with epidural analgesia in children
related to the systemic toxicity of the local anesthetic and the need to
place the catheter correctly.
• Thank you