1. Presentor :Dr.Kumar Moderator : Dr.Vamsidhar Acute pain
management
2. Acute pain Definition: Acute pain has been defined as the
normal, predicted, physiological response to an adverse chemical,
thermal, or mechanical stimulus.
3. poorly managed acute pain that can produce pathophysiologic
processes in both the peripheral and central nervous systems that
have the potential to produce chronicity Acute pain-induced change
in the central nervous system is known as neuronal plasticity. This
can result in sensitization of the nervous system resulting in
allodynia and hyperalgesia.
4. Anatomy of acute 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
5. Ascending pathway 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.)
6. classification aA/A/C is the Erlanger-Gasser classification
and refers to axon size II/III/IV is the Lloyd-Hunt classification
and is defined on conduction velocity in muscle afferents
7. 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
nociceptive-specific lamina I- noxious stimuli-
sensory-discriminative aspects of pain wide dynamic-range (WDR)
neurons-laminae IV, V, and VI -nonnoxious and noxious input -
affective-motivational component of pain
8. Axons of both nociceptive-specific and WDR neurons the
dorsal column-medial lemniscus and the anterior lateral
spinothalamic tract to synapse third-order neurons in the
contralateral thalamus somatosensory cortex perceived as pain
9. Descending pathway Descending modulatory neural pathways
function to reduce pain perception Efferent responses by inhibiting
pain transmission in the dorsal horn, PAG, brainstem
(rostroventrome-dial medulla, RVM), and other regions of the CNS. .
The cerebralcortex, hypothalamus, thalamus, PAG, nucleus raphe
magnus(NRM), and locus coeruleus (LC) all send descending axons
that synapse with and modulate pain transmission
10. 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.
11. The PAG is an enkephalinergic brainstem nucleus
respon-sible for both morphine and stimulation- produced analgesia.
Descending axons from the PAG- inhibit WDR and NS neurons Axon
terminals from NRM project to the dorsal horn- serotonin and NE.
Stimulation of the RVM activates the serotonergic system descending
to the spinal dorsal horn, resulting in analgesia Axons descending
from LC modulate nociceptive transmission in dorsal horn primarily
via release of
12. 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 fibers tend to close the GATE (inhibits trans.) while small
fibre input opens it. In otherwords A-beta fibre stimulation
activates interneurons in dorsal horn that inhibits the nociceptive
transmission. Also descending pathways from cortex and midbrain,
thermal and tactile afferents profoundly influence the GATE.
13. 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 dont reach their activity threshold, no pain is
experienced. If small fibers are active first, sg is inhibited,
both fibers increase T-activity
14. Elements of Pain 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
15. 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
16. Chemical mediators 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.
17. Allogenic substances
18. Contd..
19. Transmitters & 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.
20. The various receptors are 1. the NMDA
(N-methyl-D-aspartate) 2. the AMPA (-amino-3-hydroxy-5-
methylisoxazole-4-proprionic acid) 3. the kainate 4. the
metabotropic
21. Surgical stress response Surgical stress causes release of
cytokines (e.g., IL-1, IL-6, and TNF-) precipitates adverse
neuroendocrine and sympathoadrenal responses, resulting in
detrimental physiological responses
22. Catabolic hormones 1. Cortisol 2. Glucagon 3. Growth
hormones 4. catecholami nes Anabolic hormones 1. Insulin 2.
Testoster one hyperglycemia a negative nitrogen balance, the
consequences of which include poor wound healing, muscle wasting ,
fatigue, and impaired immunocompetency
23. Effects on the systems
24. Pre-Emptive Analgesia 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 WDR neurons in the dorsal horn leads to
central plasticity
25. To be succesful 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.
26. If not ..
27. Assessment of Acute pain 1.Visual analog score 2.Facial
Grimaces
28. McGill Pain questionnaire 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. .
29. Addressed during assessment 1. Onset of pain 2. Temporal
pattern of pain 3. Site of pain 4. Radiation of pain 5. Quality
(character) of pain 6. Intensity (severity) of pain 7. Exacerbating
factors (what makes the pain start or get worse?) 8. Relieving
factors (what prevents the pain or makes it better?) 9. Response to
analgesics (including attitudes and concerns about opioids) 10.
Response to other interventions 11. Associated physical symptoms
12. Associated psychological symptoms
30. Three Classes of acute Pain 1. Breakthrough: Pain that
escalates above a persistent background pain. 2. Transitory and
Intermittant: Pain that is episodic in the absence of background
pain. 3. Background: Pain that is persistent but may vary over
time.
32. Opiods 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,
and 3. activation of a descending inhibitory pain circuit via
inhibition of GABAergic transmission
33. Side effects Common : 1. sedation, 2. nausea and vomiting,
3. respiratory depression, 4. constipation. Less common 1.
confusion, 2. urinary retention, 3. dizziness, 4. myoclonus
34. Opioid-induced hyperalgesia (OIH) 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.16
35. Nonopioid Analgesic Adjuncts NSAIDs are among the most
commonly used drugs 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.
36. Prostaglandins : 1. Prostaglandin E2 is the key mediator of
both peripheral and central pain sensitization 2. Peripherally,
prostaglandins do not directly mediate pain; rather, they
contribute to hyperalgesia by sensitizing nociceptors 3. 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.
37. NMDA receptor antagonists 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, 3.
opioid-induced tolerance, and 4. Opoiod induced hyperanalgesia
38. ketamine and dextromethorphan are commonly used. Ketamine :
Low-dose ketamine (0.25- to 0.5-mg intravenous bolus followed by an
infusion of 2 to 4 g/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
39. 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
40. 2-adrenergic agonists clonidine and dexmedetomidine It
provide analgesia, sedation, and anxiolysis The presynaptic
activation of 2-receptors that results in the decreased release of
norepinephrine is believed to mediate analgesia.
41. CLONIDINE : selective partial agonist for the
2-adrenoreceptor Analgesia is mediated supraspinally (locus
coeruleus), spinally (substantia gelatinosa), and peripherally can
be administered orally, transdermally, intravenously, and
neuraxially for perioperative pain management.
42. Premedication with 5 g/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 g/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 g
43. Dexmedetomidine: highly selective 2-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
44. loading dose of 1 g/kg i.v over 10 minutes followed by an
infusion of 0.2 to 0.7 g/kg/hr i.v dexmedetomidine infusion (0.2 to
0.7 g/kg/hr) combined with peripheral nerve blockade may provide
superb analgesia, anxiolysis, and sedation during prolonged
procedures infusions as high as 5 to 10 g/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
45. 2- subunit calcium 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 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
46. Patient-Controlled Analgesia 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
49. Neuroaxial 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
50. Efficacy of an epidural technique is determined by numerous
factors 1. catheter incision site congruency 2. choice of analgesic
drugs 3. rates of infusion 4. duration of epidural analgesia 5.
type of pain assessment (Rest vs Dynamic)
51. Ideally, the epidural catheter is positioned congruent 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
52. 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