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AAGLAdvancing Minimally Invasive Gynecology Worldwide
Didactic: Chronic Pelvic Pain 2.0: Decoding Peripheral and Central Factors
to Optimize Patient Outcomes
PROGRAM CHAIR
Sawsan As-Sanie, MD, MPH
Michael Hibner, MD, PhD Georgine M. Lamvu, MD, MPHTracy Sher, MPT Frank F. Tu, MD, MPH
Professional Education Information Target Audience This educational activity is developed to meet the needs of residents, fellows and new minimally invasive specialists in the field of gynecology. Accreditation AAGL is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The AAGL designates this live activity for a maximum of 3.75 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. DISCLOSURE OF RELEVANT FINANCIAL RELATIONSHIPS As a provider accredited by the Accreditation Council for Continuing Medical Education, AAGL must ensure balance, independence, and objectivity in all CME activities to promote improvements in health care and not proprietary interests of a commercial interest. The provider controls all decisions related to identification of CME needs, determination of educational objectives, selection and presentation of content, selection of all persons and organizations that will be in a position to control the content, selection of educational methods, and evaluation of the activity. Course chairs, planning committee members, presenters, authors, moderators, panel members, and others in a position to control the content of this activity are required to disclose relevant financial relationships with commercial interests related to the subject matter of this educational activity. Learners are able to assess the potential for commercial bias in information when complete disclosure, resolution of conflicts of interest, and acknowledgment of commercial support are provided prior to the activity. Informed learners are the final safeguards in assuring that a CME activity is independent from commercial support. We believe this mechanism contributes to the transparency and accountability of CME.
Table of Contents
Course Description ........................................................................................................................................ 1
Disclosure ...................................................................................................................................................... 2
When Pain Persists: What Every Surgeon Should Know about the Biology and Treatment of Chronic Pelvic Pain S. As‐Sanie ..................................................................................................................................................... 4
Does This Hurt? Why Surgeons Should Learn a Musculoskeletal Exam T. Sher ......................................................................................................................................................... 14
Autonomic Nervous System in Chronic Pain States – Friend vs. Foe?
F.F. Tu ............................................................................................................................................. 24 When Sex Hurts: Evaluation and Management of Painful Intercourse in Women G.M. Lamvu ................................................................................................................................................. 26
From Dysmenorrhea to Chronic Pelvic Pain: When to Perform Surgery and What Works S. As‐Sanie ................................................................................................................................................... 36
Perioperative Care of the Chronic Pain Patient G.M. Lamvu ................................................................................................................................................. 47
You Want Me to Do What? Physiotherapy Treatments for Chronic Pelvic Pain T. Sher ......................................................................................................................................................... 55
Neuropathy: A Forgotten Cause of Chronic Pelvic Pain M. Hibner .................................................................................................................................................... 61
Cultural and Linguistics Competency ......................................................................................................... 71
PELV-610: Didactic:
Chronic Pelvic Pain 2.0: Decoding Peripheral and Central Factors
to Optimize Patient Outcomes
Presented in affiliation with the International Pelvic Pain Society (IPPS) and in cooperation with the AAGL Special Interest Group on Pelvic Pain
Sawsan As-Sanie, Chair
Faculty: Michael Hibner, Georgine M. Lamvu, Tracy Sher, Frank F. Tu Although chronic pelvic pain (CPP) is one of the most common conditions for which women seek
medical care, the evaluation and management of pelvic pain patients presents many challenges to
practicing gynecologic surgeons. This course is designed to provide participants with a practical, state-of-
the-art approach to the CPP patient that reviews the clinical evaluation, appropriate multidisciplinary
diagnostic workup, and innovations in medical and surgical treatment options. This course will also
highlight the role of surgery in the management of pelvic pain, when surgery is not likely to be helpful,
and alternative options when standard medical and surgical therapies fail. The prevention and
management of perioperative pain and chronic post-surgical pain, including post-hysteroscopic
sterilization pain, will be discussed. Course faculty will utilize clinical vignettes and video demonstrations
to enhance the interactive experience between faculty and audience. Learning Objectives: At the conclusion of this course, the clinician will be able to: 1) Discuss the
physiology and neurobiology of acute versus chronic pain; 2) formulate a comprehensive differential
diagnosis for the newly encountered chronic pelvic pain patient, including possible gynecologic, urologic,
gastrointestinal, musculoskeletal and neurologic sources; 3) describe the evaluation and management of
painful intercourse in women; 4) describe the indications and efficacy of surgical procedures used to
treat chronic pelvic pain; 5) discuss the prevention and management of perioperative and chronic
postsurgical pain; 6) describe medical and behavioral therapies for pelvic pain that is refractory to usual
therapies; and 7) integrate the evaluation and treatment of pelvic and abdominal musculoskeletal
dysfunction in the care of chronic pelvic pain patients.
Course Outline
12:30 Welcome, Introductions and Course Overview S. As-Sanie 12:35 When Pain Persists: What Every Surgeon Should Know about the
Biology and Treatment of Chronic Pelvic Pain S. As-Sanie 1:00 Does This Hurt? Why Surgeons Should Learn a Musculoskeletal Exam T. Sher 1:25 Autonomic Nervous System in Chronic Pain States – Friend vs. Foe? F.F. Tu 1:50 When Sex Hurts: Evaluation and Management of Painful Intercourse
in Women G.M. Lamvu 2:15 Questions & Answers All Faculty 2:25 Break 2:40 From Dysmenorrhea to Chronic Pelvic Pain: When to Perform Surgery
and What Works S. As-Sanie 3:05 Perioperative Care of the Chronic Pain Patient G.M. Lamvu 3:30 You Want Me to Do What? Physiotherapy Treatments for Chronic Pelvic Pain T. Sher 3:55 Neuropathy: A Forgotten Cause of Chronic Pelvic Pain M. Hibner 4:20 Questions & Answers All Faculty 4:30 Adjourn
1
PLANNER DISCLOSURE The following members of AAGL have been involved in the educational planning of this workshop (listed in alphabetical order by last name). Art Arellano, Professional Education Manager, AAGL* Sawsan As‐Sanie Consultant: Myriad Genetics Lab R. Edward Betcher* Amber Bradshaw Speakers Bureau: Myriad Genetics Lab Other: Proctor: Intuitive Surgical Sarah L. Cohen Consultant: Olympus Erica Dun* Joseph (Jay) L. Hudgens Contracted Research: Gynesonics Frank D. Loffer, Medical Director, AAGL* Suketu Mansuria Speakers Bureau: Covidien Linda Michels, Executive Director, AAGL* Karen C. Wang* Johnny Yi* SCIENTIFIC PROGRAM COMMITTEE Sawsan As‐Sanie Consultant: Myriad Genetics Lab Jubilee Brown* Aarathi Cholkeri‐Singh Consultant: Smith & Nephew Endoscopy Speakers Bureau: Bayer Healthcare Corp., DySIS Medical, Hologic Other: Advisory Board: Bayer Healthcare Corp., Hologic Jon I. Einarsson* Suketu Mansuria Speakers Bureau: Covidien Andrew I. Sokol* Kevin J.E. Stepp Consultant: CONMED Corporation, Teleflex Stock Ownership: Titan Medical Karen C. Wang* FACULTY DISCLOSURE The following have agreed to provide verbal disclosure of their relationships prior to their presentations. They have also agreed to support their presentations and clinical recommendations with the “best available evidence” from medical literature (in alphabetical order by last name). Sawsan As‐Sanie Consultant: Myriad Genetics Lab Michael Hibner* Georgine M. Lamvu* Tracy Sher* Frank F. Tu
Consultant: AbbVie Contracted Research: AbbVie Content Reviewer has no relationships. Asterisk (*) denotes no financial relationships to disclose.
When pain persists: What every surgeon should know about the biology and treatment of chronic pelvic pain.
AAGL 45th Annual Congress on Minimally Invasive GynecologyOrlando, Florida 2016
PELV-610: Chronic Pelvic Pain 2.0: Decoding Peripheral and Central Factors to Optimize Patient Outcomes
Sawsan As-Sanie, MD, MPHAssistant Professor
Department of Obstetrics and GynecologyDirector, Minimally Invasive GYN Surgery & Fellowship
Director, Endometriosis CenterThe University of Michigan
Disclosures
Consultant: Myriad Genetics Lab
I will present off-label use of medications, best evidence will be provided.
2
3
Objectives
1. Review the physiology of chronic pain, with particular emphasis on central pain disorders
2. Present evidence that endometriosis and chronic pelvic pain may be central pain disorders
3. Discuss the clinical approach to integrate treatment of central sensitization to enhance patient care
4
The challenges of caring for patients with chronic pain...
CPP Patient CPP Practitioner
5 6
Who has pelvic pain?
Pain-free
5 days/month, 3/10 pain
20 days/month, 8/10 pain
4
Burden
Institute of Medicine Report on Pain 7/2011 approximately 116 million Americans suffer from pain
Treatment of pain costs the United States more than half a trillion dollars per year
Pain is one of the most common reasons people consult a physician. Yet it frequently is inappropriately treated.
8
Definition of Chronic Pelvic Pain (CPP)
Non-cyclic pain6 or more month’s durationlocalizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocksof sufficient severity to cause functional disability or lead to medical care
American College of Obstetricians and Gynecologists, 2004
9
Epidemiology
15 - 25% of women aged 18 to 50 years have pelvic pain lasting > 6 mo during their lifetime
Primary indication for10% outpatient gynecology clinic visits12% hysterectomies40% diagnostic laparoscopies
Only 25% of UK women surveyed had sought medical evaluation in the last year
Howard FM, Ob Gyn Surv 1993, Lee NC et al AJOG 1984, Zondervan K, et al Br J Gen Prac 2001, Tu FF, AJOG 2006 10
Chronic pelvic pain negatively impacts quality of life & physical function
Among women with CPPUse 3x more medicationsHave 4x more GYN surgeriesAre 5x more likely to have a hysterectomy
58% reduce normal activity >1 day/month26% stay in bed >1 day/month15% report lost time from work48% report reduced work productivity
Mathias SD et al Obstet Gynecol 1996, Reiter R et al. Obstet Gynecol 1998
11
Challenges of endometriosis
1. Little, if any, correlation between extent of disease and severity of pain.
2. Medical therapies are non-specific & effectively treat other causes of CPP.
GnRH agonists are effective therapy for cyclic-IBS and CPP without endometriosis
3. Medical and surgical therapies are inadequate for many patients.
30% non-response rate
4. Frequency of recurrent pain is high following medical and surgical therapies.
Pain recurs often in the absence of recurrent pathology.
No brain, no painChronic Pelvic Pain
• Endometriosis• Adenomyosis• Adhesions• Chronic PID• Uterine fibroids• Pelvic congestion• Ovarian remnant• Residual ovarian syndrome• Vaginal apex pain
5
13
Mechanistic Classification of Pain
PAIN
NOCICEPTIVE NEUROPATHIC
PERIPHERAL CENTRAL
ACUTE PAIN CHRONIC PAIN14
PAIN
NEUROPATHIC
CENTRAL
Mechanistic Classification of Pain
Central disturbance in pain processing with no ongoing peripheral stimulation
NOCICEPTIVE
Chronic pain is not prolonged acute pain
Acute Pain
Symptom of injury or disease
Well defined, recent onset
Expected to end with removal of peripheral injury
Essential biological warning function
Chronic Pain
Onset often insidious and not clearly associated with specific injury
Unpredictable duration
Often progressive
Pain out of proportion to peripheral pathology
No apparent biological function
15 16
Facilitation
+
Inhibition
Supraspinal Influences on Sensory Processing = Volume Control
Substance P
Glutamate and EAA
Serotonin (5HT2a, 3a)
Neurotensin
Nerve growth factor
CCK
Descending anti-nociceptive pathways
Norepinephrine –serotonin
Opioids
GABA
Cannabanoids
Adenosine
Central amplification of pain processing can lead to chronic pain in the absence of peripheral pathology
Central amplification of pain processing can lead to chronic pain in the absence of peripheral pathology
17
Gottschalk A, Smith DS. New concepts in acute pain therapy: preemptive analgesia. Am FamPhysician. 2001 May 15;63(10):1979-84. Review
+
18
Shared features of “central” pain syndromes
Typically characterized by –Multifocal pain
Endorse “neuropathic” verbal descriptors of pain
Higher current and lifetime history of pain
Multiple somatic symptoms (fatigue, memory difficulties, sleep disturbance)
Greater sensitivity to multiple sensory stimuli (sound, light)
High rates of co-morbidities with other related syndromes
Opioids do not effectively or consistently reduce pain symptoms
6
19
1.5 – 2X more common in females
Strong familial/genetic underpinnings
Triggered or exacerbated by “stressors”
Shared features of “central” pain syndromes
Increased Pressure Pain Sensitivity in WomenWith Chronic Pelvic PainSawsan As-Sanie, MD, MPH, Richard E. Harris, PhD, Steven E. Harte, PhD, Frank F. Tu, MD, MPH,Gina Neshewat, MPH, and Daniel J. Clauw, MD
20
Obstet Gynecol, 2013, 122(5): 1047-55
Evidence of centralized pain in women with endometriosis-associated CPP
Changes in regional gray matter volume in women w ith chronic pelvic pain:A voxel-based morphometry study
Sawsan As-Sanie a, Richard E. Harrisb, Vitaly Napadow c, Jieun Kim c, Gina Neshewat a, Anson Kairysb,David Will iams b, Daniel J. Clauw b, Tobias Schmidt-Wilcke b,d,�
www.el sevi er.com/l ocat e/pai n
PAINÒ
153 (2012) 1006–1014
Dysmenorrhea Interstitial Cystitis Irritable Bowel Syndrome
Evidence of centralized pain in dysmenorrhea, bladder pain, IBS
Most chronic pain conditions are “mixed pain” conditions, with peripheral and central contributors to pain
22
Peripheral Centralized
Acute pain Osteoarthritis Fibromyalgia Rheumatoid Arthritis Tension HA
Low back pain TMJD IBSInterstitial Cystitis
Vulvodynia
CPP
Pain= balance between peripheral input and central volume control
DescendingInhibitory & Facilitatory
pathways
Central “volume control”
Peripheral signals
=
24
7
You must care, otherwise your might do more harm than good…
Identifying the underlying causes of pain should guide clinical care and decision for surgery
26
Clinical implications of central changes in pain processing
1. Chronic overlapping pain conditions… suggest common underlying pathophysiology and treatment
27
2. Patient with central pain changes respond differently to therapy
1. May be less likely to respond to “peripherally-directed” therapies (e.g. hormone suppression, surgery?)
2. More likely to experience more acute and chronic pain following surgery
28
29Brawn J, Morotti M, Zondervan KT, Becker CM, Vincent K. Central changes associated with chronic pelvic pain and endometriosis. Hum Reprod Update. 2014, Sep-Oct;20(5):737-47
3. There are many overlapping pathways that lead to chronic pain
4. Treat early to prevent transition from acute to chronic pain
30
8
31
Proposed diagnostic approach to CPP*
Gynecologic Urologic Gastrointestinal Musculoskeletal
• Endometriosis• Adenomyosis• Adhesions• Chronic PID• Uterine fibroids• Pelvic congestion• Ovarian remnant• Residual ovarian syndrome• Vaginal apex pain
• Interstitial Cystitis• Urethral syndrome• Chronic UTI• Bladder stones
• IBS• Functional Bowel
disorders• Chronic appendicitis• Inflammatory bowel
disease• Hernias• Diverticular disease• Intermittent bowel
Obstruction
• Pelvic floor myalgia• Trigger points• Idiopathic low back pain• Disc disease• SI joint disease• Coccydynia
• Nerve entrapmentsyndromes
CNS
• central pain disorder
Comorbid pain conditions: Fibromyalgia, chronic fatigue syndrome, TMD, migraines, etc.
Comorbid psychological disease: Depression, anxiety, etc.
Cognitive and psychosocial traits: Coping, personality, maladaptive behavior 32
Treatment pearls
Begin with “gold-standard” therapies for contributing factors
Ex. Hormonal suppression for cyclic pain or chronic pain with cyclic exacerbationEx. Physical therapy for abdominal wall and pelvic floor myofascial painEx. Laparoscopy for excision/ablation of endometriosis
When standard treatments fail, then reconsider the diagnosis, re-evaluate comorbid psychosocial variables
33
Treatment pearls
Abnormalities in pain processing are a common mechanism in many chronic pain disorders (IBS, IC, fibromyalgia, etc.)
It is likely to be an underlying mechanism in at least some women with CPP
Consider adding centrally-acting medication when standard “gynecology” treatments fail
Consider using centrally-acting medication as part of first-line therapy
Chronic pelvic pain with negative laparoscopyPelvic nerve entrapment syndromes (ex. Pudendal nueralgia)
Treatments for Pain Based on Underlying Mechanisms1,2
Non-inflammatory
Inflammatory Peripheral Centralized
Opioids
NSAIDs/acetaminophen
Immunosuppressants, Anti-inflammatories
Alpha-2-delta ligand anticonvulsants
TricyclicsSNRIs
1Kroenke K, et al. Gen Hosp Psychiatry. 2009;31(3):206-219. 2Dray A. Rheum Dis Clin N Am. 2008
■ Injections, surgical procedures less effective or ineffective for individuals with centralized pain
TricyclicsSNRIs
NeuropathicPeripheral
Pharmacological Therapies for Fibromyalgia (i.e. Centralized Pain)
Modified from Goldenberg et al. JAMA. 2004;292:2388-95.
StrongEvidence
■ Dual reuptake inhibitors such as ■ Tricyclic compounds (amitriptyline, cyclobenzaprine)■ SNRIs and NSRIs (milnacipran, duloxetine, venlafaxine?)
■ Anticonvulsants (e.g., pregabalin, gabapentin)
ModestEvidence
■ Tramadol■ Older less selective SSRIs or NRIs■ Gamma hydroxybutyrate■ Low dose naltrexone
WeakEvidence
■ Cannabanoids; Growth hormone, 5-hydroxytryptamine, tropisetron, S-adenosyl-L-methionine (SAMe)
NoEvidence
■ Opioids, corticosteroids, nonsteroidal anti-inflammatory drugs, benzodiazepine and nonbenzodiazepine hypnotics, guanifenesin
36
Relative Serotonin and Norepinephrine Re-uptake Amongst Antidepressants
Serotonin Mixed Norepinephrine
Citalopram
Fluvoxamine
Sertraline
Paroxetine
Fluoxetine
Venlafaxine Amitriptyline
Duloxetine Milnacipran
Imipramine
Maprotiline
Desipramine
Nortriptyline
Reboxitine
Best for pain
9
37
Antidepressant with analgesic properties
Drug Dosage Side-effects, contraindications
TCA’s Start at 5-10 mg nightly, increase by 10 mg per week up to 150 mg/day
Side effects: dry mouth, constipation, sedation, urinary retention, weight gain (tertiary amines have greater side effects).
Contraindications: cardiac conduction abnormalities, recent cardiac event, narrow-angle glaucoma
Venlafaxine Start at 37.5 mg per day, increase by 37.5 mg per week, up to 300 mg/day (BID dosing)
Side effects: headache, nausea, decreased appetite, sweating, sedation, hypertension, seizures, mania, hepatic/renal dysfunction
Duloxetine Start at 20 mg per day, increase by 20 mg per week, up to 60 (or 120 mg) per day (30 BID, 60 QD, or 60 BID)
Side effects: nausea, dry mouth, constipation, dizziness, insomnia
38
Antiepileptics with analgesic properties
Drug Dosage Side-effects, contraindications
Neurontin Start 100-300mg qhs,
Increase 100-300mg q3d
Up to 2400mg daily
(600mg, 600mg, 1200mg qhs)
Side effects: Drowsiness, dizziness, fatigue, nausea, sedation, weight gain
Pregabalin Start 50 mg BID
Increase to 100 mg BID-QIDSide effects: Drowsiness, dizziness, fatigue, nausea, sedation, weight gain
Titration protocols (examples)
39
Titration protocols
https://dl.dropboxusercontent.com/u/18727766/titration%20protocols/Cymbalta(DuloxetineHydrochloride)ChronicPain_sas.pdf
https://dl.dropboxusercontent.com/u/18727766/titration%20protocols/Elavil(AmitripylineHCL)ChronicPain_sas.pdf
https://dl.dropboxusercontent.com/u/18727766/titration%20protocols/Neurontin(gabapentin)ChronicPain_sas.pdf
40
■ Pharmacological therapies to improve symptoms
■ Increased Distress
■ Decreased activity
■ Isolation
■ Poor sleep
■ Maladaptive illness behaviors
■ Nociceptive processes (damage or inflammation of tissues)
■ Disordered sensory processing
Clauw and Crofford. Best Pract Res Clin Rheumatol. 2003;17:685-701.
Symptoms of Pain, Fatigue, etc.
Functional Consequences of Symptoms
Dually FocusedTreatment
■ Nonpharmacological therapies to address dysfunction
Nonpharmacological therapies applicable to all chronic pain conditions
Goldenberg et al. JAMA. 2004;292:2388-95.
StrongEvidence
■ Education■ Aerobic exercise■ Cognitive behavior therapy
ModestEvidence
■ Strength training■ Hypnotherapy, biofeedback, balneotherapy
WeakEvidence
■ Acupuncture, chiropractic, manual and massage therapy, electrotherapy, ultrasound
NoEvidence
■ Tender (trigger) point injections, flexibility exercise
10
Cognitive Behavioral Therapy for Chronic Pain
Shown to be effective over a wide range of pain states
Effect sizes on function (.4 - .6) are much greater than typically seen with pharmacological therapies
Despite wide agreement that these help, barriers to implementation have been:
Physicians do not strongly recommend these therapies and there is no “industry” promoting these therapies
Not generally reimbursed by third parties
Not enough trained therapists to give one-on-one CBT to all chronic pain patients
44
Program features 10 CBT modules:
Understanding Fibromyalgia
Being Active
Sleep
Relaxation
Time for You
Setting Goals
Pacing Yourself
Thinking Differently
Communicating
Fibro Fog
fibroguide.com
• In a RCT of 118 FM patients comparing the earlier version of this website plus usual care, to usual care alone, Williams demonstrated statistically significant improvements in pain (29% in the WEB group had 30% improvement in pain vs 8% in usual care, p=.009) and function (i.e., 31% in WEB-SM had .5 SD improvement in SF-36 PF vs. 6% in standard care, p<.002)
Williams et. al. Pain. 2010;151(3):694-702
Exercise to Treat Chronic Pain
Fibromyalgia. Aerobic exercise improves global well being (SMD .49), function (SMD .66) and pain (SMD .65 but very wide CIs include 0).
Strength training may also be effective although far fewer studies have been performed.
Dysmenorrhea28% decrease in pelvic and back pain, 15% decrease in depression scores.
Cochrane Database: Fransen M, et. al. 2008, Issue 3. Bartels EM et. al, 2007, Issue 4. Busch et. al. 2007, Issue 3.
Ortiz MI, Cortes-Marquez SK, Romero-Quezada LC, Murguia-Canovas G, Jaramillo-Diaz AP. (2015). Effect of a physiotherapy program in women with primary dysmenorrhea. Eur J Obstet Gynecol Reprod Biol, 152: 73-7.
Patients with chronic pain have dysfunctional sleep
• Chronic pain patients have reduced short-wave sleep and abnormal α-rhythms, suggestive of wakefulness during non-REM (rapid eye movement) sleep.
• Sleep deprivation in healthy individuals can cause symptoms of fibromyalgia, including myalgia, tenderness and fatigue.
• sleep deprivation impairs descending pain-inhibition pathways that are important in controlling and coping with pain.
Choy EH. The role of sleep in pain and fibromyalgia. Nat Rev Rheumatol. 2015 Sep;11(9):513-20.
Improve sleep = improve pain
• Clinical trials of pharmacological and nonpharmacologicaltherapies have shown that improving sleep quality can reduce pain and fatigue
• Provide instruction on sleep hygiene and limit the drugs that alter restorative sleep
• Prevent REM sleep: long acting opioids, beta blockers, clonidine, SSRIs
• Prevents paralysis and timing of sleep: Dopaminergic blockers
• Vitamin D deficiency (and toxicity) associated with poor sleep
Choy EH. The role of sleep in pain and fibromyalgia. Nat Rev Rheumatol. 2015 Sep;11(9):513-20.
Neurostimulatory Therapies
Peripheral
1. TENS (Transcutaneous electrical nerve stimulation)■ Conventional TENS (C-TENS) is given at high stimulation frequency
with low intensity, and pain relief is almost immediate both short-lived.
■ Acupuncture like TENS (AL-TENS) is given at low frequency and high intensity (which is uncomfortable to many individuals), and generally has a longer lasting analgesic effect.
■ Improvement in pain, dyspareunia and QOL in endometriosis-CPP1, and primary dysmenorrhea2
2. Percutaneous tibial nerve stimulation Small RCT shows weekly Rx x12 = possible benefit up to 6 months
after treatment3
1Mira TA, Giraldo PC, Yela DA, Benetti-Pinto CL. Effectiveness of complementary pain treatment for women with deep endometriosis through Transcutaneous Electrical Nerve Stimulation (TENS): randomized controlled trial. Eur J Obstet Gynecol Reprod Biol. 2015 Nov;194:1-6.
2Proctor ML, Smith CA, Farquhar CM, Stones RW. Transcutaneous electrical nerve stimulation and acupuncture for primary dysmenorrhoea. Cochrane Database Syst Rev. 2002
3Istek et al. 2014. Arch Gynecol Obstet 290(2): 291-8.
11
Neurostimulatory Therapies
Central - New evidence suggests efficacy across a broad range of chronic pain conditions
Applied to scalpTranscranial magnetic stimulation (TMS)
Direct Current Stimulation (DCS)
ImplantableSpinal cord stimulation
Vagal nerve stimulation
Deep brain stimulation
SummaryCentralized pain or central sensitization can be identified in most individuals with conditions such as FM, and in sub-sets (typically at least 20 – 30%) of individuals with other chronic pain states such as CPP, RA, SLE, low back pain, osteoarthritis
Thus all chronic pain states may be “mixed” pain states with variable peripheral and central contributions in different individuals with the same clinical label
None of our pharmacological treatments of chronic pain have anything more than modest efficacy when used as stand-alone therapy in any chronic pain condition
In the US in particular, opioids, NSAIDs, injections and surgical procedures are overused (easy, high reimbursement), and centrally acting analgesics, non-pharmacological therapies e.g. exercise, CBT are underused (difficult, low to no reimbursement)
One size never fits all
51 52
53
References
1. ACOG Practice Bulletin No. 51. Chronic pelvic pain. Obstet Gynecol, 2004. 103(3): p. 589-605.
2. Schweinhardt, P. and M.C. Bushnell, Pain imaging in health and disease--how far have we come? J Clin Invest, 2010. 120(11): p. 3788-97.
3. Gottschalk, A. and D.S. Smith, New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician, 2001. 63(10): p. 1979-84.
4. As-Sanie, S., et al., Increased pressure pain sensitivity in women with chronic pelvic pain. Obstet Gynecol, 2013. 122(5): p. 1047-55.
5. As-Sanie, S., et al., Changes in regional gray matter volume in women with chronic pelvic pain: a voxel-based morphometry study. Pain, 2012. 153(5): p. 1006-14.
6. Clauw, D.J., Pain management: Fibromyalgia drugs are 'as good as it gets' in chronic pain. Nat Rev Rheumatol, 2010. 6(8): p. 439-40.
7. Clauw, D.J. and G.P. Chrousos, Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation, 1997. 4(3): p. 134-53.
8. Clauw, D.J., et al., The relationship between fibromyalgia and interstitial cystitis. J Psychiatr Res, 1997. 31(1): p. 125-31.
9. Schmidt-Wilcke, T. and D.J. Clauw, Pharmacotherapy in fibromyalgia (FM)--implications for the underlying pathophysiology. Pharmacology & therapeutics, 2010. 127(3): p. 283-94.
10. De Graaff, A.A., et al., The significant effect of endometriosis on physical, mental and social wellbeing: results from an international cross-sectional survey. Hum Reprod, 2013.
11. Lebovic, D.I., M.D. Mueller, and R.N. Taylor, Immunobiology of endometriosis. Fertil Steril, 2001. 75(1): p. 1-
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12
References12. Sutton, C.J., et al., Prospective, randomized, double-blind, controlled trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild, and moderate endometriosis. Fertil Steril, 1994. 62(4): p. 696-700.
13. Ferrero, S., et al., Irritable bowel syndrome and endometriosis. Eur J Gastroenterol Hepatol, 2005. 17(6): p. 687.
14. Sinaii, N., et al., High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome and atopic diseases among women with endometriosis: a survey analysis. Hum Reprod, 2002. 17(10): p. 2715-24.
15. Vercellini, P., et al., Repetitive surgery for recurrent symptomatic endometriosis: what to do? Eur J Obstet Gynecol Reprod Biol, 2009. 146(1): p. 15-21.
16. Mogil, J.S., The genetic mediation of individual differences in sensitivity to pain and its inhibition. Proc Natl Acad Sci U S A, 1999. 96(14): p. 7744-51.
17. Diatchenko, L., et al., Genetic basis for individual variations in pain perception and the development of a chronic pain condition. Hum Mol Genet, 2005. 14(1): p. 135-43.
18. Ablin, K. and D.J. Clauw, From fibrositis to functional somatic syndromes to a bell-shaped curve of pain and sensory sensitivity: evolution of a clinical construct. Rheum Dis Clin North Am, 2009. 35(2): p. 233-51.
19. Williams, D.A. and D.J. Clauw, Understanding fibromyalgia: lessons from the broader pain research community. J Pain, 2009. 10(8): p. 777-91.
20. Ablin K, Clauw DJ. Rheum Dis Clin North Am. 2009;35:233-251
21. Wolfe F, Michaud K. J Rheumatol. 2006;33:1516-1522
22. Kato K, et al. Psychol Med. 2008;39:497-505
23. Watson NF, et al. Arthritis Rheum. 2009;60:2839-284
24. Clauw and Chrousos. Neuroimmunomodulation. 1997;4:134-53.
25. Kato K, et. al. Arch Intern Med 2006; 166(15):1649-54.
26. Goldenberg et al. JAMA. 2004;292:2388-95
27. Williams et. al. Pain. 2010;151(3):694-702
Cochrane Database: Fransen M, et. al. 2008, Issue 3. Bartels EM et. al, 2007, Issue 4. Busch et. al. 2007, Issue 3.
55
Evaluation Question
Which of the following therapies does not have demonstrated efficacy for the treatment of “centralized” pain?
a)Aerobic exercise
b)Gabapentin
c)Oxycodone
d)Cognitive behavioral therapy
e)Education
56
13
Does This Hurt? Why Surgeons Should Learn a
Musculoskeletal Exam
AAGL – Advancing Minimally Invasive Gynecology Worldwide
45th Global Conference
Tracy Sher, MPT, CSCS
Email: [email protected]
www.pelvicguru.com
www.sherpelvic.com
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Financial DisclosuresI have no financial relationships to disclose.
AAGL – Advancing Minimally Invasive Gynecology Worldwide
45th Global Conference
Tracy Sher, MPT, CSCS
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Objectives to Discuss:
WHY the MUSCULOSKELETAL (MSK) system matters with regard to chronic pelvic pain (CPP) conditions.
HOW a GYN surgeon can integrate MSK screening into their exam.
WHAT important musculoskeletal structures and findings are associated with chronic pelvic pain
And… WHY this all matters....
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Why Surgeons Should Learn a Musculoskeletal Exam
•Your patients will feel you listened and validated concerns
•Your differential diagnosis AND outcomes will improve
•You’ll have better medical “team” communication and refer appropriately
•Hero status
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“Thermogram” Pelvic Pain Patient
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Permission to share from Visible Body
14
Why Does This Matter?• Surgery won’t “fix” a musculoskeletal issue typically (hypertonic/overactive muscle). Symptoms can become worse or additional complications happen.
• Post‐op patients may have a new‐onset MSK issue or neural issue that is presumed will get better on its own, though would benefit from timely MSK treatment to prevent longer‐term chronic pain issues
•MSK issue and only meds are provided only masking the underlying problem
• Patient may have multiple issues and if MSK is not addressed in addition to surgery, etc. – issue may not fully resolve
• So…Pelvic pain is complex and MSK should be screened.Property of Tracy Sher, MPT, CSCS. All rights reserved
Why Surgery Doesn’t Help All Pelvic Pain Patients. Examples
•Musculoskeletal source or contribution (leading to nerve compression/irritation)
•Sensitization of the nervous system (peripheral and/or central)
•Comorbidities (systemic, inflammatory, hormonal, etc)
•History of trauma
• Lack of multimodal approach to care – outcomes would improve with PT, pain management, counseling, mindfulness/meditation, etc.
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Cases
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What Pelvic Pain Patients Share
• “I wish Gynecologists would go back and do professional development in the pelvic floor muscles and nerves.
• “For years I had on and off one sided pain (that I now know was pelvic muscle pain‐ obturator internus and coccygeus). I had 2 laparoscopies to find the cause and of course nothing was found. Gynecologist told me to get a hysterectomy and it might cure me.( Thank God I didn't listen)”
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What Pelvic Pain Patients Share
• “Pelvic pain is a real concern and involves a whole team of doctors to help the patient and GYNs are often the first doctor that a woman seeks out for help/treatment/diagnosis.”
• “Gynecologists think all pelvic pain has to be associated with your uterus or ovaries or a pyschissue! It's as if no other anatomy is located in the pelvis‐ so crazy!”
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How Does a Pelvic Pain Patient Present?Complex and Multiple Issues or Specific
Painful Bladder Syndrome/IC
Vulvodynia and all of the subtypes
Coccygodynia
Endometriosis
Pudendal Neuralgia
Constipation
Dysfunctional voiding
(Comorbidity overlap)
Hartmann, Howard, Steege
Myofascial pain syndrome
Rectal pain/Proctalgia Fugax
Vaginismus
Dyspareunia
IBS
Urethral Pain
PGAD
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15
Somatic NEURAL Visceral
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http://wehelpwhathurts.homestead.com/nongastricabdominalpain.html
HOW Do We Assess Musculoskeletal?
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Types of Musculoskeletal Findings
1. Extrapelvic Exam
2. Internal Pelvic Floor – Vaginal and/or Rectal
3. sEMG /Biofeedback
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Muscles – “CORE” Pressure System
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Understand Your Back & Pelvic Girdle Pain Written by Diane Lee Physiotherapist
Lee, D. The Pelvic Girdle, 3rd and 4th Elsevier 2011
Extrapelvic Exam
•Breathing Patterns/Diaphragmatic Excursion
•Positions Matter – “Always hurts when I sit vs. when I change positions”
•Bony Landmark Pain / Asymmetry
•Muscle Tightness/Tenderness
•Neural Sensitization/ Neural Tension•Spinal Mobilization Testing
•ROM Hip/Extremities & Pelvic Floor Excursion
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Palpation Matters
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16
Palpation, Palpation, Palpation. Based on History!
Palpation is VALIDATION for patient…and you. •Neuropathy? Neural pattern of referral? vs.•Tender everywhere? vs• Muscular
• tender to palpation: ”That’s my pain”
• tightness/shortness Hypertonic/overactive•Can possibly be reproduced with contracting the muscle or not able to relax muscle
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Study (Tu 2008): CPP Musculoskeletal Findings
Women with chronic pelvic pain had more musculoskeletal dysfunction (20 control/19 cases)
• Asymmetrical iliac crests height
• Pubis symphysis height
• Positive posterior pelvic provocation test (SIJ)
• Higher abdominal and pelvic muscle tender points (R Psoas, B Rectus, L Obliques)
• More difficulty relaxing pelvic floor muscles after contract/relax 2/4 and 10/10
Common Findings in Other CPP StudiesPelvic floor muscle tenderness found more often in women with chronic pelvic pain (Fitzgerald 2011)
Myofascial pain and hypertonic pelvic floor dysfunction are present in more than 50% of patients with IC and/or CPPS. (FitzGerald MP 2009)
Men with CPPS have more abnormal pelvic floor muscular findings (Hetrick2003)
Key findings: (King 1991)
• “Pelvic pain posture: Lumbar lordosis, anterior pelvic tilt
• + Thomas test and/or decreased spine ROM in 75%
• Loss of 15‐25° hip internal rotation
• Poor sit, stand, sleep mechanics
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General Extrapelvic Musculoskeletal Exam
Some of the Muscles that Attach or Influence the Pelvis
•Abdominals •Gluteals•Hamstrings •Piriformis•4 Hip Rotators
Fitzgerald, Lee
•Quadratus lumborum
•5 Hip Adductors •Ilioposas•Erector Spinae•Quadratus
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MSK Extrapelvic Screening Helps with Differential DiagnosisPain Patterns Can be very distinct MSK source “That’s my pain” at muscle belly or tendinous(muscular/bony) area. Poor Discrimination in the pelvis – May think bladder, ovary. Could be diffuseMultiple referral patterns Possibly multiple sources Long‐term can have MSK symptoms and findings from another source (hx UTIs, Endo…)
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17
Abdominal Wall – 3 Key Assessments
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http://medicfrom.com/publicpress/Massage/Basic_Clinical_Massage_11.html
• Palpation – Tenderness, Tissue/muscle mobility, Trigger points with referral pattern, Reproduces Pain
• Abdominal Wall Stability –Diastasis Recti
• Scars – Mobility / Restrictions?
Scar Mobility
Near Bladder or other organs?
Reproduce pain with touch/pressure?
Sensitive to touch?
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Types of Musculoskeletal Findings•Trigger Point – Focal, hyperirritable spots located in a taut band of skeletal muscle. They produce pain locally and in a referred pattern and often accompany chronic musculoskeletal disorders.
•Tender Point – Pain at the site of palpation only
•Spasm – Persistent increased tension and shortness in a muscle that cannot be released voluntarily
Property of Tracy Sher, MPT, CSCS. All rights reservedTravell and Simons; Alvarez (2002) ; Rummer, E.
Types of Musculoskeletal Findings
•Connective Tissue Restriction‐•Increased texture thickness with acute tenderness upon pinch‐rolling in the skin and subcutaneous tissue
•Hyperalgesia and trophic changes may be present
Property of Tracy Sher, MPT, CSCS. All rights reservedPrendergast and Rummer; Kotarinos
Abdominal/Pelvic Pain – Musculoskeletal?
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DAVID D. ORTIZ, MD, CHRISTUS Santa Rosa Family Medicine Residency Program, San Antonio, TexasAm Fam Physician. 2008 Jun 1;77(11):1535‐1542.
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Abdominal Pain – Carnett’s Test (Screening)(Takada, T 2011)
• 130 consecutive outpatients with abdominal tenderness. (Functional GI/IBS excluded)
• 84% + Test: Abdominal
Wall Pain
• 86% + Test: Psychogenic
Abdominal Pain
• 13% + Test:
Intra‐Abdominal
Source
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http://clindx.wordpress.com/2011/05/26/carnetts‐test‐for‐excluding‐intra‐abdominal‐origens‐of‐abdominal‐tenderness/
External Muscles – Quadratus Lumborum
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External Muscles – Psoas and Iliacus
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External Muscles –Gluteals, Hamstrings, Piriformis
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External/Internal Muscle- Obturator Internus
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“Hips Don’t Lie”?: Sacroiliac Joint and Hips
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Sacral Thigh Thrust
19
HIP LABRAL TEAR?
•Basic hip mobility testing•Research has produced NO tests with sufficient specificity to help confidently RULE IN dx of hip labrallesion.
•Negative finding for certain tests provides clinician with evidence‐based confidence that a hip labral tear is ABSENT.
Lebold, RM J Man Manip Ther. 2008; 16(2): E24–E41.PMCID: PMC2565117Concurrent Criterion‐Related Validity of Physical Examination Tests for Hip Labral Lesions: A Systematic Review
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2. Internal: Pelvic Floor Muscle Assessment
Pelvic Pain and Pelvic Floor Connection?
•Majority of pelvic pain conditions involve some kind of pelvic floor muscle dysfunction
•Patients with pain usually have muscle spasms/hypertoncity/shortening, NOT weakness (but can have both)
•Many unable to actively contract pelvic floor muscles
•Difficulty with release of contraction
•Poor awareness – “am I even contracting?”
Fitzgerald, Howard, Tu
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Pelvic Floor – Muscle Function
External and Internal Observation/Palpation –Can you: Contract, Relax, Bulge? NOT just a KEGEL
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Pelvic Floor – Muscle Function
Palpation
•Layers 1‐3. Tender, Trp, Decreased tissue mobility
•Differential ‐ Specific muscles or with cotton swab at vestibule only?
•Asymmetries ‐ each side?
•Referral to another place – to bladder, abdomen, etc.?
•Does it feel tight in spasm or “shortnened?”
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Features of Pelvic Floor Muscle Dysfunction – Overactive, Hypertonicity, Shortened Pain with or after voiding – NOT like a UTI
Pain with penetration vaginally –tampon, digit, intercourse.
Urinary hesitancy/frequency Incomplete urinary voiding
Incomplete or difficulty passing stool and constipation via outlet obstruction
Not common to have urinary incontinence
Usually worse with “core” strengthening
Worse with KegelsProperty of Tracy Sher, MPT, CSCS. All rights reserved
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Pelvic Floor Muscles
Functions of Pelvic Floor Muscles
•Core stability in conjunction with the respiratory diaphragm, back and abdominal muscles
•Transfer loads generated by body wt. and gravity •Sexual/reproductive function•Urinary and colorectal function
•Superficial layer: (pudendal nerve)•Bulbocavernosus•Ischiocavernosus•Superficial transverse perineal•External anal sphincter (EAS)Property of Tracy Sher, MPT, CSCS. All rights reserved Property of Tracy Sher, MPT, CSCS. All rights reserved
Pelvic Floor Muscles
•Second layer - Urogenital: pudendalnerve•External urethral sphincter•Compressor uretherae•Sphincter urethrovaginalis
•Deep transverse perineal
Property of Tracy Sher, MPT, CSCS. All rights reserved Property of Tracy Sher, MPT, CSCS. All rights reserved
Pelvic Floor Muscles
•Deep layer /Pelvic diaphragm: sacral nerve roots S3-S5•Levator ani: Pubococcygeus(Pubovaginalis, Puborectalis), Illiococcygeus
•Coccygeus/ischiococcygeus•Piriformis•Obturator internus
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Property of Tracy Sher, MPT, CSCS. All rights reserved Property of Tracy Sher, MPT, CSCS. All rights reserved
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3. Pelvic Floor sEMG /Biofeedack Testing
Vulvodynia.com
What Can YOU Do for MSK Evaluation ?
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GYNs and MSK Evaluation Connection ?
Specific Evaluation for Pain Patient
Look for tissue that doesn’t move or hurts when you move it – external or internal
Looking for muscle spasms and “trigger points” which may be a source of pain.
Look for muscle dysfunction – can they contract, release and elongate muscles as needed?
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GYNs and MSK Evaluation Connection ?
Typical Findings on Vaginal Exam Difficulty tolerating vaginal exam May only be able to use child speculum if any Pain with palpation of muscles – improved
differential with specific muscle identification. Residual pain following examination Reproduction of abdominal pain with palpation
of muscles Apparent weak or minimal contraction of muscles on command Paradoxical contraction with attempts to push
out or elongate muscles. Property of Tracy Sher, MPT, CSCS. All rights reserved
22
Recommendations if Patients Have MSK FindingsDo NOT start on Kegels and send them away
Consider holding off on surgeries planned until MSK treatment
Refer to Pelvic Physical Therapy if possible Will screen to rule out Back/Hip and other differentials
Restore Tissue mobility
Train patient in toileting postures, muscle re‐education, self help strategies
Suggestions for self care –
massage, meditation, counseling
(but do not infer they are ”crazy”
or it is “all in your head.”
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References
Alvarez, DJ, Rockwell, PG. Trigger Points: Diagnosis and Management. Am FamPhysician. 2002 Feb 15;65(4):653‐661
Butler and Mosely, Explain Pain, 2003
FitzGerald MP, Anderson RU, Potts J, et al. Randomized multicenter feasibility trial of myofascial physical therapy for treatment of urologic chronic pelvic pain syndrome. J Urol. 2009;182:570–580.FitzGerald MP, Kotarinos, ER. Rehabilitation of the short pelvic floor. I: Background and patient evaluation. Int Urogynecol J (2003) 14: 261–268
Hilton S, Vandyken C. Clinical Commentary. The puzzle of pelvic pain – a rehabilitation framework for balancing tissue dysfunction and central sensitization, I: Pain physiology and evaluation for the physical therapist J Women’s Health PT. 2011;35(3):103‐113
Lee, D. The Pelvic Girdle, 3rd and 4th Elsevier, 2004/ 2011.
Louw A, et al. The Effect of Neuroscience Education on Pain, Disability, Anxiety, and Stress in Chronic Musculoskeletal Pain. Arch. Phys. Med. and Rehab 2011; 92(12):2041‐2056
Mannion AF, et al. [Increase in strength after active therapy in chronic low back pain (CLBP) patients: muscular adaptations and clinical relevance] Schmerz 2001;15(6): 468‐73.
Property of Tracy Sher, MPT, CSCS. All rights reserved
References
Takada T, Ikusaka M, Ohira Y, Noda K, & Tsukamoto T (2011). Diagnostic usefulness of Carnett’s test in psychogenic abdominal pain. Internal medicine (Tokyo, Japan), 50 (3), 213‐7 PMID: 21297322
Tu, FF. Physical therapy evaluation of patients with chronic pelvic pain: a controlled study. American Journal of Obstetrics & Gynecology Volume 198, Issue 3 , Pages 272.e1‐272.e7, March 2008
Travell, and Simon. Myofascial Pain and Dysfunction: The Trigger Point Manual, Volume 2, 1992
vanMiddelkoop M, et al. Exercise therapy for chronic nonspecific low‐back pain. Best Pract Res ClinRheumatol 2010;24(2):193‐204
Vandyken C, Hilton S. The puzzle of pelvic pain‐a rehabilitation framework for balancing tissue dysfunction and central sensitization, II: A review of treatment considerations. J Women's Health PT. 2012;36(1):44‐54
Wall LL. The muscles of the pelvic floor. Clin Obstet Gynecol 1993;36:910‐25
Weiss J.Chronic pelvic pain and myofascial trigger points. Complim Med and Pain. 2000 Dec:13‐18
Weiss JM, Prendergast SA. Screening for musculoskeletal causes of pelvic pain. Clin Obstet Gynecol. 2003;46(4):773‐82
Hip References• Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis of Sacroiliac Joint Pain: Validity of Individual Tests and Composites of Tests. Manual Therapy. 2005: 10; 207‐18.
• van der Wurff P, Hagmeijer RH, Meyne W. Clinical tests of the sacroiliac joint: A systematic methodological review. Part 1: Reliability. Man Ther. 2000;5:30–36.
• Robinson HS, Brox JI, Robinson R, Bjelland E, Solem S, Telje T. The reliability of selected motion and pain provocation tests for the sacroiliac joint. Man Ther. 2007;12:72–79.
Property of Tracy Sher, MPT, CSCS. All rights reserved
Website References
http://clindx.wordpress.com/2011/05/26/carnetts‐test‐for‐excluding‐intra‐abdominal‐origens‐of‐abdominal‐tenderness/
http://medicfrom.com/publicpress/Massage/Basic_Clinical_Massage_11.html
http://wehelpwhathurts.homestead.com/nongastricabdominalpain.html
http://medicfrom.com
23
Autonomic Nervous System in CPP States-- Friend or Foe?
Frank F. Tu, MD, MPH
Clin Assoc Prof
Dept of Ob/Gyn
Disclosures
• Consultant: AbbVie
• Contracted Research: AbbVie
• Off label use of medications will be reviewed
Objectives
• Identify the pertinent components of the autonomic nervous system for CPP states
• Recognize significant features of prior studies of ANS dysfunction in CPP states
• Discuss 3 potential ANS medication therapies of potential value for treating CPP
Uterine pain and CPP need more effective treatments
• Dysmenorrhea– OCPs I
– NSAIDs I – 15% of cases refractory
• CPP/endometriosis– Hormonal suppression (OCPs, progestins, GnRH
agonists and antagonists, AIs) Ib
– Surgical removal of endometriosis implants (Ib
– General neuromodulator drugs (III)
Autonomic targeting of visceral pain -rationale
Visceral innervation is autonomic
• Sympathetic and parasympathetic– arise from the sympathetic trunk and the sacral
spinal nerves,
• Converge on abdominopelvic plexus extending thoracoabdominal diaphragm superiorly to the pelvic diaphragm inferiorly.
• Initially only efferent aspects described
24
Sympathetic pelvic neuroanatomy
•SHP and IHP are major integrative center
•IHP Fans into middle rectal/ vesical/ pelvic plexi
•These supply most pelvic GU/GI/ reproductive structures
•Anterior part is paracervical ganglia
•Corpora cavernosa, vagina, periurethral tissues
Wesselmann U et al, Pain 73:3, 1997
Key constituents
Sympathetic
• Sympathetic trunk connections to…
• Lumbar (L1-L2) and sacral splanchnic nerves to
Parasympathetic
• Pelvic splanchnics (S2-S4)
• Through IHP to target pelvic organs, ganglia in walls, the postganglionic fibers to deeper layers –smooth muscle and glands
Overview of afferent visceral pathways
• 1. Pelvic splachnics – PS from IHP, anterior rami of S2-S2 (nervi erigentes) – uterus, bladder, vagina and inferior rectum
• 2. Sacral splanchnics – S from IHP, visa sympath chain to L1, L2, white rami comm to SC, also uterus, vagina, rectum
• 3. IHP -> hypogastrics to SHP, then pre-aortic plexus, then T and L splanchnics to sympathetic chain at T7-L2
• 4. S and PS bypass in adnexa to thoracic splanchnics, but also vagal PS
• 5. Middle and superior rectal S t along vessel to infemes plexus, then to lumbar splachnics
Complexity the norm
• Vs somatic fibers, visceral fibers are
• more divergent on entering SC, contacting multiple DH neurons.
• Visceral afferent fibers ascend and descend many more levels than typical somatosensory afferent fibers.
• Almost all visceral afferent fibers are convergent on DHneurons that also receive somatic primary afferent fibers.
Understanding the big scheme
• PFC-> RM -> NTS -> vagus -> bladder
• Bladder to thalamus to PFC
• RM to DH -> bladder (symp)
• Absence of vagal tone worsens things
• Gain of function
Background on parasympathetic contribution to wellness
• Reliable individual differences in cardiac vagal tone exist (Cacioppo et al., 1994) – Reduction with age (Craft and Schwartz, 1995).
• Unknown if impaired vagal tone is a cause or consequence of chronic disease
Cacioppo JT, et al. Psychophysiology 31, 412–419. Craft N, Schwart JB. American Journal of Physiology 268, 2005:H1441–H1452.
25
Autonomic ganglia contributions
• axon collaterals in an autonomic ganglion from pathologic organ afferents could excite ganglionic secretory and motor neurons innervating other organ
• several neuropeptides exert facilitatory/ inhibitory effects @ autonomic ganglia
Delepine, L., Aubineau, P., 1997. Exp. Neurol.147, 389–400; Brumovsky P & Gebhart GF. Auton Neurosci. 2010;153(1-2):106-15.
• El-Henafy – 2015 Urology 25917730 - SHG vs. HD for PBS
• C Rapp 2016 BJOG - 27292167 - postop hypogastric block for hysterectomy
So what is going on with ANS in chronic visceral pain?
• Output is exaggerated due to chronic hyperarousal– Clinical treatment goal
? wipe out sympathetic efferent drive TO uterus (ischemia, contraction, pain)
• DNIC is impaired
• Linked to comorbid conditions– Sleep impairment
– Fatigue
– Mood /anxiety d/o
Baseline and stress response
• Increased HR in IC (82) vs HC (63), 14 vs. 14 females (mean age 49)
• maintained during 25 min stressor application (∆ 19, p < 0.0001), but not different.– Speech, Stroop, and
serial subtractionLutgendorf S et al J Urol2004
ANS-R is GOOD
• greater capacity for context and goals to modulate emotion (output of vmPFC) vmPFC –system of systems” linking conceptualization, context, emotion and response. – Via connection to PAG bias more caudal brainstem
networks to specific modes that reflect particular behavior patterns and their autonomic accompaniments.
– ANS-R may be the “poor man’s” marker of vmPFCoutflow to the PAG
Resting HF-HRV – marker for emotional regulation?
• indicator of capacity for cognitive and affective regulation– low HF-HRV reflecting reduced ability to
psychologically modulate physiological responses4
• BUT, if decreased autonomic outflow predisposes to the development of IC/BPS, one might consider whether the vagal anti-inflammatory pathway has a role27
Williams, J Urol 2015
26
Causal role in CPP?
• unique ANS changes in response to stress occur in IC/BPS absent from other CPP disorders underlie the bladder dysfunction that characterizes IC/BPS
ANS responsiveness (ANS-R) in patients with IC/BPS, both at rest and during orthostatic challenge• in vagal tone, measured by high-frequency heart rate
variability (hfHRV)• in sympathetic reactivity, via baroreflex sensitivity (BRS)
Chelimsky -
Is exag SNS output more a predisposing issue?
• Sympathetic activity adverse chronic influence– Tissue vasoconstriction
– Facilitate pain pathways in DH (NE on a circuit is more synaptic conductance – Wolff)
HRV and functional somatic disorders
• lower PNS activity in FSD patients regardless of type of FSD (i.e., CFS, FM or IBS).
• Reliability limited by unexplained heterogeneity in effect sizes and potential publication bias.
• Key study design features– Appropriate controls, blinding personnel for HRV
measurements, reporting adequate HRV outcomes, and adjustment for potential confounders.
• Must consider influence of time of day, smoking, alcohol intake, caffeine intake, water or food ingestion
Tak et al Biol Psych 2009
IBS and ANS
• 24-h recording IBS patients vs. HC mean lnHF; mean square root LF/HF index
– shift in sympathetic/ parasympathetic balance toward sympathetic dominance, but due to vagal withdrawal.
Heitkemper M, et al. Dig Dis Sci 1998; 43: 2093–8.
Diagnostic/therapeutic blocks
Malignant
• Plancarte et al. 1997
• “vague, dull, poorly localized pain”
• Dx – 159/227 with “good pain relief”
• Tx – 115/227 with “good pain relief”
• Some 2nd procedures attempted
43% avg opioid dosage
Non-malignant
• Bosscher, 1996-2000
• Dx - 50% pain relief > 4 hrs – 10/22
• Tx – 50% relief > 1 mth4/11, only 1 with complete, long-lasting relief
Plancarte R et al. Reg Anesth. 1997;22(6):562-8; Bosscher H, Pain Practice; 1(2), 2001: 162–170
Pelvic pain in women Kindel 1939
• Review PSN
• 2 deaths.
27
Presacral neurectomy
• Italian RCT 2003– 162 women with >6 mths severe
dysmenorrhea + dx of endometriosis
– Tx with (A) EOE or (B) EOE + PSN
– Outcomes (12 mths F/U)» Dysmenorrhea – (B) 85.7% cured
vs. (A) 57.1%» Dyspareunia» Pelvic pain
– Complications (12 mths F/U)» 9/63 (14%) with constipation» 3/63 (5%) with urinary urgency
Zullo F et al, AJOG 2003
Case studies suggest efficacy for CPP states, clinical experience says not effective
Model of dysmenorrhea to CPP progression at target organ.
Brain RVM
UterusBladder
Severe menses
Regulation of pain/homeostasis
Sympathetic modulation of perfusion/ contractiility
∆ PGs, LTs, vasopressin, PAF concentration
Ascending pain pathways
Implications
• Diaphragmatic breathing can restore vagal tone – reverse LF/HF imbalance in FAP.
• Resonant frequency breathing in pilot study improves FM symptoms and transiently improves abnl HRV imbalance – N=12 , 50% achieved 50% improvement in 3 mths
in 10 session trial
– Baroreflex stimulation optimizes autonomic and emotion mediated reflexes (hypothal/limbic projections)
Sowder E. et al, Appl Psychophysiol Biofeedback Sep;35(3):199-206, 2010); Hasset A et al, Appl Psychophysiol Biofeedback. 2007 Mar;32(1):1-10.
Add’l thoughts
• Exercise, CBT similarly?
• benefits of autonomically focused psychosocial-behavioral interventions with respect to HTN and CHD have been demonstrated in a number of trials in adults
• Find solutions to reduce threat with reducing PFC -> PAG, RM (RM produces 80% of NE)
» Beta blockade?
Sanudo B et al, Clin Exp Rheumatol, 33 (suppl.) (2015), p. S41; ; Linden W et al, Ann Behav Med. 1994;16:35–45.
Acknowledgements
• Work funded by NIH R01 DK100368
• Thanks to
• Kevin Hellman, PhD
• Katlyn Dillane
• Ellen Garrison, RN
• Julia Kane, MS
• Nicole Steiner
28
When Sex Hurts Georgine Lamvu, MD, MPH
Gynecologic Surgeon and Pelvic Pain Specialist
Orlando VA Medical Center
Associate Clinical Professor University of Central Florida
Disclosure
I have no financial relationships to disclose.
Objectives
Identify the diagnostic criteria for sexual pain
Explain the impact of this very prevalent chronic pain syndrome
Describe the benefits of both physical and psychosocial therapies
54 yo married female presents to your office for management of fibromyalgia and her pain and medications. You are done with your visit, and as you are walking out the door she says ”I know you don’t have time but…” and she proceeds to report that over the last several months she has been experiencing pain during intercourse and loss of desire which is worrying her. She tells you she has no medical problems and her only medications (besides her pain meds) is her hormone pill. You perform a brief vaginal exam and you tell her you ‘see nothing wrong’. Which of the following should be your next step?
Test your knowledge
• A. You order a UA which is negative and you give her a short course of your favorite antibiotic
• B. You ask her some additional questions such as whether she has been experiencing any vaginal dryness, itching, hot flashes, insomnia
• C. You tell her you don’t see anything wrong and you recommend she go home and have more sex to see if it gets better
• D. You ask her whether she is being abused and if she denies you tell her there is nothing you can do.
Test your knowledge Sexual Pain Terminology• Dyspareunia – recurrent or persistent vaginal pain associated with sexual intercourse
• Vulvodynia – chronic vaginal or vulvar pain that can be unprovoked or provoked by contact such as intercourse
• Vestibulitis – pain localized to the vestibule, provoked or unprovoked,
• Both are usually a symptoms of an underlying condition rather than just a diagnosis in and of itself. But technical definitions are based on the ability to exclude ‘organic’ causes such as infection, neoplasm or dermatoses
• Vaginismus – involuntary muscle spams and fear of touch
• Hypoactive sexual desire disorder, arousal disorder‐ diagnoses that do not involve pain
Boardman L, et al. Clinical Obstetrics and Gynecology. 2009; 52(4), 682.Lamvu G, et al. Vulvodynia: a prevalent yet underdiagnosed chronic pain syndrome. Painweek Journal. 2015; Q1, 14.Kingsberg S, et al. Female Sexual Dysfunction. Obstetrics and Gynecology. 2015 125(2); 477.
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Dyspareunia: Additional Terminology
• Situational dyspareunia: pain with intercourse that is limited to specific situations, positions or a particular partner
• General dyspareunia ‐ pain that is not situational
• Primary dyspareunia ‐ pain that presents with or since first intercourse
• Secondary dyspareunia ‐ pain with intercourse that occurs after a period of pain‐free intercourse
• Superficial dyspareunia ‐ pain limited to the vulvar vestibule or vaginal introitus
• Deep dyspareunia ‐ pain with deep penetration
MacNeill C. Dyspareunia. Obstetrics and Gynecology Clinics of North America. 2006; 33 (4):565Howard F. Dyspareunia. In Pelvic Pain: Diagnosis and Management. Lippincott New York 200.
Vulvodynia
• Chronic lower genital pain of “unknown etiology” that manifests as pain and occasional erythema of the vulva without obvious infectious, dermatologic, or neurologic disease
• Generalized vulvodynia – to the entire vulva
• Localized vulvodynia – to the vestibule
• Provoked vulvodynia – occurring with touch (tampon, sexual activity)
• Unprovoked vulvodynia‐ occurring spontaneously or continuous pain
Dyspareunia VulvodyniaSuperficial Generalized
ProvokedUnprovokedMixed
Deep LocalizedProvokedUnprovokedMixed
Epidemiology
• Mixed populations of vulvodynia and dyspareunia
• Vulvodynia prevalence estimated at 8.3%; 14 million women will experience pain at some point
• Dyspareunia 12‐21% in women and 1‐5% in men in U.S.
• Dyspareunia 8‐21% in women around the world
Pitts M, et al. The journal of sexual medicine. 2008; 5(5):1223.Reed BD, et al. American Journal of Obstetrics and Gynecology. 2012; 206(2):170.Latthe P, et al. BMC Public Health. 2006; 6:177.
54 Studies, 35,973 womenPrevalence: 8%-21%; 1.1% (Sweden) to 45% (US)
USA
Latthe P, 2006: WHO systematic review of prevalence of chronic pelvic pain: a neglected reproductive health morbidity
Social and Economic Impact
• Poor health‐related quality of life, sexual dysfunction and high rates of psychological distress
• Vulvodynia patients 2‐3x more likely to have one or more chronic pain conditions such as fibromyalgia, PBS, TMD and IBS.
• Vulvodynia impact on U.S. healthcare system: 31‐72 Billion in direct, indirect and non‐healthcare costs
Reed BD, et al. American Journal of Obstetrics and Gynecology. 2012; 206(2):170.Xie Y, et al. Current Medical Research and Opinion. 2012; 28(4): 601.
Normal Vaginal Anatomy
30
Healthy Sexual Response
Masters and Johnson
• Relaxation of pelvic floor muscles• Vaginal canal lengthens by 3‐4 cm, widens by ~6cm
• Pelvic organs elevate ‘up and out’ of the way
• Clitoral retraction under the clitoral hood
• Labia minora enlarge and become red
• Contraction of pelvic floor muscles at the vaginal entrance during ‘orgasmic’ phase
Emotional Intimacy
Sexual Stimuli
Sexual Arousal
Emotional and
Physical Satisfaction
Arousal and Sexual Desire
Spontaneous Sexual Drive
Spontaneous Sexual Drive
Basson Intimacy – Based Model of Sexual Response Cycle -2001
Conditions Associated with Sexual Pain
Superficial / Insertional• Vulvar Dermatoses
• Lichen sclerosis• Lichen Planus• Contact dermatitis
• Vaginitis / Infections / Inflammatory
• Candidiasis• Bacterial vaginosis• DIV
• Vaginal atrophy / Hormonal
• Myalgias
• Neuralgia
Deep• Reproductive
• Endometriosis / Adenomyosis• Uterine or Ovarian Masses (Cysts, Fibroids)• Pelvic congestion• PID• Adhesions
• Myalgias / Spasm
• Neuralgia
• Trauma (vaginal surgery, mesh, hysterectomy)• Obstetrical• Surgical
• Urinary• IC / PBS• Urethral diverticulum
• Bowel• IBS• IBD• Constipation• Adhesions
How Do We Figure Out Diagnosis?90% History and Physical Examination
The Biopsychosocial Model Of Pain
Chronic Pain
Psychological Factors
Biological Factors
Social Factors
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Timing
• Pain lasting >3 months
• Primary vs. Secondary; Constant vs. Intermittent; Provoked vs. Unprovoked
Impact
• Associated with disability, poor QOL (activity, sleep, distress)
• Poor sexual function
• Associated symptoms, itching vs. burning pain, bleeding, discharge, bladder and bowel symptoms
Location• Insertional vs. Deep; Generalized vs. Localized
Therapies• Pain not‐responsive to 'simple' therapies
TILT
THE BIOPSYCHOSOCIAL MODEL OF PAIN ASSESSMENT Screen for Reported Risk Factors that May Actually Impact Outcome
• Recurrent vulvovaginal infections
• Hormonal status
• Onset of pain prior to initiating intercourse
• Presence of dysmenorrhea
• Co‐morbid pain and psychiatric disorders
• Adverse life experiences
Physical Exam
Mood Affect Distress
Musculoskeletal Back Abdomen
External Visual External SensorySingle Digit Internal /
Musculoskeletal
Internal Speculum exam
Gynecologic Examination For Pain• Trust• Relaxation and decrease anxiety• Patient properly covered• Patient should have a sense of control
• Educate patient on what is examined during the evaluation• Explain sensory exam and pain severity scales• Explain difference between exam and ‘what you feel at home’• Give the option to stop and any point, may break up examination into two visits• Give the option of deferring speculum exam if no abnormal bleeding or discharge• Use the smallest speculum possible• Must have a ‘chaperone’
External Visual
• Fissures
• Dryness
• Erythema
• Hyperkatosis
• Ulcerations
• Derm 101: raised lesions, irregular edges, discolored lesions
External Sensory
• Sensory test with cotton tipped applicator to ‘soft’ and ‘pin prick’
• Anal wink reflex, allodynia, hyperalgesia in S1‐T12 distribution
• Allodynia to static ‘pressure’ or dynamic ‘brushing’ touch of the vestibule
NVR: 90% had pain localized to the vestibule, 10% had generalized pain
Lamvu et al. The Evidence –based Vulvodynia Assessment Project: A National Registry for the Study of Vulvodynia. The Journal of Reproductive Medicine. 2015; 60:223.
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Single Digit Internal / Musculoskeletal
NVR: 90% had pain on palpation of vaginal muscles, 65% had high tone, 38% had low strength
• Single well lubricated digit
• Slow insertion
• Voluntary contraction, strength and tone
• “Deep” palpation of the pelvic floor muscles
• Palpation of the cervix, uterus and adnexa
Lamvu et al. The Evidence –based Vulvodynia Assessment Project: A National Registry for the Study of Vulvodynia. The Journal of Reproductive Medicine. 2015; 60:223.
Internal Speculum
• Well lubricated speculum
• Small, clear speculum to allow full visualization with less distention
• Slow insertion
• Vaginal pH
• Wet prep
• Vaginal cultures
• Vaginal biopsy only if vulvar cancers or dermatoses are suspected
Diagnostic Tests
• Urinalysis• Vaginal cultures / wet prep
• Pelvic imaging• Transvaginal ultrasound• Pelvic MRI
• Pelvic function imaging• Dynamic MRI• Defecography• Sitz Marker study• Urodynamics• Cystoscopy
• Colposcopy• Biopsy
• Neural blocks• Pudendal and pudendal branches• Prineal• Genifemoral• Ilioinguial• Iliohypogastric
Treatments: Treatment Plan• Define Expectations
• Patient expectations• Provider expectation• Derive a common ground
• Define Goals• Decreased pain vs. “cure” and pain free vs. sexually active• Improved quality of life
• Define Treatment Duration• Treatment duration varies (e.g. 6‐12 months)• “Treatment” is actually may involve a variety of therapies used at the same time
• Educate on Patient Participation
Available treatments of Dyspareunia and Vulvodynia• Education and vulvar care• Topical applications (lidocaine, estradiol, steroids)• Oral Therapy (analgesics, neuroleptics, TCA, SSRIs)• Intravaginal therapy• Physical Therapy• Behavioral Therapy: Cognitive‐Behavioral Therapy, Sex Therapy, Relationship Counseling
• Injections: Neuronal blocks & Trigger points• Surgical Therapy (vestibulectomy)
• Treatment often involves multiple therapies and is often highly individualized
Andrews JC. Vulvodynia Interventions‐ systematic review and evidence grading. Obstet & Gyn Survey, 2011
Treatment
Dermatoses / Inflammatory
Topical Steroids
Triamcinolone, Clobetasol
Emollient / Vulvar Care
Antimicrobials for chronic
superimposed vaginitis
Oral steroids for patients who fail topical therapy
Topical or oral immunosuppressant
Tacrolimus
Clinical Pearl•Non irritating bases and emollients: versa base, coconut oil, hydrophilic petrolatum – re-compound any topical that ‘burns’•Use ‘ointments’ vs. ‘creams’•Additional estradiol to promote regeneration of new mucosa•Anti-histamines to prevent scratching and itching
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TreatmentAllodynia / Neuropathy
Topical anesthetics
2.5%‐5% Lidocaine
Oral TCAs e.g.
Amitriptyline Nortriptyline
Oral Anticonvulsants
e.g.
Gabapentin Pregabalin
Neural Blocks e.g.
Pudendalbranch blocks
Clinical Pearl•Non irritating bases and emollients: versa base, coconut oil, hydrophilic petrolatum – re-compound any topical that ‘burns’•Use ‘ointments’ vs. ‘creams’•Additional estradiol to promote regeneration of new vaginal mucosa•TCAs and Neuroleptics may be compounded for vaginal application•Vaginal pain that is localized to the ‘top’ of the vagina may require different blocks
TreatmentMyalgias
Muscle Relaxants e.g.
Oral or Intravaginal e.g.
Cyclobenzaprine Baclofen Diazepam
Physical therapy Vaginal Dilator Therapy
Intramuscular vaginal trigger point injection with anesthetics or Onabotulinum toxinA
Clinical Pearl• Change muscle relaxant if patient does not notice
effect• Dilators should be incremental in size up to the
partner size• Physical therapy should focus on voluntary and
involuntary relaxation techniques… make sure you have the right physical therapist
Treatments
Vaginal Atrophy / Hormonal
Premenopausal
Topical estrogens, low dose, uterine
protection not needed if still menstruating
Postmenopausal
Topical estrogens, uterine protection and HT side effects should
be considered
Oral SERMS Intravaginal estradiol
Vagifem Estring
Cancer Survivors
Topical lidocaine only for breast cancer
survivors
Clinical Pearl•Hypo-estrogenic effects can be seen before ‘menopause’
•Pre-formulated compounds, e.g. Estrace, Premarin are often too low dose•Start with daily application for 4-6 weeks and then decrease to maintenance 3x/week- it takes a long time to regenerate vaginal mucosa•Compounded estradiol doses 0.1-0.2mg/g base•May combine with anesthetic to provide pain relief•If the vaginal introitus is contracted consider dilator therapy, and physical therapy•Vulvar care and lubrication for maintenance
Treatments
Psychosocial
Treat mood disorders such as
anxiety and depression
CBT Relaxation Coping Stress control Sleep Relationship
Clinical Pearls• Many of these psychosocial issues do not become evident until providers
really ‘get to know’ their patients• Anxiety, poor coping may be more common than depression• Relationship therapy involves the partner
Assessing for Centralized Pain
• Pain body map (screen for co‐morbid pain syndromes)
• Somatic symptoms (fatigue, insomnia, dizziness)
• Psychological function (anxiety, depression, catastrophizing, rumination)
• Quantitative sensory testing at extra genital sites
Vulvar Care
• Avoid over‐washing and harsh cleansers
• Avoid ‘wiping’ emphasize gentle ‘pat’
• Avoid drying agents focus on lubrication during daily activities and intercourse
• Lubricants should be water based or ‘ointment’ that are preservative free, alcohol free, non irritating
• Avoid tight clothing
• Avoid over ‘analyzing’ and examination of the vagina
• Resuming intercourse only when not pain free
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Physical Therapy
• Decrease hypertonicity THEN restore normal muscle function and strength
• Focus on voluntary and involuntary pelvic floor muscle relaxation• Internal manipulation
• Biofeedback with focus on relaxation
• Pelvic floor stretches
• Internal vaginal dilators
Sexual Cycle and ‘Fear of Intercourse’: Cognitive –Motivational
• Models explaining how patients become ‘trapped’ in a vicious circle of fear and pain that go beyond obvious physical markers:
• Pain and resultant anticipatory anxiety leads to fearful reactions, inhibit genital arousal, vaginal dryness, and pelvic floor hypertonicity
• Inhibition of automatic responses (outside awareness) that would lead sexually meaningful stimuli that normally lead to arousal
• Women may ‘like’ intercourse but not necessarily ‘want’ to have intercourse due to anticipation of pain
• Women have intercourse in spite of pain, because they want to avoid the consequence of relationship discord more than the consequence of pain
Dewitte M, et al. Pain. 2011; 152: 251
Treatment: CBT and “Desensitization”
• Before overcoming fear of pain, patients have to experience non‐painful insertion
• Vaginal dilators, internal PT and internal examination should be non‐painful before patients can overcome ‘fear of pain’
• Address motivational factors for avoiding pain or for continuing to have intercourse in spite of pain
• Identify factors that help reduce fear but also increase arousal and desire
• Address relationship issue that result from being in chronic pain (e.g. partners that don’t ‘believe’ the pain or partners that use pain for ‘gain’
Summary
• Dyspareunia is often multifactorial
• Treatment is usually involves the multidisciplinary approach: organic and psychosocial dysfunctions must be addressed
• Resolution of pain does not ensure return to normal sexual function; psychosocial and ‘fear of intercourse’ factors must be considered
• Chronic sexual or vaginal pain IS VERY SIMILAR to other chronic pain syndromes
• A. You order a UA which is negative and you give her a short course of your favorite antibiotic
• B. You ask her some additional questions such as whether she has been experiencing any vaginal dryness, itching, hot flashes, insomnia
• C. You tell her you don’t see anything wrong and you recommend she go home and have more sex to see if it gets better
• D. You ask her whether she is being abused and if she denies you tell her there is nothing you can do.
Test your knowledge
35
From dysmenorrhea to chronic pelvic pain: when to perform surgery and what works.
AAGL 45th Annual Congress on Minimally Invasive GynecologyOrlando, Florida 2016
PELV-610: Chronic Pelvic Pain 2.0: Decoding Peripheral and Central Factors to Optimize Patient Outcomes
Sawsan As-Sanie, MD, MPHAssistant Professor
Department of Obstetrics and GynecologyDirector, Minimally Invasive GYN Surgery & Fellowship
Director, Endometriosis CenterThe University of Michigan
Disclosures
1. Consultant: Myriad Genetics Lab
1. I will present off-label use of medications, best evidence will be provided.
2
3
Objectives
1. Identify the indications for laparoscopy in women with dysmenorrhea or chronic pelvic pain
2. Describe the efficacy of various surgical procedures for the treatment of chronic pelvic pain
3. Review the evidence regarding the utility of hysterectomy and/or bilateral salpingo-oophorectomy for the treatment of CPP
4. Review the incidence of and risk factors for persistent pelvic pain following hysterectomy
4
Case study
JD is a 24 year old G0 female who presents with complaints of progressive dysmenorrhea. She had previously been on OCPs, ages 15-22, for dysmenorrhea and cycle control. But her pain is no longer controlled on this regimen.
5
Clinical Scenario (continued)
JD’s history is notable for daily pelvic pain (mid-pelvic crampy pain) that worsens shortly before and during menses. +deep dyspareunia.
Physical exam is notable for small, retroverted tender uterus, shortening of right uterosacral ligament with nodularity, and right adnexal tenderness and fullness.
6
Test your knowledge
Prior to proceeding with surgery, you treat JD with 3 months of DepoLupron. Her pain improves. Does this establish the diagnosis of endometriosis?
A. yes
B. no
36
7
Does response to GnRHa diagnose endometriosis?
RCT, n=95, Lupron vs. PlaceboPain relief at 3 mo: p ≤ .001
81% of GnRHa treated group39% of placebo treated group, NNT 2.3
After 3 mo of Lupron treatment, pain relief in:82% of women with endometriosis73% of women without endometriosis
Ling FW. Randomized controlled trial of depot leuprolide in patients with chronic pelvic pain and clinically suspected endometriosis. Pelvic Pain Study Group. Obstet Gynecol. 1999 Jan;93(1):51-8.
8
Test your knowledge
What are the indications for laparoscopy in a patient with dysmenorrhea or CPP?
A. Persistent complex adnexal mass
B. Pelvic pain refractory to medical therapy
C. Family history of endometriosis
D. A & B
E. All of the above
9
Indications for laparoscopic surgery in the evaluation of dysmenorrhea or CPP
To investigate an adnexal mass
To establish a diagnosis of endometriosis (and surgically treat endometriosis if present)
Decision Algorithm for dysmenorrhea or CPP with cyclic exacerbation
10
Actively trying for pregnancy
? Persistent adnexal mass
Laparoscopy
Comprehensive evaluation for all sources of pain
yes
Pain severe,Unresponsive to NSAIDs and
other eligible medical therapies
yes
no
Pain severe,Unresponsive to medical Rx
(including hormone suppression)
yesno
11
Endometriosis
Presence of endometrial stroma and glands outside of the endometrial cavity and musculature
UterusOvary
endometriosis
adhesions
12
Variable appearance of endometriosis
37
13
Misdiagnosed as endometriosis:
Hemangiomas
old suture
ovarian carcinoma
carbon deposits
adrenal rest
Walthard rest
carcinoma
breast
ovary
epithelial inclusions
Reaction of oil based HSG medium
inflammation with or without Psammoma bodies
splenosis
endosalpingiosis
submesothielial microbleeding
normal peritoneum
14
Characteristic PPV Sensitivity NPV Specificity Location
Anterior cul-de-sac 32 100 100 66 Posterior cul-de-sac 65 100 100 76 Uterosacral ligament (l) 61 100 100 77 All sites 45 97 99 77
Lesion appearance Any abnormality 62 100 100 33 Puckered-pigmented only 85 74 75 86
Walter AJ, et al. Endometriosis: correlation between histologic and visual findings at laparoscopy. Am J Obstet Gynecol. 2001 Jun;184(7):1407-11
Surgical biopsy is recommended because accuracy of visual inspection is poor
Accuracy of visual inspection for the diagnosis of endometriosis
Diagnosis requires histological confirmation
15
Test your knowledge
You identify endometriosis at the time of laparoscopy and perform biopsy to confirm the diagnosis and fulguration of the remaining lesions. What proportion of women report improved pain after this procedure?
A. 15-20%
B. 30-50%
C. 60-80%
D. >90%16
Laparoscopy for pelvic pain associated with endometriosis…RCT #1
Sutton et al. 1994Study design
RCT, double blindedN=63 ♀ stage I-III endometriosis[Laparoscopic laser ablation + LUNA] vs. expectant management
ResultsNo difference at 3 months (48% of expectant group with improved pain)Significant improvement with laser ablation at 6 months (63% vs. 23%, p<0.01)
0
1
2
3
4
5
6
7
8
9
10
Before 3 mo 6 mo
Expectant
Laser
VAS
pain
sco
re (0
-10)
Sutton et al. Fertil Steril 1994; 62(4):696-700.
*
* p=0.01, laser vs. expectant
17
83%
53%
32%
80%
N=196 mos 6 mos
N=20 6 mos 6 mos
83%
80%
Diagnostic L/S
Operative L/S
Abbot et al. Fertil Steril 2004; 82(4):878-884.
RCT, blinded, crossoverLaparoscopic excision more effective than placebo30% placebo rate20% not responsive to surgery
Laparoscopy for pelvic pain associated with endometriosis…RCT #2
18
Test your knowledge
At the time of laparoscopy, is it preferable to excise or ablate suspected endometriosis lesions?
A. excise
B. ablate
C. it depends on the location and depth of the lesion
D. it doesn’t matter
38
Excision vs. ablation?
Advantages:histological confirmation
may be more effective??
Disadvantages:Requires greater surgical skill
More bleeding
More operative time
Advantages:Surgeon comfort
Less bleeding
Less operative time
Disadvantages:increase risk of thermal damage
may be less complete
Excision Ablation
20
Excision vs. ablation: Is one superior for pain symptoms?
Wright 2005RCT, double-blinded
N=24
Stage 1-2 endo
Healy 2005RCT, double-blinded
N=103
Stage 1-4 endo
0
10
20
30
Before 6 month
Excision(n=12)
Ablation(n=12)
Wright J, Lotfallah H, Jones K, Lovell D. A randomized trial of excision versus ablation for mild endometriosis. FertilSteril. 2005 Jun;83(6):1830-6. Healey M, Ang WC, Cheng C. Surgical treatment of endometriosis: a prospective randomized double-blinded trial comparing excision and ablation. Fertil Steril. 2010 Dec;94(7):2536-40.
Mea
n Pa
in S
core
Mea
n Pa
in S
core
02468
Before 12 month
Excision(n=54)
Ablation(n=49)
P=0.94
21
Test your knowledge
JD reports that her pain is much improved at her postop visit. What is the likelihood that she will experience recurrent pelvic pain in the next year?
A. <5%B. 25%C. 75%D. 90%
22
Pain recurrence after 1st surgery
Vercellini et al. The effect of surgery for symptomatic endometriosis: the other side of the story. Hum Repro Update 2009; 15: 177-188.
Mean 25% (range 15-50%)
23
Time to recurrent pain after 1st surgery
Vercellini et al. The effect of surgery for symptomatic endometriosis: the other side of the story. Hum Repro Update 2009; 15: 177-188.
24
Test your knowledge
What if JD had a 6cm ovarian endometrioma. What is the best surgical approach?
A. drain the endometriomaB. drain and ablate the endometrioma wallC. excise the endometrioma cyst wallD. it doesn’t matter, all of the above are equivalent.
39
25
Endometriomas: excise or drain & ablate?
Outcome OR (95% CI)
Recurrence of Pain Symptoms:
Dysmenorrhea 0.15 (0.06, 0.38)
Non-menstrual pain 0.10 (0.02, 0.56)
Dyspareunia 0.08 (0.01, 0.51)
Recurrence of endometrioma 0.41 (0.18, 0.93)
1 10 1000.1OR
Favors excision Favors ablation
Hart RJ, Hickey M, Maouris P, Buckett W. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev. 2008 Apr 16;(2):CD004992.
26
Test your knowledge
Following laparoscopic ovarian cystectomy of an endometrioma, JD wonders: will going back on OCPs prevent the development of another endometrioma?
A. No
B. Yes
27
Post cystectomy medical therapy reduces rate and size of recurrent endometrioma
In those with recurrent endometriomas, users of OCPs had smaller cysts.
Non-users
Cyclic
Continuous
Seracchioli R et al, Fertility and Sterility, 2010.
Recurrence free survival is higher in users vs. non-
users of OCPs.
Continuous
Cyclic
Non-users
RCT, n=239, 24 month follow-up.
28
Postop OCP: continuous or cyclic?
Outcome OR (95% CI)
Recurrence of Pain Symptoms:
Dysmenorrhea (n=287) 0.24 (0.06, 0.91)
Non-menstrual pain (n=209) 0.61 (0.36, 1.03)
Dyspareunia (n=180) 0.77 (0.52, 1.12)
Recurrence of endometrioma (n=154) 0.54 (0.28, 1.05)
1 2 50.5OR
Favors continuous Favors cyclicMuzii L, et al. Continuous versus cyclic oral contraceptives after laparoscopic excision of ovarian endometriomas: a systematic review and metaanalysis. Am J Obstet Gynecol. 2016 Feb;214(2):203-11.
0.2
29
Test your knowledge
Four years later, JD reports that she has recurrent dysmenorrhea and is unable to tolerate hormone suppression. She says she read about nerve ablation surgeries and wonders if it is an option for her. Is there evidence to support these procedure?
A. No
B. Yes
30
Presacral neurectomy & LUNA
1. Presacral neurectomy: surgical transection of presacral nerves
=superior hypogastric nerve in the interiliac triangle
2. Laparoscopic uterosacral nerve ablation (LUNA)
Sensory pain fibers from the midline pelvis
Do NOT receive input from ovaries or lateral structures
Indication for CENTRAL MIDLINE PAIN, especially dysmenorrhea
40
No evidence to support LUNA as a treatment for CPP or dysmenorrhea
Daniels 2009 (JAMA)• Double blind RCT
• N=487
• 69 month follow-up
• No difference in:• Worst pain
• Noncyclic pain
• Dysmenorrhea
• dyspareunia
31Daniels J, et al. Laparoscopic uterosacral nerve ablation for alleviating chronic pelvic pain: a randomized controlled trial. JAMA. 2009 Sep 2;302(9):955-61.
Presacral neurectomy associated with modest benefit and substantial risk
Zullo 2003• Single blinded RCT
• N=141
• 1 year follow-up
• 15x adverse events:• 15% constipation
• 5% urinary urgency
32
Zullo F, et al. Effectiveness of presacral neurectomy in women with severe dysmenorrhea caused by endometriosis who were treated with laparoscopic conservative surgery: a 1-year prospective randomized double-blind controlled trial. Am J Obstet Gynecol. 2003 Jul;189(1):5-10.
33
Test your knowledge
JD decides that nerve ablation surgery is not for her. But she is worried that “scar tissue around her uterus and ovaries” is causing her recurrent pain and requests surgery. Is there evidence to support lysis of adhesions as a therapy for CPP?
A. No
B. Yes
34
Pelvic & Abdominal Adhesions
~ 25% prevalence among CPP patients
80% of patients undergoing pain mapping reported pain when adhesions palpated
Nerves, sensory neuron markers found in adhesions of both pain & pain-free patients
Howard F, Ob Gyn Surv 1993; Sulaiman et al. Ann Surg 2001
35
Adhesiolysis is not an effective treatment for chronic abdominal pain
RCT of laparoscopic lysis of adhesions vs. diagnostic laparoscopy100 participants with chronic abdominal pain (> 6 months)
Participants, assessors maskedOutcome: overall improvement in pain, functionNo difference in groups at one year
Swank DJ, et al. Laparoscopic adhesiolysis in patients with chronic abdominal pain: a blinded randomised controlled multi-centre trial. Lancet. 2003 Apr 12;361(9365):1247-51.
Pain scores
hrQOL scores
36
Is adhesiolysis an effective treatment for women with CPP?
Cheong 2014• Double blind RCT• N=50• Study stopped early due to
lack of enrollment• Adhesiolysis group had
more adhesions and more pain at baseline
• Results suggest decreased pain and QOL in adhesiolysis group
Cheong YC, Reading I, Bailey S, Sadek K, Ledger W, Li TC. Should women with chronic pelvic pain have adhesiolysis? BMC Womens Health. 2014 Mar 4;14(1):36. doi: 10.1186/1472-6874-14-36.
41
37
Test your knowledge
Twenty years after her first surgery, JD returns and requests hysterectomy for definitive management. She reports persistent daily pelvic pain despite hormone suppression, physical therapy, and various treatments for interstitial cystitis. What should you recommend?
A. Total hysterectomyB. Total hysterectomy + BSOC. Supracervical hysterectomyD. Supracervical hysterectomy + BSOE. Hysterectomy is not likely to be helpful
78-86% of all women undergoing hysterectomy report improvement after surgery
50% report improvement in mental health, physical or social function
60% report improvement in dyspareunia
38Hartmann KE, Ma C, Lamvu GM, Langenberg PW, Steege JF, Kjerulff KH. Quality of life and sexual function after hysterectomy in women with preoperative pain and depression. Obstet Gynecol. 2004 Oct;104(4):701-9.
Hysterectomy:Most women are satisfied
Hysterectomy:Most women are satisfied, but there are risks
78-86% of all women undergoing hysterectomy report improvement after surgery
50% report improvement in mental health, physical or social function
60% report improvement in dyspareunia
39
Potential for serious morbidity
Regret over loss of fertility
and...significant risk of persistent pain
Hartmann KE, Ma C, Lamvu GM, Langenberg PW, Steege JF, Kjerulff KH. Quality of life and sexual function after hysterectomy in women with preoperative pain and depression. Obstet Gynecol. 2004 Oct;104(4):701-9.
Incidence of persistent pain after hysterectomy
40 Brandsborg B. Pain following hysterectomy: epidemiological and clinical aspects. Dan Med J 2012; 59(1):B4374.
Persistent postop pain = ~25% (6.7 – 31.9%)
New or increased postop pain = ~5% (1-15%)
Risk factors for persistent pain in large prospective observational study
1. Preoperative pelvic pain
2. Pain problems elsewhere
3. Pain is primary indication for hysterectomy
41 Brandsborg B. Pain following hysterectomy: epidemiological and clinical aspects. Dan Med J 2012; 59(1):B4374.
= 3x risk of persistent pelvic pain after hysterectomy
N=1135
Factors associated with persistent pelvic pain after hysterectomy
42
Pain elsewhere (Brandsborg 2007, VanDenKerkhof 2012)
Younger age (Shakiba 2008, MacDonald 1999, Hillis 1995)
Lack of private insurance (Hillis 1995)
Lack of pelvic pathology (Hillis 1995)
Depression (Kjerulff 2000, Hartmann 2004)
Pain catastrophizing (Martin 2011, Carey 2013)
42
Route of hysterectomy (Brandsborg 2009)
Preoperative dysmenorrhea (Stovall 1990)
Preoperative uterine tenderness (Stovall 1990)
Uterine fibroid symptom score (Brandsborg 2009)
Uterine weight (Stovall 1990, Brandsborg 2009)
Adenomyosis (Stovall 1990)
43
…i.e. clinical factors that often guide physicians to offer hysterectomy
Factors NOT associated with persistent pelvic pain after hysterectomy What about the ovaries?
Preserve ovaries
Unilateral oophorectomy
Bilateral oophorectomy
44
?
BSO should not be taken lightly
45
• Relief of pelvic pain
• Prevent recurrent ovarian cysts
• Prevent recurrent endometriosis
• Hot flashes• Vaginal
dryness• Osteoporosis• Cardiovascular
disease• Dementia• All cause
mortality
PROS CONS
BSO
46Parker WH, Feskanich D, Broder MS, Chang E, Shoupe D, Farquhar CM, Berek JS, Manson JE. Long-term mortality associated with oophorectomy compared with ovarian conservation in the nurses' health study. Obstet Gynecol. 2013 Apr;121(4):709-16.
Level II-2Large, prospective observation study
Summary
47
Effectiveness of Hysterectomy
KRISTEN H. KJERULFF, MS, PhD, PATRICIA W. LANGENBERG, PhD,
JULIA C. RHODES, MS, LYNN A. HARVEY, GAY M. GUZINSKI, MD, AND
PAUL D. STOLLEY, MD, MPH
A prospective study of 3 years of outcomes af terhysterectomy with and without oophorectomy
Cynthia M. Farquhar, MBChB, FRANZCOG, MD, CREI, MPH,a,b Sally A. Harvey, RN,RMidwife,a Yi Yu, MSc,a Lynn Sadler, MBChB, MRANZCOG, MPH,a,b
Alistair W. Stewart , BScb
1
2
3
4
5
6
Single site, retrospective, endo only Favors BSO
Single site, retrospective, any CPP No benefit of BSO
Multi site, prospective, any CPP Favors BSO
Multi site, prospective, any CPP BSO increases risk of CPP
Multi site, prospective, any CPP No benefit of BSO
Single site, survey, endo only No benefit of BSO in age<40 48
Likelihood of Success (no reoperation) depends on age and ovarian preservation
Hysterectomy only
Hysterectomy + BSO
Age 30-39 89.6 (76.0–100.0) 85.7 (70.7–100.0)
≥ 40 yrs old 64.3 (33.0–95.7) 96.0 (88.3–100.0)
=
<
Shakiba K, Bena JF, McGill KM, Minger J, Falcone T. Surgical treatment of endometriosis: a 7-year follow-up on the requirement for further surgery. Obstet Gynecol. 2008 Jun;111(6):1285-92
43
If ovaries are removed, what is the risk of recurrent pain and recurrent endometriosis with hormone replacement therapy?
49
Summary guidelines from Expert Reviews (2006, 2010)
Limited data, mostly expert opinion
Level of evidence: III
50
1. Benefits of HRT likely outweigh risk, in select populations
2. No reason to delay HRT after surgery, can start immediately
3. Consider combined estrogen-progestin methods in women with endometriosisUnopposed estrogen may stimulate recurrence of endometriosis and/or stimulate malignant transformation of residual endometriosis
51 52
So, before considering hysterectomy…
• Recognize that chronic pelvic pain is generally multifactorial, often with multiple organ systems involved
• Systematically treat all sources of pain before considering hysterectomy
If a patient fails medical therapy and chooses hysterectomy
She should be well informed regarding the risk of persistent pain (Grade B)
Retain the ovaries when possible (Grade B)Suggested when ovaries are visibly normal, superficial endometriosis, or ovarian endometrioma <5 cm (?)
If BSO is performed, patient should be fully counseled regarding risks associated with surgical menopause and persistent pain
53 54
Test your knowledge
JD undergoes TLH, BSO and was found to have extensive endometriosis and an obliterated posterior culdesac. She initially reported resolution of her pelvic pain, but then returns 3 years later with recurrent pelvic pain. Pelvic ultrasound demonstrates a 4 cm complex left ovarian mass. What do you recommend?
A. No interventionB. Hormone suppression and repeat ultrasoundC. LaparoscopyD. Laparotomy
44
55
Ovarian remnant syndrome
Definition:Histologically confirmed ovarian tissue in a women who has previously undergone bilateral salpingo-oophorectomy
PrevalenceUp to 18% of women with persistent pelvic pain, who previously underwent hysterectomy-BSO for endometriosis/pelvic pain
Abu-Rafeh, et al. J Am Assoc Gynecol Laparosc 2003. 10: 33-37 56
Ovarian remnant syndrome
Clinical presentation:Chronic pelvic pain: 84%Dyspareunia: 26%Cyclic pelvic pain: 9%Dysuria: 7%Pain with defecation: 6%
Risk factors are all related to history of difficult hysterectomy:
EndometriosisPelvic adhesive disease or h/o pelvic inflammatory diseaseMultiple prior abdominal or pelvic surgeries
57
Diagnosis of ovarian remnant
History of prior BSOPelvic pain and/or pelvic mass on exam or imaging
… not all remnants are hormonally active:~ 30% of patients with surgically documented remnants have postmenopausal values of serum estradiol (<35 pg/mL) and FSH (>30 IU/dL).
Magtibay PM, Magrina JF. Ovarian remnant syndrome. Clin Obstet Gynecol. 2006 Sep;49(3):526-34.\; Kho RM, Abrao MS. Ovarian remnant syndrome: etiology, diagnosis, treatment and impact of endometriosis. Curr Opin Obstet Gynecol. 2012 Aug;24(4):210-4.
58
Management of ovarian remnant
Asymptomatic, low risk of malignancy:Surveillance, expectant management
59
Management of ovarian remnant
Asymptomatic, low risk of malignancy:
Surveillance, expectant management
Concern for malignancy (complex appearance, increasing size, etc)
Surgical excision with anticipation of extensive sidewall and retroperitoneal dissection
Laparoscopic approach is feasible, safe and associated with lower morbidity.
Zapardiel I, Zanagnolo V, Kho RM, Magrina JF, Magtibay PM. Ovarian remnant syndrome: comparison of laparotomy, laparoscopy and robotic surgery. Acta Obstet Gynecol Scand. 2012 Aug;91(8):965-9. 60
Management of ovarian remnant
Asymptomatic, low risk of malignancy:Surveillance, expectant management
Concern for malignancy (complex appearance, increasing size, etc)
Chronic pelvic pain, low risk of malignancyConsider medical management with hormonal suppressionLook for other sources of painIf above fails, surgical excision with anticipation of extensive sidewall and retroperitoneal dissection
45
61
Surgical excision of ovarian remnant
Laparoscopic approach is feasible for the experienced surgeon
Significant improvement and/or resolution of pain in ~80%
Recurrence of remnant in 0-20%
Kho RM, Magrina JF, Magtibay PM. Pathologic findings and outcomes of a minimally invasive approach to ovarian remnant syndrome. Fertil Steril. 2007 May;87(5):1005-9
Thank you
62“Wait, those weren’t lies. That was spin…”
References
63
References
64
References
65
Evaluation Question
Which of the following is NOT a risk factor for persistent pelvic pain after hysterectomy?
a) Pain elsewhere in the body prior to hysterectomy
b) Adenomyosis
c) Younger age
d) Normal uterine pathology
e) Depression
66
46
Pre‐operative, Post‐Operative and Chronic Pain Management
Georgine Lamvu, MD, MPH, CPE
Gynecologic Surgeon and Pelvic Pain Specialist, Orlando VA Medical Center
Associate Professor
University of Central Florida
Disclaimer
I have no financial relationships to disclose.
Objectives
• Briefly review pain physiology as it relates to surgical pain
• Describe the evidence available for pain management as it applies to surgical intervention
• Describe new guidelines for pain managmentWHY ARE WE DOING THIS LECTURE TODAY?
Challenges of Operative Pain Management
• 73 million surgeries done in the U.S. annually
– 80% experience acute pain and 20% experience severe pain
• 2001 US Congress “A decade of pain control”
• APS considers pain as the “fifth vital sign”
Hutchinson, Rob. Challenges in acute post-operative pain management, 2007.
Dolin SJ, et al. Effectiveness of acute post‐operative pain management I. Br J Anaesth 2002
• Meta‐analysis of 165 studies, nearly 20,000 patients
• Using VAS score for pain evaluation
– 11% experienced severe pain
– 30% experienced moderate to severe pain
0
10
20
30
40
50
60
70
80
% Severe Pain
% Moderate to Severe Pain
IM
IV PCA
Epidural
47
A History of Ineffective Pain Treatment
0
10
20
30
40
50
60
70
80
90
Any Pain Slight Pain Moderate Pain Severe Pain Extreme pain
% Patients With Acute Post Operative Pain: Hutchinson 2007
Hutchinson, Rob. Challenges in acute post-operative pain management, 2007.
Factors That Contribute to Inadequate Pain Management
Factors That Contribute to Inadequate Pain Management
Impact of Inadequate Pain Relief:
• Diminished patient functioning and increased risk for complications
– diminished immune response
– Avoidance of movement and ambulation increasing risk of DVT
– Anxiety, stress, demoralization, depression
• Extended lengths of stay, readmission, poor satisfaction
• Increased resource utilization and healthcare costs
• Development of chronic pain syndrome
Hutchinson, Rob. Challenges in acute post-operative pain management, 2007.Anesthesiology 2004; 100: 1573.Anesthesiology 2000; 93: 1123
Sinatra, Raymond. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, pp. 20. Professional Communications Inc. 2012.
Impact of Inadequate Pain Relief
• Over‐reliance on opioid therapy monotherapy
How Did We Contribute to the Opioid Epidemic?
• Heroin has been used for all types of ailments since 1900s
• In 2011 Oxycontin was the #1 most prescribed drug in the U.S.
• By 2010 Cochrane reported that 62 RCTs demonstrated that opioids are more effective than placebo for SHORT‐TERM acute pain control but the evidence is weak for its long‐term use
48
49
Monotherapy
Over‐reliance on single class analgesia commonly results in
• Limited efficacy
• Intolerable adverse events
• Diminished patient satisfaction
• Example of opioid monotherapy
– Nausea, vomiting, constipation, ileus, urinary retention
– Opioid induced hyperalgesia
– Long term‐side effects such as mood instability, insomnia, tolerance and withdrawal
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
Development of Chronic Pain Syndrome After Surgery
• 10‐50% of patients undergoing operations later develop persistent pain
– 14% of women after hysterectomy develop newonset pain after surgery
Kehlet H, et al. Persistent Postsurgical Pain: Risk Factors and Prevention. Lancet, 2006Pluijms, WA, et al. Chronic post-thoracotomy pain: A retrospective Study. Acta Anaesthsiol Scand, 2006Brandsborg B, Nikolajsen L, Hansen CT, Kehlet H, Jensen TSSO. Risk factors for chronic pain after hysterectomy: a nationwide questionnaire and database study. Anesthesiology. 2007.
What Should Surgeons Do?
Neurobiology of Pain
• Peripheral nociceptors
• Signal propagation and conduction to the spinal cord
• Cortical perception: identification and localization of pain
• Descending inhibition: suppression of pain transmission by descending contacts from the brainstem, midbrain and cerebral cortex
• Supraspinal reactions: cortical responses including fear, anxiety, depression
Sinatra, Raymond , Larach S, Ramammorthy Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.Julius and Basbaum Nature Sept, 2001;413 :203-210. Drysdaleosteopathy.wordpress.com
Predictive Factors of Postoperative Pain Intensity
Hui et al. Predictors of Postoperative Pan and Analgesic Consumption: A QualitativeSystemic Review. Anesthesiology 111; 657-77. 2009.
Predictive Factors of Postoperative Analgesic Consumption
Hui et al. Predictors of Postoperative Pan and Analgesic Consumption: A QualitativeSystemic Review. Anesthesiology 111; 657-77. 2009.
50
A Model to Identify Patients at Risk for Prescription Opioid Abuse,
Dependence and Misuse
• Pain Med 2012; (13)9:1162
Guide to Pain Managment
• These recommendations are based on CDC, Va/DoD and APS pain management guidelines
• Evidence about opioid therapy– Benefits of long‐term opioid therapy for chronic pain not well
supported by evidence– Short term benefits small to moderate for pain; inconsistent for
function– Insufficient evidence for long‐term benefits in low back pain,
headache and fibromyalgia
• Non‐opioid therapies– May be used alone or in combination– Non‐opioid medication, e.g. NSAIDS, TCA, SNRIs, anti‐convulsants– Topical analgesics, injections (e.g. steroids) and blocks– Physical treatments, e.g. physical therapy, exercise– Behavioral therapy, e.g. counseling, CBT
Four Steps to Pain Management*
1. Assess: History, Exam and Risk Assessment
2. Check: what other medications are being taken, possible interactions, opioids, benzodiazepines, high doses, obtaining medications from multiple providers
3. Discuss: Expectations, potential risks
4. Observe: Look for clinical improvement, overuse and misuse, go slow with dose increases, consult support pain management teams if needed
* A must before surgery
Risk Assessment for Pain Chronicity*
• Poorly controlled pain
• Psychiatric co‐morbidities
• Pre‐operative anxiety
• Having surgery
• Poorly controlled post operative pain
• If the patient has multiple pain co‐morbidities
* A must before surgery
Risk Assessment*
• Urine Drug Screen
– Check to confirm presence of prescribed substances or for undisclosed prescription drug or illicit substances
• Prescription drug monitoring program
– Check for opioids or benzodiazepines from other sources
* A must before surgery
Patient Education*
• Opioids are not first‐line or routine therapy for chronic pain and for acute pain they are used only in severe pain and in short amounts
• Establish realistic goals for improvements in pain and function
• Discuss benefits and risks and availability of non‐opioid therapies with patients
* A must before surgery
51
Key Points For Patient / Family Education*
• Analgesics will not make you pain free, they only help alleviate some pain, most pain medications take 1‐2 hours to take effect; the goal is not to cure pain but rather to improve function
• We expect about a 30% improvement in pain and function for most therapies• Recovery from surgical or acute traumatic injury is expected to take 2‐4 weeks, it is not immediate• Don’t take extra doses beyond what is prescribed, tell all you providers what medications you are
taking• Don’t stop opioids suddenly, instead taper slowly as instructed by your provider• Do not drive or operate heavy machinery, don’t drink alcohol or take other street drugs with you
pain medications• Protect your pain medications from damage, loss or theft• Report any side effects such as sleepiness, confusion, constipation, itching, nausea and vomiting,
difficulty breathing to your provider• Your prescriptions are registered in a state monitoring program that is accessible to all of your
providers• To monitor your medication intake, your provider may recommend a urine drug screen when you
are evaluated
* A must before surgery
Surgical Pain Management
Multimodal Analgesia
• Defined as the simultaneous use of different analgesic agents or forms of analgesic delivery to suppress pain transmission in the peripheral and Central Nervous System (CNS). Regimens can be designed to:
– Inhibit release of noxious mediators
– Block conduction in sensory nerves
– Suppress pain perception in the CNS
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
Multimodal Analgesia
Advantages• Addresses multiple mechanisms of pain
• Allows for use of lower nontoxic does of medications
• It can be used in acute and chronic pain management
• In some cases can avoid use of opioids completely
• 52 RCTs vs. opioid monotherapy show
– Improved mobilization and rehabilitation
– Better pain control
– Improved patient satisfaction
– Less 15‐55% decrease in opioid dosing
Disadvantages
• Requires knowledge of multiple drugs and pain mechanisms
• Potential for interaction
• Requires skills in regional and neuraxial analgesia
• Possible post discharge patient confusion and compliance issues
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
Pain Management
American Society for Anesthesiology Postsurgical Pain Practice Guidelines
and Recommendations
Perioperative Techniques for Pain Management Guidelines
• The literature supports the use of epidural or intrathecal opioid analgesia, PCA with systemic opioids, regional anesthetic blocks ( intercostal, plexus) and peripheral anesthetic blocks (intercostal, ilioinguinal, interpleural, femoral)
• The literature supports post‐incisional infiltration with local anesthetics
• The literature is equivocal on benefits of pre‐incisional infiltration
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
52
• The literature supports the administration of two analgesic agents that act by two different mechanisms. Examples include:
– Epidural opioids combined with epidural local anesthetics or clonidine
– IV opioids combined with Ketorolac or Ketamine
– Unless contraindicated, all patients should receive an around –the‐clock regimen of NSAIDS, COXIBs or acetominophen, in addition regional blockade with local anesthetics should be considered
Perioperative Techniques for Pain Management Guidelines
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
Non‐Opioid Treatments for Pain
Medication Harms Comments
Acetominophen Hepatotoxic
NSAIDS Cardiac, GI, Renal
Gabapentin/pregabalin
Sedation, dizziness, ataxia
Neuropathic pain, fibromyalgia
TCAs and SNRIs TCAs anticholinergic and cardiac
Neuropathy, fibromyalgia, headaches
Topical agents (Lidocaine, Capsaicin, NSAIDs)
Capsaicin burning Lidocaine for neuropathic pain, NSAIDS for arthritis
Muscle Relaxants
Steroids
Opioid : Higher Dose=Higher Risk• Start with immediate release instead of extended‐release• Increase slowly and keep dose below 50MME/day. What is
50MME/d?– 50mg of hydrocodone (10 tabs of 5/300)– 33mg of oxycodone (2 tabs of oxycodone sustained release, 15mg)– 12 mg methadone (<3 tabs of 5mg)
• Start with 3‐7 days with a taper (by about 30% at a time)• Prescribe exact doses and instructions, avoid “PRN”• Avoid concurrent benzodiazepine use• Prescribe naloxone when concerned about risk of overdose• Have an explicit (and document it) conversation with the patient
about risks, benefits and expectations for pain relief Opioid Morphine Equivalent
1mg Codeine 0.1mg Morphine
1mg Hydrocodone 1mg Morphine
1mg Hydromorphone 4mgMorphine
1mg Methadone 4mg‐12 mgMorphine
1mg Oxycodone 1.5mgMorphine
1mg Oxymorphone 3mgMorphine
1 mcg Fentanyl 2.4 mg Morphine
=
Keys to Opioid Start, Continuation and Discontinuation
• Repeated or long‐term use of opioids requires
– Periodic re‐assessment– Urine drug screen– Checking the prescription drug
monitoring program
• Start low and increase dose slow by 10%
• Decrease slow by 10‐30%, patients can have severe withdrawal
• Document the dose, total # of pills given and the instructions for use every time
Recommendations for Post‐Surgical Pain
• Acetaminophen, NSAIDS first (PO or IV)
• Preferably use oral vs. IV opioids if patients can take PO, avoid IM
• Use anesthetic epidurals or spinals for thoracic and abdominal surgery
• Use PCA without basal rate• Pre‐operative celecoxcib• Pre or Post‐operative
gabapentin• Infiltrate surgical sites with
anesthetic, nerve blocks or topical anesthetics
• Physical Therapy / Occupational Therapy
• Heat or cold therapy• Acupuncture• Chiropractic• TENS‐ Nerve stimulation• Relaxation • Cognitive behavioral therapy
Preemptive Analgesia
• Benefits associated with preemptive analgesia are gained only when:
– Pre‐operative dosing occurs prior to surgical incision
– There is continued dosing during anesthesia
– Post‐surgical maintenance of therapy is maintained for 24‐48 hours for outpatient surgery and 96 hours for longer more invasive procedures
• I.e. preemptive analgesia does not work without post‐operative pain control
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
53
In Patients With Difficult‐to‐Manage Pain Consider
• Skeletal muscle spasm
• Visceral muscle spasm
• Inflammation
• Neuropathic pain
• Opioid induced hyperalgesia
• Anxiety
• Insomnia
Sinatra, Raymond , Larach S, Ramammorthy S. Surgeon’s Guide to Postsurgical Pain Management: Colorectal and Abdominal Surgery. First Edition, Professional Communications Inc. 2012.
For Patients With Difficult‐to‐Manage Post Surgical or Chronic Pain
• Start with NSAIDS, Acetominophen unless contraindicated, then add one or more of the following:
– Local anesthetics: lidocaine, marcaine, bipuvacaine via local injection, transdermal or long acting local injection
– Alpha 2 agonists: clonidine provides sedation, anxiolysis and analgesia, via oral, transdermal or IV or epidural, most effective when combined with opioids
For Patients With Difficult‐to‐Manage Post Surgical or Chronic Pain
– Anticonvulsants: Neurontin and Pregabalin oral approved for long term treatment neuralgias and also recommended for acute surgical pain management
• Gabapentin 600mg‐900mg pre‐op and 600‐900mg tid for 24‐72 hours post op
• Pregabalin 75‐100mg preoperatively followed by 75‐100mg bid for 24‐72 hours
For Patients With Difficult‐to‐Manage Post Surgical or Chronic Pain
– NMDA receptor antagonists: Ketamine potentiates opioid‐mediated analgesia and provides opioid‐sparing effect. IV, PCA
– Muscle relaxants: Methocarbamol, cyclobenzaprine, tizanidine, benzodiazepines such as diazepam and lorazepam
• Carisoprodol ranked 14th or the 20 most abused mood‐altering drugs in the US
– Corticosteroids: anti‐inflammatory actions useful in post‐surgical pain relief, comparable to NSAIDS and acetominophen, may be useful in patients who cannot tolerate NSAIDS
– TCAs: unclear mechanisms of pain relief, used for management of depression and chronic pain (neuropathic, fibromyalgia, neck and low back pain)
• Lower doses needed for pain control than for management of depression
For Patients With Difficult‐to‐Manage Post Surgical or Chronic Pain
54
You Want Me to Do What? Physiotherapy Treatments for
Chronic Pelvic Pain
AAGL – Advancing Minimally Invasive Gynecology Worldwide
45th Global Conference
Tracy Sher, MPT, CSCS
Email: [email protected]
www.pelvicguru.com
www.sherpelvic.com
Property of Tracy Sher, MPT, CSCS. All rights reserved
Financial DisclosuresI have no financial relationships to disclose.
AAGL – Advancing Minimally Invasive Gynecology Worldwide
45th Global Conference
Tracy Sher, MPT, CSCS
Property of Tracy Sher, MPT, CSCS. All rights reserved
Objective
Discuss physical therapy for the treatment of chronic pelvic pain.
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So WHAT IS Pelvic Physical Therapy?
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What My Mom Thinks We Do
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55
What Patients Think We Do
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What Potential Dates Think We Do
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Pelvic Physical Therapy / Physiotherapy
What We Actually Do * we have time
Property of Tracy Sher, MPT, CSCS. All rights reservedhttp://personcentredcare.health.org.uk/overview‐of‐person‐centred‐care/overview‐of‐person‐centred‐care/overview‐of‐person‐centred‐care/se‐0
Treating the Whole PersonOverlapping Conditions with Pelvic Pain
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2015 Report: Impact of Chronic Overlapping Pain Conditions on Public Health and the Urgent Need for Safe and Effective Treatment 2015 Analysis and Policy Recommendations
Somatic NEURAL Visceral
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http://wehelpwhathurts.homestead.com/nongastricabdominalpain.html
Treatment Umbrella- Key Points
Brain and Pain – Neural Education
Manual Therapy
Therapeutic Exercise
Integrating Downtraining / Desensitization
sEMG Biofeedback
Lifestyle Modifications – Bladder, Bowel, Hygiene, Cushions
Modalities
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Motivational Interviewing, Neural Education, and “Cheerleading.” Biopsychosocial
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Neuro Education- Pain Management
Conclusions: For chronic musculoskeletal disorders there is compelling evidence that an educational strategy addressing neurophysiology and neurobiology of pain can have a positive effect on pain, disability, catastrophizing, and physical performance.
Property of Tracy Sher, MPT, CSCS and Loretta J. Robertson, PT, MS. Permission required to reproduce or share. 14
Louw, Adriaan. The effect of neuroscience education on pain disability, anxiety, and stress in chronic musculoskeletal pain. 2011; 92. (12)
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Manual Therapy
Myofascial release /
Soft tissue mobiization
Trigger point release
(Dry Needling TrP)
Connective tissue manipulation
Visceral mobilization
Joint mobilization / Manipulation
Muscle energy techniques
Strain‐Counterstrain
Pelvic Physical Therapy Treatment
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Manual Therapy Local and Central:
• “direct effect on tissue dysfunction…muscles, fascia, and neural tissue “
• “…may also directly impact the state of the autonomic nervous system, specifically by interrupting the viscera‐somatic reflex arc, which is an autonomic reflex.”
• So, “treatment may have an important effect not only on local tissue dysfunction but also on the sensitized nervous system”
CMT Connective Tissue Mobilization:
Property of Tracy Sher, MPT, CSCS and Loretta J. Robertson, PT, MS. Permission required to reproduce or share. 18
(Hilton and Vandyken 2012)
57
Manual Therapy
• “Manual therapy techniques may unload the peripheral nerve by increasing the space or fluid motion in the tissues around the nerve.”
• the nerve has a better chance of moving well within the space surrounding it.
Local Tissue and Peripheral Nerve:
Property of Tracy Sher, MPT, CSCS and Loretta J. Robertson, PT, MS. Permission required to reproduce or share. 19
(Hilton and Vandyken 2012)
Therapeutic ExerciseKey Findings:
• Exercise therapy improved post‐treatment pain intensity and disability
• There is no evidence that one particular type of exercise therapy is clearly more effective than others.
LBP (van Middlekoop 2010)
• “The value of supervised active therapy programs…not…specific muscular deficiencies, but rather…encouragement for the patient, that movement is not harmful…
• Decreased catastrophizing had positive effect.
• Authors ask‐ do stabilization exercises have some sort of "central" effect, unrelated to abdominal muscle function per se?
Spine Stab/ LBP (Mannion 2012)
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Muscles – “CORE” Pressure System
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Understand Your Back & Pelvic Girdle Pain Written by Diane Lee Physiotherapist
Lee, D. The Pelvic Girdle, 3rd and 4th Elsevier 2011
Self-Care and Lifestyle Modifications
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If Patients Have MSK Findings as the Source or a Part of Their Pelvic Pain…
Do NOT start on Kegels and send them away
Do NOT suggest surgery will fix all of the issues
Do NOT tell them Barry White, wine or “just relaxing” will cure them
Refer to Pelvic Physical Therapy if possible Will screen to rule out Back/Hip and other differentialsRestore Tissue mobility and improved movement (decrease kineseophobia)Train patient in toileting postures, muscle re‐education, self help strategies Help ”downregulate” nervous system
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If Patients Have MSK Findings as the Source or a Part of Their Pelvic Pain…
If You Have to Do This Alone
Start patient on deep breathing, Yoga, relaxation, meditation to help relax
Toilet posture – feet supported Self massage for abdomen Don’t just tell them to get dilators. They need more guidance (do follow‐up)
Get an Ortho PT to rule out hip/back involvement if you suspect that
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58
Find a Pelvic PT (and Other Pelvic Pain Professionals)
International Pelvic Pain Society www.pelvicpain.org
Women’s Health APTA/SOWHwww.womenshealthapta.org
Pelvic Guru:https://pelvicguru.com/2016/02/13/find‐a‐pelvic‐health‐professional/
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Pelvic PT – Part of a Team Approach• Best approach is a team approach. Multimodal!
• Lots of hope. Even if past failure, were they having a multimodal approach at same time?
• At the point that it is chronic, there’s likely local, central and psychological impact.
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THANK YOU!!
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www.pelvicguru.com www.sherpelvic.com
References
Alvarez, DJ, Rockwell, PG. Trigger Points: Diagnosis and Management. Am FamPhysician. 2002 Feb 15;65(4):653‐661
Butler and Mosely, Explain Pain, 2003
FitzGerald MP, Anderson RU, Potts J, et al. Randomized multicenter feasibility trial of myofascial physical therapy for treatment of urologic chronic pelvic pain syndrome. J Urol. 2009;182:570–580.FitzGerald MP, Kotarinos, ER. Rehabilitation of the short pelvic floor. I: Background and patient evaluation. Int Urogynecol J (2003) 14: 261–268
Hilton S, Vandyken C. Clinical Commentary. The puzzle of pelvic pain – a rehabilitation framework for balancing tissue dysfunction and central sensitization, I: Pain physiology and evaluation for the physical therapist J Women’s Health PT. 2011;35(3):103‐113
Lee, D. The Pelvic Girdle, 3rd and 4th Elsevier, 2004/ 2011.
Louw A, et al. The Effect of Neuroscience Education on Pain, Disability, Anxiety, and Stress in Chronic Musculoskeletal Pain. Arch. Phys. Med. and Rehab 2011; 92(12):2041‐2056
Mannion AF, et al. [Increase in strength after active therapy in chronic low back pain (CLBP) patients: muscular adaptations and clinical relevance] Schmerz 2001;15(6): 468‐73.
Property of Tracy Sher, MPT, CSCS. All rights reserved
References
Takada T, Ikusaka M, Ohira Y, Noda K, & Tsukamoto T (2011). Diagnostic usefulness of Carnett’s test in psychogenic abdominal pain. Internal medicine (Tokyo, Japan), 50 (3), 213‐7 PMID: 21297322
Tu, FF. Physical therapy evaluation of patients with chronic pelvic pain: a controlled study. American Journal of Obstetrics & Gynecology Volume 198, Issue 3 , Pages 272.e1‐272.e7, March 2008
Travell, and Simon. Myofascial Pain and Dysfunction: The Trigger Point Manual, Volume 2, 1992
•vanMiddelkoop M, et al. Exercise therapy for chronic nonspecific low‐back pain. Best Pract Res ClinRheumatol 2010;24(2):193‐204
Vandyken C, Hilton S. The puzzle of pelvic pain‐a rehabilitation framework for balancing tissue dysfunction and central sensitization, II: A review of treatment considerations. J Women's Health PT. 2012;36(1):44‐54
Wall LL. The muscles of the pelvic floor. Clin Obstet Gynecol 1993;36:910‐25
Weiss J.Chronic pelvic pain and myofascial trigger points. Complim Med and Pain. 2000 Dec:13‐18
Weiss JM, Prendergast SA. Screening for musculoskeletal causes of pelvic pain. Clin Obstet Gynecol. 2003;46(4):773‐82
Hip References• Laslett M, Aprill CN, McDonald B, Young SB. Diagnosis of Sacroiliac Joint Pain: Validity of Individual Tests and Composites of Tests. Manual Therapy. 2005: 10; 207‐18.
• van der Wurff P, Hagmeijer RH, Meyne W. Clinical tests of the sacroiliac joint: A systematic methodological review. Part 1: Reliability. Man Ther. 2000;5:30–36.
• Robinson HS, Brox JI, Robinson R, Bjelland E, Solem S, Telje T. The reliability of selected motion and pain provocation tests for the sacroiliac joint. Man Ther. 2007;12:72–79.
Property of Tracy Sher, MPT, CSCS. All rights reserved
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Website References
http://clindx.wordpress.com/2011/05/26/carnetts‐test‐for‐excluding‐intra‐abdominal‐origens‐of‐abdominal‐tenderness/
http://medicfrom.com/publicpress/Massage/Basic_Clinical_Massage_11.html
http://wehelpwhathurts.homestead.com/nongastricabdominalpain.html
http://medicfrom.com
2015 Report: Impact of Chronic Overlapping Pain Conditions on Public Health and theUrgent Need for Safe and Effective Treatment 2015 Analysis and Policy Recommendations http://www.chronicpainresearch.org/public/CPRA_WhitePaper_2015‐FINAL‐Digital.pdf
www.visiblebody.com
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Michael Hibner, MD, PhD, FACOG, FACS
Director, Division of Surgery and Pelvic Pain
St. Joseph’s Hospital and Medical Center, Phoenix, Arizona
Professor of Obstetrics and Gynecology
Creighton University School of Medicine
I have no financial relationships to disclose. Diagnosis and treatment of neuropathic pain.
Annual cost to US economy for treating chronic
pain conditions is 600 billion dollars/year
Greater than combined treatment for diabetes,
cancer and heart disease
Neuropathic pain 0.9% to 17.9% of pain patients
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Pain caused by a lesion or disease of
somatosensory system
Affects 8% of population
Compression
Transection
Contusion
Stretch
Crush
Blunt Trauma
• Falls
• Accidents
• Pelvic fractures
Obstetrical
• Prolonged second stage of
labor
• Positioning
• Traumatic Delivery
Surgery
• Incisions
• Compression from
retractors
• Stretching from positioning
• Mesh
Radiation Therapy
• Fibrosis
Medical conditions
Tingling (“pins and needles” or “prickling”)
Burning (“hot”)
Shooting (“electrical shocks”)
If motor nerve – numbness, weakness, loss of
reflexes
Hypoesthesia (abnormally reduced sensation to touch
or cold)
Hypoalgesia (abnormally reduced pain sensation to
noxious stimulus)
Hyperalgesia (abnormally increased sensation to
noxious stimulus)
Allodynia (pain sensation to a nonnoxious stimulus)
Diagnosis and treatment of neuropathic pain
has to be done in timely fashion to minimize
central and peripheral sensitization
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Description of injury
Description of distribution of motor, sensory and
autonomic changes
Pain quality
Additional pain generators
Palliative and provocative positions
Neurological exam testing sensory, motor and
autonomic fibers
Hypo and hyper sensitivity, allodynia
Tinel’s sign – percussion tenderness over
affected nerve – distal migration of axonal
cone
Guided nerve blocks
MRI
EMG
Nerve conduction studies/PNMTL
Pain must be present
• Patients must have pain at the time of the injection
Evaluate for technical success
• Anatomical position, diffusion of solution, and achieved
analgesia
Interpretation
• Relief of symptoms, the specificity of the block, and the
possibility of placebo effect
Local anesthetic
• Lidocaine 1 – 2% with epinephrine
• Bupivacaine 0.5% with epinephrine
Sodium Bicarbonate 8.4% (10:1 ratio)
Three to five milliliters, to minimize spread
Image guidance (ultrasound, CT, etc…)
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Multidisciplinary approach
Avoidance of offending factors
Pharmacotherapy
Physical therapy
Holistic treatments – acupuncture
Psychological – counseling, biofeedback
Botox and steroid injections
Antidepressants
Anticonvulsants
Local anesthetics
NMDA receptor
antagonists
Opioids
Cannabinoids
Botulinum toxin
Topical capsacin
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Neurolysis
Neurectomy
Nerve repair/reconstruction
Static
• Within rigid fibro‐osseus tunnel
• Between ligaments
• Scarring in or apart of the tunnel
Dynamic
• Narrowing of the nerve from muscle contractions
• Angulation during positioning
Freeing the nerve from:
• Scar tissue
• Ligaments
• Surgical material
Transposition of the nerve
Prevention of re‐scarring
For purely sensory nerves
Permanent numbness ‐ diminishes over one year
as surrounding nerves take over
Risk of stump neuroma (tangle of regenerating
axons and Schwann cells without end destination
• Implantation into the muscle may diminish the risk
Neurolysis – 70‐88%
Neurectomy – 64‐75%Inferior rectal nerve
Cutaneous branch of obturator nerve
Lateral cutaneous branch of iliohypogastric nerve
Femoral branch of genitofemoral nerve
Posterior femoral cutaneous nerve
Lateral femoral cutaneous nerve
Iliohypogastricnerve
Clitoral/perinealnerves
Femoral nerve
Genital branch of genitofemoral nerve
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Overall any neuropathy – 1.9%
Obturator – 39%,
Ilioinguinal/iliohypogastric – 21%
Genitofemoral – 17%
Femoral ‐ 7.5%
Lumbosacral plexus – 0.2%
Overall recovery rate – 73%
Honig, 2002
Originates from S2‐S4
Sensory
• Rectum
• Perineum
• Scrotum / Vulva
• Penis / Clitoris
Motor
• Sphincters (anal, urethral)
• Muscles of the urogenital triangle
Autonomic
Pain in the area of innervation of the pudendal nerve
Pain is neuropathic in nature
• Paresthesia – burning, tingling, prickling, numbness sensation
• Allodynia – pain in response to non painful stimulus
• Hyperalgesia – pain out of proportion to the stimulus
Pain is more severe with sitting
Pain absent or significantly less when lying down
Pain less when sitting on the toilet vs. chair
Sensation of foreign body in the rectum or vagina (allotriesthesia)*
Urinary symptoms – frequency, urgency, hesitancy
Dyschesia
Dyspareunia
Pain with orgasm
Pain with sexual arousal
Persistent sexual arousal
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Surgery
• Direct mesh injury
• Indirect – hysterectomy, cystocele repair, prolapse repair
Vaginal childbirth
Trauma
• Falls
• Cycling
• Intense lower extremity exercise
(abductor machine)
• Excessive masturbation
• Excessive use of anal vibrators
100 patients – 8 lost to follow up
Cured – 13/91 (14%)
Better – 45/91 (49%)
Same – 28/91 (31%)
Worse – 6/91 (6%)
63%
37%
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Originates from L1
Sensory:
• Posterior lateral glute
• Suprapubic skin
Motor:
• Transverse abd.
• Internal oblique
Burning numbing pain in the lower abdomen
radiating to the labia (scrotum)
Worsened by lumbar extension
Transection, entrapment, crush injury, neuroma formation
Ilioinguinal nerve
• to ASIS
• 3.1 cm medial
• 3.7 cm inferior
• to symphisis pubis
• 2.7 cm lateral
• 1.7 cm superior
Iliohypogastric nerve
• to ASIS
• 2.1 cm medial
• 0.9 cm inferior
• to symphysis pubis
• 3.7 cm lateral
• 5.2 cm superior
Whiteside et al., 2003
Sensory sparing
• Nerve Blocks – 25%
Sensory non sparing
• Alcohol Ablation – 70%
• Neurectomy – 87%
Loos et al. 2008
Originates from L1‐L2
Divides into genital and femoral branches
Sensory:
• Labium majus
• Anteromedial thigh
Motor:
• Cremaster
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Compression from self retaining retractor
Genitofemoral n.
IVC
Genitofemoral Nerve
67 to 100% resolution of pain
Chen DC, Hiatt JR, Amid PK. Operative management of refractory neuropathic inguinodynia by a laparoscopic retroperitoneal approach. JAMA Surg. 2013;148(10):962‐7.
Emerges from S1‐4
Sensory:
• Inferior buttocks
• Lateral perineum
• Proximal medial thigh
• Labia majora
• Clitoris
Often confused with the
pudendal nerve
Darnis B, Robert R, Labat JJ, et al. Perineal pain and inferior cluneal nerves: anatomy and surgery. SurgRadiol Anat. 2008;30(3):177‐83.
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Emerges form L2‐4
Sensory
• Medial thigh
Motor
• Pectineus
• Abductor longus/brevis
• Gracillis
87% improvement
50% complete resolution of pain
Rigaud J, Labat J‐J, Riant T, Hamel O, Bouchot O, Robert R. Treatment of obturator neuralgia with laparoscopic neurolysis. J Urol. 2008;179(2):590‐4; discussion 594‐5.
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CULTURAL AND LINGUISTIC COMPETENCY Governor Arnold Schwarzenegger signed into law AB 1195 (eff. 7/1/06) requiring local CME providers, such as
the AAGL, to assist in enhancing the cultural and linguistic competency of California’s physicians
(researchers and doctors without patient contact are exempt). This mandate follows the federal Civil Rights Act of 1964, Executive Order 13166 (2000) and the Dymally-Alatorre Bilingual Services Act (1973), all of which
recognize, as confirmed by the US Census Bureau, that substantial numbers of patients possess limited English proficiency (LEP).
California Business & Professions Code §2190.1(c)(3) requires a review and explanation of the laws
identified above so as to fulfill AAGL’s obligations pursuant to California law. Additional guidance is provided by the Institute for Medical Quality at http://www.imq.org
Title VI of the Civil Rights Act of 1964 prohibits recipients of federal financial assistance from
discriminating against or otherwise excluding individuals on the basis of race, color, or national origin in any of their activities. In 1974, the US Supreme Court recognized LEP individuals as potential victims of national
origin discrimination. In all situations, federal agencies are required to assess the number or proportion of LEP individuals in the eligible service population, the frequency with which they come into contact with the
program, the importance of the services, and the resources available to the recipient, including the mix of oral
and written language services. Additional details may be found in the Department of Justice Policy Guidance Document: Enforcement of Title VI of the Civil Rights Act of 1964 http://www.usdoj.gov/crt/cor/pubs.htm.
Executive Order 13166,”Improving Access to Services for Persons with Limited English
Proficiency”, signed by the President on August 11, 2000 http://www.usdoj.gov/crt/cor/13166.htm was the genesis of the Guidance Document mentioned above. The Executive Order requires all federal agencies,
including those which provide federal financial assistance, to examine the services they provide, identify any
need for services to LEP individuals, and develop and implement a system to provide those services so LEP persons can have meaningful access.
Dymally-Alatorre Bilingual Services Act (California Government Code §7290 et seq.) requires every
California state agency which either provides information to, or has contact with, the public to provide bilingual
interpreters as well as translated materials explaining those services whenever the local agency serves LEP members of a group whose numbers exceed 5% of the general population.
~
If you add staff to assist with LEP patients, confirm their translation skills, not just their language skills.
A 2007 Northern California study from Sutter Health confirmed that being bilingual does not guarantee competence as a medical interpreter. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2078538.
US Population
Language Spoken at Home
English
Spanish
AsianOther
Indo-Euro
California
Language Spoken at Home
Spanish
English
OtherAsian
Indo-Euro
19.7% of the US Population speaks a language other than English at home In California, this number is 42.5%
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