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IBS - AGA

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Douglas A. Drossman, M.D. Co-Director UNC Center for Functional GI & Motility Disorders Chapel Hill, NC, USA However, we are now conducting research in an time where ... – PowerPoint PPT presentation

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Title: IBS - AGA


1
Narcotic Bowel Syndrome
Douglas A. Drossman, M.D. Co-Director UNC Center
for Functional GI Motility DisordersChapel
Hill, NC, USA
2
Adverse Effects of Opioids on the Bowel
  • Opioid bowel dysfunction (OBD)
  • Constipation, nausea, vomiting, bloating, ileus,
    and sometimes pain
  • Narcotic bowel syndrome (NBS)
  • Abdominal pain is the predominant symptom
  • Progressive and paradoxical increase in pain
    despite continued or escalating dosages of
    narcotics prescribed to relieve the pain
  • Underrecognized

Pappagallo. Am J Surg 200118211S18S
Grunkenmeier et al. Clin Gastro Hep
200751126-1139 Mehendale, Yuan. Dig Dis
200624105112
2124
3
Narcotic Bowel Syndrome
A Case of Narcotic Bowel Syndrome Successfully
Treated with Clonidine Voishim Wong, George
Sobala, and Monty Losowsky Postgrad Med Journal
1994 70138
Editorial The Narcotic Bowel Syndrome M. Rogers
and J. Cerda, J Clin Gastroenterol, 1989
11(2)132
Narcotic Bowel Treated with Clonidine John E.
Sandgren, Mark S. McPhee, and Norton J.
Greenberger Ann of Int Med 1984 101331
1987
4
Narcotic Bowel Syndrome
The Narcotic Bowel Syndrome Clinical Features,
Pathophysiology, and Management David M. S.
Grunkemeier, Joseph E. Cassara, Christine B.
Dalton, and Douglas A. Drossman
Seminal paper for 2007 American College of
Physicians
Grunkemeier, DMS et al., Clin Gastroenterology
and Hepatology 2007 51126
1988
5
Typical Clinical Presentation for NBS
  • Patient presents with chronic or recurrent
    abdominal pain which is treated with narcotics
  • Narcotics may have relieved pain initially but
    then tachyphylaxis occurs
  • Pain worsens when the narcotic effect wears off
  • Shorter pain-free periods result in increasing
    narcotic doses
  • Increasing doses further alter motility and
    aggravate pain
  • Can occur with in patients FGID, organic disease
    or otherwise health subjects (e.g., post
    operative)

Grunkenmeier et al. Clin Gastro Hep 2007 51126
2125
6
Case 1 NBD Developing in FBD
  • 42 yo woman with h/o IBS for gt 20yrs but
    worsening lower abdominal pain x 3 yrs
  • PCP was prescribing oxycodone (10 mg tid) for
    pain and clonazepam and paroxetine for anxiety
    and depression
  • Pain seemed different from her more typical IBS
    symptoms more persistent and not relieved by
    defecation
  • Pain associated with abdominal bloating, nausea,
    vomiting, and depressive symptoms
  • Twice tried to stop narcotics but was
    unsuccessful due to increasing pain
  • Was placed on outpatient detoxification and 1
    year later she remained off narcotics with only
    mild IBS symptoms

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2126
7
Functional Pain Disorders Particularly Vulnerable
to Being Treated with Narcotics
  • Abdominal pain is a key feature and associated
    with
  • Pain is a strong predictor of health care seeking
  • 43 of patients admitted for abdominal pain are
    discharged from hospitals with no specific
    explanation for their pain
  • Perception of no other treatment options
  • Narcotics are more likely prescribed when
    symptoms are severe and patient demands pain
    relief

Spiegel et al. Arch Intern Med 20041641773-1780
Lembo A et al. CGH 20053717725
Grunkemeier D.M.S. et al. CGH 2007, 51126 Gray
DW et al. Br J Surg 198774239242
2127
8
Case 2 NBS with Crohns Disease
  • 20 yo woman with a 16 mo h/o narcotic use
    (methadone 260 mg/d) for low back pain
  • Admitted with obstipation methadone tapered to
    230 mg/d and enemas given
  • 3 days later, patient returned with N/V, RLQ pain
  • Studies
  • CT scan short segment of TI thickening and
    retained fecal material
  • Colonoscopy congested TI without obstruction
    biopsies showed mild chronic active ileitis
  • SBFT20 cm of thickened, non-obstructing TI

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2128
9
Case 2 NBD with Crohns Disease
  • Narcotics reinstituted for pain presumed due to
    Crohns disease and pain got worse
  • The GI service was consulted and determined that
    although the patient had Crohns disease, the
    pain pattern was related clinically to NBS
  • Corticosteroids and 5-ASA were started and
    methadone was tapered gradually over 11 days
  • Pain improved with withdrawal of narcotics
  • Patient continued to use narcotics ? worsening
    pain that improved with withdrawal of narcotics
    (unrelated to CD activity)

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2129
10
NBS Can Occur in Organic GI disorders
  • The pain is attributed to an underlying disease
  • The physician feels justified to use narcotics
    even when disease activity is not sufficient to
    explain pain
  • Assessment of disease activity relative to the
    patients pain behavior is needed

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2130
11
Case 3 NBD Developing Postoperatively
  • 40 yo lawyer admitted with severe abdominal pain,
    n/v fever
  • No history of previous GI symptoms
  • Severe RLQ tenderness and leukocytosis ? surgery
    ? normal
  • Postoperatively given 40 mg/day of IV Morphine
    Sulphate
  • 2 weeks later increasing pain and obstipation
    x-ray showed partial small bowel obstruction ?
    2nd surgery
  • 6 cm. small bowel resected due to adhesions and
    SBO
  • 1 wk later?peritonitis from anastamotic
    perforation?3rd surgery
  • Continued in hospital for 2 months on 40?60?80
    mg/day IV morphine sulfate for severe pain n/v
    with pseudo-obstruction
  • GI consult diagnosed NBS and patient detoxified
    over 6 days
  • Patient discharged?continued abdominal pain,
    bloating for 1 yr
  • No difficulties over subsequent 10 years

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2131
12
NBS Can Occur in Otherwise Healthy Persons
  • Can occur postoperatively from high dosages of IV
    narcotics
  • Narcotics are justified because the pain and N/V
    is attributed to surgical injury and
    postoperative ileus
  • Surgery ? visceral hypersensitivity ? enhanced
    pain
  • Increased narcotics ? ileus ? pseudoobstruction
  • NBS develops

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2132
13
Challenges for Physicians
  • Physicians are ambivalent about prescribing
    narcotics for non-malignant chronic pain
  • Patients requests for pain relief ? difficult
    dialog about narcotic use. This can interfere
    with discussion of other treatment options
  • The physician may then feel unwilling or unable
    to manage the clinical condition ? negative
    interaction
  • Patient may feel hopeless and angry at the
    physician when the request for narcotics is
    rejected

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126 Drossman DA. Am J
Gastroenterol 1997 921418
2133
14
Challenges for Physicians (cont.)
  • Nonverbal communication of pain most predictive
    of narcotic prescribing
  • Time constraints for clinical visit increases
    diagnostic testing ? reduces effective
    communication and information gathering?
    improper-decision making
  • Patients may be discharged from ER or released
    from clinic with narcotic Rx for pain without a
    diagnosis or treatment plan or follow-up
  • PCP must deal with lack of diagnosis and pressure
    to prescribe narcotics

Turk DC et al. Clin J Pain 1997 13330 Drossman
DA. Gastroenterology 2004 126952
2134
15
Narcotic Bowel Syndrome
Pain
Narcotics
Narcotics
Vicious Cycle of Patient - Physician Interactions
Maladaptive Therapeutic Interaction
Narcotic Bowel Syndrome
Patient Frustration
Physician Frustration
Negative evaluations
Furor Medicus
Healthcare / Societal Pressures
Increased Healthcare Utilization
Emergency Room Visits
1888b
16
Narcotic Prescribing in the Health Care Setting
  • The USA (4.6 of world population) prescribes 80
    of worlds opioids.
  • 1997?2002 gt400 increase in retail sales of
    oxycodone and methadone
  • 1993?1999 100 increase in hydrocodone
    associated ED visits
  • Prescribing has shifted from acute severe pain or
    palliative care of malignancies to prolonged use
    in chronic nonmalignant pain (e.g. IBD, FGIDs)
  • Pain treatment centers shifted to narcotic
    treatments for non-malignant pain ? emphasizes
    quick fix over multidisciplinary pain treatment
  • There is no scientific evidence for long-term
    benefit of narcotics in non-malignant pain
  • Greater sensitivity of bowel in FGIDs ? more side
    effects from narcotics
  • These changing practice patterns are enabled by
    3rd party payers due to greater cost benefit with
    shorter visits and expensive delivery systems
  • The net effect is increased annual health care
    expenditures

Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007 51126
2135
17
Retail Sales of Opioid Medications 1997-2002
1997 2002 change Morphine 5,922,872 10,264,264
73.3 Hydrocodone 8,669,311 18,822,618 117.1 Oxycod
one 4,449,562 22,376,891 402.9 Methadone
518,737 2,649,559 410.8
Trescot et al. Pain Physician 2006 9(1)1
2136
18
Opiate Prescriptions in Ambulatory Visits NHAMCS
1994-2005
Ambullatory visits
Choung et al. in preparation
2138
19
Drug Abuse Related Emergency Department Visits
Visits
US Department of Health and Human Services. April
2004 Trescot et al. Pain Physician. 2006 Jan
9(1)1-39
2140
20
Potential Physiological Mechanisms for NBS
  • Bimodal (Excitatory/Inhibitory) Opioid Modulation
    in Dorsal Horn
  • Activation of opioid receptors generally
    considered to inhibit afferent neurons ? reduced
    signaling (via Gi/Go protein receptor)
  • Newly identified Gs protein excitatory receptor ?
    hyperalgesia
  • Gs excitatory receptor activates with low dose
    opioids (1-10?mol/L) or and acutely is inhibited
    with high dose opioids (gt1µmol/L)
  • Gi/Go inhibitory receptor activates with high
    dose opioids but is inhibited with chronic opioid
    use
  • Chronic opioid use?hyperalgesia due to Gi/Go
    inhibition and Gs activation
  • Low dose narcotic antagonists (e.g.
    Suboxonebuprenorphine/naloxone) ? analgesia with
    lower dosages by blocking Gs protein excitatory
    activation

Crain SM et al. Pain 2000 84121 Crain SM et al.
Brain Res 1992 575
Grunkemeier D.M.S. et al. CGH 2007 51126
2141
21
a
b
c
Low-dose opioid 1-10 nM
High-dose opioid gt1 mM
Chronic opioid use
Gi
Gi
Gi
Go
Go
Go
Gs
Gs
Gs
Inhibitory
Inhibitory
Inhibitory
Excitatory
Excitatory
Excitatory
Low-dose masks inhibitory effects
High-dose masks excitatory effects
Sensitized excitatory receptor
Tolerance to inhibitory receptor
Hyperalgesia
Hyperalgesia
Analgesia
1890
22
Potential Physiological Mechanisms for NBS
  • Bimodal (Excitatory/Inhibitory) Opioid Modulation
    in Dorsal Horn
  • Descending Pain Facilitation at RVM and via
    Dynorphin and CCK Activation
  • Cingulate and prefrontal cortex and rostral
    ventral medulla (RVM) and PAG modulate incoming
    pain signals at the level of the spinal cord
  • These areas can produce antinociception via
    descending inhibitory pathways
  • RVM in particular can activate descending tracts
    to enhance nociception at the spinal cord
  • Dynorphin (endogenous opioid) is found in
    inflammatory conditions, with nerve injury or in
    opiate induced pain states ?increases excitatory
    neurotransmitters from primary afferent neurons
  • Cholecystokinin (CCK) and CCK receptors in CNS
    overlap with distribution of opioid peptides and
    can facilitate descending pain pathways

Grunkemeier D.M.S. et al. CGH 2007 51126
Porreca F et al. Trends Neurosci 2002 25319
Vanderah TW et al. J Neurosci 2000 207074
Heinricher MM et al. J Neurophysiol 2004 921982
2142
23
Glia of Brain and Spinal Cord
Microglia
Astrocytes
2284
24
Potential Physiological Mechanisms for NBS
  • Bimodal (Excitatory/Inhibitory) Opioid Modulation
    in Dorsal Horn
  • Descending Pain Facilitation at RVM and via
    Dynorphin and CCK Activation
  • Effects of Glial Cell Activation on Pain and
    Facilitation by Opioids
  • Glial cells (astrocytes and microglia) in dorsal
    horn can amplify pathologic pain and produce
    hyperalgesia
  • Infection/chronic inflammation activates glial
    cells ? releases inflammatory cytokines ?
    enhances neuronal excitability
  • Chronic narcotics bind to glia via µ receptors ?
    release of proinflammatory cytokines
  • Opiates can also activate dynorphin release ?
    glial cell activation

Grunkemeier D.M.S. et al. CGH 2007,
51126 Watkins LR et al. Trends Neurosci
200528661 Hutchinson MR et al. Sci World J
2007798
2143
25
Effects of Opioids on Glia and Pain
  • Opioids acutely activate neuronal receptors ?
    analgesia
  • Chronic opioid use activates glia via toll-like
    receptors (TLR4, TLR2)
  • TLR dependent glial activation produces
    pro-inflammatory cytokines (IL-1, IL-6, TNFa) and
    other inflammatory mediators
  • Inflammatory cytokines increase neuronal
    excitability, produce neuropathic pain, reduce
    opioid analgesia and chronically, lead to opioid
    induced hyperalgesia.

Hutchinson M et al. Scientific World J 2007 798
2285
26
Opioids Neuronal Analgesia and Glial Activation
TLR4
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
ANALGESIA
IL-1
Analgesia
2286
Hutchinson M et al. Scientific World J 2007798
27
Effects of Opioids on Glia and Pain
  • Opioids acutely activate neuronal receptors ?
    analgesia
  • Chronic opioid use activates glia via toll-like
    receptors (TLR4, TLR2)
  • TLR dependent glial activation produces
    pro-inflammatory cytokines (IL-1, IL-6, TNFa) and
    other inflammatory mediators
  • Inflammatory cytokines increase neuronal
    excitability, produce neuropathic pain, reduce
    opioid analgesia and chronically, lead to opioid
    induced hyperalgesia.
  • Low dose opioid antagonists (e.g., naloxone) can
    block TLR activation of glia and enhance opioid
    analgesia
  • Future pain treatment may reduce detrimental
    (i.e., glial inflammatory) effects while
    preserving beneficial (neuronal opioid receptor
    analgesic) effects

Hutchinson M et al. Scientific World J 2007 798
2287
28
Potential Benefit of Opioid Antagonists
TLR4
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
ANALGESIA
2288
Hutchinson M et al. Scientific World J 2007798
29
Neuron-to-glia chemokine Fractalkine
Sensory afferent neuron ATP, NO, SP, CGRP
Immune / infectious challenges Virus, bacteria,
trauma
CNS signals
Dorsal horn glial cell
Other glial cells
Chronic opiod use Pro-inflammatory cytokine,
dynorphin release
Proinflammatory cytokines, PG, NO excitatory
amino acids
Neuron excitability upregulates NMDA release
Enhanced pain
1889
30
Diagnostic Criteria Narcotic Bowel Syndrome
Chronic or frequently recurring abdominal pain
treated with acute high dose or chronic narcotics
and
  • The pain worsens or incompletely resolves with
    continued or escalating dosages of narcotics
  • There is marked worsening of pain when the
    narcotic dose wanes and improvement when
    narcotics are reinstituted (Soar and Crash)
  • There is a progression of the frequency, duration
    and intensity of the pain episodes
  • The nature and intensity of the pain is not
    explained by a current or previous GI diagnosis

A patient may have a structural diagnosis
(e.g., IBD, chronic pancreatitis, but the
character or activity of the disease process is
not sufficient to explain the pain
Grunkemeier D.M.S. et al. Clin Gastro and
Hepatology 2007, 51126
2144
31
Narcotic Bowel Syndrome
Pain
Narcotics
Narcotics
Vicious Cycle of Patient - Physician Interactions
Maladaptive Therapeutic Interaction
Narcotic Bowel Syndrome
Patient Frustration
Physician Frustration
Negative evaluations
Furor Medicus
NBS treatment, Narcotics withdrawal
Healthcare / Societal Pressures
Increased Healthcare Utilization
Emergency Room Visits
1888a
32
Narcotic Withdrawal Protocol
Physician Patient Relationship
-3 -2 -1 0 1 2 3 4 5 6 7 8 9 10 . . . 21
Day of taper
1887
33
Clinician-Patient Process and Techniques
  • Accept the pain as real (validate) and treatable
  • I can see the pain has really affected your
    life
  • We can work together on this

2145
34
Clinician-Patient Process and Techniques
  • Accept the pain as real and treatable
  • Elicit the patients concerns and expectations
  • What are your biggest worries or concerns about
    being on narcotics (and going off narcotics)?
  • What do you expect will happen when you stop
    narcotics?

2146
35
482
36
Clinician-Patient Process and Techniques
  • Accept the pain as real and treatable
  • Elicit the patients concerns and expectations
  • Provide information through a dialog
  • Address the patients stated concerns and
    expectations
  • Provide a physiologic basis for the pain
  • Pain in the body is experienced in the brain
    where it can turn pain volume up or down
    depending on the circumstances (give examples)
  • Discuss the effects of narcotics on pain and GI
    function
  • Narcotics slow the bowels producing the
    constipation, bloating and vomiting you are
    having they also sensitize the nerves to turn up
    the pain volume thus making the pain worse
  • Explain the rationale for and process of
    withdrawal
  • It is likely you will be better and certainly no
    worse when you are off the narcotics. We will be
    substituting other pain control methods while we
    gradually taper the narcotics (so you wont be
    abandoned in pain)

2147
37
Clinician-Patient Process and Techniques
  • Accept the pain as real and treatable
  • Elicit the patients concerns and expectations
  • Provide information through a dialog
  • Present the withdrawal program
  • Use illustrations or graphics
  • Involve a responsible family member
  • Indicate that someone will be available to
    address possible side effects or flare-ups

2148
38
Clinician-Patient Process and Techniques
  • Accept the pain as real and treatable
  • Elicit the patients concerns and expectations
  • Provide information through a dialog
  • Present the withdrawal program
  • Clinical setting
  • Outpatient
  • Patient must be highly motivated
  • Withdrawal can take days to weeks
  • Inpatient
  • If complicated by nausea, vomiting, ileus or
    pseudo-obstruction
  • Limited motivation or social support
  • Requires monitoring
  • Withdrawal can occur over several days

2210
39
Clinician-Patient Process and Techniques
  • Accept the pain as real and treatable
  • Elicit the patients concerns and expectations
  • Provide information through a dialog
  • Present the withdrawal program
  • Clinical setting
  • Gauge the patients response
  • Willingness to go through the program
  • Degree of participation
  • Keep a log?
  • Be aware of Whatever you say doc
  • Assess Non-verbal behaviors and meta-language
  • Address challenging questions
  • How do you know youre still not missing
    something?
  • What if I get a bad attack?
  • What if these other medicines make me sick?

2149
40
Narcotic Withdrawal Protocol
  • Accept pain as real and treatable
  • Elicit patients concerns/expectations
  • Provide information through a dialog
  • Present the withdrawal program
  • Gauge the patients response

TCA or SNRI
PEG 3350 17g PO BID
Physician Patient Relationship
-3 -2 -1 0 1 2 3 4 5 6 7 8 9 10 . . . 21
Day of taper
1887
41
Antidepressants
  • Tricyclics (e.g., Desipramine, Nortriptyline,
    Amitriptyline)
  • Pain benefit
  • Side effects (sedation, constipation) reduce
    adherence
  • 20 amines (desipramine/nortriptyline) have fewer
    side effects
  • SNRIs (e.g., Duloxetine, Venlafaxine,
    Desvenlafaxine)
  • Pain benefit
  • Nausea side effects
  • Specific effects
  • Duloxetine first to be marketed for pain with
    depression
  • Venlafaxine requires higher dosage (e.g., 225
    mg.) for pain benefit
  • SSRIs (e.g., Paroxetine, Citalopram,
    Escitalopram)
  • Anxiolysis (social phobia, agoraphobia, OCD)
  • /- pain benefit (but augments TCA effect via
    anxiolysis)
  • Side effects (anxiety, diarrhea)
  • Specific effects

2060
42
Narcotic Withdrawal Protocol
  • Accept pain as real and treatable
  • Elicit patients concerns/expectations
  • Provide information through a dialog
  • Present the withdrawal program
  • Gauge the patients response

Lorazepam 1mg PO q 6hrs.
TCA or SNRI
220 200 180 160 140 120 100 80 60 40 20 0
Morphine equiv. Dose (mg)
PEG 3350 17g PO BID
Physician Patient Relationship
-3 -2 -1 0 1 2 3 4 5 6 7 8 9 10 . . . 21
Day of taper
1887
43
Narcotic Withdrawal
  • Start medium acting benzodiazepine (e.g.,
    lorazepam)
  • Involve psychologist to help with withdrawal
    program
  • Narcotic tapering
  • Start with maximal daily dose of medium to long
    acting narcotic (more frequent dosing needed for
    short acting opiates)
  • Standardize all narcotics to one dose (morphine
    equivalents)
  • Non-contingently reduce 10-33 each day
  • (e.g., off on 4th day with 33 reduction qd)
  • No prn or breakthrough dosing)

2151
44
Narcotic Withdrawal Protocol
Accept pain as real and treatable Elicit patients
concerns/expectations Provide information through
a dialog Present the withdrawal program Gauge the
patients response
Clonidine 0.1mg PO q 6 hrs.
Lorazepam 1mg PO q 6hrs.
TCA or SNRI
220 200 180 160 140 120 100 80 60 40 20 0
Morphine equiv. Dose (mg)
PEG 3350 17g PO BID
Physician Patient Relationship
-3 -2 -1 0 1 2 3 4 5 6 7 8 9 10 . . . 21
Day of taper
1887
45
Centrally Acting Augmentation
  • Clonidine
  • a2-adrenergic against with central (anxiety
    reduction) and peripheral (pain reduction via
    bowel compliance) effects
  • Helps reduce diarrhea
  • Prevents adrenergic effects of narcotic
    withdrawal
  • Mirtazepine
  • Serotonergic and noradrenergic drug with 5HT2 and
    5HT3 effects can have pain benefit
  • Use with nausea, anorexia, weight loss, diarrhea
  • Some sedation
  • Buspirone
  • Azaprione with anti-anxiety effects acting on non
    BZD GABA receptors
  • Has 5HT1 and 5HT2 effects
  • May augment the effect of the antidepressant
  • Quetiapine
  • Atypical antipsychotic in high doses with complex
    effects
  • Dopamine (D1, D2) and Serotonin (5HT1a, 5HT2)
    antagonism and some a2-adrenergic effect
  • Benefits include sleep, anti-anxiety, analgesia
    augmentation

2152
46
If I dont think its going to work, will it
still work?
2021
47
When Will Program Work?
  • The patient
  • Has no history of drug seeking behavior or other
    substance use
  • Recognizes the adverse effects of the narcotics
  • Understands there are other treatment options for
    pain relief
  • Is motivated at start and throughout treatment
    (no bargaining)
  • The physician
  • Believes in and communicates commitment to the
    patient and the treatment plan
  • Is comfortable in coordinating the treatment
    (medications, availability)
  • Will personally follow up or set up resources
    (psychologist, primary care doc, PA or FNP) to do
    so
  • The treatment interaction is collaborative
  • Health care resources are available
  • Psychologist
  • Primary care clinician

2155
48
Interferences With Successful Outcome
  • Negotiation (Just one more day)
  • Determine if it relates to anxiety about
    treatment failure, ambivalence, lack of desire to
    continue or malingering
  • Explore and discuss patient concerns
  • May not have been previously addressed
  • May fear being abandoned in the care
  • Provide solutions
  • Continue discussions
  • Reduce time between dosing maintaining daily
    dosage
  • Adjust or add other medications (.e.g. Ketorolac)
  • Rapidly tapers or abruptly withdraws narcotics
  • Patient may not have understood protocol
  • Trying to prove he/she can do it or to get it
    over with
  • Sabotage (See it does not work)

2156
49
Interferences With Successful Outcome
  • Seeks additional help elsewhere
  • May be due to lack of trust with diagnosis
  • Risk of seeing physicians who again prescribe
    narcotics
  • Provide solutions
  • Encourage patient to work with one treating
    physician
  • Identify and communicate with other physicians
    involved
  • Copy records to other physicians
  • Be vigilant to drug seeking behaviors

2157
50
Case 4 Unsuccessful Treatment
  • 26 yo medical student sent by father (prominent
    academic physician) for detoxification
  • 2 year history of pain beginning acutely as sharp
    and severe in RLQ followed by N/V which has
    progressed in frequency and severity
  • Extensive evaluation with HIDA, MRI/MRCP, ERCP,
    CT, Liver bx all normal
  • Diagnosed with cyclic vomiting syndrome and Rx
    with amitriptyline with 8 mo relief
  • Pain recurred while on taking night call ? began
    taking fentanyl patch ? improvement ? gradual
    increase in dosing for relief ? now self
    medicates 2 mg. dilaudid SQ q4 hrs.
  • Currently with severe constipation (BM q2-3 wks),
    pain relieved only 1-2 hrs on narcotic, n/v
  • Psychologist consulted to help with
    detoxification program
  • Psychosocial
  • Lost control of life because of frequent
    hospitalizations
  • Engaged for 2 yrs and fiance lives out of state
  • Current problem has delayed wedding and he has
    contemplated dropping out of school
  • Brother developed appendicitis and quit medicine
    soon after graduation Best choice he ever
    made Father upset
  • Denies stress related to symptoms or in his life
    illness is positive brings him closer to
    mother and fiance

2153
51
Case 4 Unsuccessful Treatment, Cont.
  • Admitted for detoxification program with taper to
    occur by 25 daily
  • While patient acknowledged desire to go off
    narcotics, he repeatedly asked what he will get
    if pain recurs.
  • On 1st day before when getting full narcotic
    dosing he asked for delay in taper because he ate
    fried chicken the night before
  • During taper he requested to leave hospital to go
    to his hotel room
  • Later mother noted narcotics stashed in his room
  • Patients mother reported that he told her he
    would go back on narcotics at home if he has pain
  • One night before completion of taper patient
    reported increased pain and demanded to go back
    on narcotics and to slow down taper
  • This was refused and narcotics completely tapered
    off
  • That night prior to discharge the patient signed
    out against medical advice
  • A follow up appointment was given in 6 weeks but
    patient did not return
  • 6 months later the patient contacted Dr. Drossman
    stating he now felt he was ready to come off
    narcotics.
  • Inpatient detoxification rescheduled

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Case 4 Unsuccessful Treatment (cont.)
  • Rehospitalized for detoxification 10/08
  • Psychosocial / Clinical data
  • Claimed that had bowel obstructions from
    adhesions after leaving UNC records obtained
    and not documented laparoscopy showed some
    adhesions but no obstruction
  • Patient said engagement was off, mother said he
    is still seeing her
  • Mother closely involved in care
  • Psychologist saw patient and saw little
    motivation for detox refused several visits
  • Protocol instituted with more delayed detox
    program 15 reduction daily
  • On 2nd day patient stated it was too fast and
    asked for 10 reduction refused
  • By 4th day patient said he was having pain and
    asked for just one shot
  • Patient noted to house staff that after discharge
    he would go to ER to get pain shot if he had pain
  • Narcotics tapered off by 6th day
  • That evening he went down to basement of hospital
    to find the ER to get a pain shot. was escorted
    back but that evening and later found to be very
    sedated
  • Patient discharged the next morning

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Summary Narcotic Bowel Syndrome
  • NBS is a subset of opioid bowel dysfunction
  • Chronic or recurrent abdominal pain which worsens
    or incompletely resolves with continued or
    escalating dosages of narcotics
  • Can occur in patients with FGID or organic
    diseases
  • Limitations in health care use of narcotics for
    non-malignant pain, poor communication, improper
    decision-making and lack of recognition of NBS,
    contribute to escalating narcotic use
  • Treatment involves a protocol driven
    detoxification that requires a motivated patient
    and clinical team

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It sort of makes you stop and think, doesnt it?
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