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Narcotic Bowel Syndrome. Definitions, history, how frequent?

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Presentation on theme: "Narcotic Bowel Syndrome. Definitions, history, how frequent?"— Presentation transcript:

1 Narcotic Bowel Syndrome

2 Definitions, history, how frequent?

3 Definition NBS Definition NBS Note: not yet defined in Int. Classification of diseases or Rome Criteria of FGID Progressive and paradoxical increase in abdominal pain despite continued or escalating doses of narcotics prescribed to relieve the pain Progressive and paradoxical increase in abdominal pain despite continued or escalating doses of narcotics prescribed to relieve the pain Less common than but may be associated with Less common than but may be associated with opioid bowel disorder, a dose related dysmotility opioid bowel disorder, a dose related dysmotility Grunkemeier, Drossman, et al Clin Gast and Hep 2007;5:

4 Opioid Bowel Disorder or Dysfunction (OBD) A Dysmotility Disorder Central effects also implicated, but interaction with opioid receptors in the gut felt to be primary Central effects also implicated, but interaction with opioid receptors in the gut felt to be primary Nausea Nausea Bloating, distension Bloating, distension Ileus Ileus Constipation Constipation Abdominal Pain Abdominal Pain GERD GERD Pseudo-obstruction Pseudo-obstruction Interference with oral drug absorption Interference with oral drug absorption

5 First described Narcotic Bowel Syndrome Treated with Clonidine: Narcotic Bowel Syndrome Treated with Clonidine: CAP, Pseudo-obstruction, vomiting, wt loss- resolution after discontinuing narcotics Annals of IM Sandgren et al U of KS 1984;101:334-8 CAP, Pseudo-obstruction, vomiting, wt loss- resolution after discontinuing narcotics Annals of IM Sandgren et al U of KS 1984;101:334-8 Editorial: The Narcotic Bowel Syndrome: Editorial: The Narcotic Bowel Syndrome: Pain and pseudo-obstruction described- “although helpful initially, the pain returns requiring more and more narcotic for control of symptoms” J Clin Gastro Michael Rogers and James Cerda U of Fl 1989;11:132-5 Pain and pseudo-obstruction described- “although helpful initially, the pain returns requiring more and more narcotic for control of symptoms” J Clin Gastro Michael Rogers and James Cerda U of Fl 1989;11:132-5 A Case of Narcotic Bowel Syndrome Successfully Treated with Clonidine: CAP worsening treated with narcotics and followed by increasing doses need for pain relief, resolution of pain upon withdrawal of narcotics aided by Clonidine A Case of Narcotic Bowel Syndrome Successfully Treated with Clonidine: CAP worsening treated with narcotics and followed by increasing doses need for pain relief, resolution of pain upon withdrawal of narcotics aided by Clonidine Wong et al Postgrad Med J 1994;70:138-40

6 Opiate Use in the US Study of Narcotic Use in IBD Estimated: 80% of world’s opioid used in USA (4.6%) Estimated: 80% of world’s opioid used in USA (4.6%) Rx’s for methadone ↑ 1177% Rx’s for methadone ↑ 1177% Estimated: ~5-13% IBD pts on chronic narcotics as opt Estimated: ~5-13% IBD pts on chronic narcotics as opt ~ 8% IBS “ “ ~ 8% IBS “ “ Estimated: Prevalence of IBS symptoms in IBD 2-3x Estimated: Prevalence of IBS symptoms in IBD 2-3x > general population > general population ~57% CD ~33% UC report IBS-like symptoms ~57% CD ~33% UC report IBS-like symptoms Study result: 70% of hospitalized pts received narcotics Study result: 70% of hospitalized pts received narcotics ↑ CD, duration of IBD, prior psych dx, prior outpt use of ↑ CD, duration of IBD, prior psych dx, prior outpt use of narcotics, smoking, prior IBD surgery, and prior dx of narcotics, smoking, prior IBD surgery, and prior dx of IBD/IBS IBD/IBS *Not associated with disease severity on CT or endoscopy *Not associated with disease severity on CT or endoscopy Long et al, Inflamm Bowel Dis V 18 #5 May from UNC

7 OBD and NBS in the Mayo Olmstead County Population (~ 124,000 total, ~5000 participated in the study) Opioids mainstay of Rx in cancer pain and increasingly used as the main or only source of pain relief for non cancer pain Opioids mainstay of Rx in cancer pain and increasingly used as the main or only source of pain relief for non cancer pain Few studies on GI effects in non cancer pain in outpts Few studies on GI effects in non cancer pain in outpts Results: 4% of population on prescription narcotics Results: 4% of population on prescription narcotics 8.5 % on narcotics were for cancer pain 8.5 % on narcotics were for cancer pain.17% met criteria of NBS (5 cases).17% met criteria of NBS (5 cases) Increased symptoms of abd pain, and laxative use Increased symptoms of abd pain, and laxative use OBD symptoms prevalence from previous studies: OBD symptoms prevalence from previous studies: (ca and non ca pain) constip 20-40% prior meta: 80% at least 1 symp (ca and non ca pain) constip 20-40% prior meta: 80% at least 1 symp nausea 8-40% (non ca pain) constip 41% nausea 32% nausea 8-40% (non ca pain) constip 41% nausea 32% Talley et al, AJG V104 May

8 What is prevalence in pts on chronic narcotics? 146 subjects, on narcotics for CNCP (non GI origin) CAP 58.2%, 19.4% daily Constipation 47% correlated with duration, not dose Nausea 27% Vomiting 9% no cor with dose/dur GERD 33% HB 25% NBS6.4% NBS 6.4% Neurogastro Motil V e Tuteja et al Univ of Utah

9 Features of NBS Increasingly recognized with increased use of narcotics for non cancer pain over the last decade Increasingly recognized with increased use of narcotics for non cancer pain over the last decade Initially narcotics relieve pain, but continued use in a subset (?) with chronic use → NBS Initially narcotics relieve pain, but continued use in a subset (?) with chronic use → NBS Pts first develop tolerance or tachyphylaxis followed by hyperalgesia even with dose escalation Pts first develop tolerance or tachyphylaxis followed by hyperalgesia even with dose escalation Genetic or pharmacogenomic factors, vary pt to pt Genetic or pharmacogenomic factors, vary pt to pt

10 Not specific to any disorder Not associated with any specific medical condition Not associated with any specific medical condition Seen in a wide variety of disorders Seen in a wide variety of disorders Can be seen when high dose narcotics are used postoperatively Can be seen when high dose narcotics are used postoperatively

11 5 Criteria for Dx 1.Chronic or frequently recurring GI pain treated with acute high dose or continual narcotics 2.Pain worsens or incompletely resolves with continued or increased dosages of narcotics 3.There is marked worsening when the narcotic dose wanes and improvement when reinstituted (“soar and crash”) 4.There is progression of the frequency, duration and intensity of GI pain episodes 5.The nature and intensity of the pain is not explained by a current or previous GI Dx *

12 Dx of NBS Dr. Drossman’s group recommends Dx of NBS be strongly considered: Dr. Drossman’s group recommends Dx of NBS be strongly considered: When patients with abdominal pain are on When patients with abdominal pain are on narcotics and fulfill 3 of the other 4 criteria narcotics and fulfill 3 of the other 4 criteria Dose of narcotic: equiv of 100mg MS/d Dose of narcotic: equiv of 100mg MS/d Talley et al report dosage of >10mg/d is “high” Talley et al report dosage of >10mg/d is “high” Am J Surg 2001;182:11s-8s Am J Surg 2001;182:11s-8s

13 What causes NBS

14 ENS Neurotransmitters Largest collection of neurons outside the CNS AcH (acetylcholine) AcH (acetylcholine) Serotonin (5-hydroxytryptamine) Serotonin (5-hydroxytryptamine) Adrenergic Adrenergic Tachykinins (substance P, neurokinin A) Tachykinins (substance P, neurokinin A) NO (nitric oxide) NO (nitric oxide) ATP ATP Opioid peptides- endorphins, endomorphins, dynorphins, enkephalins, and nociceptin Opioid peptides- endorphins, endomorphins, dynorphins, enkephalins, and nociceptin Neuropeptide Y Neuropeptide Y

15 Opioid Receptors delta (OP1) kappa (OP2) mu (OP3) All 3 contribute to opiate-induced inhibition of muscle activity All 3 contribute to opiate-induced inhibition of muscle activity Symptoms of OBD are predominantly mediated by mu-opioid receptors in humans Most effective opioid analgesics are mu- opioid receptor-selective agonists Given the presence of delta and kappa receptors, selective opioid analgesics for these receptors would not help reduce GISE….thus Given the presence of delta and kappa receptors, selective opioid analgesics for these receptors would not help reduce GI SE….thus

16 Opioid Receptors delta (OP1) kappa (OP2) mu (OP3) Selectively targeting peripheral mu opioid receptors has been a goal of pharmacological research Methylnaltrexone non selective mu receptor preferring antagonist Alvimopan selective mu opioid receptor antagonist ex. of peripheral mu receptor antagonists Loperamide ex. of peripheral gut selective mu receptor agonist

17 Central Opioid Receptors OP1……………………OP4 (OPL-1, CNS only) OP1……………………OP4 (OPL-1, CNS only) OP4: Nociceptin Receptor: anxiety, depression, appt OP4: Nociceptin Receptor: anxiety, depression, appt tolerance to μ agonists tolerance to μ agonists Location in multiple locations in the brain and spinal cord Location in multiple locations in the brain and spinal cord Effects multiple: analgesia, physical dependence, euphoria, respiratory depression, anti-depressive, are examples Effects multiple: analgesia, physical dependence, euphoria, respiratory depression, anti-depressive, are examples

18 Adverse effects of opioid analgesics on the GI tract: Expression of opioid peptides and opioid receptors by distinct enteric neurons and intestinal muscle cells Expression of opioid peptides and opioid receptors by distinct enteric neurons and intestinal muscle cells When released from these neurons opioid peptides play a transmitter role in enteric regulation of propulsive motility and secretory processes When released from these neurons opioid peptides play a transmitter role in enteric regulation of propulsive motility and secretory processes Inhibitory effects on peristalsis primarily from interruption of transmission ENS pathways governing muscle contractions via pre and post synaptic modulation: AcH, other excitatory neurotransmitters attenuated Inhibitory effects on peristalsis primarily from interruption of transmission ENS pathways governing muscle contractions via pre and post synaptic modulation: AcH, other excitatory neurotransmitters attenuated

19 Adverse effects of opioid analgesics on the GI tract: Inhibit peristalsis- ↓AcH and other excitatory NT release, and tonic contractions induced which block propulsive activity Inhibit peristalsis- ↓AcH and other excitatory NT release, and tonic contractions induced which block propulsive activity Tonic Spasms: depression of NO from inh neurons or direct activation of muscles cells that express opioid receptors Tonic Spasms: depression of NO from inh neurons or direct activation of muscles cells that express opioid receptors Alters intestinal fluid balance- ↓ ion and fluid secretion Alters intestinal fluid balance- ↓ ion and fluid secretion ↑ intestinal fluid absorption ↑ intestinal fluid absorption Constipation: stationary segmentations + inhibition of peristalsis + depression of secretory activity Constipation: stationary segmentations + inhibition of peristalsis + depression of secretory activity

20 Mechanisms for NBS How does narcotic use cause and aggravate the pain being treated How does narcotic use cause and aggravate the pain being treated 4 mechanisms proposed: 4 mechanisms proposed: 1.bimodal opioid regulation system 2.counter regulatory mechanisms 3.glial cell activation 4.microglia (CNS macrophage) cell activation

21 Summary of proposed mechanisms for opioid induced hyperalgesia Activation of excitatory antianalgesia pathways in the opioid regulatory system Activation of excitatory antianalgesia pathways in the opioid regulatory system Descending facilitation of pain at the rostral ventral medulla Descending facilitation of pain at the rostral ventral medulla Dorsal Horn glial cell activation leading to morphine tolerance via inflammatory pathways Dorsal Horn glial cell activation leading to morphine tolerance via inflammatory pathways Microglia (CNS macrophages) that release inflammatory factors and may upregulate neural signals Microglia (CNS macrophages) that release inflammatory factors and may upregulate neural signals

22 Bimodal (Excitatory and Inhibitory) Opioid Modulation in the Dorsal Horn & Afferent Neurons Inhibitory mode: analgesia- opioids activate proteins (G1,G0) that inhibit neurotransmission Inhibitory mode: analgesia- opioids activate proteins (G1,G0) that inhibit neurotransmission Excitatory mode: hyperalgesia- opioids also activate proteins (Gs) that activates neurotransmission----- antianalgesia and tolerance Excitatory mode: hyperalgesia- opioids also activate proteins (Gs) that activates neurotransmission----- antianalgesia and tolerance Effects depend in part on concentration and duration Effects depend in part on concentration and duration of the opioids acting on the action potential of the opioids acting on the action potential At the Dorsal Horn- At the Dorsal Horn- Low conc prolong AP and excitatory effects (enhance NT release) Low conc prolong AP and excitatory effects (enhance NT release) High conc.---- shorten AP and inhibit NT release ** (typical therapeutic High conc.---- shorten AP and inhibit NT release ** (typical therapeutic doses of opioids) doses of opioids)

23 Bimodal Mechanism High concentration of opioids typical for pain relief lead to high concentration of opioids and pain relief initially (inhib effect > excit effect) High concentration of opioids typical for pain relief lead to high concentration of opioids and pain relief initially (inhib effect > excit effect) Over time, Gs coupled excitatory opioid receptors become sensitized with chronic exposure at the DRG- & chronic use will thus lead to tolerance of inhibitory pain effects and ultimately hyperalgesia Over time, Gs coupled excitatory opioid receptors become sensitized with chronic exposure at the DRG- & chronic use will thus lead to tolerance of inhibitory pain effects and ultimately hyperalgesia

24 Narcotic antagonists, pain relief, and bimodal modulation Also note: low doses of antagonists selectively inhibit the excitatory (Gs) pathways which can enhance opioid analgesia Also note: low doses of antagonists selectively inhibit the excitatory (Gs) pathways which can enhance opioid analgesia Examples- naltrexone, naloxone, buprenorphone Examples- naltrexone, naloxone, buprenorphone & is basis for the combination: & is basis for the combination: Suboxone- buprenorphine/naloxone Suboxone- buprenorphine/naloxone Note: combo meds can be used for detox as well Note: combo meds can be used for detox as well

25 Counter regulatory Mechanisms A CNS effect Specific areas of the brain modulate incoming pain signals at the level of the spinal cord ↑ or ↓ Specific areas of the brain modulate incoming pain signals at the level of the spinal cord ↑ or ↓ cingulate and prefrontal cortex cingulate and prefrontal cortex rostral ventral medulla (RVM) ** rostral ventral medulla (RVM) ** periaqueductal gray periaqueductal gray Responses occur in part via activation or inactivation of on and off cells in the RVM Responses occur in part via activation or inactivation of on and off cells in the RVM Chronic use may lead sensitization of the on signals Chronic use may lead sensitization of the on signals ? Role in a rebound effect when opioid analgesia wears off ? Role in a rebound effect when opioid analgesia wears off

26 Counter regulatory mechanisms Endogenous neuromodulators in the brainstem and spinal cord Endogenous neuromodulators in the brainstem and spinal cord dynorphin, CCK → dynorphin, CCK → increase in excitatory NT’s from 1° afferents in increase in excitatory NT’s from 1° afferents in nociceptive tracts → hyperalgesia nociceptive tracts → hyperalgesia

27 Spinal cord glial cell activation- Newly found mechanism of pain amplification Dorsal horn glia (astrocytes and microglia) Dorsal horn glia (astrocytes and microglia) When activated produce hyperalgesia in response to: When activated produce hyperalgesia in response to: **drugs such as morphine **drugs such as morphine inflammation or infection inflammation or infection peripheral injury peripheral injury signals from the CNS--- possibly stress signals from the CNS--- possibly stress When blocked can decrease pain When blocked can decrease pain

28 Glia and opioids Glia have μ (OP3) receptors ** (as well as other NT and NM receptors) Glia have μ (OP3) receptors ** (as well as other NT and NM receptors) Opioids can release dynorphin that also can activate glia ** Opioids can release dynorphin that also can activate glia ** Glial cells produce and release NT’s, proinflammatory cytokines (IL-1, IL-6, TNF) others Glial cells produce and release NT’s, proinflammatory cytokines (IL-1, IL-6, TNF) others e.g. NO, PG’s, excitatory aa’s, growth factors → hyperalgesia Chronic (not acute) use of morphine increases spinal levels of dynorphin → hyperalgesia Chronic (not acute) use of morphine increases spinal levels of dynorphin → hyperalgesia

29 Microglia Newer information CNS microglia- inflammatory cells that release cytokines the upregulate neural signals CNS microglia- inflammatory cells that release cytokines the upregulate neural signals Concept of Toll-like-receptor-mediated glial cell activation: Concept of Toll-like-receptor-mediated glial cell activation: - may be central to neuropathic pain - may be central to neuropathic pain - and impairment in opioid analgesia - and impairment in opioid analgesia - as well as development of unwanted opioid - as well as development of unwanted opioid side effects side effects

30 Opioids and Glial Cells Opioid agents possess Toll-like-receptor-4 agonist activity Opioid agents possess Toll-like-receptor-4 agonist activity Opioids thus act not only at classical opioid receptors but also via TLR4 to activate glial cells to release cytokines and other pronociceptive agents leading to a reduction in analgesia and then increase in hyperalgesia Opioids thus act not only at classical opioid receptors but also via TLR4 to activate glial cells to release cytokines and other pronociceptive agents leading to a reduction in analgesia and then increase in hyperalgesia

31 Narcotic induced hyperalgesia Possible new roads to pain management: Possible new roads to pain management: These mechanisms may help to explain NBS first described 20 years ago, and are avenues for research. These mechanisms may help to explain NBS first described 20 years ago, and are avenues for research. May lead to improved pharmacologic treatment of chronic pain and NBS May lead to improved pharmacologic treatment of chronic pain and NBS

32 Treatment of NBS

33 The Basics

34 Overview of Therapy Physician –Patient Relationship: Physician –Patient Relationship: Accept pain as real Accept pain as real Provide information to the pat and family- basis of pain in Provide information to the pat and family- basis of pain in NBS, effect of narcotics on pain and GI function NBS, effect of narcotics on pain and GI function Present the rationale of and plan for withdrawal Present the rationale of and plan for withdrawal Elicit pt concerns and gauge willingness to proceed Elicit pt concerns and gauge willingness to proceed Review with family Review with family NBS withdrawal protocol NBS withdrawal protocol Post therapy issues: Post therapy issues: Pt negotiates to go back on narcotics Pt negotiates to go back on narcotics Pt seeks drugs elsewhere Pt seeks drugs elsewhere

35 Treatment- Psychobiological Effective physician patient relationship Effective physician patient relationship Consistent plan for narcotic withdrawal Consistent plan for narcotic withdrawal Effective alternative treatments to manage pain and bowel symptoms Effective alternative treatments to manage pain and bowel symptoms Initiate treatment when dx of NBS made and no other dx explains symptoms Initiate treatment when dx of NBS made and no other dx explains symptoms NBS is a positive Dx NBS is a positive Dx Does not exclude existing inactive abd pathology ** Does not exclude existing inactive abd pathology **

36 Physician-patient relationship Validate pain is real, empathize with impact Validate pain is real, empathize with impact Dialogue- not lecture or written materials Dialogue- not lecture or written materials Discuss the physiologic basis Discuss the physiologic basis It’s not in your head * It’s not in your head * Visceral hypersensitivity Visceral hypersensitivity Brain-gut dysfunction & filter mechanism Brain-gut dysfunction & filter mechanism Effects of narcotic- slowing the bowel: Effects of narcotic- slowing the bowel: Constip, bloating, N/V, narcotics sensitize Constip, bloating, N/V, narcotics sensitize nerves and make the pain worse nerves and make the pain worse

37 Review the plan and rationale with the patient Assess patient concerns Assess patient concerns Expectations Expectations Willingness to participate in the program ** Willingness to participate in the program ** Review with family Review with family Review the therapeutic plan Review the therapeutic plan

38 “You could you be missing something” “What are you going to do for the pain” 1. NBS is a Dx that needs treatment but that the doctor will stay vigilant to eval new findings 1. NBS is a Dx that needs treatment but that the doctor will stay vigilant to eval new findings 2. Withdrawal is gradual, other treatments will be started, will not abandon pt with their pain 2. Withdrawal is gradual, other treatments will be started, will not abandon pt with their pain 3. Will address any flair ups or side effects as they occur 3. Will address any flair ups or side effects as they occur

39 Expectations Be realistic in explaining expectations Be realistic in explaining expectations Some pts become pain free Some pts become pain free More likely pts will feel better off narcotics than on and this may improve with time as More likely pts will feel better off narcotics than on and this may improve with time as other treatments are added other treatments are added Review plan with family Review plan with family Treatment is an ongoing process and not a cure- there will be ups and downs Treatment is an ongoing process and not a cure- there will be ups and downs

40 Follow up Emotional support with continuity of care Emotional support with continuity of care Psychologist, psychiatrist, pain management, other ancillary personnel Psychologist, psychiatrist, pain management, other ancillary personnel Visits in q 1-2 wks, then monthly x 2-3 months Visits in q 1-2 wks, then monthly x 2-3 months

41 Basics of Medical therapy Gradual withdrawal of narcotics Gradual withdrawal of narcotics Substituting other treatments to reduce the immediate withdrawal symptoms Substituting other treatments to reduce the immediate withdrawal symptoms Treat psychological comorbidity Treat psychological comorbidity Other treatments for pain control Other treatments for pain control **Note: not intended for habitual users of **Note: not intended for habitual users of recreational narcotics or those with drug recreational narcotics or those with drug seeking behaviors seeking behaviors

42 Inpatient vs Outpatient Inpt: N/V, pseudo-obstruction, ileus Inpt: N/V, pseudo-obstruction, ileus Limited motivation or social support Limited motivation or social support Outpt: Chronic narcotic use without acute Outpt: Chronic narcotic use without acute medical problems medical problems

43 Time Frame Developed over a shorter time frame: Developed over a shorter time frame: e.g. NBS in the postoperative setting e.g. NBS in the postoperative setting Developed over a longer time frame Developed over a longer time frame e.g. former IV narcotics user on e.g. former IV narcotics user on accelerated doses of methadone accelerated doses of methadone

44 Components of therapy

45 Concomitant treatments Prevent withdrawal Prevent withdrawal Reduce Anxiety Reduce Anxiety Treat psychological comorbidity Treat psychological comorbidity Provide long term central analgesia Provide long term central analgesia

46 1. Antidepressants to assist with pain control and treat depression when present Start optimally 1 week before withdrawal (start at lower doses) Start optimally 1 week before withdrawal (start at lower doses) (can ↑ over time) (can ↑ over time) Continue indefinitely for pain management Continue indefinitely for pain management Provides improved well being and reduces abd pain Provides improved well being and reduces abd pain TCA’s favored- use 2°amines over 3° (desip, nortr over imip, amitrip) TCA’s favored- use 2°amines over 3° (desip, nortr over imip, amitrip) desipramine, nortriptyline mg qhs (higher doses for depression) desipramine, nortriptyline mg qhs (higher doses for depression) SNRI can be substituted, e.g. duloxetine 30-90mg/d SNRI can be substituted, e.g. duloxetine 30-90mg/d **SSRI’s- less benefit in pain management (norepinephrine- import in pain Rx) **SSRI’s- less benefit in pain management (norepinephrine- import in pain Rx)

47 Other Psychotropic Medicines to treat pain and depression Mirtazapine 15-30mg hs: Mirtazapine 15-30mg hs: - consider instead of or better in addition to a TCA or SNRI if - consider instead of or better in addition to a TCA or SNRI if nausea is a prominent feature nausea is a prominent feature Quetiapine (Seroquel) mg hs: Quetiapine (Seroquel) mg hs: - adjunctive treatment for pain either in hospital or - adjunctive treatment for pain either in hospital or add after several weeks as opt if the antidepressant add after several weeks as opt if the antidepressant is not sufficient for pain management is not sufficient for pain management - also helpful for sleep problems, anxiety, and pain Rx - also helpful for sleep problems, anxiety, and pain Rx

48 2. Narcotic Withdrawal Convert total daily dose to morphine equivalents Convert total daily dose to morphine equivalents Inpt: use IV route: Inpt: use IV route: - Continuous drip of MS with PCA pump - Continuous drip of MS with PCA pump - Reduce dosage by 10-33% q24 hours - Reduce dosage by 10-33% q24 hours Use the slower taper for more extended user Use the slower taper for more extended user Typical duration is 4-11 days Typical duration is 4-11 days

49 Starting Dose Start with maximal dose that will achieve pt comfort Start with maximal dose that will achieve pt comfort Those receiving IV should continue the IV route for a few days and can switch to an equivalent oral dose Those receiving IV should continue the IV route for a few days and can switch to an equivalent oral dose Those on oral narcotics continue same Those on oral narcotics continue same

50 Narcotic Withdrawal Outpatient regimen: Outpatient regimen: - taper with oral medications - taper with oral medications - reduce by one dose (about 10-20%) / wk - reduce by one dose (about 10-20%) / wk

51 Withdrawal Rate 3-10 days 10 to 33% per day using medium to long acting narcotic 10 to 33% per day using medium to long acting narcotic Given in equal divided regular doses Given in equal divided regular doses For shorter acting agents e.g. oxycodone, hydrocodone: Convert to long term narcotic For shorter acting agents e.g. oxycodone, hydrocodone: Convert to long term narcotic such as methadone when pt is such as methadone when pt is or or Give more frequently e.g. q 3 hours Give more frequently e.g. q 3 hours

52 Equivalent Dosages of Common Opioids Drug SC/SQ/IV po morphine morphine codeine codeine fentanyl fentanyl patch- careful as conversion data underestimate strength patch- careful as conversion data underestimate strength hydrocodone hydrocodone hydromorphone hydromorphone meperidine meperidine methadone *acute/op naive; for chronic- goes methadone *acute/op naive; for chronic- goes down and depends on daily dose down and depends on daily dose oxycodone oxycodone Source: Epocrates- Opioid Equivalents

53 3. Block withdrawal symptoms The role of clonidine Reduces sympathetic activation: Reduces sympathetic activation: anxiety, restlessness, muscle pain, chills anxiety, restlessness, muscle pain, chills CNS: reduces anxiety (locus ceruleus) CNS: reduces anxiety (locus ceruleus) Intestinal effects: ↓ Ach release presynaptic terminals Intestinal effects: ↓ Ach release presynaptic terminals reduces gut motor activity- cramps reduces gut motor activity- cramps Relieves pain & diarrhea Relieves pain & diarrhea

54 Clonidine in NBS Dosage: Dosage: - start at 0.1 BID or TID - start at 0.1 BID or TID - can titrate to 0.6mg/day - can titrate to 0.6mg/day - alternative is patch: same daily dose - alternative is patch: same daily dose - begin when dose ↓ 50% or 1 st sign of withdrawal - begin when dose ↓ 50% or 1 st sign of withdrawal Can be tapered off rapidly or maintained for several weeks, even indefinitely depending on perceived risk of relapse & overall clinical benefit Can be tapered off rapidly or maintained for several weeks, even indefinitely depending on perceived risk of relapse & overall clinical benefit May have independent effects on FGID symptoms May have independent effects on FGID symptoms e.g. pain and diarrhea e.g. pain and diarrhea

55 4. Benzodiazepines Temporary use of medium to long acting benzo’s: Temporary use of medium to long acting benzo’s: Clonazepam or lorazepam Clonazepam or lorazepam Start at beginning of withdrawal and give at regular intervals throughout Start at beginning of withdrawal and give at regular intervals throughout Addresses sympathetic activation of withdrawal Addresses sympathetic activation of withdrawal Taper off when withdrawal is complete Taper off when withdrawal is complete Example: Lorazepam 1 mg q 6-8 hours Example: Lorazepam 1 mg q 6-8 hours

56 5. Constipation PEG based preferred 1-3 glasses/day PEG based preferred 1-3 glasses/day Avoid PO4, Mg based, stimulant types Avoid PO4, Mg based, stimulant types Colonoscopy prep for complete flush if severe constipation and KUB reveals large stool burden Colonoscopy prep for complete flush if severe constipation and KUB reveals large stool burden Methylnaltrexone if constipation is severe and not initially responsive to PEG solution Methylnaltrexone if constipation is severe and not initially responsive to PEG solution

57 6. Psychotherapy (Vital) part of comprehensive approach (Vital) part of comprehensive approach CBT and other behavioral therapies CBT and other behavioral therapies Dx and Rx rec of underlying psychopathology Dx and Rx rec of underlying psychopathology

58 Outcomes

59 Prospective study of 3 month outcomes after Detox in 39 Pts with NBS Pts: 92% F Pts: 92% F Dx: 21% IBS Dx: 21% IBS 37% IBD 37% IBD 29% FM/functional somatic/orthopedic 29% FM/functional somatic/orthopedic 13% post op/other 13% post op/other MS equivalent 75mg +/- 78mg with pain scores severe MS equivalent 75mg +/- 78mg with pain scores severe Common psychosocial problems: catastrophizing, anxiety, depression, poor daily function scores Common psychosocial problems: catastrophizing, anxiety, depression, poor daily function scores Drossman et al AJG 107 Sept 2012

60 Patient’s Clinical Features Mostly young to middle age females Mostly young to middle age females Variety of functional, structural, GI disorders and post operative status Variety of functional, structural, GI disorders and post operative status Pain avg ~ 15 yrs, narcotic use ~ 5 yrs Pain avg ~ 15 yrs, narcotic use ~ 5 yrs Despite MS equiv of 75mg/d, abd pain rated as more severe than labor or post op pain Despite MS equiv of 75mg/d, abd pain rated as more severe than labor or post op pain Other severe symptoms: N, fatigue, bloating, sleep disturbances Other severe symptoms: N, fatigue, bloating, sleep disturbances 1/3 signif anxiety, depression, high catastrophizing scores 1/3 signif anxiety, depression, high catastrophizing scores 80% out of work, > 6 hosp/2yrs, mult MD’s seen, high H.C. costs 80% out of work, > 6 hosp/2yrs, mult MD’s seen, high H.C. costs

61 Outcomes Detox successful 89.7% side effects 81%- narcotic withdrawal: anxiety, n, HA, sleep disturbances Abdominal pain reduced by 35% post detox Nonabdominal pain reduced by 42% Catastrophizing improved At 3 months: 45.8% returned to using narcotics For those who remain off- pain score at 3 mo ↓ 75% from pretreatment compared to those back on narcotics

62 Why did pts resume narcotic if most had reduced abd pain ¼ in 1 wk, ½ by ~3 mo, ¾ by ~8 mo ¼ in 1 wk, ½ by ~3 mo, ¾ by ~8 mo Reasons postulated other than pain relief: Reasons postulated other than pain relief: Some report being “numb from life issues” Some report being “numb from life issues” Some value being high Some value being high Other acknowledge some desire to stay off narcotics but can’t resist taking them again when prescribed by their doctors Other acknowledge some desire to stay off narcotics but can’t resist taking them again when prescribed by their doctors Higher COMM scores (Current Opioid Misuse Measure) Higher COMM scores (Current Opioid Misuse Measure) Successful detox and good clinical response assoc with low abuse potential Successful detox and good clinical response assoc with low abuse potential

63 Functional Abdominal Pain Syndrome

64 Functional Abdominal Pain Syndrome (FAPS) Present for at least 3 mo, onset at least 6 mo before dx of: Present for at least 3 mo, onset at least 6 mo before dx of: 1. Continuous or nearly continuous abd pain 1. Continuous or nearly continuous abd pain 2. No or only occ relationship with physiologic events (e.g. eating, defecation, or menses) and 2. No or only occ relationship with physiologic events (e.g. eating, defecation, or menses) and 3. Some loss of daily functioning and 3. Some loss of daily functioning and 4. The pain is not feigned (e.g. malingering) 4. The pain is not feigned (e.g. malingering) 5. Insufficient symptoms to meet criteria for another dx of GI function that would explain the pain 5. Insufficient symptoms to meet criteria for another dx of GI function that would explain the pain

65 Clues on PE Paradoxical “closed eyes” sign- acute pain of intestinal origin eyes open- anxious, FAP may close eyes to communicate pain Paradoxical “closed eyes” sign- acute pain of intestinal origin eyes open- anxious, FAP may close eyes to communicate pain Carnett’s sign or test- Pain increases with raising the head and contracting the rectus abdominus muscle, with visceral pain it decreases. Carnett’s sign or test- Pain increases with raising the head and contracting the rectus abdominus muscle, with visceral pain it decreases. Abd wall contraction leads to increased pain, central sensitization due to viscerosomatic referral Abd wall contraction leads to increased pain, central sensitization due to viscerosomatic referral

66 FAPS If exam is negative and with a history of extensive negative testing, avoid ordering further tests. If exam is negative and with a history of extensive negative testing, avoid ordering further tests. This reinforces concept something has been missed This reinforces concept something has been missed Further tests may aggravate pt’s visceral hypersensitivity Further tests may aggravate pt’s visceral hypersensitivity

67 Background factors with FAPS Severe and disabling pain without a structural Dx Confluence of factors Confluence of factors Brain-gut interactions Brain-gut interactions Peripheral measures e.g. intestinal inflam and altered immune function Peripheral measures e.g. intestinal inflam and altered immune function Central effects of stress on neural signaling Central effects of stress on neural signaling Background: Family distress, emotional, physical sexual abuse Background: Family distress, emotional, physical sexual abuse Often h/o of recurrent abd pain in childhood Often h/o of recurrent abd pain in childhood Perhaps post infectious IBS in a setting of emotional distress Perhaps post infectious IBS in a setting of emotional distress Prior surgeries that can lead to abd-pelvic nerve injury, mucosal inflam from infection that can activate mucosal mast and immune cells that secrete proteases, cytokines, and other mediators that activate sensory neurons, and promote visceral hypersensitivity Prior surgeries that can lead to abd-pelvic nerve injury, mucosal inflam from infection that can activate mucosal mast and immune cells that secrete proteases, cytokines, and other mediators that activate sensory neurons, and promote visceral hypersensitivity

68 Central mechanisms Activation of certain brain regions e.g. mid-cingulate cortex Activation of certain brain regions e.g. mid-cingulate cortex This leads to disinhibition- an inability to down regulate incoming sensory input from the viscera This leads to disinhibition- an inability to down regulate incoming sensory input from the viscera Pain + noxious experiences can encode a linkage of emotional distress with the pain in this part of the brain Pain + noxious experiences can encode a linkage of emotional distress with the pain in this part of the brain In chronic and severe pain peripheral factors e.g. visceral hypersensitivity may become secondary to central sensitization, the alteration of central pain control centers In chronic and severe pain peripheral factors e.g. visceral hypersensitivity may become secondary to central sensitization, the alteration of central pain control centers Therefore management must include centrally mediated treatments Therefore management must include centrally mediated treatments

69 Effective doctor patient relationship Challenges for the physician : - frustration, anger, perception of decreased effectiveness in the absence of a treatable disorder, failure of pt improvement perceived as failure by the physician, stress of the pt demands for narcotics for pain relief, realities of large time commitments needed and low reimbursement rates Physician to treat himself or herself first: - Accept that FAPS is a + dx and further studies not needed - Accept chronicity - Reduce expectations for cure or rapid recovery - Understand role: to provide support, guidance, and hope, facilitate pt acceptance of the as a chronic disorder requiring personal responsibility for management

70 Equianalgesic dosage table Buprenorphine (IM/IV): 0.4 Butorphanol (IM/IV): 2.0 Codeine (IM/IV): 120 Codeine (PO): 200 Fentanyl (IM/IV): 0.1 Fentanyl (Transdermal): 0.2 Hydrocodone (PO): 30 Hydromorphone (IV/IM/SC): 1.5 Hydromorphone (PO): 7.5 Levorphanol (acute PO): 4.0 Levorphanol (chronic PO): 1.0 Meperidine (IV/IM/SC): 75 Meperidine (PO): 300 Methadone (acute IV): 5.0 Methadone (acute PO): 10 Morphine (IV/IM/SC): 10 Morphine (acute PO): 60 Morphine (chronic PO): 30 Nalbuphine (IV/IM/SC): 10 Oxycodone (PO): 20 Oxymorphone (IV/IM/SC): 1.0 Oxymorphone (PO): 10 Tapentadol (PO): Methadone Chronic dosing: 0-99 mg: 4: mg: 8: mg: 12: mg: 15:1 >1000 mg: 20:1

71 Opioid Conversion Data: Equi-Analgesic Dosing Guide Equivalency Table

72 Mechanism of Glial cell activation and pain Glial cells express receptors for NT’s and NM’s Glial cells express receptors for NT’s and NM’s This can enhance pain transmission and counter pain inhibitory effects of morphine This can enhance pain transmission and counter pain inhibitory effects of morphine Fractalkine: neuron to glial cell chemokine- may be involved in exaggerated nociceptive pain response to visceral stimuli Fractalkine: neuron to glial cell chemokine- may be involved in exaggerated nociceptive pain response to visceral stimuli


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