1. 1. Presentor :Dr.Kumar Moderator : Dr.Vamsidhar Acute pain management
2. 2. Acute pain Definition: Acute pain has been defined as the normal, predicted, physiological response to an adverse chemical, thermal, or mechanical stimulus.
3. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 17. Allogenic substances
18. 18. Contd..
19. 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. 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. 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. 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. 23. Effects on the systems
24. 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. 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. 26. If not ..
27. 27. Assessment of Acute pain 1.Visual analog score 2.Facial Grimaces
28. 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. 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. 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.
31. 31. MANAGEMENT DRUGS : Opiods Non opiods (NSAIDS) NMDA receptor antagoinsts Alpha-2 agonists 2- subunit calcium channel ligands Invasive Procedures : Neuroaxial blockade Peripheral nerve blockade
32. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
47. 47. Opioids regimens for PCA
48. 48. Relative Risk factors 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
49. 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. 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. 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. 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