phatass
Bluelighter
if you, like me have come out of pretty serious surgery and are in quite a lot of pain and are given tramadol, when on MMT , you might be interested in this part of an article i found... i'll definately be showing this to my doctor
Common Misconceptions
Four common misconceptions of health providers result in the undertreatment of acute pain in patients receiving OAT: 1) The maintenance opioid agonist (methadone or buprenorphine) provides analgesia; 2) use of opioids for analgesia may result in addiction relapse; 3) the additive effects of opioid analgesics and OAT may cause respiratory and central nervous system (CNS) depression; and 4) the pain complaint may be a manipulation to obtain opioid medications, or drug-seeking, because of opioid addiction.
Misconception 1: The Maintenance Opioid Agonist (Methadone or Buprenorphine) Provides Analgesia
There are pharmacokinetic and pharmacodynamic explanations for why patients do not receive adequate analgesia from maintenance opioids prescribed for addiction treatment. Not only do the analgesic and addiction treatment profiles of these opioids differ, but the neuroplastic changes associated with long-term opioid exposure (that is, tolerance and hyperalgesia) may effectively diminish their analgesic effectiveness (45).
Analgesic Properties of Maintenance Opioids
Patients receiving maintenance therapy with opioids for addiction treatment do not derive sustained analgesia from it. Methadone and buprenorphine, potent analgesics, have a duration of action for analgesia (4 to 8 hours) that is substantially shorter than their suppression of opioid withdrawal (24 to 48 hours) (46–50). Because most patients receiving OAT are given a dose every 24 to 48 hours, the period of even partial pain relief with these medications is small.
Opioid Tolerance
Tolerance is one factor that explains why these patients derive little pain relief from maintenance opioids. Tolerance, the need for increasing doses of a medication to achieve its initial effects, develops with continuous opioid use but differentially affects specific opioid properties. For example, tolerance readily develops to the respiratory and CNS depressive effects of opioids but not to their constipating effects (51, 52). Analgesic tolerance develops for different medications within the opioid class, a phenomenon called cross-tolerance (53, 54). Doverty and colleagues (55) found that patients receiving maintenance methadone therapy were cross-tolerant to the analgesic effects of morphine and that pain relief, when obtained, did not last as long as expected. Therefore, cross-tolerance between the opioids used for maintenance therapy and other opioids used for analgesia may explain why patients receiving OAT often require higher and more frequent doses of opioid analgesics to achieve adequate pain control.
Opioid-Induced Hyperalgesia
An alternative explanation for the lack of analgesia derived from maintenance opioids may be the presence of opioid-induced hyperalgesia. This is the result of neuro-plastic changes in pain perception that yield an increase in pain sensitivity. The outcome is that opioids have less potent analgesic effects (45, 56–58). Empirical evidence supports increased sensitivity to experimental pain in patients receiving OAT (33, 38, 55, 59–62), such that patients receiving maintenance methadone therapy tolerate cold-pressor pain only half as long as do matched controls (55, 59). Accumulating evidence suggests that maintenance with buprenorphine therapy has similar and statistically significant effects on pain tolerance, although to a lesser degree than methadone (63). The pain intolerance of patients receiving methadone and buprenorphine maintenance therapy can be conceptualized as a latent hyperalgesia secondary to long-term opioid exposure.
The presence of hyperalgesia with ongoing opioid use has resulted in reexamination of the previously described phenomenon of opioid analgesic tolerance. Both hyperalgesia and opioid tolerance involve neuroplastic changes associated with excitatory amino acid (N-methyl-D-aspartate) and opioid receptors (64–70). The hyperalgesic processes precipitated by opioid administration serve to counteract opioid analgesia (56, 71–73); thus, it is possible that what seems to be opioid analgesic tolerance may in fact be an expression of an opioid-induced increased sensitivity to pain.
Therefore, despite the benefits of OAT for the opioid-dependent person, the accompanying hyperalgesia (or analgesic tolerance) counteracts the analgesic effects of opioids and complicates pain management. At clinically effective doses for the treatment of opioid dependence, patients do not experience analgesia to experimental pain but demonstrate the hyperalgesic effects of OAT. Thus, from a theoretical and experimental basis, it is clear that the perception of pain is not decreased in OAT patients.
Misconception 2: Use of Opioids for Analgesia May Result in Addiction Relapse
A common concern of physicians is that the use of opioids for analgesia in patients receiving OAT May result in relapse to active drug use. However, there is no evidence that exposure to opioid analgesics in the presence of acute pain increases rates of relapse in such patients. A small retrospective study (74) of patients enrolled in maintenance methadone programs who received opioid analgesics after surgery did not find a difference in relapse indicators compared with matched patients receiving maintenance methadone therapy. Similarly, no evidence of relapse was seen in 6 patients receiving methadone maintenance therapy who were treated with opioid analgesics for cancer-related pain (75). In fact, relapse prevention theories would suggest that the stress associated with unrelieved pain is more likely to be a trigger for relapse than adequate analgesia. In a study by Karasz and colleagues (76), patients receiving methadone maintenance therapy stated that pain played a substantial role in their initiating and continuing drug use.
Misconception 3: The Additive Effects of Opioid Analgesics and OAT May Cause Respiratory and CNS Depression
Physicians’ concerns that opioid analgesics will cause severe respiratory or CNS depression in patients receiving OAT is a theoretical risk, which has never been clinically demonstrated. As previously noted, tolerance to the respiratory and CNS depressant effects of opioids occurs rapidly and reliably (50–52). Similarly, patients with worsening cancer-related pain who require dose escalations typically do not exhibit respiratory and CNS depressant effects when additional opioids are administered (75, 77–79). It has been suggested that acute pain serves as a natural antagonist to opioid-associated respiratory and CNS depression (15, 43). This purported effect is supported by the observation that a patient with chronic pain who was treated with opioids developed signs of respiratory depression after a successful nerve block procedure (80). Therefore, the concern about severe drug toxicity with analgesic opioid treatment is not supported by clinical or empirical experience.
Misconception 4: Reporting Pain May Be a Manipulation To Obtain Opioid Medications, or Drug-Seeking, because of Opioid Addiction
Physicians’ concerns about being manipulated by drug-seeking patients is substantial, difficult to quantify, and emotion-laden. It is a powerful motive underlying physicians’ reservations about prescribing opioid analgesia for acute pain to patients receiving OAT for opioid dependence. Pain is always subjective, making assessment of its presence and severity difficult. A careful clinical assessment for objective evidence of pain will decrease the chance of being manipulated by a drug-seeking patient and will support the use of opioid analgesics in patients with a history of opioid dependence. Reports of acute pain with objective findings are less likely to be manipulative gestures than are reports of chronic pain with vague presentations. Furthermore, patients receiving OAT typically receive treatment doses that block most euphoric effects of coadministered opioids, theoretically decreasing the likelihood of opioid analgesic abuse (81, 82).
Not uncommonly, patients dependent on opioids are perceived by health care providers to be demanding when hospitalized with acute pain. This scenario develops in part because of the patients’ distrust of the medical community, concern about being stigmatized, and fears that their pain will be undertreated or that their OAT may be altered or discontinued (76, 83). Patient anxiety related to these concerns, which can be profound and well-founded, can complicate provision of adequate pain relief.
Requests for opioid analgesia from patients receiving OAT may be labeled as drug-seeking behaviors, which are defined as concerted efforts on the part of the patient to obtain opioid medication, including engaging in illegal activities (44). It is important to keep in mind that there may be appropriate reasons for a patient to seek medication. The distinction between appropriate drug-seeking and addiction is harder to discern when the patient requests a drug with known abuse potential, such as opioid analgesics, regardless of the apparent validity of the complaint. In the case of unrelieved pain, drug-seeking behaviors arise when a patient cannot obtain tolerable relief with the prescribed dose of analgesic and seeks alternate sources or increased doses, a phenomenon referred to as pseudoaddiction (84). Alternately, patients receiving good pain relief may exhibit drug-seeking behaviors because they fear not only the reemergence of pain but perhaps also the emergence of withdrawal symptoms. Rather than indicating addictive disease, such behaviors, termed therapeutic dependence (85), are actually efforts to maintain a tolerable level of comfort. Other patients with adequate pain control may continue to report persistent severe pain to prevent reduction in current effective doses of opioid analgesics, a behavior termed pseudo-opioid resistance (86).
Conclusion
Addiction elicits neurophysiologic, behavioral, and social responses that worsen the pain experience and complicate provision of adequate analgesia. These complexities are heightened for patients with opioid dependency who are receiving OAT, for whom the neural responses of tolerance or hyperalgesia may alter the pain experience. As a consequence, opioid analgesics are less effective; higher doses administered at shortened intervals are required. Opioid agonist therapy provides little, if any, analgesia for acute pain. Fears that opioid analgesia will cause addiction relapse or respiratory and CNS depression are unfounded. Furthermore, clinicians should not allow concerns about being manipulated to cloud good clinical assessment or judgment about the patient’s need for pain medications. Reassurance regarding uninterrupted OAT and aggressive pain management will mitigate anxiety and facilitate successful treatment of pain in patients receiving OAT.
source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1892816/
Common Misconceptions
Four common misconceptions of health providers result in the undertreatment of acute pain in patients receiving OAT: 1) The maintenance opioid agonist (methadone or buprenorphine) provides analgesia; 2) use of opioids for analgesia may result in addiction relapse; 3) the additive effects of opioid analgesics and OAT may cause respiratory and central nervous system (CNS) depression; and 4) the pain complaint may be a manipulation to obtain opioid medications, or drug-seeking, because of opioid addiction.
Misconception 1: The Maintenance Opioid Agonist (Methadone or Buprenorphine) Provides Analgesia
There are pharmacokinetic and pharmacodynamic explanations for why patients do not receive adequate analgesia from maintenance opioids prescribed for addiction treatment. Not only do the analgesic and addiction treatment profiles of these opioids differ, but the neuroplastic changes associated with long-term opioid exposure (that is, tolerance and hyperalgesia) may effectively diminish their analgesic effectiveness (45).
Analgesic Properties of Maintenance Opioids
Patients receiving maintenance therapy with opioids for addiction treatment do not derive sustained analgesia from it. Methadone and buprenorphine, potent analgesics, have a duration of action for analgesia (4 to 8 hours) that is substantially shorter than their suppression of opioid withdrawal (24 to 48 hours) (46–50). Because most patients receiving OAT are given a dose every 24 to 48 hours, the period of even partial pain relief with these medications is small.
Opioid Tolerance
Tolerance is one factor that explains why these patients derive little pain relief from maintenance opioids. Tolerance, the need for increasing doses of a medication to achieve its initial effects, develops with continuous opioid use but differentially affects specific opioid properties. For example, tolerance readily develops to the respiratory and CNS depressive effects of opioids but not to their constipating effects (51, 52). Analgesic tolerance develops for different medications within the opioid class, a phenomenon called cross-tolerance (53, 54). Doverty and colleagues (55) found that patients receiving maintenance methadone therapy were cross-tolerant to the analgesic effects of morphine and that pain relief, when obtained, did not last as long as expected. Therefore, cross-tolerance between the opioids used for maintenance therapy and other opioids used for analgesia may explain why patients receiving OAT often require higher and more frequent doses of opioid analgesics to achieve adequate pain control.
Opioid-Induced Hyperalgesia
An alternative explanation for the lack of analgesia derived from maintenance opioids may be the presence of opioid-induced hyperalgesia. This is the result of neuro-plastic changes in pain perception that yield an increase in pain sensitivity. The outcome is that opioids have less potent analgesic effects (45, 56–58). Empirical evidence supports increased sensitivity to experimental pain in patients receiving OAT (33, 38, 55, 59–62), such that patients receiving maintenance methadone therapy tolerate cold-pressor pain only half as long as do matched controls (55, 59). Accumulating evidence suggests that maintenance with buprenorphine therapy has similar and statistically significant effects on pain tolerance, although to a lesser degree than methadone (63). The pain intolerance of patients receiving methadone and buprenorphine maintenance therapy can be conceptualized as a latent hyperalgesia secondary to long-term opioid exposure.
The presence of hyperalgesia with ongoing opioid use has resulted in reexamination of the previously described phenomenon of opioid analgesic tolerance. Both hyperalgesia and opioid tolerance involve neuroplastic changes associated with excitatory amino acid (N-methyl-D-aspartate) and opioid receptors (64–70). The hyperalgesic processes precipitated by opioid administration serve to counteract opioid analgesia (56, 71–73); thus, it is possible that what seems to be opioid analgesic tolerance may in fact be an expression of an opioid-induced increased sensitivity to pain.
Therefore, despite the benefits of OAT for the opioid-dependent person, the accompanying hyperalgesia (or analgesic tolerance) counteracts the analgesic effects of opioids and complicates pain management. At clinically effective doses for the treatment of opioid dependence, patients do not experience analgesia to experimental pain but demonstrate the hyperalgesic effects of OAT. Thus, from a theoretical and experimental basis, it is clear that the perception of pain is not decreased in OAT patients.
Misconception 2: Use of Opioids for Analgesia May Result in Addiction Relapse
A common concern of physicians is that the use of opioids for analgesia in patients receiving OAT May result in relapse to active drug use. However, there is no evidence that exposure to opioid analgesics in the presence of acute pain increases rates of relapse in such patients. A small retrospective study (74) of patients enrolled in maintenance methadone programs who received opioid analgesics after surgery did not find a difference in relapse indicators compared with matched patients receiving maintenance methadone therapy. Similarly, no evidence of relapse was seen in 6 patients receiving methadone maintenance therapy who were treated with opioid analgesics for cancer-related pain (75). In fact, relapse prevention theories would suggest that the stress associated with unrelieved pain is more likely to be a trigger for relapse than adequate analgesia. In a study by Karasz and colleagues (76), patients receiving methadone maintenance therapy stated that pain played a substantial role in their initiating and continuing drug use.
Misconception 3: The Additive Effects of Opioid Analgesics and OAT May Cause Respiratory and CNS Depression
Physicians’ concerns that opioid analgesics will cause severe respiratory or CNS depression in patients receiving OAT is a theoretical risk, which has never been clinically demonstrated. As previously noted, tolerance to the respiratory and CNS depressant effects of opioids occurs rapidly and reliably (50–52). Similarly, patients with worsening cancer-related pain who require dose escalations typically do not exhibit respiratory and CNS depressant effects when additional opioids are administered (75, 77–79). It has been suggested that acute pain serves as a natural antagonist to opioid-associated respiratory and CNS depression (15, 43). This purported effect is supported by the observation that a patient with chronic pain who was treated with opioids developed signs of respiratory depression after a successful nerve block procedure (80). Therefore, the concern about severe drug toxicity with analgesic opioid treatment is not supported by clinical or empirical experience.
Misconception 4: Reporting Pain May Be a Manipulation To Obtain Opioid Medications, or Drug-Seeking, because of Opioid Addiction
Physicians’ concerns about being manipulated by drug-seeking patients is substantial, difficult to quantify, and emotion-laden. It is a powerful motive underlying physicians’ reservations about prescribing opioid analgesia for acute pain to patients receiving OAT for opioid dependence. Pain is always subjective, making assessment of its presence and severity difficult. A careful clinical assessment for objective evidence of pain will decrease the chance of being manipulated by a drug-seeking patient and will support the use of opioid analgesics in patients with a history of opioid dependence. Reports of acute pain with objective findings are less likely to be manipulative gestures than are reports of chronic pain with vague presentations. Furthermore, patients receiving OAT typically receive treatment doses that block most euphoric effects of coadministered opioids, theoretically decreasing the likelihood of opioid analgesic abuse (81, 82).
Not uncommonly, patients dependent on opioids are perceived by health care providers to be demanding when hospitalized with acute pain. This scenario develops in part because of the patients’ distrust of the medical community, concern about being stigmatized, and fears that their pain will be undertreated or that their OAT may be altered or discontinued (76, 83). Patient anxiety related to these concerns, which can be profound and well-founded, can complicate provision of adequate pain relief.
Requests for opioid analgesia from patients receiving OAT may be labeled as drug-seeking behaviors, which are defined as concerted efforts on the part of the patient to obtain opioid medication, including engaging in illegal activities (44). It is important to keep in mind that there may be appropriate reasons for a patient to seek medication. The distinction between appropriate drug-seeking and addiction is harder to discern when the patient requests a drug with known abuse potential, such as opioid analgesics, regardless of the apparent validity of the complaint. In the case of unrelieved pain, drug-seeking behaviors arise when a patient cannot obtain tolerable relief with the prescribed dose of analgesic and seeks alternate sources or increased doses, a phenomenon referred to as pseudoaddiction (84). Alternately, patients receiving good pain relief may exhibit drug-seeking behaviors because they fear not only the reemergence of pain but perhaps also the emergence of withdrawal symptoms. Rather than indicating addictive disease, such behaviors, termed therapeutic dependence (85), are actually efforts to maintain a tolerable level of comfort. Other patients with adequate pain control may continue to report persistent severe pain to prevent reduction in current effective doses of opioid analgesics, a behavior termed pseudo-opioid resistance (86).
Conclusion
Addiction elicits neurophysiologic, behavioral, and social responses that worsen the pain experience and complicate provision of adequate analgesia. These complexities are heightened for patients with opioid dependency who are receiving OAT, for whom the neural responses of tolerance or hyperalgesia may alter the pain experience. As a consequence, opioid analgesics are less effective; higher doses administered at shortened intervals are required. Opioid agonist therapy provides little, if any, analgesia for acute pain. Fears that opioid analgesia will cause addiction relapse or respiratory and CNS depression are unfounded. Furthermore, clinicians should not allow concerns about being manipulated to cloud good clinical assessment or judgment about the patient’s need for pain medications. Reassurance regarding uninterrupted OAT and aggressive pain management will mitigate anxiety and facilitate successful treatment of pain in patients receiving OAT.
source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1892816/
