Transcript IBS - AGA - UNC School of Medicine

Narcotic Bowel
Syndrome
Douglas A. Drossman, M.D.
Co-Director
UNC Center for Functional GI & Motility Disorders
Chapel Hill, NC, USA
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 2001;182:11S–18S
Mehendale, Yuan. Dig Dis 2006;24:105–112
Grunkenmeier et al. Clin Gastro Hep 2007;5:1126-1139
2124
Narcotic Bowel Syndrome
A Case of Narcotic Bowel Syndrome
Successfully Treated with Clonidine
Voishim Wong, George Sobala,
and Monty Losowsky
Postgrad Med Journal 1994; 70:138
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; 101:331
1987
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; 5:1126
1988
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; 5:1126
2125
Case 1: NBD Developing in FBD
 42 yo woman with h/o IBS for > 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; 5:1126
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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 2004;164:1773-1780
Lembo A et al. CGH 2005;3:717–725
Grunkemeier D.M.S. et al. CGH 2007, 5:1126
Gray DW et al. Br J Surg 1987;74:239–242
2127
Case 2: NBS with Crohn’s 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
– SBFT:20 cm of thickened, non-obstructing TI
Grunkemeier D.M.S. et al. Clin Gastro and Hepatology 2007; 5:1126
2128
Case 2: NBD with Crohn’s Disease
 Narcotics reinstituted for pain presumed due to Crohn’s
disease and pain got worse
 The GI service was consulted and determined that although
the patient had Crohn’s 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; 5:1126
2129
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
patient’s pain behavior is needed
Grunkemeier D.M.S. et al. Clin Gastro and Hepatology 2007; 5:1126
2130
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; 5:1126
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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; 5:1126
2132
Challenges for Physicians
 Physicians are ambivalent about prescribing
narcotics for non-malignant chronic pain
 Patient’s 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; 5:1126
Drossman DA. Am J Gastroenterol 1997; 92:1418
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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; 13:330
Drossman DA. Gastroenterology 2004; 126:952
2134
Narcotic Bowel Syndrome
Pain
Narcotics
Narcotics
Maladaptive
Therapeutic
Interaction
Vicious Cycle
of Patient Physician
Interactions
Physician
Frustration
Narcotic Bowel
Syndrome
Patient
Frustration
“Negative”
evaluations
“Furor
Medicus”
Healthcare /
Societal
Pressures
Emergency
Room Visits
Increased
Healthcare
Utilization
1888b
Narcotic Prescribing in the Health Care Setting
 The USA (4.6% of world population) prescribes 80% of world’s opioids.
 19972002: >400% 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 nonmalignant 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; 5:1126
2135
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
Oxycodone
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
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Opiate Prescriptions in Ambulatory Visits
NHAMCS 1994-2005
8
7
6
%
Ambullatory
visits
5
4
3
2
1
0
1994 1995
Choung et al. in preparation
1996 1997
1998 1999
2000 2001
2002 2003
2004 2005
2138
Drug Abuse Related Emergency Department Visits
110,000
100,000
Narcotic analgesics
Benzodiazepines
80,000
60,000
Visits
40,000
20,000
0
1995
1996
1997
1998
US Department of Health and Human Services. April 2004
Trescot et al. Pain Physician. 2006 Jan; 9(1):1-39
1999
2000
2001
2002
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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 (110ηmol/L) or and acutely is inhibited with high dose opioids
(>1μmol/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. Suboxone–
buprenorphine/naloxone)  analgesia with lower dosages by
blocking Gs protein excitatory activation
Crain SM et al. Pain 2000; 84:121
Crain SM et al. Brain Res 1992; 575:
Grunkemeier D.M.S. et al. CGH 2007; 5:1126 2141
a
b
Low-dose opioid
c
High-dose opioid
>1 mM
1-10 nM
Gi
Gi
Go
Go
Inhibitory
Gs
Excitatory
Low-dose
masks
inhibitory
effects
Hyperalgesia
Chronic opioid
use
Gi
Gs
Inhibitory
Excitatory
High-dose
masks
excitatory
effects
Analgesia
Go
Inhibitory
Tolerance
to
inhibitory
receptor
Gs
Excitatory
Sensitized
excitatory
receptor
Hyperalgesia
1890
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; 5:1126
Vanderah TW et al. J Neurosci 2000; 20:7074
Porreca F et al. Trends Neurosci 2002; 25:319
Heinricher MM et al. J Neurophysiol 2004; 92:1982
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Glia of Brain and Spinal Cord
Microglia
Astrocytes
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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, 5:1126
Hutchinson MR et al. Sci World J 2007;7:98
Watkins LR et al. Trends Neurosci 2005;28:661
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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, TNFα) 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; 7:98
2285
Opioids: Neuronal Analgesia and Glial Activation
TLR4
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
Analgesia
ANALGESIA
IL-1
Hutchinson M et al. Scientific World J 2007;7:98
IL-1
2286
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, TNFα) 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; 7:98
2287
Potential Benefit of Opioid Antagonists
TLR4
IL-1
IL-1
IL-1
IL-1
IL-1
IL-1
ANALGESIA
Hutchinson M et al. Scientific World J 2007;7:98
2288
Neuron-to-glia chemokine
Fractalkine
Immune / infectious
challenges
Virus, bacteria, trauma
Sensory afferent neuron
ATP, NO, SP, CGRP
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
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, 5:1126
2144
Narcotic Bowel Syndrome
Pain
Narcotics
Narcotics
Maladaptive
Therapeutic
Interaction
Vicious Cycle
of Patient Physician
Interactions
Physician
Frustration
Patient
Frustration
“Negative”
evaluations
“Furor
Medicus”
NBS
treatment,
Narcotics
withdrawal
Narcotic Bowel
Syndrome
Healthcare /
Societal
Pressures
Emergency
Room Visits
Increased
Healthcare
Utilization
1888a
Narcotic Withdrawal Protocol
Physician – Patient Relationship
Day of taper
-3
-2
-1
0
1
2
3
4
5
6
7
8
9
10 . . . 21
1887
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
Clinician-Patient Process and Techniques
 Accept the pain as real and treatable
 Elicit the patient’s 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
482
Clinician-Patient Process and Techniques
 Accept the pain as real and treatable
 Elicit the patient’s concerns and expectations
 Provide information through a dialog:
Address the patient’s 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 won’t be
abandoned in pain)”
2147
Clinician-Patient Process and Techniques
 Accept the pain as real and treatable
 Elicit the patient’s 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
Clinician-Patient Process and Techniques
 Accept the pain as real and treatable
 Elicit the patient’s 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 pseudoobstruction
• Limited motivation or social support
• Requires monitoring
• Withdrawal can occur over several days
2210
Clinician-Patient Process and Techniques
 Accept the pain as real and treatable
 Elicit the patient’s concerns and expectations
 Provide information through a dialog
 Present the withdrawal program
 Clinical setting
 Gauge the patient’s 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 you’re still not missing something?”
 “What if I get a bad attack?”
 “What if these other medicines make me sick?”
2149
Narcotic Withdrawal Protocol
 Accept pain as real and treatable
 Elicit patients concerns/expectations
 Provide information through a dialog
 Present the withdrawal program
 Gauge the patient’s response
TCA or SNRI
PEG 3350 17g PO BID
Physician – Patient Relationship
Day of taper
-3
-2
-1
0
1
2
3
4
5
6
7
8
9
10 . . . 21
1887
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
Narcotic Withdrawal Protocol





Accept pain as real and treatable
Elicit patients concerns/expectations
Provide information through a dialog
Present the withdrawal program
Gauge the patient’s response
Lorazepam 1mg PO q 6hrs.
TCA or SNRI
Morphine equiv. Dose (mg)
220 200 180 160 140 120 100
80
60
40
20
0
PEG 3350 17g PO BID
Physician – Patient Relationship
Day of taper
-3
-2
-1
0
1
2
3
4
5
6
7
8
9
10 . . . 21
1887
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
Narcotic Withdrawal Protocol
Accept pain as real and treatable
Elicit patients concerns/expectations
Provide information through a dialog
Present the withdrawal program
Gauge the patient’s response
Clonidine 0.1mg PO q 6 hrs.
Lorazepam 1mg PO q 6hrs.
TCA or SNRI
Morphine equiv. Dose (mg)
220 200 180 160 140 120 100
80
60
40
20
0
PEG 3350 17g PO BID
Physician – Patient Relationship
Day of taper
-3
-2
-1
0
1
2
3
4
5
6
7
8
9
10 . . . 21
1887
Centrally Acting Augmentation
 Clonidine
 α2-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 α2adrenergic effect
 Benefits include – sleep, anti-anxiety, analgesia augmentation
2152
“If I don’t think it’s going to work, will it still work?”
2021
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
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
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
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
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mother and fiance
Case 4: Unsuccessful Treatment, Con’t.
 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
 Patient’s 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 nonmalignant pain, poor communication, improper decisionmaking 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, doesn’t it?”
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