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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

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slide1

Narcotic Bowel Syndrome

Douglas A. Drossman, M.D.

Co-Director

UNC Center for Functional GI & Motility DisordersChapel Hill, NC, USA

slide2

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 Grunkenmeier et al. Clin Gastro Hep 2007;5:1126-1139

Mehendale, Yuan. Dig Dis 2006;24:105–112

2124

slide3

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

slide4

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

slide5

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

slide6

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

2126

slide7

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

Grunkemeier D.M.S. et al. CGH 2007, 5:1126

Gray DW et al. Br J Surg 1987;74:239–242

Spiegel et al. Arch Intern Med 2004;164:1773-1780

Lembo A et al. CGH 2005;3:717–725

2127

slide8

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

slide9

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

slide10

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

slide11

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

2131

slide12

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

slide13

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

2133

slide14

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
slide15

Narcotic Bowel Syndrome

Pain

Narcotics

Narcotics

Vicious Cycle

of Patient - Physician Interactions

Maladaptive Therapeutic Interaction

Narcotic Bowel Syndrome

Physician Frustration

Patient Frustration

“Negative” evaluations

“Furor Medicus”

Healthcare / Societal Pressures

Increased Healthcare Utilization

Emergency Room Visits

1888b

slide16

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 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; 5:1126

2135

slide17

Retail Sales of Opioid Medications1997-2002

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

2136

slide18

8

7

6

5

4

3

2

1

0

1994 - 1995

1996 - 1997

1998 - 1999

2000 - 2001

2002 - 2003

2004 - 2005

Opiate Prescriptions in Ambulatory Visits NHAMCS 1994-2005

%

Ambullatory visits

Choung et al. in preparation

2138

slide19

110,000

100,000

Narcotic analgesics

Benzodiazepines

80,000

60,000

40,000

20,000

0

1995

1996

1997

1998

1999

2000

2001

2002

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

slide20

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 (1-10ηmol/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

slide21

a

b

c

Low-dose opioid

1-10 nM

High-dose opioid

>1 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

Tolerance to inhibitory receptor

Sensitized excitatory receptor

Hyperalgesia

Hyperalgesia

Analgesia

1890

slide22

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 Porreca F et al. Trends Neurosci 2002; 25:319 Vanderah TW et al. J Neurosci 2000; 20:7074 Heinricher MM et al. J Neurophysiol 2004; 92:1982

2142

slide23

Glia of Brain and Spinal Cord

Microglia

Astrocytes

2284

slide24

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 Watkins LR et al. Trends Neurosci 2005;28:661 Hutchinson MR et al. Sci World J 2007;7:98

2143

slide25

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

slide26

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 2007;7:98

slide27

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

slide28

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 2007;7:98

slide29

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

slide30

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

slide31

Narcotic Bowel Syndrome

Pain

Narcotics

Narcotics

Vicious Cycle

of Patient - Physician Interactions

Maladaptive Therapeutic Interaction

Narcotic Bowel Syndrome

Physician Frustration

Patient Frustration

“Negative” evaluations

“Furor Medicus”

NBS treatment, Narcotics withdrawal

Healthcare / Societal Pressures

Increased Healthcare Utilization

Emergency Room Visits

1888a

slide32

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

slide33

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

slide34

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

slide36

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

slide37

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

slide38

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 pseudo-obstruction
      • Limited motivation or social support
      • Requires monitoring
      • Withdrawal can occur over several days

2210

slide39

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

slide40

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

-3 -2 -1 0 1 2 3 4 5 6 7 8 9 10 . . . 21

Day of taper

1887

slide41

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

slide42

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

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

slide43

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

slide44

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

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

slide45

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 α2-adrenergic effect
    • Benefits include – sleep, anti-anxiety, analgesia augmentation

2152

slide47

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

slide48

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

slide49

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

slide50

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

slide51

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 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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