discussed the definition of acute pain

1. Radhwan Hazem Alkhashab
Consultant anesthesia & ICU
2020

2. • Acute pain has been defined as “the normal, predicted,
physiological response to an adverse chemical, thermal, or
mechanical stimulus.”
• Acute pain is self-limited discomfort that typically lasts from a
few moments to several weeks but less than 3 to 6 months.
Types of Acute Pain
• Acute pain can vary significantly and may be categorized into
two main types: spontaneous insult or trauma and elective or
planned procedures.

3. 1) Mildly painful spontaneous conditions include headache, upper
respiratory infection, or backache , and may be self-treated with
rest-ice-compression-elevation (RICE) therapy and over the
counter analgesics.
2) Moderately painful conditions include a sprained ankle, strained
ligament, deep laceration, or simple bone fracture. These may
require interventions such as minor outpatient surgery or
splinting, but are generally managed with nonsteroidal anti-
inflammatory drugs (NSAIDs), acetaminophen, and RICE.
3) Severely painful conditions include trauma such as a motor vehicle
accident, traumatic amputation, or burn, and will likely involve
surgery and a hospital stay. A stronger combination of analgesics,
including opioids, may be required.

4. 1) Office procedures, including immunizations, phlebotomy, or
catheter placement, tend to result in mild acute pain that is usually
eased with application of topical lidocaine/prilocaine (EMLA),
lidocaine, ice, or devices like a Buzzy, which combines the
application of ice and vibration.
2) Moderately painful procedures include same-day dental,
arthroscopic, laparoscopic, or podiatric surgeries. This type of pain
may be managed with simple analgesics, such as NSAIDs and
acetaminophen. At most, a total of 6 to 8 doses of an opioid and
acetaminophen combination might be needed if the patient’s
discomfort is not controlled with simple analgesics.
3) Severely painful procedures include surgeries requiring inpatient
stays, such as orthopedic joint replacement, spine surgery, or
colorectal surgery. These will require a combination of analgesics
and stronger opioids, possibly starting preoperatively

5. Acute pain
1) Comes on suddenly .
2) Caused by something
specific.
3) Sharp in quality.
4) Usually does not last
longer than six months.
5) Goes away when there is
no longer an underlying
cause for the pain.
Chronic pain
1. Chronic pain that is
ongoing and usually lasts
longer than six months.
2. Can continue even after
the injury or illness that
caused it has healed or
gone away.
3. Pain signals remain active
in the nervous system for
weeks, months, or years.

6. • Poorly managed acute pain that can produce pathophysiologic
processes in both the peripheral and central nervous systems
that have the potential to produce chronicity
• People who have chronic pain can have physical effects that
are stressful on the body. These include tense muscles, limited
ability to move around, a lack of energy, and appetite changes.
Emotional effects of chronic pain include depression, anger,
anxiety, and fear of re-injury. Such a fear might limit a person's
ability to return to their regular work.

7. Acute pain
• Surgery
• Broken bones
• Dental work
• Burns or cuts
• Labor and childbirth
Chronic pain
• Headache
• Arthritis
• Cancer
• Nerve pain
• Back pain
• Fibromyalgia pain

8. 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

9.  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 -first pain- sharp or stinging – well localized.
 Polymodal C fibers -“second pain- diffuse (associated with the
affective and motivational aspects of pain).

11. • 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

12. Descending modulatory neural pathways function to reduce pain perception:
• Efferent responses by inhibiting pain transmission in the dorsal horn,
periaqueductal gray (PAG) & brainstem
( PAG area can produce analgesia, demonstrated through electrophysiological
and pharmacological studies that descending influences on spinal nociceptive
processing involves the PAG and the rostral ventromedial medulla (RVM).
• 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
• The PAG is an enkephalinergic brainstem nucleus responsible for both
morphine and stimulation produced analgesia.

13. 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.

14.  Nociceptive afferets Fibres were
subjected to modulating influence of
GATE at the first synaptic contact in
the spinal cord.
Large fibers tend to close the GATE
(inhibits trans.) while small fibre
input opens it.
In other words A-beta fibre
stimulation activates interneurons in
dorsal horn that inhibits the
nociceptive transmission.

15. • 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

16. 1. Transduction- event whereby noxious thermal, chemical, or
mechanical stimuli are converted into an action potential
2. 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

17. 3. 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
4.Perception :
Perception of pain is the final common pathway, which results
from the integration of painful input into the somatosensory and
limbic cortices

18. N-methyl-D-aspartate

19. Tissue damage following surgical procedures leads to the
activation of small nociceptive nerve endings and local
inflammatory cells. This chemical milieu will both directly
produce pain transduction via nociceptor stimulation as well as
facilitate pain transduction by increasing the excitability of
nociceptors.
Peripheral sensitization of polymodal C fibers and high-threshold
mechanoreceptors by these chemicals leads to primary
hyperalgesia, which by definition is an exaggerated response to
pain at the site of injury.

22. 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.

23. 1. The NMDA (N-methyl-D-aspartate)
2. The AMPA (α-amino-3-hydroxy-5- methylisoxazole-4-
proprionic acid)
3. The kainate
4. The metabotropic

24. Surgical stress causes release of cytokines (e.g., IL-1, IL-6, and
TNF-α) precipitates adverse neuroendocrine and
sympathoadrenal responses, resulting in detrimental
physiological responses

25. • Catabolic hormones
1. Cortisol
2. Glucagon
3. Growth hormones
4. Catecholamines
Anabolic hormones
1. Insulin
2. Testosterone
•Hyperglycemia
•A negative nitrogen balance,
the consequences of
which include:
•Poor wound healing.
•Muscle wasting.
•Fatigue.
•Impaired immunocompetency

27. The goal of pre-emptive analgesia is to prevent NMDA receptor
activation in the dorsal horn, which 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

28. Three critical principles
1. The depth of analgesia must be adequate enough to block all
nociceptive input during surgery,
2. The analgesic technique must be extensive enough to include
the entire surgical field
3. The duration of analgesia must include both the surgical and
postsurgical periods.

30. 1.Visual analog score
2.Facial Grimaces

31. 1. Breakthrough: Pain that escalates above a persistent
background pain.
2. Transitory and Intermittent: Pain that is episodic in the
absence of background pain.
3. Background: Pain that is persistent but may vary over time.

32. DRUGS :
1. Opiods
2. Non opiods (NSAIDS)
3. NMDA receptor antagoinsts
4. Alpha-2 agonists
5. α 2-δ subunit calcium channel ligands
Invasive Procedures :
Neuroaxial blockade
Peripheral nerve blockade

33. Opioids are the mainstay for the treatment of acute
postoperative pain, and morphine is the “goldstandard.”
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

34. Common :
1. Sedation.
2. Nausea and vomiting.
3. Respiratory depression.
4. Constipation.
Less common
1. Confusion.
2. Urinary retention.
3. Dizziness.
4. Myoclonus.

35. 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 thwart OIH. evidence that coadministration of an
NMDA receptor antagonist can abolish opioid-induced
tolerance and OIH.

36. NSAIDs are among the most commonly used drugs anti-
inflammatory, analgesic, and antipyretic effects

37. Prostaglandin E2 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.

41. 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, wind-up and allodynia(Allodynia is a condition
where pain is caused by a stimulus that does not normally elicit pain. For
example, bad sunburn can cause temporary allodynia).
3. Opioid-induced tolerance.
4. Opioid induced hyperanalgesia.

42. 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.
Ideal intravenous PCA morphine-ketamine combination ratio is
1:1

43. 1. Does not have a direct analgesic affect; rather, analgesia is
likely mediated by its NMDA receptor antagonism.
2. It has been used for many years as an antitussive
3. It can be administered orally, intravenously, and
intramuscularly.
4. Inhibit secondary hyperalgesia following peripheral burn
injury .Preoperative administration of 150 mg of oral
dextromethorphan can reduce the PCA morphine
requirements

44. Clonidine and dexmedetomidine
It provide analgesia, sedation, and anxiolysis
The presynaptic activation of α2-receptors that results in the
decreased release of norepinephrine is believed to mediate
analgesia.
CLONIDINE :
• selective partial agonist for the α2-adrenoreceptor
• Analgesia is mediated supraspinally (locus coeruleus), spinally
(substantia gelatinosa), and peripherally also.
• Can be administered orally, transdermally, intravenously, and
neuraxially for perioperative pain management.

45. • 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 µg

46. Dexmedetomidine:
1. Highly selective α2-agonist
2. Does not interact with the GABA-mimetic system
3. Does not depress the respiratory drive.
4. Analgesic and anxiolysis.
5. The centrally mediated reduction in sympathetic tone is
reported to have a cardioprotective effect.
6. It is a useful adjunct to both opioid and nonopioid analgesics
as part of a multimodal analgesic protocol

47. loading dose of 1 µg/kg i.v over 10 minutes followed by an
infusion of 0.2 to 0.7 µg/kg/hr i.v
dexmedetomidine infusion (0.2 to 0.7 µg/kg/hr) combined with
peripheral nerve blockade may provide good 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

48. 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 be synergistic in attenuating the hyperalgesia
associated with peripheral inflammation.
Prevents the development of central excitability and is
antihyperalgesic.
Side effects - somnolence, dizziness, confusion, and ataxia

49. • Menthol, camphor, methyl salicylate, or a combination of
these counterirritants can be useful in managing localized
musculoskeletal injuries, particularly when they can be
massaged into the painful area. As long as the skin is intact,
these can offer short-term relief of muscle pain.

50. PCA is any technique of pain management that allows the
patients to administer their own analgesia on demand.
Five variables associated with all modes of PCA include:
1. Bolus dose.
2. Incremental (demand) dose.
3. Lockout interval.
4. Background infusion rate.
5. 1- and 4-hour limits.

52. 1. Pulmonary disease
2. Obstructive sleep apnea
3. Renal or hepatic dysfunction
4. Congestive heart failure
5. Closed head injury
6. Altered mental status
7. Lactating mothers

53. 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

54. Efficacy of an epidural technique is determined by numerous
factors
1. Catheter incision site.
2. Choice of analgesic drugs
3. Rates of infusion
4. Duration of epidural analgesia
5. Type of pain assessment .

55. Ideally, the epidural catheter is positioned with the surgical
incision.
Thoracic epidural catheter placement is recommended for both
thoracic and upper abdominal surgical procedures.
Because of
1. Improvement in coronary artery blood flow.
2. Attenuation of pulmonary complications.
3. The reduction in the duration of postoperative ileus.

56. 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.
Other than analgesia, epidural infusions lasting <24 hours do not
appear to offer any clear cardiovascular advantages.

57. Epidurally administered opioids have the distinct advantage of
producing analgesia without causing significant sympatholytic
effect or motor blockade.
Analgesia occurs by way of a spinal mechanism and through a
supraspinal mechanism following systemic adsorption.
Hydrophilic opioids tends to have a slow onset, long duration,
and a mechanism of action that is primarily spinal in nature.
Lipophilic opioids, on the other hand, have a quick onset, short
duration, and a mechanism of action that is primarily
supraspinal, secondary to rapid systemic uptake

58. 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

59. a) Brachial Plexus Blockade
b) The Lumbar Plexus
c) Psoas Compartment Block
d) Femoral nerve block
e) Sacral Plexus

61. Acute pain management in children undergoing surgery or
invasive procedures offers several specific and unique challenges
for the anesthesiologist.
1. Child's parents and siblings relative to their child's responses
to the operative environment.
2. Unavoidable preoperative fear and anxiety in the child.
3. Difficulties in evaluating pain and the effectiveness of
treatment.
4. The patient's reaction to pain, surgery, and the environment
manifest as active crying and screaming resistance to care

62. 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 absence.
6. Parent's reactions to the care.

63. The use of non opioid analgesics administered orally or by rectal
suppository are important adjuvant analgesic therapies.
Non parenteral 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.

64. 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

65. 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 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.

66. End of session
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