Chronic Pelvic Pain E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Serie: GIP - Gynaecology in Practice
• Sprache: Englisch

Seitenzahl: 478

Veröffentlichungsjahr: 2011

Beschreibung

A new addition to the Gynecology in Practice series, Chronic Pelvic Pain provides a practical guide to diagnosing and treating chronic pelvic pain in women. Emphasizing diagnosis, management and psychological aspects, the book assists gynecologists to better care for their patients suffering from this condition. As a part of the series, various feature boxes are highlighted throughout. "Tips and Tricks" give suggestions on how to improve outcomes through practical technique or patient questioning. In addition, "Caution" warning boxes supply helpful advice on how to avoid problems and "Science Revisited" boxes offer quick reminders of the basic science principles necessary for understanding the presented concepts.

Leseprobe

Table of Contents

Cover

Table of Contents

Half title page

Title page

Copyright page

Series Foreword

Preface

Contributors

1 Neurobiology of Chronic Pelvic Pain

Introduction

Nociception and pain

Mechanisms of chronic pelvic pain

2 The Differential Diagnosis of Chronic Pelvic Pain

Introduction

Reproductive system diagnoses

Urinary system diagnoses

Musculoskeletal system diagnoses

Summary

3 Psychogenic Causes of Chronic Pelvic Pain, And Its Impact on Psychological Status

Introduction

What does “psychogenic” really mean?

How do psychogenic causes translate into physical pain?

Psychogenic causes of chronic pelvic pain

Criteria for the diagnosis of psychogenic pain

Common mistakes

Psychological and sexual consequences of CPP

Conclusions

4 Endometriosis: Pathogenesis and Management of Pain

Introduction

Pathogenesis

Symptoms

Treatment options

5 Pelvic Infections and Chronic Pelvic Pain

Introduction

Epidemiology and risk factors

Pathology

Clinical presentation and diagnosis

Treatment and prevention

Complications

Relationship to chronic pelvic pain

Evaluation of the patient with chronic pelvic pain

Medical management of chronic pelvic pain

Dyspareunia

6 Pelvic Congestion Syndrome

Introduction

Pelvic congestion syndrome

Symptoms

Pathophysiology

Investigations

Use of dihydroergotamine in pelvic congestion

Treatment

Conclusions

7 Chronic Pelvic Pain and Adhesions

Introduction

Incidence of de novo adhesion formation and adhesion reformation

Relationship of adhesion to pelvic pain

Clinical trials examining efficacy of adhesiolysis

Conclusions

8 Fibroids, Adenomyosis, and Chronic Pelvic Pain

Introduction

Adenomyosis

Fibroids

9 Bladder Pain Syndrome and Other Urological Causes of Chronic Pelvic Pain

Introduction

Well-characterized urologic causes of pelvic pain

Idiopathic bladder pain—interstitial cystitis/bladder pain syndrome

Pelvic floor muscle dysfunction

Dyspareunia

Conclusions

10 Chronic Pelvic Pain of Enterocolic Origin

Introduction

Epidemiology

Enterocolic and pelvic innervation

Evaluation of chronic pelvic pain with enterocolic symptoms

Irritable bowel syndrome

Postinfectious IBS

Functional abdominal pain syndrome

Functional bloating syndrome

Diverticular disorders

Inflammatory bowel disease

Enterocolic endometriosis

Celiac sprue

Colorectal cancer

Conclusions

11 Musculoskeletal Causes of Pelvic Pain

Introduction

Epidemiology

Anatomy

Pathophysiology

Diagnostics

Treatment

Home therapy

12 Dyspareunia: Causes and Treatments (Including Provoked Vestibulodynia)

Introduction

Causes/correlates of dyspareunia

Assessment of dyspareunia

Treatment of dyspareunia

Conclusions

13 Management of Chronic Pelvic Pain in the Adolescent Woman

Introduction

Evaluation

14 Multidisciplinary Management of Chronic Pelvic Pain Without Obvious Pathology

Introduction

The initial encounter: special considerations when evaluating women with CPP without an identifiable cause

Multidisciplinary pain management

Pharmacologic management of pain

Adjuvant therapies

Combination therapy

Addressing psychopathology and improving quality of life

Cognitive-behavioral therapy

Conclusions

15 The Role of Definitive Surgery in the Management of Chronic Pelvic Pain and Posthysterectomy Pain

Introduction

General principles of hysterectomy

The role of definitive surgery in specific gynecologic conditions

Pain that remains after hysterectomy

Conclusions

16 Alternative Treatments for Chronic Pelvic Pain

Introduction

Acupuncture

Spinal manipulation

Chinese herbal medicine

Conclusions

Index

Chronic Pelvic Pain

This edition first published 2011, © 2011 by Blackwell Publishing Ltd

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Library of Congress Cataloging-in-Publication Data

Chronic pelvic pain / edited by Paolo Vercellini.

p. ; cm. – (Gynecology in practice)

 Includes bibliographical references and index.

 ISBN 978-1-4443-3066-3 (pbk. : alk. paper)

 1. Pelvic pain. 2. Generative organs, Female–Diseases. I. Vercellini, Paolo. II. Series: Gynecology in practice.

[DNLM: 1. Pelvic Pain. 2. Chronic Disease. WP 155]

RG483.P44C46 2011

618.1–dc22

2010036365

A catalogue record for this book is available from the British Library.

This book is published in the following electronic formats: ePDF 9781444391831; Wiley Online Library 9781444391855; ePub 9781444391848

Series Foreword

In recent decades, massive advances in medical science and technology have caused an explosion of information available to the practitioner. In the modern information age, it is not unusual for physicians to have a computer in their offices with the capability of accessing medical databases and literature searches. On the other hand, however, there is always a need for concise, readable, and highly practicable written resources. The purpose of this series is to fulfill this need in the field of gynecology.

The Gynecology in Practice series aims to present practical clinical guidance on effective patient care for the busy gynecologist. The goal of each volume is to provide an evidence-based approach for specific gynecologic problems. “Evidence at a glance” features in the text provide summaries of key trials or landmark papers that guide practice, and a selected bibliography at the end of each chapter provides a springboard for deeper reading. Even with a practical approach, it is important to review the crucial basic science necessary for effective diagnosis and management. This is reinforced by “Science revisited” boxes that remind readers of crucial anatomic, physiologic or pharmacologic principles for practice.

Each volume is edited by outstanding international experts who have brought together truly gifted clinicians to address many relevant clinical questions in their chapters. The first volume in the series is the volume on Chronic Pelvic Pain, one of the most challenging problems in gynecology. Following volumes cover the subjects of Disorders of Menstruation, Infertility, Contraception, Sexually Transmitted Diseases, Menopause, Urinary Incontinence, Endoscopic Surgeries, and Fibroids, to name a few. I would like to express my gratitude to all the editors and authors, who, despite their other responsibilities, have contributed their time, effort, and expertise to this series.

Finally, I greatly appreciate the support of the staff at Wiley-Blackwell for their outstanding editorial competence. My special thanks go to Martin Sugden, PhD; without his vision and perseverance, this series would not have come to life. My sincere hope is that this novel and exciting series will serve women and their physicians well, and will be part of the diagnostic and therapeutic armamentarium of practicing gynecologists.

Aydin Arici, MD

Professor

Department of Obstetrics, Gynecology, and

Reproductive Sciences

Yale University School of Medicine

New Haven, USA

Preface

Chronic pelvic pain (CPP) is a common gynecologic problem that may negatively affect health-related quality of life. Prevalence figures for CPP in the general female population vary greatly according to several variables, including definition, country, and socioeconomic status. Overall, CPP has an estimated prevalence of 38 per 1,000 in women aged 15–73 years, a rate higher than that of migraine (21 per 1,000) and comparable to that of asthma (37 per 1,000) and chronic back pain (41 per 1,000). CPP is the single most common indication for referrals to gynecology clinics, accounting for 20% of all appointments in secondary care, and constitutes the indication for 12% of all hysterectomies and over 40% of gynecologic diagnostic laparoscopies. In a Gallup poll of 5,325 US women, 16% reported CPP, 11% limited their home activity, 12% limited their sexual activity, 16% took medications, and 4% missed at least 1 day of work per month.

An estimated $274 million is spent annually on the management of this condition in the UK National Health System, and $881 million a year on its outpatient management in the United States. Direct and indirect costs may total over $2 billion per year. CPP may cause prolonged suffering and disability, with consequent loss of employment, family conflicts, repetitive unsuccessful treatments, and serial ineffective surgical procedures.

In women, several causes of CPP are recognized, although in a not negligible proportion of patients, a definite diagnosis cannot be made. Different neurophysiologic mechanisms are involved in the pathophysiology of CPP. Pain may be classified as nociceptive or non-nociceptive. In the former, the symptom originates from stimulation of a pain-sensitive structure, whereas in latter, pain is considered neuropathic or psychogenic. The patient’s history is crucial and is generally of the utmost importance for a correct diagnosis, being sometimes more indicative of the condition than several diagnostic investigations. The main contributing factors in women with CPP can still be identified by history and physical examination in most cases.

Many disorders of the reproductive tract, urologic organs, and gastrointestinal, musculoskeletal, and psychoneurologic systems may be associated with CPP. Indeed, CPP is a symptom and not a disease, and rarely reflects a single pathologic process. When multiple factors are present, treatment of only some of them will lead to incomplete relief and frustration for both patient and clinician. Therapy for CPP, different from that of acute pain, generally requires acceptance of the concept of managing rather than curing the symptoms. Gaining women’s trust and developing a strong patient–physician relationship is of the utmost importance in determining the long-term outcome of care and may reveal itself to be no less important than drugs or surgery.

Given this background, we deemed it of interest to review, with the collaboration of authoritative experts in the field, the pathophysiology and etiology of CPP, as well as the various proposed therapies targeted at both general pain relief and the treatment of specific disorders associated with CPP. Our aim is to define a rational approach to the differential diagnosis and long-term management of this distressing condition. Specific clinical situations, such as CPP in the adolescent woman, dyspareunia, and CPP without obvious pathology, have been included, as has an evaluation of the effects of complementary treatments and definitive surgery.

I warmly thank the colleagues that have dedicated their precious time in order to offer readers a concentrate of their vast knowledge, and trust that this book will provide a practical guide to effective patient care for gynecologists, limiting the number of undue procedures that women undergo and avoiding prolonged suffering. Finally, I wish to express my gratitude to the Editor, who, since the the very beginning, has stimulated, supported, and coordinated this initiative with uncommon devotion and efficiency.

Paolo Vercellini

June 2010

Contributors

A. Arici, MD, Professor, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, Connecticut, USA

David Ashley Hill, MD, Associate Director, Department of Obstetrics and Gynecology, Florida Hospital Graduate Medical Education, Florida Hospital, Orlando, Florida, USA

Stefano Bianchi, MD, Professor and Head of Department of Obstetrics and Gynecology, Fondazione IRCCS Ca Granda Ospedale Maggiore Policlinico, University of Milan, Italy

Yitzchak M. Binik, PhD, Professor, Department of Psychology, McGill University; Director, Sex and Couple Therapy Service, McGill University Health Center, Montreal, Quebec, Canada

Ying Cheong, MD, MRCOG Senior Lecturer in Obstetrics and Gynaecology and Subspecialist in Reproductive Medicine/Surgery, University of Southampton, Southampton, UK

J. Quentin Clemens, MD, FACS MSCI, Associate Professor of Urology; Director, Division of Neurourology and Pelvic Reconstructive Surgery, University of Michigan, Ann Arbor, Michigan, USA

Liza Marie Colimon, MD, Fellow, Division of Advanced Gynecology and Minimally Invasive Surgery, Department of Obstetrics and Gynecology, Florida Hospital Graduate Medical Education, Florida Hospital, Orlando, Florida, USA

Michael P. Diamond, MD, Associate Chair and Kamran S. Moghissi Professor of Obstetrics and Gynecology; Director, Division of Reproductive Endocrinology and Infertility; Assistant Dean for Clinical and Translational Research, Wayne State University School of Medicine, Detroit, Michigan, USA

Tommaso Falcone, MD, Professor and Chairman, Department of Obstetrics and Gynecology, Cleveland Clinic, Cleveland, Ohio, USA

Cindy Farquhar, MD, Postgraduate Professor of Obstetrics and Gynaecology, Department of Obstetrics and Gynaecology, University of Auckland, Auckland, New Zealand

Luigi Fedele, MD, Professor and Head of Department of Obstetrics, Gynecology and Neonatology, Fondazione IRCCS Ca Granda Ospedale Maggiore Policlinico, University of Milan, Italy

Colleen Fitzgerald, MD, Rehabilitation Institute of Chicago and Feinberg School of Medicine at Northwestern University, Chicago, Illinois, USA

Giada Frontino, MD, Assistant, Department of Obstetrics, Gynecology and Neonatology, Fondazione IRCCS Ca Granda Ospedale Maggiore Policlinico, University of Milan, Italy

Alessandra Graziottin, MD, Director, Center of Gynecology and Medical Sexology, H. San Raffaele Resnati, Milan, Italy; Consultant Professor, University of Florence, Italy; President, Alessandra Graziottin Foundation, Milan, Italy

Jennifer Gunter, MD, FRCS(C), FACOG, DABPM, Director, Pelvic Pain, Kaiser San Francisco, San Francisco, California, USA

Fred Howard, MS, MD, Professor and Associate Chair in Obstetrics and Gynecology, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA

John Jarrell, MSc, MD, FRCSC, Professor, Department of Obstetrics and Gynecology, University of Calgary, Calgary, Alberta, Canada

Jennifer L. Kulp, MD, Instructor, Department of Obstetrics, Gynecology and Reproductive Sciences, Division of Reproductive Endocrinology and Infertility, Yale University School of Medicine, New Haven, Connecticut, USA

Georgine Lamvu, MD, MPH, Medical Director of Gynecology; Director of the Fellowship in Advanced Gynecology and Minimally Invasive Surgery, Department of Obstetrics and Gynecology, Florida Hospital Graduate Medical Education, Orlando, Florida, USA

Marta Meana, PhD, Professor, Department of Psychology, University of Nevada, Las Vegas, Nevada, USA

David L. Olive, MD, Medical Director, Wisconsin Fertility Institute, Middleton, Wisconsin, USA

Nicole Paterson, BSc, MSc, MD, Department of Obstetrics and Gynecology, University of Calgary, Calgary, Alberta, Canada

Kristen Pozolo, BS, Clinical Research Coordinator, Northshore University HealthSystem, Evanston, Illinois, USA

Elizabeth E. Puscheck, MD, Professor of Obstetrics and Gynecology, Wayne State University School of Medicine/Detroit Medical Center, Detroit, Michigan, USA

Andrea J. Rapkin, MD, Professor, Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA

Brett A.H. Schultz, DO, MBA, Fellow, Minimally Invasive Gynecologic Surgery, Department of Obstetrics and Gynecology, St Elizabeth Medical Center, Utica, New York, USA

Sangeeta Senapati, MD, MS, Clinical Assistant Professor of Obstetrics and Gynecology, Pritzker School of Medicine, University of Chicago, Chicago, Illinois; Northshore University HealthSystem, Evanston, Illinois, USA

Manvinder Singh, MD, Associate Professor, Department of Obstetrics and Gynecology, Wayne State University School of Medicine/Detroit Medical Center, Detroit, Michigan, USA

Tevy Tith, MD, Resident, Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA

Frank Tu, MD, MPH, Clinical Assistant Professor of Obstetrics and Gynecology, Pritzker School of Medicine, University of Chicago, Chicago, Illinois; Northshore University HealthSystem, Evanston, Illinois, USA

Aarti Umranikar, MRCOG, MFFP, Specialist Registrar in Obstetrics and Gynaecology, Southampton University Hospitals NHS Trust, Southampton, UK

Daniela Wittmann, LMSW, CST, Clinical Social Worker and Sexual Health Coordinator, Department of Urology, University of Michigan Medical Center, Ann Arbor, Michigan, USA

1

Neurobiology of Chronic Pelvic Pain

Jennifer Gunter

Kaiser San Francisco Medical Center, San Francisco, California, USA

Introduction

The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of that damage. Chronic pelvic pain is defined as pain in the pelvis present for at least 2 weeks out of every month for at least 6 months.

Chronic pain is much more than noxious nociception; it is a complex condition with sensory, adaptive, and affective components. While acute pain has biologic utility, chronic pain does not appear to confer any evolutionary advantage.

Many of the complexities of chronic pelvic pain are born from the complex neuroanatomy of the pelvis and corresponding responses of both the peripheral and central nervous systems; therefore a thorough understanding of the neurobiology is essential.

tips & tricks

All structures in the pelvis should be considered as potential pain generators. In addition to the uterus and adnexa, it is also important to consider the bladder, the bowel, muscles of the pelvic floor, the skin, and both the peripheral and central nervous systems as potential pain generators. When evaluating a patient with chronic pelvic pain, make a list of all the potential pain generators in the painful area and consider the possible contribution of each one. Remember that, for many patients with chronic pelvic pain, there may be more than one pain generator in addition to changes in the central nervous system that enhance pain (central sensitization).

Nociception and Pain

The nocioceptors of somatic structures (e.g. muscle, skin, and bone) are undifferentiated nerve endings of myelinated A-delta and unmyelinated C fibers.

Mechanical, chemical, or thermal stimulation results in an influx of sodium across the sodium/potassium ion channels resulting in depolarization, which converts the noxious stimulus into an electrical impulse. The wave of depolarization is transmitted along the afferent sensory neuron, where it triggers the release of excitatory neurotransmitters at the synapse with second-order neurons in laminae I–V of the dorsal horn of the spinal cord. Some afferent nerves travel up or down for several segments in the spinal cord before making contact with second-order neurons, while others synapse at their level of entry.

The muscles of the pelvic floor and the skin of the vulva are innervated by spinal segments L4–S4, although the mons and labia also receive sensory innervation from L1 and L2 via the ilioinguinal and genitofemoral nerves.

Nociceptive input from the uterus and bladder is transmitted via the sympathetic nervous system. The sympathetic afferents also transmit some sensory input from the vagina, pelvic muscles, and skin. Sympathetic sensory axons are either thinly myelinated A-delta or unmyelinated C fibers. The pelvic viscera contain three categories of nocioceptors: stimulus specific, intensity responsive, and silent. Visceral nociceptors are unresponsive to stimuli such as cutting and crushing but very responsive to distension, traction, ischemia, and inflammation. The viscera have fewer afferent neurons compared with somatic structures.

Afferent neurons from the pelvic viscera converge with sympathetic afferents from the enteric nervous system forming a series of retroperitoneal plexuses that pass through the sympathetic chain without synapsing. These afferents enter the dorsal roots at T1–L2. Like the somatic sensory afferents, the cell bodies of the visceral afferents are located in the dorsal root ganglia. These sympathetic afferents synapse with second-order neurons, primarily in laminae I, V, and X, on both sides of the spinal cord. Parasympathetic primary afferents travel from the enteric nervous system to the central nervous system (CNS) via the vagus nerve.

Somatic and sympathetic afferents both synapse on the second-order neurons of the spinothalamic tract. There are three types of spinothalamic tract neuron in the dorsal horn: low-threshold mechanoreceptors, high-threshold nociceptors, and wide dynamic range neurons (WDRs).

WDR neurons are found in laminae I, II, V, and VI of the dorsal horn. They are multireceptive, gathering somatic input from A-delta and C fibers, with some input from A-beta fibers (touch), as well as input from visceral afferents. This convergence of both somatic and visceral afferents on the same second-order neurons results in a loss of visceral specificity, contributing to the vague and poorly localized qualities of visceral pain. Convergence is also responsible for the phenomenon of referred pain.

The second-order neurons receiving afferent input cross over to the contralateral side of the spinal cord and ascend to the brain as part of the spinothalamic, spinoreticular, and spinomesencephalic tracts. When depolarization in these ascending tracts reaches the thalamus, excitatory neurotransmitters are released that trigger depolarization of third-order neurons. These neurons are the final step in relaying nociceptive input to the somatosensory cortex, where nociception is translated into pain. As each somatic afferent has cortical representation, somatic pain is well localized; however, there is no direct visceral representation in the somatosensory cortex.

science revisited

Visceral pain is typically poorly localized because viscera have no direct projections to the cerebral cortex. Well localized pain is more likely to be somatic or neuropathic in origin.

Once pain is perceived by the brain, descending pathways are activated at many levels including the cortex, thalamus, periaqueductal gray matter, nucleus raphe magnus, and locus coeruleus–subcoeruleus complex. Inhibitory pathways descend in the dorsal column and stimulate inhibitory neurons in the dorsal horn, which synapse on both the primary sensory afferents the second-order dorsal horn neurons. These descending pathways release endogenous opioids, which have an antinociceptive effect, as well as inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA).

Mechanisms of Chronic Pelvic Pain

The nervous system responds dynamically to pain—this is an integral part of the pain response system. When peripheral nociceptors receive a noxious stimulus of sufficient intensity, the subsequent depolarization displaces magnesium from its binding site on the N-methyl-D-aspartate (NMDA) receptors. The open NMDA receptors are now free to bind the neurotransmitter glutamate, which increases the excitability of second-order neurons. The clinical effect is that, after an initial noxious stimulus, less input is required to trigger second-order neurons. This phenomenon is termed wind-up and is a normal response with a biologic purpose: creating hypersensitivity after injury increases the likelihood that the area will be protected from reinjury.

It is this ability of the nervous system to adapt in response to nocioceptive input that is the foundation for the mechanisms of chronic pain. Maladaptive responses and reorganization in both the peripheral and the CNS increase both somatosensory burden and nociceptive excitability, resulting in a self-sustaining cycle of pain and neurogenic inflammation (Figure 1.1).

Figure 1.1 Cycle of chronic pain.

Peripheral Sensitization

Peripheral sensitization is a heightened response of primary afferent nerves to nociceptive input. It plays a prominent role in the genesis and maintenance of many pelvic pain syndromes. Peripheral nociceptors may become sensitized by inflammatory neurotransmitters such as calcitonin gene-related peptide (CGRP), substance P, histamine, prostaglandins, and bradykinin. Local inflammatory changes may also activate silent nociceptor, upregulate of sodium channels, as well as trigger other genomic changes resulting in ectopic activity at the nociceptors or cell body. Endometriosis and interstitial cystitis, two conditions associated with chronic pelvic pain, have pronounced local inflammatory changes possibility facilitating peripheral sensitization. Nocioceptor sensitization has been described in women with vulvodynia.

Abnormal or excessive sprouting of peripheral nerve terminals at the site of injury or disease can also increase sensitivity to excitatory neurotransmitters, resulting in depolarization at a lower threshold or even spontaneous firing of nociceptors.

Changes in the peripheral nerves can also occur proximally at the site of synapse in the dorsal horn with second-order neurons. After peripheral nerve injury, there is greater loss of smaller C fibers than larger diameter A-beta fibers, so surviving A-beta fibers sprout new branches, making connections to second-order neurons vacated by the lost C fibers in the substantia gelatinosa (lamina II). As a result, A-beta fibers may take on a primary nociceptive role. For many patients, this is an important contributor to allodynia, the perception of light touch as pain.

Sympathetically Maintained Pain

Sympathetically maintained visceral pain is an important component of chronic pelvic pain for many patients. Like their somatic counterparts, sympathetic nociceptors may become unregulated and sensitized by injury or ongoing neurogenic inflammation, lowering the threshold for response to sympathetic stimuli such as stretching and distension. Another important mechanism of sympathetically mediated pain is activation of silent nociceptors. This phenomenon has been described in chronic bladder pain.

Abnormal sprouting is also a mechanism of sympathetically mediated pain. This may occur in neuromas at the site of injury and also in the dorsal root ganglia, where the somatic and sympathetic afferents run in close proximity. Abnormal sympathetic sprouting is reported in endometriosis implants.

Estrogen may affect vulnerability to sympathetically mediated pain. Estrogen alters mictu­rition thresholds in rats, and in humans the menstrual cycle influences bladder pain and urgency. In animal studies, the proliferation of sympathetic neurons in the lower reproductive tract is affected by estrogen, with a significant decrease noted in ovariectomized rats.

Central Sensitization

Central sensitization refers to the changes in the CNS that facilitate, enhance, or distort pain. It is largely mediated by WDR neurons.

WDR neurons are found in lamina V. They receive input from four types of presynaptic afferents: C, A-delta, A-beta, and sympathetic. They are particularly sensitive to changes in stimulus intensity and do not normally respond to non-noxious or subthreshold stimuli. Under abnormal conditions, the WDR neurons begin to respond inappropriately to low-threshold A-beta input and may even begin to discharge spontaneously. They can also develop abnormal synapses, sprouting into other areas of the dorsal horn in response to injury and neuroinflammatory changes. Other central changes that contribute to central sensitization are recruitment of previously silent synapses in the dorsal horn and activation of glia.

Neuroinflammatory transmitters, such as CGRP, tachykinins, and glutamate, mediate changes in the dorsal horn that lead to central sensitization. Activation of NMDA receptors by glutamate, also plays a major role in the excit­ability of WDR neurons. Input from inhibitory interneurons (largely mediated by GABA and glycine) is also decreased, further enhancing WDR output.

Some nociceptive inputs are more likely to lead to central changes. Muscle pain is a more potent inducer of the intraspinal changes of central sensitization compared to skin. This is an important consideration as high-tone somatic dysfunction of the pelvic floor, localized myalgias, and fibromyalgia are common among patients with chronic pelvic pain. Visceral pain is also a highly effective mechanism for inducing central sensitization, producing more dorsal horn excitability when compared to cutaneous tissues.

Neuroinflammation in the spinal cord, which facilitates central sensitization, is also a key mechanism behind the multiorgan system involvement of chronic pelvic pain. Close neural connections in the sacral spinal cord are essential for the complex coordinated visceral functions of the pelvis. However, these intimate connections also allow neuroinflammation to spread from involved to uninvolved neurons via the dorsal horn. Once the end terminal of the previously uninvolved afferent is stimulated in the dorsal horn, the excitatory neurotransmitter substance P travels in a retrograde fashion down C and A-delta fibers, leading to increased expression of sodium channels and sensitization distally at the terminal nociceptors. This phenomenon is seen in animal models: rats with surgically induced endometriosis demonstrate a reduced bladder capacity, vaginal hyperalgesia, and increased visceral pain compared to animals who were subject to a sham procedure.

These central connections do more than allow pain to spread from organ system to organ system; they also allow the spread of pathology. In the murine model, an attenuated Bartha strain of pseudorabies virus (PRV) can be used to initiate a neuroinflammatory response in the spinal cord, leading not only to bladder pain, but also to inflammatory bladder pathology. As PRV is incapable of antidromic spread down either sensory or motor neurons, this effect is not mediated directly by the PRV itself but rather indirectly via neuroinflammation that spreads between shared spinal segments. This centrally-induced peripheral neurogenic inflammation is then translated into mast cell activation in the lamina propria of the bladder, resulting in local cystitis. If a hypogastric neurectomy is performed, the effect on the bladder is prevented.

Therefore, both pain and pathology can be triggered solely by central neurogenic inflammation, explaining the presence of not only of chronic pain, but also end-organ disease in multiple somatic and visceral structures.

Loss of Inhibitory Control

The affective processing of pain is mediated by neurotransmitters and involves input from the periaqueductal grey, amygdala, anterior cingulate cortex, and anterior insula. Both descending spinally projecting neurons and inhibitory interneurons inhibit neurotransmitter release from primary afferents, modulating nociceptive input. Important neurotransmitters in descending modulation include mu-opioids, GABA, neurokinin 1, and norepinephrine.

Altered activity of the descending pathways has an important role in the maintenance of chronic pain states and can be a mechanism by which changes in mood, anxiety, and depression influence common pain via shared neurotransmitters.

Other Systemic Factors

Systemic Immune Activation

Abnormal activation of the systemic immune system may have a role in the pathogenesis of some pelvic pain syndromes. Conco­mitant inflammatory and autoimmune conditions are significantly more common with interstitial cystitis. Patients with interstitial cystitis are 100 times more likely to have inflammatory bowel disease (Crohn’s disease or ulcerative colitis) and 30 times more likely to have systemic lupus erythematosus than the general population. Sjögren syndrome, present in 0.6% of the population, has a prevalence of up to 28% among patients with interstitial cystitis, and the incidence of other rheumatologic disorders, such as rheumatoid arthritis and fibromyalgia, is also significantly higher. Women with endometriosis have a higher incidence of atopy, allergies, and asthma. It is conceivable that widespread inflammation from a rheumatologic or other source may trigger the neurogenic inflammation of chronic pain. Alternatively, there may be a common genetic component.

caution

For women, cyclic pain does not necessarily imply endometriosis. Cyclic pain is a common phenonomenon as estrogen and progesterone have a complex relationship with pain. The best example is menstrual migraines, which are clearly not an endometriosis-related phenomenon. Exacerbations of bladder and muscle pain with the menstrual cycle are common.

Depression

Depression, anxiety, and catastrophizing all have a role in the neurobiology of chronic pain. Chronic pain can lead to mood disorders but the reverse is also true, that negative mood and emotion can exacerbate pain. Patients with depression are three times more likely to develop chronic pain, and patients with chronic pain have a higher incidence of major depression and generalized anxiety disorder.

Depression lowers both somatic and visceral pain thresholds, possibly via changes in neurotransmitters such as norepinephrine, serotonin, and substance P or by activation of the hypothalamic–adrenal–pituitary access. Depression and hostility are also known to have an effect on circulating levels of inflammatory markers, and markers of chronic inflammation, such as interkeukin-6, are elevated after an immune challenge. These changes may facilitating end-organ inflammation in conditions, as well as stimulate or enhance both peripheral and central neurogenic inflammation.

Selected Bibliography

Berkley KJ, Hubscher CH, Wall PD. Neuronal responses to stimulation of the cervix, uterus, colon, and skin in the rat spinal cord. J Neurophysiol 1993;69:545–56.

Chen H, Lamer TJ, Rho R et al. Contemporary management of neuropathic pain for the primary care physician. Mayo Clin Proc 2004; 79:1533–45.

Fields HL, Basbaum AI, Heinricher MM. Central nervous mechanisms of pain modulation. In: McMahon S, Koltzenburg M, eds. Wall and Melzack’s textbook of pain, 5th ed. St. Louis: Elsevier; 2005. pp. 125–42.

Giamberardino MA, Berkleyt, KJ, Affaiti G et al. Influence of endometriosis on pain behaviors and muscle hyperalgesia. Pain 1995;61: 459–69.

Gunter J. Neurobiology of chronic pelvic pain. In: Potts J, ed. Genitourinary pain and inflammation. Totowa, NJ: Humana Press; 2008. pp. 3–17.

Moshiree B, Zhou Q, Price DD, Verne GN. Central sensitization in visceral pain disorders. Gut 2006;55:905–8.

Powell-Boone T, Ness TJ, Cannon R, Lloyd LK, Weigent DA, Fillingim RB. Menstrual cycle affects bladder pain sensation in subjects with interstitial cystitis. J Urol 2005;174: 1832–6.

Roberts M. Clinical neuroanatomy of the abdomen and pelvis: implications for surgical treatment of prolapse. Clin Obstet Gynecol 2005;48:627–38.

Robinson DR, Gebhart GF. Inside information – the unique features of visceral sensation. Mol Interv 2008;8:242–53.

Salter MW. Cellular neuroplasticity mechanisms mediating pain persistence. J Orofasc Pain 2004;18:318–24.

Siddall PJ, Cousins MJ, Neurobiology of pain. Int Anesthesiol Clin 1997;35:1–26.

Sinaii N, Cleary SD, Ballweg ML, Nierman LK, Stratton P. High rates of autoimmune and endocrine disorders, fibromyalgia, chronic fatigue syndrome, and atopic diseases among women with endometriosis. Hum Reprod 2002;17:2715–24.

Wesselman U. Neurogenic inflammation and chronic pelvic pain. World J Urol 2001;19: 180–5.

Wiech K, Tracey I. The influence of negative emotions on pain: behavioral effects and neural mechanisms Neuroimage 2009;47:987–94.

Winnard KP, Bmitrieva N, Berkley KJ. Cross-organ interactions between reproductive, gastrointestinal, and urinary tracts: modulation by estrous stage and involvement of the hypogastric nerve. Am J Physiol Regul Integr Comp Physiol 2006;291:R1592–601.

2

The Differential Diagnosis of Chronic Pelvic Pain

Fred M. Howard

University of Rochester of Rochester School of Medicine and Dentistry, Rochester, New York, USA

Introduction

Chronic pelvic pain (CPP) is a common condition in women. Its prevalence in the general population may be as high as 15%. In about 4% of women, CPP is of sufficient severity that it causes them to seek medical care. CPP has a prevalence that is comparable to the prevalence of migraine, asthma, and low back pain in women. It is the fourth most common benign disorder evaluated in gynecologic practices. In spite of being a common condition, the evaluation of CPP remains a complex and perplexing diagnostic problem.

science revisited

The following are important definitions:

Pain: an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.Chronic pelvic pain: noncyclic pain of 6 or more months’ duration that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, lumbosacral back, or buttocks and is of sufficient severity to cause functional disability or lead to medical care.

At least one of the difficulties in the diagnostic evaluation of CPP is the common assumption that it is a symptom of a single disease or disorder. Although this is sometimes true, in many cases CPP (like other chronic pain disorders) is due to inflammatory or neuropathic changes of the central and/or peripheral nervous system. This may be at least one reason that so many patients with CPP have more than one pain-related diagnosis. In such cases, it is clinically more productive to view CPP as a diagnosis, not a symptom, and to view other pain-related diagnoses as pain generators.

tips and tricks

General guidelines for the evaluation of chronic pelvic pain:

1. Take a thorough history.

2. Perform a pain-directed physical examination—a “pain-mapping” examination (Tables 2.1–2.4)

3. Laboratory and imaging studies should be obtained specifically to confirm or refute those pain-related diagnoses derived from the history and physical examination.

4. Laparoscopy has a limited role as a diagnostic modality.

5. Those diagnoses with level A evidence of association with chronic pelvic pain should always be considered first.

Table 2.1 Components of the standing physical examination of the woman with chronic pelvic pain and general problems or diagnoses that may be suggested based on these components of the examination

Standing examinationPossible problems diagnosedGaitShort leg syndrome Herniated disc General musculoskeletal problemsPosture with and without forward bendingTypical pelvic pain posture Scoliosis One-leg standingStanding on one leg with and without hip flexionLaxity of the pubic symphysis Laxity of the pelvic girdle Weakness of the hip and pelvisIliac crest symmetryShort leg syndrome One-leg standingGroin evaluation with and without Valsalva maneuverInguinal hernia Femoral hernia(Incisional evaluation with and without Valsalva maneuver)Incisional herniaPubic symphysis evaluation, including trigger pointsPeripartum pelvic pain syndrome Trigger points Osteitis pubis Osteomyelitis pubisHip and sacroiliac evaluation, including trigger pointsArthritis of hip Trigger pointsButtocks (gluteus and piriformis) evaluation, including trigger pointsPiriformis syndrome Pelvic floor pain syndrome Gluteal trigger points(Fibromyalgia tender point evaluation)Fibromyalgia(Pelvic floor relaxation evaluation)Enterocele Rectocele Cystocele Uterine descent

Table 2.2 Components of the sitting physical examination of the woman with chronic pelvic pain and general problems or diagnoses that may be suggested based on these components of the examination

Sitting examinationPossible problems diagnosedPostureLevator ani spasm Pelvic floor pain syndromePalpation of the upper and lower backTrigger points Myalgia ArthritisPalpation of the sacrumTrigger points SacroiliitisPalpation of the gluteal and piriformis musclesTrigger points MyalgiaPalpation of the posterior superior iliac crestsPeripartum pelvic pain syndromeBasic sensory testing to sharpness, dullness, and light touchHerniated discMuscle strength testing and deep tendonsHerniated disc

Table 2.3 Components of the supine physical examination of the woman with chronic pelvic pain and general problems or diagnoses that may be suggested based on these components of the examination

Supine examinationPossible problems diagnosedPosture for lordosis or pelvic tiltLordosis Pelvic tilt Abdominal weakness Stiffness of the lumbar spineActive leg flexion, knee to chestLow back dysfunction Low back pain Abdominal muscle weakness DeconditioningObturator and psoas sign testingShortening, dysfunction, or spasm of the obturator or iliopsoas muscles or fasciaHead raise and leg raiseHerniated disc Abdominal muscle weakness DeconditioningLight abdominal palpationReferred visceral pain Nerve entrapment NeuropathyGentle pinchingReferred visceral pain Nerve entrapment NeuropathyHead maneuverReferred visceral pain Nerve entrapment NeuropathyDermographism evaluationReferred visceral pain Nerve entrapment NeuropathySingle digit palpationTrigger points Myofascial pain Hernias Nerve entrapmentsAbdominal wall tenderness testAbdominal wall pain Visceral painGroin and abdominal evaluation with and without Valsalva maneuverInguinal hernia Spigelian hernia Epigastric hernia Diastasis recti(Incisional evaluation with and without Valsalva maneuver)Incisional herniaPubic symphysis evaluationTrigger points Osteitis pubis Osteomyelitis pubisTraditional abdominal examination for distension, masses, ascites, bowel sounds, shifting dullness, vascular bruits, deep tenderness, guarding, or rigidityAcute disease

Table 2.4 Components of the lithotomy physical examination of the woman with chronic pelvic pain and general problems or diagnoses that may be suggested based on these components of the examination

Lithotomy examinationPossible problems diagnosedVisual inspection of the external genitaliaInflammatory and infectious diseases Vulvar abscess Trauma Fistula Ulcerative disease Pigmented lesions (neoplasias) Condylomas Atrophic changes FissureBasic sensory testing to sharpness, dullness, and light touchNerve entrapment Neuropathy Spinal cord lesionCotton-tipped swab evaluation of the vestibuleVulvar vestibulitisSingle-digit palpation of the vulva and pubic archTrigger points(Colposcopic evaluation of the vulva and vestibule)NeoplasiaSims retractor or single-blade speculum examination of the vagina and pelvic musclesEnterocele Cystocele Rectocele Uterine descensusCotton-tipped swab evaluation of the cervical os, paracervical, and cervical tissuesTrigger points(Cotton-tipped swab evaluation of the vaginal cuff)Trigger points NeuromaSingle-digit pelvic examination of the introitusVulvar vestibulitis Vaginismus Trigger pointsSingle-digit pelvic examination of levator aniPelvic floor pain syndrome Trigger pointsSingle-digit pelvic examination of coccygeusPelvic floor pain syndrome Trigger pointsSingle-digit pelvic examination of piriformis with and without abductionPiriformis syndromeSingle-digit pelvic examination of anterior vaginal urethral and trigonal evaluationChronic urethral syndrome Urethritis Cystitis Interstitial cystitis Trigonitis Urethral diverticulum Vaginal wall cystSingle-digit pelvic examination of the cervix, paracervical areas, and vaginal fornicesTrigger points Endometriosis Cervicitis Repeated cervical trauma Pelvic infection Pelvic infection Ureteral painSingle-digit pelvic examination of the uterusAdenomyosis Pelvic congestion syndrome Pelvic infection Premenstrual syndrome AdhesionsSingle-digit pelvic examination of the coccyxCoccydyniaSingle-digit pelvic examination of adnexaPelvic congestion syndrome EndometriosisBimanual pelvic examinationSee textRectovaginal examinationSee text

Women suffering from CPP are a heterogeneous group, and the possible pain-related diagnoses are numerous and varied (Table 2.5). There is a tendency for patients and clinicians to assume that most women with CPP have a gynecologic etiology for their pain. There are data suggesting, however, that this is not the case, and that gastroenterologic and urologic disorders may be more common than gynecologic disorders. Also, most clinicians look for one diagnosis to account for CPP, but, as noted above, many women with CPP have more than one pain-related diagnosis. For example, data from a primary care database showed that, of patients with a diagnosis, 54% had more than one diagnosis. In our center, a tertiary referral practice specializing in CPP, 72% of patients have more than one diagnosis. Studies of patients with endometriosis suggest that up to 65% may also have interstitial cystitis/painful bladder syndrome (IC/PBS).

Table 2.5 Diagnoses that may be pain generators or etiologies of chronic pelvic pain in women by level of the evidence

Gynecologic

Level AEndometriosisGynecologic malignanciesOvarian retention syndromeOvarian remnant syndromePelvic congestion syndromePelvic inflammatory diseaseTuberculous salpingitisLevel BAdhesionsBenign cystic mesotheliomaFallopian tube prolapse after hysterectomyLeiomyomasPostoperative peritoneal cystsLevel CAdenomyosisAtypical dysmenorrheaAdnexal cystsCervical stenosisChronic ectopic pregnancyChronic endometritisEndometrial or cervical polypsEndosalpingiosisIntrauterine contraceptive deviceOvulatory painResidual accessory ovarySpilled retained gallstonesSymptomatic pelvic relaxation

Urologic

Level ABladder neoplasmInterstitial cystitis/painful bladder syndromeRadiation cystitisLevel BDetrusor dyssynergiaUrethral diverticulumUrethral syndromeLevel CChronic urinary tract infectionRecurrent, acute cystitisRecurrent, acute urethritisStone/urolithiasis

Gastrointestinal

Level ACarcinoma of the colonConstipationInflammatory bowel diseaseIrritable bowel syndromeLevel BCeliac diseaseDiverticular diseaseLevel CChronic intermittent bowel obstructionColitis

Musculoskeletal

Level AAbdominal wall myofascial pain (trigger points)Chronic coccygeal or back painFaulty or poor postureFibromyalgiaNeuralgia of the iliohypogastric, ilioinguinal, pudendal, or genitofemoral nervesPelvic floor tension myalgiaPeripartum pelvic pain syndromeLevel BHerniated nucleus pulposusLow back painNeoplasia of spinal cord or sacral nervePiriformis syndromeRectus abdominis painLevel CCompression of lumbar vertebraeDegenerative joint diseaseHernias: ventral, inguinal, femoral, spigelianMuscular strains and sprainsSpondylosis

Others

Level AAbdominal cutaneous nerve entrapment in a surgical scarSomatization disorderPrior pelvic surgeryLevel BPorphyriaShinglesSleep disturbancesLevel CAbdominal epilepsyAbdominal migraineBipolar disordersFamilial Mediterranean fever

Level A: good and consistent scientific evidence of a causal relationship to chronic pelvic pain.

Level B: limited or inconsistent scientific evidence of a causal relationship to chronic pelvic pain.

Level C: causal relationship to chronic pelvic pain based on expert opinions.

Reproductive System Diagnoses

The number of reproductive tract diagnoses that approach level A evidence of association with CPP is relatively small (Table 2.5). Endometriosis is by far the most common of these diagnoses (Chapter 4). CPP subsequent to pelvic inflammatory disease (PID) is also common—published data suggest that one third of women develop CPP after PID—but it is usually diagnosed as severe adhesive disease at the time of evaluation for CPP (see Chapters 5 and 7). Ovarian retention syndrome, ovarian remnant syndrome, and pelvic congestion syndrome are less commonly diagnosed, and their classification as having level A evidence is somewhat controversial. Tuberculous salpingitis is rare in developed countries but still must be considered in the differential diagnosis. CPP as a manifestation of gynecologic malignancies is a late manifestation and will not be covered in this discussion.

As previously stated, it is most appropriate to evaluate patients for these seven diagnoses with higher levels of evidence to support an association with CPP before considering the diagnoses with lower levels of evidence (Table 2.5).

Endometriosis

Definition

The presence of tissue with the histologic appearance of endometrial glands and stroma located outside the uterine endothelium or myometrium (see also Chapter 4 for more on this condition).

History

Endometriosis is a disease of women of reproductive age; most women with endometriosis-associated pain are 20–45 years of age at the time of diagnosis. However, it has been reported in girls as young as 10 years and may be a more common cause of pain in teenagers than is generally recognized. It may also occur in postmenopausal women, particularly if they are on estrogen replacement. About 70% of women with endometriosis and CPP are nulligravid.

Most often, patients with endometriosis-associated pelvic pain initially have pain at the time of menses, followed by the development of premenstrual and midcycle ovulatory pain. This history precedes the presence of CPP in at least 90% of women with endometriosis-associated pelvic pain. Dyspareunia is present in 40–50% of women with endometriosis-associated pain. Intestinal involvement occurs in about 10–20% of women and may cause tenesmus, dyschezia, constipation, diarrhea, low back pain, and, rarely, hematochezia or symptoms of bowel obstruction. Urinary tract involvement occurs in 10–20% of women with endometriosis and often causes no bladder symptoms, although frequency, pressure, dysuria, or hematuria occasionally are present.

Abnormal uterine bleeding, particularly intermenstrual bleeding, may occur in women with endometriosis.

Physical Examination

Some women have persistent areas of tenderness in the pelvis consistent with sites of endometriosis, but in many women with endometriosis-associated pelvic pain, the physical examination is completely normal. In some, there is tenderness only during menses. For this reason, it is sometimes helpful to do the examination during the first day or two of menstrual flow in women with suspected endometriosis.

Some specific findings that suggest endometriosis are: a fixed retroverted uterus with posterior tenderness; tender nodularity of the uterosacral ligaments and cul-de-sac; narrowing of the posterior vaginal fornix; asymmetrically enlarged, tender ovaries that are fixed to the broad ligaments or pelvic side walls; and lateral cervical deviation.

Diagnostic Studies

At the present time, an accurate diagnosis of endometriosis can only be made by histologic confirmation. This is usually accomplished through biopsies at the time of diagnostic laparoscopy. Many gynecologic surgeons believe it appropriate to exclude or diagnose endometriosis solely on the basis of visual findings. However, recent studies have clearly shown that endometriosis presents with a variety of appearances, which may make laparoscopic visual diagnosis inaccurate in many cases.

A preoperative ultrasound seems prudent before a laparoscopic evaluation for CPP, specifically to evaluate for possible endometriomas and colorectal or bladder involvement. About 15–20% of women with endometriosis have endometriomas, generally ranging in size from 2 to 8 cm, so they are not always palpable on examination. However, it is important to recognize that only 60% of chocolate cysts are endometriomas.

In patients in whom intestinal endometriosis is suspected, endoscopic evaluation of the intestinal tract is usually normal, as most patients have involvement of the serosa or muscularis and not the mucosa. Imaging studies are more useful in identifying colonic involvement preoperatively. The choice of ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI) scans appears to somewhat depend on the expertise of the radiologist and gynecologist with each modality.

In patients with suspected urinary tract involvement, cystoscopy and intravenous pyelography or CT of the kidney, ureters, and bladder may be indicated. MRI and ultrasound imaging may also be useful.

Ovarian Retention Syndrome

Definition

The presence of persistent pelvic pain or dyspareunia attributed to one or both ovaries that were deliberately conserved at the time of hysterectomy (also called residual ovary syndrome).

History

Often there is a history of pelvic surgery prior to hysterectomy in patients with ovarian retention syndrome. The time of onset of symptoms and presentation following hysterectomy is quite varied, ranging from less than 6 months to greater than 20 years. Patients also often have a history of pelvic pain prior to their hysterectomy. If the prehysterectomy pain was due to another pain-associated disorder, such as pelvic congestion, pelvic adhesions, or endometriosis, persistent or recurrent pain due to that diagnosis must be considered. Another possible explanation for persistent pain after hysterectomy may be the pre-existence of inflammatory or neuropathic pain. A history of unilateral versus bilateral ovarian preservation at hysterectomy does not seem to influence the subsequent development of ovarian retention syndrome.

The intensity of pain may vary in a cyclic pattern in some patients, but this is not a consistent finding. Pain is usually unilateral in patients with one retained ovary, and may be unilateral or bilateral in patients with both ovaries. The pain can also radiate to the lower back and down into the legs. Deep dyspareunia occurs in at least one fifth of patients with ovarian retention syndrome. It is usually not a solitary complaint, but when it is the only symptom, pain with intercourse usually is located directly at the site of the retained ovary.

Physical Examination

The abdominal examination usually is normal, although there may be tenderness to deep palpation in the lower abdomen. Pelvic examination reveals tenderness at the vaginal vault or upon palpation of the ovary. Pelvic examination may also reproduce the pain of dyspareunia at the retained ovary or ovaries.

Diagnostic Studies

A diagnostic approach using gonadotropin-releasing hormone (GnRH) agonists has been suggested based on the theory that, since functional ovaries are an integral part of ovarian retention syndrome, suppressing their function should produce an amelioration of symptoms. Published evaluations of this approach are limited but suggest it may be predictive of successful pain relief after oophorectomy.

Laparoscopy may also be used as a diagnostic test and has the advantage of being diagnostically and therapeutically beneficial. At laparoscopy, the surgeon is able to identify any pathology of the retained ovary. Conscious laparoscopic pain mapping may be useful in cases where the diagnosis is not clear.

Ovarian Remnant Syndrome

Definition

The presence of pelvic pain with a persistence of ovarian tissue inadvertently not removed at the time of intended extirpation of one or both ovaries, with or without hysterectomy.

History

Ovarian remnant syndrome occurs due to persistence of ovarian fragments unintentionally left in situ during oophorectomy, so by definition there is always a past history of unilateral or bilateral oophorectomy. Most often there is a history of hysterectomy and bilateral salpingo-oophorectomy, but the syndrome may occur in women who have a history of bilateral or unilateral oophorectomy, with or without hysterectomy. A history of prior surgery for treatment of an ovarian remnant should make the physician highly suspicious of recurrent ovarian remnant syndrome.

A patient with ovarian remnant syndrome may present any time from a few months to 5 years or more after her oophorectomy. It is a disorder that occurs in the reproductive years. Patients usually present with chronic abdominopelvic pain. Most often pain occurs in the lower abdomen and pelvis and is ipsilateral to the remnant, although it can be diffuse or variable in its location. Deep dyspareunia is sometimes also present. Patients may complain of flank pain in the rare cases that have ureteral obstruction due to the remnant. Since most of the patients have undergone multiple surgeries, including a hysterectomy and bilateral salpingo-oophorectomy, the possibility of a gynecologic cause is usually not recognized, and they often suffer for years before their diagnoses are made.

The absence of hot flashes in a woman with a history of bilateral oophorectomy who is not using hormonal replacement therapy is an important signal to investigate carefully for ovarian remnant syndrome. However, more than 70% of women with ovarian remnant syndrome do not have hot flashes in spite of not receiving hormonal replacement therapy. In a patient who has undergone bilateral oophorectomy without hysterectomy, cyclic vaginal bleeding in the absence of hormonal replacement therapy is suggestive of endogenous ovarian estrogen production by an ovarian remnant.

Physical Examination

Tenderness to deep palpation may be present and is usually on the same side as the remnant. Ovarian remnants are usually too small to be palpated abdominally. At pelvic examination, inspection of the external genitalia and vagina usually reveals signs of estrogen effect, with normal-sized labia and moist, well-cornified vaginal mucosa. Pelvic palpation may reveal tenderness in one or both fornices. Bimanual pelvic examination may reveal a palpable mass, although its absence does not preclude the diagnosis. If a mass is palpable, it is usually tender and small (less than 5 cm) and located on the pelvic side wall or at the lateral vaginal apex.

Diagnostic Studies

A follicle-stimulating hormone (FSH) level less than 40 mIU/mL and an estradiol level greater than 30 pg/mL in a patient who has not had hormonal replacement therapy for at least 2–3 weeks are diagnostic in most cases. However, premenopausal levels of FSH and estradiol are present in only 50% of women with an ovarian remnant, so postmenopausal levels cannot be used to exclude the diagnosis.

When ovarian remnant syndrome is suspected and FSH and estradiol levels are postmenopausal, the GnRH agonist stimulation test is useful. GnRH agonists initially stimulate gonadotropin production and therefore ovarian estrogen production. This observation is used in the GnRH agonist stimulation test, in which a baseline level of estradiol is measured and a GnRH agonist (e.g., depot leuprolide, 3.75 mg intramuscularly once, or leuprolide 1 mg a day for 3 days subcutaneously) is administered, followed by a repeat measurement of estradiol four 4–7 days later. If hormonally responsive ovarian tissue is present, a significant rise in estradiol occurs. This test will not be reliable if exogenous hormones are being taken.

Imaging studies are important both diagnostically and preoperatively. Vaginal ultrasound shows a pelvic mass in more than 50% of cases. The diagnostic accuracy of ultrasound may be improved by pretreatment with clomiphene citrate. A 5–10 day course of clomiphene citrate, 100 mg daily, appears to stimulate follicular formation in up to 90% of cases, and this may permit easier sonographic visualization. Not all ovarian remnants have functional follicles, so this technique is not always helpful.

CT scanning, particularly with intravenous contrast to evaluate the urinary tract, can be extremely useful. If there is ureteral dilatation, hydronephrosis, or ureteral deviation, it is likely the ovarian remnant will be directly over the ureter.

In some cases, the diagnosis of ovarian remnant can only be made at the time of surgery, and even then it can be difficult. Laparoscopy is an inconsistent diagnostic tool as dense adhesions frequently hide the ovarian remnant. If diagnostic laparoscopy is used in the evaluation of a patient with a suspected ovarian remnant, the surgeon must be prepared to perform extensive and potentially complicated adhesiolysis. The most common locations are along the pelvic side wall and the vaginal cuff. In both of these locations, the remnant is likely to be on the ureter (Figure 2.1) On the left pelvic side wall, ovarian remnants are often covered by an adherent rectosigmoid colon. Further complicating the operative diagnosis is the fact that ovarian remnants may be bilateral and there may be multiple remnants unilaterally.

Figure 2.1 Example of an ovarian remnant with endometriosis located over the ureter.

Pelvic Congestion Syndrome

Definition

A syndrome characterized by pelvic pain, pelvic varicosities, and pelvic venous congestion with delayed emptying of the pelvic veins.

History

Pelvic congestion syndrome remains a controversial disorder. Substantial research suggests that when the diagnosis is accurately confirmed by the triad of pelvic pain, pelvic varicosities, and pelvic venous congestion with delayed emptying of the pelvic veins, it is a legitimate diagnosis and is responsible for pelvic pain in a substantial number of women. Using this triad of diagnostic criteria, one study found that pelvic congestion syndrome could be a source of pelvic pain in up to 40%, and potentially the only source in 30%, of women with CPP.

Symptoms of pelvic congestion syndrome are usually limited to the reproductive years. Pelvic pain is generally described as dull, aching pain in the pelvic area, similar to the quality of pain described in the legs of people with symptomatic leg varicosities. Pain is exacerbated by physical activity. A typical characteristic of pain of pelvic congestion syndrome is that it varies in its location. It is also most severe premenstrually, which has been termed “congestive dysmenorrhea.” Occasionally, acute paroxysmal exacerbations of sharp pain may occur, at times severe enough to result in emergent evaluation, and may lead to mistaken diagnoses such as acute appendicitis or PID.

Deep dyspareunia is another consistent symptom of pelvic congestion syndrome, occurring in 70–80% of patients. Postcoital pelvic aching, lasting in some cases up to 24 hours, also is typical of pelvic congestion syndrome and occurs in about 65% of cases.

Physical Examination

Abdominal palpation reveals tenderness at the ovarian point in about 75% of women with pelvic congestion syndrome. The ovarian point lies at the junction of the upper and middle thirds of a line drawn from the anterior superior iliac spine to the umbilicus (Figure 2.2). On inspection of the external genitalia, superficial vulvar and paravulvar varices may be observed but are not consistently present. Palpation of the cervix frequently elicits pain and tenderness on movement. The uterosacral ligaments and the parametrium are often also tender to palpation. Uterine and adnexal tenderness to palpation is characteristic of pelvic congestion syndrome.

Figure 2.2 The ovarian point; tenderness at this location is commonly found in women with pelvic congestion syndrome.

Diagnostic Studies

Pelvic venography is the current “gold standard” diagnostic test for pelvic congestion syndrome. Although invasive, it provides a detailed picture of the pelvic venous anatomy, accurate measurements of venous diameters, assessment of venous dysfunction and delayed emptying, and grading of the degree of venous plexuses. A variety of techniques has been used, but the most common techniques are selective retrograde ovarian venography and transuterine venography.

Transuterine venography is the method best validated for accurate diagnosis. Water-soluble contrast medium is introduced into the uterine venous system via injection into the myometrium of the uterine fundus. This is facilitated by using a special single-lumen needle and metal sheath (a reusable system is available from Rocket Needle, Rocket Co., London, United Kingdom; a disposable system is available from Cook Women’s Health, Bloomington, Indiana, United States).